id,title,created_at,updated_at,common_name,type,synonyms,description,organism,cas,pubchem,uniprot,kegg_compound,omim,chebi,biocyc,supertoxic,ctd,stitch,actor,pdb,drugbank,wikipedia,inchi,iupac,mol,smiles_isomeric,smiles_canonical,chemical_formula,weight,appearance,melting_point,boiling_point,density,solubility,specific_gravity,flash_point,vapour_pressure,route_of_exposure,interacting_proteins,mechanism_of_action,metabolism,toxicity,lethaldose,carcinogenicity,use_source,min_risk_level,health_effects,symptoms,treatment,targets
2,T3D0001,2009-03-06 18:57:53 UTC,2009-08-26 21:35:14 UTC,Arsenic,Inorganic Compound;Metalloid;Arsenic Compound,"ARSARSENIC, 99.999%ASAgent saArsenArsen [german,polish]Arsenic [UN1558] [Poison]Arsenic and arsenic compoundsArsenic and certain arsenic compoundsArsenic and compoundsArsenic atomic absorption standard solutionArsenic blackArsenic compoundsArsenic elementalArsenic hydrideArsenic hydride (AsH3)Arsenic trihydrideArsenic, elementalArsenic, inorganicArsenic, organic compoundsArsenic, water-soluble compounds, n.o.sArsenic, water-soluble compounds, n.o.s.Arsenic-75ArsenicalsArsenicoArsenicumArsenicum Album 3ch-30ch GranulesArsenicum Drops D3-C1000Arsenicum Iodatum 3ch-30chArseniuretted hydrogenArsenous hydrideArsenowodor [polish]Arsenwasserstoff [german]ArsineArsine [UN2188] [Poison gas]CACColloidal arsenicCompounds, arsenicFowler's solutionGray arsenicGrey arsenicHydrogen arsenideMetallic arsenicTrisenox","Arsenic is a chemical element that has the symbol As and atomic number 33. This is a notoriously poisonous metalloid that has many allotropic forms: yellow (molecular non-metallic) and several black and grey forms (metalloids) are a few that are seen. Three metalloidal forms of arsenic with different crystal structures are found free in nature (the minerals arsenopyrite and the much rarer arsenolamprite and pararsenolamprite), but it is more commonly found as arsenide and arsenate compounds. Several hundred such mineral species are known. 
(R004)",,7440-38-2,5359596,,C06269,"",27563,CPD-763,,D001151,Arsenic,6367,,,http://en.wikipedia.org/wiki/Arsenic,InChI=1/As/q+3,arsenic,http://www.biospider.ca/saved_files/mol/,[As+3],[As+3],[As]3+,74.921600,Grey metallic solid.,> 615 °C,614 °C ,5.778 g/cm3,"",5.727,Not flammable,7.5x10-3 mmHg at 280 °C,Oral Inhalation Dermal (R009),"Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Arsenite methyltransferase (Q9HBK9) (R164)","Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carcinogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (R001, R054)","Arsenic is absorbed mainly by inhalation or ingestion, as to a lesser extent, dermal exposure. It is then distributed throughout the body, where it is reduced into arsenite if necessary, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant. (R055)","LD50: 763 mg/kg (Oral, Rat) (R263) 
LD50: 13.4 ug/kg (Intraperitoneal, Rat) (R263)",130 mg for an adult human. (R265),"1, carcinogenic to humans. (R264)","Arsenic is used in pesticides, wood preservatives, paints/pigments, and various metal alloys (electronics). Small amounts of arensic can be found in contaminated air, water, and some meat products, especially seafood. (R009)","Acute Oral: 0.005 mg/kg/day (R260)
Chronic Oral: 0.0003 mg/kg/day (R260)
Chronic Inhalation: 0.01 mg/m3 (R260)","Arsenic poisoning can lead to death from multi-system organ failure, probably from necrotic cell death, not apoptosis. Arsenic is also a known carcinogen, especially in skin, liver, bladder and lung cancers. (R001, R055)","Exposure to lower levels of arsenic can cause nausea and vomiting, decreased production of red and white blood cells, abnormal heart rhythm, damage to blood vessels, and a sensation of “pins and needles” in hands and feet. Breathing high levels of inorganic arsenic can give you a sore throat or irritated lungs. Arsenic also affects the brain, causing neurological disturbances such as headaches, confusion, and drowsiness. (R002)","Arsenic poisoning can be treated by chelation therapy, using chelating agents such as dimercaprol, EDTA or DMSA. Charcoal tablets may also be used for less severe cases. In addition, maintaining a diet high in sulfur helps eliminate arsenic from the body. (R055)",P29803;P68871;P69905;P00738;P03372;P04150;P00390;Q14145;P09874;P07437;Q16881;Q9NNW7;Q86VQ6;P23025;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;P10515;P08559;P11177;O00330;P60709;P63261;P68032;P68133;P62736;P63267;A6NHL2;A6NNZ2;A6NKZ8 ;Q99867;Q9H853
3,T3D0002,2009-03-06 18:57:54 UTC,2009-08-26 21:41:46 UTC,Lead,Inorganic Compound;Metal;Lead Compound,"C.I. Pigment metal 4GloverHaro Mix CE-701Haro Mix CK-711Haro Mix MH-204Lead (II) ionLead S2Lead ionLead ion (Pb2+)Lead(2+)Lead(2+) ionLead(2+) ionsLead(2+)ionsLead(II) cationLead, ion (Pb2+)Lead, isotope of mass 239Metallic elementOLOWOmahaPBPlumbumPlumbum Pwr 6xPlumbum aceticumPlumbum iodatumPlumbum phosphoricum","Lead is a heavy metal and stable element with the symbol Pb and the atomic number 82, existing in metallic, organic, and inorganic forms. It is mainly found in nature as the mineral galena (PbS), cerussite (PbCO3) or anglesite (PbSO4), usually in ore with zinc, silver, or copper. Lead is highly malleable and corrosion-resistant, with its use being traced back to ancient times. Inicidences of lead poisoning have also been documented in these ancient Greek, Roman, and Chinese societies. (R056)",,7439-92-1,73212,"",C06696,150500,27889,CPD-527,,D007854,Lead,6472,,,http://en.wikipedia.org/wiki/Lead,InChI=1/Pb/q+2,lead,http://www.biospider.ca/saved_files/mol/2bbe569d4154ae1585c0c597135dabe2_1237932030.mol,[Pb++],[Pb++],[Pb]2+,207.976654,"Bluish-white metallic solid, turns grey when exposed to air.",327.5 °C,1740 °C ,11.34 g/cm3,"",11.3,Not flammable,1.77 mmHg at 1000 °C,"Oral 
Inhalation 
Dermal 
(R266)","Delta-aminolevulinic acid dehydratase (P13716) 
Serum albumin (P02768) 
Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083)
(R266)","Lead mimics other biologically important metals, such as zinc, calcium, and iron, competing as cofactors for many of their respective enzymatic reactions. For example, lead has been shown to competitively inhibit calcium's binding of calmodulin, interferring with neurotransmitter release. It exhibits similar competitive inhibition at the NMDA receptor and protein kinase C, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Lead also affects the nervous system by impairing regulation of dopamine synthesis and blocking evoked release of acetylcholine. However, it's main mechanism of action occurs by inhibiting delta-aminolevulinic acid dehydratase, an enzyme vital in the biosynthesis of heme, which is a necesssary cofactor of hemoglobin. (R008, R061, R063, R266)","Lead is absorbed following inhalation, oral, and dermal exposure. It is then distributed mainly to the bones and red blood cells. In the blood lead may be found bound to serum albumin or the metal-binding protein metallothionein. Organic lead is metabolized by cytochrome P-450 enzymes, whereas inorganic lead forms complexes with delta-aminolevulinic acid dehydratase. Lead is excreted mainly in the urine and faeces. (R266)","","","2B, possibly carcinogenic to humans. (R264)","Lead is used extensively in building construction and can also be found in batteries, ammunition, non-Western cosmetics, solder, and pipes. Old paints and ceramic products may also contain lead, though recent legislation has banned its use. (R266)",Chronic Inhalation: 0.05 mg/m3 (R260),"Lead is a neurotoxin and has been known to cause brain damage and reduced cognitive capacity, especially in children. Lead exposure can result in nephropathy, as well as blood disorders such as high blood pressure and anemia. Lead also exhibits reproductive toxicity and can results in miscarriages and reduced sperm production. (R056)","Symptions of chronic lead poisoning include reduced cognitive abilities, nausea, abdominal pain, irritability, insomnia, metal taste in the mouth, excess lethargy or hyperactivity, chest pain, headache and, in extreme cases, seizures, comas, and death. There are also associated gastrointestinal problems, such as constipation, diarrhea, vomiting, poor appetite, weight loss, which are common in acute poisoning. (R007, R056)","Lead poisoning is usually treated with chelation therapy using DMSA, EDTA, or dimercaprol. (R056)",P22830;P13716;Q05586;Q13224;Q12879;O60391;Q14957;O15399;P62158;P62328;P07108;P17252;P05771;P05129;Q05655;P41743;Q02156;P24723;Q04759;Q05513;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P54710;Q8TCU5
4,T3D0003,2009-03-06 18:57:54 UTC,2009-08-26 21:53:40 UTC,Mercury,Inorganic Compound;Metal;Mercury Compound,"AzogueBlue massBlue pillCaswell No. 546Colloidal mercuryHGHGNHydrargyrumKWIKKwik [dutch]Liquid silverMarceroMercureMercure [french]MercurioMercurio [italian]Mercurius Drops C6-C1000Mercurius Vivus 4ch-30ch Gran and GlobMercury [UN2809] [Corrosive]Mercury atomic absorption standard solutionMercury atomic spectroscopy standard concentrate 1.00 g HgMercury massMercury metal [mercury and mercury compounds]Mercury vaporMercury vapor (as HG)Mercury(II) chloride solutionMercury(II) nitrate solutionMercury, elementalMercury, elemental and inorganic formsMercury, metallicMercury, vaporMetallic mercuryQuecksilberQuecksilber [german]Quick silverQuicksilverRCRA waste no. U151RTECRathjeRcra waste number U151Rtec [polish]UN 2024 (liquid compounds)mercury(0)","A heavy, silvery d-block metal, mercury is one of six elements that are liquid at or near room temperature and pressure. It is a naturally occuring substance, and combines with other elements such as chlorine, sulfur, or oxygen to form inorganic mercury compounds (salts). Mercury also combines with carbon to make organic mercury compounds. It is mostly obtained by reduction from the mineral cinnabar. (R005)",,7439-97-6,23931,,C01319,"",16170,CPD-29,,D008628,Mercury,6477,,,http://en.wikipedia.org/wiki/Mercury,InChI=1/Hg,mercury,http://www.biospider.ca/saved_files/mol/05fb46ec3f5a13fb5558261feed933fc_1237932209.mol,[Hg++],[Hg++],[Hg]2+,201.970642,Silver metallic liquid.,-38.8 °C,"","","6e-05 mg/mL at 25 °C [ROSENBLATT,DH et al. (1975)]","","","","Inhalation 
Ingestion 
(R022)","Metallothionein-2 (P02795) Metallothionein-1G (P13640) Metallothionein-1H (P80294) Metallothionein-3 (P25713) Metallothionein-1F (P04733) Metallothionein-1E (P04732) Metallothionein-1X (P80297) Metallothionein-1A (P04731) Metallothionein-1B (P07438) Metallothionein-1M (Q8N339) Metallothionein-4 (P47944) Metallothionein-1L (Q93083) Catalase (P04040) Hemoglobin subunit alpha (P69905) Hemoglobin subunit beta (P68871) Hemoglobin subunit gamma-1 (P69891) Hemoglobin subunit gamma-2 (P69892) Hemoglobin subunit delta (P02042) Hemoglobin subunit epsilon (P02100) Hemoglobin subunit theta-1 (P09105) Hemoglobin subunit zeta (P02008) Hemoglobin subunit mu (Q6B0K9) (R022, R164)","High-affinity binding of the divalent mercuric ion to thiol or sulfhydryl groups of proteins is believed to be the major mechanism for the activity of mercury. Through alterations in intracellular thiol status, mercury can promote oxidative stress, lipid peroxidation, mitochondrial dysfunction, and changes in heme metabolism. Mercury is known to bind to microsomal and mitochondrial enzymes, resulting in cell injury and death. For example, mercury is known to inhibit aquaporins, halting water flow across the cell membrane. It also inhibits the protein LCK, which causes decreased T-cell signalling and immune system depression. Mercury is also believed to inhibit neuronal excitability by acting on the postsynaptic neuronal membrane. It also affects the nervous system by inhibiting protein kinase C and alkaline phosphatase, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Organic mercury exerts developmental effects by binding to tubulin, preventing microtubule assembly and causing mitotic inhibition. Mercury also produces an autoimmune response, likely by modification of major histocompatibility complex (MHC) class II molecules, self peptides, T-cell receptors, or cell-surface adhesion molecules. (R022, R025, R066, R067)","Mercury is absorbed mainly via ingestion and inhalation, then distributed throughout the body via the bloodstream, where a portion binds to sulfhydryl groups on haemoglobin. Being lipid soluble, mercury vapor readily enters the red blood cells and the central nervous system following inhalation exposure. Once inside the cell, mercury vapor can undergo oxidation to mercuric mercury, which takes place via the catalase–hydrogen peroxide pathway. The mercury atom is able to diffuse down the cleft in the catalase enzyme to reach the active site where the heme ring is located. Oxidation most likely occurs in all tissue, as the catalase hydrogen peroxide pathway is ubiquitous. Following oxidation, mercury tends to accumulate in the kidneys. Organic and elemental mercury can also penetrate the placenta and blood-brain barrier, and thus also accumulate in the brain. Mercury is excreted mainly by exhalation and in the faeces. (R021, R022)","",Lethal dose is 1 to 4 grams or 14 to 57 mg/kg for a 70-kg adult human. (R024),"3, not classifiable as to its carcinogenicity to humans. (R264)","Metallic mercury is used to produce chlorine gas and caustic soda, and is also used in thermometers, dental fillings, and batteries. Mercury salts are sometimes used in skin lightening creams and as antiseptic creams and ointments. (R022)",Chronic Inhalation: 0.0002 mg/m3 (R260),"Mercury mainly affects the nervous system. Exposure to high levels of metallic, inorganic, or organic mercury can permanently damage the brain, kidneys, and developing fetus. Effects on brain functioning may result in irritability, shyness, tremors, changes in vision or hearing, and memory problems. Acrodynia, a type of mercury poisoning in children, is characterized by pain and pink discoloration of the hands and feet. Mercury poisoning can also cause Hunter-Russell syndrome and Minamata disease. (R022)","Common symptoms include peripheral neuropathy (presenting as paresthesia or itching, burning or pain), skin discoloration (pink cheeks, fingertips and toes), edema (swelling), and desquamation (dead skin peels off in layers). (R020)","Mercury poisoning is treated by immediate decontamination and chelation therapy using DMSA, DMPS, DPCN, or dimercaprol. (R023)",P05186;P29972;Q96PS8;Q8NBQ7;Q8IXF9;A6NM10;P41181;Q92482;P55087;P55064;Q13520;O14520;O94778;O43315;P30301;P17252;P05771;Q05655;Q02156;P24723;P05129;P41743;Q04759;Q05513;P06239;A6NKZ8 ;Q99867;Q9H853;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2;Q9UJT1;Q9UJT0;P23258;Q9NRH3
5,T3D0004,2009-03-06 18:57:54 UTC,2009-08-04 21:27:25 UTC,Vinyl chloride,Organic Compound;Industrial Precursor/Intermediate;Organochloride,"1-ChloroethyleneArmodourAron TS 700Atactic poly(vinyl chloride)BakeliteBoltaronC2H3ClCarinaChloretheneChlorethyleneChloride, vinylChloroetheneChloroethene homopolymerChloroethyleneChloroethylene homopolymerise [french]Chloroethylene polymerChloroethylene, polymerChlorure de vinyleChlorure de vinyle [french]CloroetilenoCloruro de viniloCloruro di vinileCloruro di vinile [italian]Corvic 55/9DacovinDarvic 110DynadurEkavyl SD 2Ethene, chloro-, homopolymerEthylene monochlorideEthylene, chloro-Ethylene, chloro-, polymerExpanded polyvinyl chlorideFlocorGEON 51GenothermHalvic 223HostalitInChI=1/C2H3Cl/c1-2-3/h2H,1HMonochloroetheneMonochloroethyleneMonovinyl chloridePVCPoly(vinyl chloride)Poly(vinyl chloride) carboxylatedPoly(vinyl chloride-co-acrylic acid)Polyvinyl chloridePolyvinyl chloride resinPolyvinylchloridePolyvinylchloride latexRCRA waste no. U043Rcra waste number U043Resinite 90TrovidurVCVCMVinileVinile (cloruro di) [italian]Vinyl cVinyl c monomerVinyl chlorideVinyl chloride chloroethyleneVinyl chloride monomerVinyl chloride, inhibitedVinyl chlorineVinylchloridVinylchlorid [german]VinylchlorideVinyle(chlorure de)Vinyle(chlorure de) [french]Winylu chlorekWinylu chlorek [polish]","Vinyl chloride is a man-made organic compound, formed when other substances such as trichloroethane, trichloroethylene, and tetrachloroethylene are broken down. In its monomer form it is acutely hazardous, thus it is primarily used for the production of polymers. At room temperature it is a flammable, colorless gas with a sweet odor, but it is easily condensed and usually stored as a liquid. (R010)",,75-01-4,6338,,C06793,"",28509,11-DCE,,D014752,Vinyl chloride,1466,,,,"InChI=1/C2H3Cl/c1-2-3/h2H,1H2",chloroethene,http://www.biospider.ca/saved_files/mol/2b811af09c998820d8fe98805eb12908_1237932391.mol,C=CCl,C=CCl,C2H3Cl,61.992330,"Colorless gas, usually stored as a liquid.",-153.7 °C,-13.37 °C,0.91 g/ml,"8.8 mg/mL at 25 °C [DELASSUS,PT & SCHMIDT,DD (1981)]",0.9121,-78 °C,2600 mmHg at 25 °C,Oral Inhalation Dermal (R010),"Cytochrome P450 2E1 (P05181) 
Glutathione S-transferase P (P09211) 
Glutathione S-transferase Mu 1 (P09488) 
Glutathione S-transferase A1 (P08263) 
Glutathione S-transferase theta-2 (P30712) 
Glutathione S-transferase Mu 4 (Q03013) 
Glutathione S-transferase theta-1 (P30711) 
Glutathione S-transferase A4 (O15217) 
Glutathione S-transferase A2 (P09210) 
Glutathione S-transferase A3 (Q16772) 
Glutathione S-transferase Mu 3 (P21266) 
Glutathione S-transferase omega-1 (P78417) 
Glutathione S-transferase kappa 1 (Q9Y2Q3) 
Glutathione S-transferase Mu 2 (P28161) 
Glutathione S-transferase omega-2 (Q9H4Y5) 
Glutathione S-transferase A5 (Q7RTV2) 
Glutathione S-transferase Mu 5 (P46439) 
Glutathione S-transferase theta-4 (A8MPT4) 
Maleylacetoacetate isomerase (O43708) 
Microsomal glutathione S-transferase 1 (P10620) 
Microsomal glutathione S-transferase 2 (Q99735) 
Microsomal glutathione S-transferase 3 (O14880) 
(R010)","Vinyl chloride poisoning exhibits many of the characteristics of autoimmune diseases. This is believed to be the result of a reactive vinyl chloride intermediate metabolite binding to an immunoglobulin, altering the protein and initiating an immune response. The metabolites of vinyl chloride, especially choloroethylene oxide, are mutagenic and act by covalently binding to DNA. This produces cyclic etheno-adducts, which cause base-pair transitions during transcription and DNA crosslinks. Metabolites also may cause oxidative stress and affecting tumor supressor genes, as vinyl chloride has been known to produce specific mutations in the p53 and Ki-ras genes. Vinyl chloride metabolites are also believed to exert toxic effects in the liver by covalently binding to liver proteins, resulting in cellular toxicity. (R010, R202)","Vinyl chloride absorbed primarily via inhalation or ingestion is rapidly distributed throughout the body. It is metabolized mainly in the liver by cytochrome P-450 monooxygenases, first into chloroethylene oxide, then into chloroacetaldehyde, which are the main toxic metabolites. Chloroacetaldehyde is further converted into chloroethanol and monochloroacetic acid. Detoxification occurs in conjunction with glutathione, producing mainly thiodiglycolic acid, which is excreted in the urine. At high doses vinyl chloride may also be excreted by exhalation. (R010, R011)","LD50: 500 mg/kg (Oral, Rat) (R265)","120,000 ppm in an adult human. (R268)","1, carcinogenic to humans. (R264)","Vinyl chloride is used primarily to make polyvinyl chloride (PVC). PVC is used in a variety of plastic products, such as pipes, wire and cable coatings, and packaging materials. Small amounts of vinyl chloride is sometimes used in furniture and automobile upholstery, wall coverings, housewares, and automotive parts. (R010)","Acute Inhalation: 0.5 ppm (R260)
Intermediate Inhalation: 0.03 ppm (R260)
Chronic Oral: 0.003 mg/kg/day (R260)","Exposure to vinyl chloride results in liver damage, nerve damage, and immune reactions, as well as depression of the central nervous system and cardiac arrhythmias. Long term exposure may result in damage to the sperm and testes of males. Vinyl chloride is also a known carcinogen. (R010)","Symptoms of acute vinyl chloride exposure include headache, nausea, dizziness, and drowsiness, possibly resulting in loss of conciousness, coma or cardiac arrhythmias at higher levels. Chronic exposure can lead to lung and kidney irritation, inhibition of bloodclotting, numbness and pain in the fingers, memory loss, and sleep disurbances. (R010)",Vinyl chloride has no tested antidote. Poisoning is usually handled by preventing further exposure and treating the observed symptoms. (R010),P01857;P01859;P01860;P01861;DNA;P98194;O75185;P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P78334;Q8N1C3;P18507;Q99928;O00591;P24046;P28476;A8MPY1;Q9UN88;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;P54710;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P03372;Q92731
6,T3D0005,2009-03-06 18:57:54 UTC,2009-08-11 15:45:55 UTC,Polychlorinated biphenyls,Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 3,3',4,4',5,5'-hexachloro-1,1'-Biphenyl, 3,3',4,4',5,5'-hexachloro- (9CI)3,3',4,4',5,5'-Hexachloro-1,1'-biphenyl3,3',4,4',5,5'-Hexachlorobiphenyl3,4,5,3',4',5'-HEXACHLOROBIPHENYL3,4,5,3',4',5'-Hexa coplanar polychlorinated biphenylBiphenyl, 3,3',4,4',5,5'-hexachloro-Polychlorinated biphenyls (PCBS)","Polychlorinated biphenyls (PCBs) are a group of 209 synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. PCBs were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate in the environment and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,1336-36-3,36231,,"","","","",,,Polychlorinated biphenyls,6513,,,,InChI=1/C12H4Cl6/c13-7-1-5(2-8(14)11(7)17)6-3-9(15)12(18)10(16)4-6/h1-4H,"1,2,3-trichloro-5-(3,4,5-trichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=C(C=C(C(=C1Cl)Cl)Cl)C2=CC(=C(C(=C2)Cl)Cl)Cl,C1=C(C=C(C(=C1Cl)Cl)Cl)C2=CC(=C(C(=C2)Cl)Cl)Cl,C12H4Cl6,357.844420,Oily liquids or solids that are colorless to light yellow. ,"","","","0.0007 mg/mL at 25 °C [GRIFFIN,RA & CHOU,SFJ (1981)]","","","","Oral
Inhalation 
Dermal 
(R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly by inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disruption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are transported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) 
LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)","","2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refrigerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 µg/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P35869;P49888;P03372;P11684;P20711;P07101;Q92731
7,T3D0006,2009-03-06 18:57:54 UTC,2009-08-04 21:27:25 UTC,Benzene,Organic Compound;Solvent;Gasoline Additive/Component;Industrial Precursor/Intermediate;Aromatic Hydrocarbon,"(6)Annulene1hyz1swi:benzeneAmsco h-SBAmsco h-jAnnuleneAromatic alkaneAromatic solventAsphaltAsphalt (bitumen)fume as benzene-soluble aerosolAsphalt (cut)Asphalt (cutback)Asphalt (petroleum)Asphalt [bitumens]Asphalt cementsAsphalt fumesAsphalt, liquid medium-curingAsphalt, liquid rapid-curingAsphalt, liquid slow-curingAsphaltic bitumenAsphaltumBNZBP 2 (solvent)Base oilBenzeenBenzeen (dutch)Benzeen [dutch]BenzenBenzen (polish)Benzen [polish]Benzene (including benzene from gasoline)Benzene + aniline comboBenzene [UN1114] [Flammable liquid]Benzene, labeled with carbon-14Benzene, labeled with carbon-14 and tritiumBenzene, pureBenzene-U-14CBenzinBenzin (obs.)Benzin B70BenzineBenzine (light petroleum distillate)Benzine (obs.)BenzinumBenzolBenzol 90Benzol diluentBenzoleBenzoleneBenzolineBenzoloBenzolo (italian)Benzolo [italian]BenzolumBenzyna do lakierow c [polish]Bicarburet of hydrogenBitumenBitumens, asphaltBituminous materials, asphaltCanadolCarbon oilCaswell No. 062Caswell No. 077Caswell No. 106Caswell No. 632ACaswell No. 802Coal naphthaCoal oil [oil, misc.]Coal tarCrankcase oil, usedCrankcase oil, used mineral-basedCrude oilCrude oil [oil, misc.]Crude oil, petroleumCrude oilsCrude petroleumCyclohexatrieneDeutero benzeneFenzenFenzen (czech)Fenzen [czech]HSDB 35HerbitoxHi-flash naphthaHi-flash naphthayethylenHydrocarbons, C4-8Hydrotreated naphthaIsoparaffinic hydrocarbonsJudean pitchLight ligroinLigroinLigroineMineral naphthaMineral oils, highly-refined oils [mineral oils]Mineral pitchMineral rubber (van)Mineral spiritsMineral spirits No. 10Mineral thinnerMineral turpentineMotor benzolNaphthaNaphtha 49 degree be-coal tar typeNaphtha VM & P, 50 degree flashNaphtha VM & pNaphtha VM & p, high flashNaphtha VM & p, regularNaphtha, hydrotreatedNaphtha, ligroineNaphtha, petroleumNaphtha, solventNaphtha, stoddard solventNaphtha, varnish makers' and painters'Nitration benzeneOil, crudeOrganic slvents, stoddard solventPainters' naphthaParaffinic oilPetroleumPetroleum [waxes]Petroleum asphaltPetroleum benzinPetroleum bitumenPetroleum crudePetroleum crude oil [UN1267] [Flammable liquid]Petroleum distillatePetroleum distillatesPetroleum distillates (naphtha)Petroleum distillates naphtha, rubber solventPetroleum etherPetroleum naphthaPetroleum pitchPetroleum refining residues, asphaltsPetroleum roofing tarPetroleum, lightPetroleum-derived naphthaPhenePhenyl hydridePolystreamPyrobenzolPyrobenzoleRCRA waste no. U109RNGRcra waste number U019Refined solvent naphthaRoad asphaltRoad tarRock oilRubber solventRubber solvent (naphtha)Seneca oilSkelly-solve S-66Skelly-solve hSkelly-solve rSkelly-solve sSkellysolve fSkellysolve gSolvent naphthaSolvents, naphthasStoddard solventStoddard solvent (naphtha)Super VMPTransgenic model evaluation II (benzene)Trinidad pitchUnleaded gasolineUsed mineral-based crankcase oilV.m. and p. naphthaVM & p naphthaVM and p naphthaVarnish makers' and painters naphthaVarnish makers' naphthaVarnish makers' naphtha and painters' naphthaVarnish marker's naphthaVarsolVirolWLN: RHWhite spiritWhite spirits[6]Annulenebenzene (ACD/Name 4.0){[6]Annulene}","Benzene is an aromatic hydrocarbon formed both naturally and from human activities. It can be found in crude oil, gasoline, and cigarette smoke, and made mostly from petroleum sources. Benzene is a highly flammable, colorless liquid with a sweet odor. (R016)",,71-43-2,241,,C01407,111300,16716,BENZENE,,D001554,Benzene,136,,,http://en.wikipedia.org/wiki/Benzene,InChI=1/C6H6/c1-2-4-6-5-3-1/h1-6H,benzene,http://www.biospider.ca/saved_files/mol/b673b58431ea0c5edc03eaea489d54c1_1237932620.mol,C1=CC=CC=C1,C1=CC=CC=C1,C6H6,78.046950,Colorless liquid.,5.5 °C,80.1 °C,0.8786 g/cm3,"1.79 mg/mL at 25 °C [MAY,WE et al. (1983)]",0.88,−11 °C,75 mmHg at 20 °C,Inhalation (R016),"Cytochrome P450 2E1 (P05181)
(R016)","The toxic agents of benzene are its metabolites. Benzene is able increase its toxicity by inducing cytochrome P450 2E1, its main metabolic enzyme. Benzene's primary toxic effects are decreases in haematological cell counts and bone marrow cellularity. The decrease in blood cell count may be due to the binding of metabolites such as benzene oxide to the blood proteins albumin and haemoglobin. In the bone marrow, phenolic metabolites can be metabolized by bone marrow peroxidases to highly reactive semiquinone radicals and quinones that stimulate the production of reactive oxygen species. This and direct metabolite binding leads to damage to tubulin, histone proteins, and topoisomerase II. Some metabolites also exert mutagenic effects by inhibiting other DNA associated proteins, such as mitochondrial DNA polymerase and ribonucleotide reductase, as well as covalently binding to DNA itself, causing effects such as strand breakage, mitotic recombination, chromosome translocations, and aneuploidy. (R016)","Benzene is absorbed readily following inhalation or oral exposure. It enters the bloodstream and is rapidly distributed throughout the body, tending to accumulate in fatty tissues. Benzene is exhaled unchanged by the lungs, as well as metabolized in the liver to benzene oxide by cytochrome P450 enzymes. Benzene oxide is further converted into phenol, catechol, and hydroquinone, which are excreted in the urine as glucuronide or sulfate conjugates. (R017)","LD50: 3306 mg/kg (Oral, Rat) (R263)
LD50 340 mg/kg (Intraperitoneal, Mouse) (R263)
LC50: 9980 ppm (Inhalation, Mouse) (R263)",50-500 mg/kg (oral) or 20000 ppm (inhaled) for adult humans. (R270),"1, carcinogenic to humans. (R264)","Benzene is often used as an intermediate to make chemicals needed for the production of plastics, resins, and nylon and other synthetic fibers. It is also used to make some types of rubbers, lubricants, dyes, detergents, drugs, and pesticides. Natural sources of benzene include emissions from volcanoes, forest fires, crude oil, gasoline, and cigarette smoke. (R016)","Acute Inhalation: 0.009 ppm (R260)
Intermediate Inhalation: 0.006 ppm (R260)
Chronic Inhalation: 0.003 ppm (R260) 
Chronic Oral: 0.0005 mg/kg/day (R260)","Benzene causes harmful effects on the bone marrow and also decreases blood cell counts, leading to blood disorders such as anemia. It can also cause excessive bleeding and affect the immune system, increasing the chance for infection. Benzene is also a known carcinogen, as chronic exposure to high levels has been shown to cause leukemia, particularly acute myelogenous leukemia. (R016)","Breathing benzene can cause drowsiness, dizziness, rapid heart rate, headaches, tremors, confusion, and unconsciousness. Ingestion can result in vomiting, irritation of the stomach, dizziness, sleepiness, convulsions, and rapid heart rate. (R016)","There is no known antidote for benzene and poisoning is first treated by preventing further exposure. If inhalated, respiratory assist may be necessary. If ingested, gastric lavage may be performed, or activated charcoal can be administered. (R018)",P69905;P68871;P69891;P69892;P02042;P02100;P09105;P02008;P02768;P62805;P68431;Q16695;P84243;P54098;P23921;P31350;P68363;Q13748;P68366;P07437;Q13885;P68371;Q13509;P04350;P23258;P11388;Q02880;Q71U36;Q9BQE3;Q6PEY2;Q9NY65;Q9H4B7;Q9BVA1;Q9BUF5;Q3ZCM7;Q9UJT1;Q9UJT0;Q9NRH3;Q71DI3;Q7LG56;Q9UHN1;A6NHL2;A6NNZ2;A6NKZ8 ;Q99867;Q9H853;P07305;Q02539;P16403;P16402;P10412;P16401;Q8IZA3;P22492;Q92522;P0C0S8;Q96QV6;P04908;Q93077;P20671;Q96KK5;Q99878;O60814;Q6FI13;Q8IUE6;Q16777;Q7L7L0;P0C5Y9;P0C5Z0;Q9BTM1;Q71UI9;P16104;P0C0S5;Q96A08;P33778;P62807;P58876;Q93079;P06899;Q99880;Q99879;Q99877;P23527;Q16778;Q5QNW6;Q8N257;P0C1H6;P57053;Q7Z2G1;Q6NXT2;P49450;Q99525;Q75WM6;Q6DN03	;Q6DRA6;DNA
8,T3D0007,2009-03-06 18:57:54 UTC,2009-08-26 21:52:13 UTC,Cadmium,Inorganic Compound;Metal;Cadmium Compound,"AQUANAL-plus cadmium (Cd) 0.02-1.2 mg/LCADMIUM, 99.95%CDCadmioCadmium Metallicum 6x - TabCadmium Sulphuricum Liquid (S No. 43)Cadmium [cadmium and cadmium compounds]Cadmium [cadmium and certain cadmium compounds]Cadmium atomCadmium atomic absorption standard solutionCadmium bromatumCadmium compoundsCadmium elementalCadmium iodatumCadmium ion standard solutionCadmium metallicumCadmium muriaticumCadmium nitrate solutionCadmium standard for icCadmium sulfuratumCadmium sulfuricumCadmium sulphuratumCadmium sulphuricumCadmium, elementalColloidal cadmiumKadmiumKadmium [german]","Cadmium is a transition metal and chemical element with the symbol Cd and atomic number 48. Cadmium is found naturally in the earth's crust, though rarely on it's own. It is usually extracted as a byproduct from mining, smelting, and refining sulfide ores of zinc, lead, and copper. (R019)",,7440-43-9,23973,,C01413,"",22977,CD%2b2,,D002104,Cadmium,6393,,,http://en.wikipedia.org/wiki/Cadmium,InChI=1/Cd/q+2,cadmium,http://www.biospider.ca/saved_files/mol/c667f27184181f7f6efc084ec868b63e_1237932827.mol,[Cd++],[Cd++],[Cd]2+,113.903358,Bluish-white metallic solid.,"594.22 K
(321.07 °C, 609.93 °F)","1040 K
(767 °C, 1413 °F)",8.65  g·cm−3,"","","","","Oral 
Inhalation 
Dermal
(R019)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Serum albumin (P02768)
(R019, R164)","Cadmium initially binds to metallothionein and is transported to the kidney. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Accumulation of cadmium in the kidney results in increased excretion of vital low and high molecular weight proteins. Cadmium is a high affinity zinc analog and can interfere in its biological processes. It also binds to and activates the estrogen receptor, likely stimulating the growth of certain types of cancer cells and causing other estrogenic effects, such as reproductive dysfunction. Cadmium causes cell apoptosis by activating mitogen-activated protein kinases. (R026, R058, R059, R069)","Cadmium is absorbed from oral, inhalation, and dermal routes. Cadmium initially binds to metallothionein and albumin and is transported mainly to the kidney and liver. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Cadmium is not known to undergo any direct metabolic conversion and is excreted unchanged, mainly in the urine. (R019)","LD50: 225 mg/kg (Oral, Rat) (R263) 
LD50: 5700 µg/kg (Intraperitoneal, Mouse) (R263)","150 mg (oral) or 39 mg/m3 over 20 minutes (inhalation) for adult humans. (R263, R271)","1, carcinogenic to humans. (R264)","Cadmium is used mainly in the electroplating of other metals and the production of metal alloys. It can be found in batteries, pigments, metal coatings, and plastics. Exposure usually occurs in an industrial setting, but can also result from breathing cigarette smoke and eating contaminated foods. (R019)","Acute Inhalation: 0.00003 mg/m3 (R260)
Chronic Inhalation: 0.00001 mg/m3 (R260)
Intermediate Oral: 0.0005 mg/kg/day (R260)
Chronic Oral: 0.0001 mg/kg/day (R260)","Chronic exposure to cadmium fumes can cause chemical pneumonitis, pulmonary edema, and lung diseases such as bronchitis and emphysema. Cadmium also accumulates in the kidneys, causing permanent damage. Loss of bone density also occurs. (R019)","Acute inhalation of cadmium fumes results in metal fume fever, which is characterized by chills, fever, headache, weakness, dryness of the nose and throat, chest pain, and coughing. Ingestion of cadmium causes vomiting and diarrhea. (R019)","Cadmium poisoning is treated by removal from exposure and supportive care. If ingested, induced vomiting or gastric lavage may be performed. (R272)",P03372;Q92731;P28482;P27361;P31152;Q16659;Q13164;P45983;P45984;P53779;Q15759;P53778;O15264;Q16539;Q13387;O60271;Q9UQF2;Q9UPT6;Q8TD08
10,T3D0009,2009-03-06 18:57:54 UTC,2009-08-04 21:27:25 UTC,Benzo[a]pyrene,Organic Compound;Industrial By-product/Pollutant;Aromatic Hydrocarbon;Polycyclic Aromatic Hydrocarbon,"1,2-Benzpyrene3, 4-Benzopirene (ITALIAN)3, 4-Benzypyrene3,4 Benzopyrene3,4 Benzpyrene3,4-Benz(a)pyrene3,4-Benz[a]pyrene3,4-Benzo(a)pyrene3,4-Benzopirene3,4-Benzopirene [Italian]3,4-Benzopyrene3,4-Benzopyrene (carcinogen)3,4-Benzpyren3,4-Benzpyren (GERMAN)3,4-Benzpyren [German]3,4-Benzpyrene3,4-Benzypyrene3,4-benzylpyrene4,5-Benzpyrene6, 7-Benzopyrene6,7-BenzopyreneB(a)pB1760_SIGMABAPBENZO(A)PYRENE (SEE ALSO: BENZO(E)PYRENE (CAS 192-97-2))BPB[a]pBenz(a)pyreneBenz[a]pyreneBenzo(3,4)pyrene, radical ion(1+)Benzo(a)pyreneBenzo(a)pyrene [polycyclic aromatic compounds]Benzo(a)pyrene [polycyclic aromatic hydrocarbons]Benzo(a)pyrene radical cationBenzo(a)pyrene, labeled with tritiumBenzo(a)pyrene, radical ion(1+)Benzo(d,e,f)chryseneBenzo(def)chryseneBenzo[α]pyreneBenzo[PQR]tetrapheneBenzo[a]pyrene solutionBenzo[d,e,f]chryseneBenzo[def]chryseneBenzopyreneBenzpyreneCoal tar pitch volatiles: benzo(a)pyreneRCRA waste no. U022Rcra waste number U022WLN: L D6 B6666 2AB TJbenzo[def]chrysene (ACD/Name 4.0){3,4-Benz[a]pyrene}{b[a]p}{benz[a]pyrene}{benzo[a]pyrene}{benzo[d,e,f]chrysene}","Benzo[a]pyrene is one of over 100 different polycyclic aromatic hydrocarbons (PAHs). PAHs are chemicals that are formed during the incomplete burning organic substances, such as fossil fuels. They are usually found as a mixture containing two or more of these compounds. (R028)",,50-32-8,2336,,C07535,"",29865,"",,D001564,Benzo[a]pyrene,141,,,http://en.wikipedia.org/wiki/Benzo(a)pyrene,InChI=1/C20H12/c1-2-7-17-15(4-1)12-16-9-8-13-5-3-6-14-10-11-18(17)20(16)19(13)14/h1-12H,benzo[a]pyrene,http://www.biospider.ca/saved_files/mol/b01123dfec59b4c5a94115e8eaf70665_1237933157.mol,C1=CC=C2C3=C4C(=CC2=C1)C=CC5=C4C(=CC=C5)C=C3,C1=CC=C2C3=C4C(=CC2=C1)C=CC5=C4C(=CC=C5)C=C3,C20H12,252.093900,Pale yellow solid.,176.5 °C,495 °C,1.24 g/cm³,"1.62e-06 mg/mL at 25 °C [MAY,WE et al. (1983)]","","","","Oral 
Inhalation 
(R028)","Serum albumin (P02768) 
Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 1B1 (Q16678) 
(R060)","The ability of PAH's to bind to blood proteins such as albumin allows them to be transported throughout the body. Many PAH's induce the expression of cytochrome P450 enzymes, especially CYP1A1, CYP1A2, and CYP1B1, by binding to the aryl hydrocarbon receptor or glycine N-methyltransferase protein. These enzymes metabolize PAH's into their toxic intermediates. The reactive metabolites of PAHs (epoxide intermediates, dihydrodiols, phenols, quinones, and their various combinations) covalently bind to DNA and other cellular macromolecules, initiating mutagenesis and carcinogenesis. The main carcinogenic metabolite of benzo(a)pyrene is the diol-epoxide trans-9,10-epoxy-7,8-dihydrodiol. (R028, R060, R068, R073)","PAH metabolism occurs in all tissues, usually by cytochrome P-450 and its associated enzymes. PAHs are metabolized into reactive intermediates, which include epoxide intermediates, dihydrodiols, phenols, quinones, and their various combinations. The phenols, quinones, and dihydrodiols can all be conjugated to glucuronides and sulfate esters; the quinones also form glutathione conjugates. (R028)","LD50: 250 mg/kg (Intraperitoneal, Mouse) (R270)","","1, carcinogenic to humans. (R264)","PAHs are released into the environment via the combustion of fossil fuels, coke oven emissions and vehicle exhausts, as well as naturally from forest fires and volcanic eruptions. PAHs from these sources may contaminate nearly water systems. They are also found in coal tar and charbroiled food. (R028)","","PAHs are carcinogens and have been associated with the increased risk of skin, respiratory tract, bladder, stomach, and kidney cancers. They may also cause reproductive effects and depress the immune system. (R028)","Acute exposure to PAHs causes irritation and inflammation of the skin and lung tissue. (R034)
",There is no known antidote for PAHs. Exposure is usually handled with symptomatic treatment. (R028),P35869;Q14749;DNA
11,T3D0010,2009-03-06 18:57:55 UTC,2009-08-04 21:27:26 UTC,Benzo[b]fluoranthene,Organic Compound;Industrial By-product/Pollutant;Aromatic Hydrocarbon;Polycyclic Aromatic Hydrocarbon,"2, 3-Benzofluoranthene2,3-Benzfluoranthene2,3-Benzofluoranthene2,3-Benzofluoranthrene3, {4-Benz[e]acephenanthrylene}3,4-Benz(e)acephenanthrylene3,4-Benz[e]acephenanthrylene3,4-Benzfluoranthene3,4-Benzofluoranthene3,4-Benzofluoranthrene4,5-BenzofluorantheneB(b)fBCR047_FLUKABFBenz(e)acephenanthryleneBenz[b]fluorantheneBenzo(b)fluorantheneBenzo(b)fluoranthene [polycyclic aromatic compounds]Benzo(b)fluoranthene [polycyclic aromatic hydrocarbons]Benzo(e)fluorantheneBenzo[b]fluorantheneBenzo[b]fluoranthene solutionBenzo[e]acephenanthryleneBenzo[e]fluorantheneWLN: L C65 K666 1A TJbenzo[e]acephenanthrylene (ACD/Name 4.0){benz[e]acephenanthrylene}{benzo[b]fluoranthene}{benzo[e]fluoranthene}","Benzo[b]fluoranthene is one of over 100 different polycyclic aromatic hydrocarbons (PAHs). PAHs are chemicals that are formed during the incomplete burning organic substances, such as fossil fuels. They are usually found as a mixture containing two or more of these compounds. (R028)",,205-99-2,9153,,C14320,"",34565,"",,C006703,Benzo[b]fluoranthene,6380,,,,InChI=1/C20H12/c1-2-7-14-13(6-1)12-19-16-9-4-3-8-15(16)18-11-5-10-17(14)20(18)19/h1-12H,"",http://www.biospider.ca/saved_files/mol/0f63752e0319d088fbe082b6fefc1003_1237933319.mol,C1=CC=C2C3=C4C(=CC=C3)C5=CC=CC=C5C4=CC2=C1,C1=CC=C2C3=C4C(=CC=C3)C5=CC=CC=C5C4=CC2=C1,C20H12,252.093900,Colorless solid.,168 °C,"","","1.5e-06 mg/mL [YALKOWSKY,SH & DANNENFELSER,RM (1992)]","","","","Oral 
Inhalation
(R028)","Serum albumin (P02768) 
Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 1B1 (Q16678) 
(R060)","The ability of PAH's to bind to blood proteins such as albumin allows them to be transported throughout the body. Many PAH's induce the expression of cytochrome P450 enzymes, especially CYP1A1, CYP1A2, and CYP1B1, by binding to the aryl hydrocarbon receptor or glycine N-methyltransferase protein. These enzymes metabolize PAH's into their toxic intermediates. The reactive metabolites of PAHs (epoxide intermediates, dihydrodiols, phenols, quinones, and their various combinations) covalently bind to DNA and other cellular macromolecules, initiating mutagenesis and carcinogenesis. (R028, R060, R068, R073)","PAH metabolism occurs in all tissues, usually by cytochrome P-450 and its associated enzymes. PAHs are metabolized into reactive intermediates, which include epoxide intermediates, dihydrodiols, phenols, quinones, and their various combinations. The phenols, quinones, and dihydrodiols can all be conjugated to glucuronides and sulfate esters; the quinones also form glutathione conjugates. (R028)","","","2B, possibly carcinogenic to humans. (R264)","PAHs are released into the environment via the combustion of fossil fuels, coke oven emissions and vehicle exhausts, as well as naturally from forest fires and volcanic eruptions. PAHs from these sources may contaminate nearly water systems. They are also found in coal tar and charbroiled food. (R028)","","PAHs are carcinogens and have been associated with the increased risk of skin, respiratory tract, bladder, stomach, and kidney cancers. They may also cause reproductive effects and depress the immune system. (R028)","Acute exposure to PAHs causes irritation and inflammation of the skin and lung tissue. (R034)
",There is no known antidote for PAHs. Exposure is usually handled with symptomatic treatment. (R028),P35869;Q14749;DNA
12,T3D0011,2009-03-06 18:57:55 UTC,2009-08-26 22:04:02 UTC,Chloroform,Organic Compound;Solvent;Reagent;Organochloride,"1,1,1-TrichloromethaneCHCl3CHLOROFORM, DEUTERATED, 99%Caswell No. 192Chloroform [NF xvII]Chloroform [UN1888] [Poison]ChloroformeChloroforme (french)Chloroforme [french]CloroformioCloroformio (italian)Cloroformio [italian]Formyl trichlorideFreon 20HSDB 56Methane trichlorideMethane, trichloro-Methenyl chlorideMethenyl trichlorideMethyl trichlorideR 20 (VAN)R 20 (refrigerant)RCRA waste no. U044Rcra waste number U044Refrigerant R20TCMTrichloormethaanTrichloormethaan (dutch)Trichloormethaan [dutch]TrichlormethanTrichlormethan (czech)Trichlormethan [czech]TrichloroformTrichloromethaneTriclorometanoTriclorometano (italian)Triclorometano [italian]Water disinfection byproducts(chloroform)chloroform (ACD/Name 4.0)","Chloroform is a chemical compound produced by heating a mixture of chlorine and either chloromethane or methane. It was originally used as an anaesthetic, but is now used mainly in refridgerants and as a solvent or reagent in the synthesis of other chemicals. (R036)",,67-66-3,6212,,C13827,"",35255,5-CHLOROFORMYCIN,,D002725,Chloroform,307,,,http://en.wikipedia.org/wiki/Chloroform,InChI=1/CHCl3/c2-1(3)4/h1H,chloroform,http://www.biospider.ca/saved_files/mol/5a750ada6ee031f3111b070eab80645f_1237933443.mol,C(Cl)(Cl)Cl,C(Cl)(Cl)Cl,CHCl3,117.914380,Colorless liquid.,-63.6 °C,61.2 °C,1.48 g/cm3,"7.95 mg/mL at 25 °C [MACKAY,D et al. (1980)]","","","","Oral 
Inhalation 
Dermal
(R036)",Cytochrome P450 2E1 (P05181) (R036),"Chloroform and the reactive intermediates of chloroform metabolism, especially phosgene, bind covalently and irreversibly to cellular macromolecules and cause cellular damage within the liver and kidney. While the exact mechanism is unknown, phosgene has been shown to react with molecules such as cysteine, deplete hepatic glutathione, form adducts with microsomal proteins, and elevate hepatic enzyme levels. Chloroform has also been shown to block HERG potassium channels, causing cardiac arrest. (R036, R037, R070)","Chloroform in absorbed mainly through the lungs. Once in the body it concentrates in lipid-containing organs such as the adipose tissue, the central nervous system, kidney and liver. It is eliminated unchanged in expired air or metabolized by the liver via a cytochrome P450 mechanism and excreted in the urine and faeces. (R037)","LD50: 36 mg/kg (Oral, Mouse) (R270)
LD50: 623 mg/kg (Intraperitoneal, Mouse) (R270)
LD50: 704 mg/kg (Subcutaneous, Mouse) (R270)
LC50: 47702 mg/m3 over 4 hours (Inhalation, Rat) (R270)",10mL for an adult human. (R273),"2B, possibly carcinogenic to humans. (R264)",Chloroform is found in refridgerants and is also used as a solvent or reagent in the synthesis of other chemicals. Exposure may results from contact with contaminated air or water. (R036),"Acute Inhalation: 0.1 ppm (R260)
Intermediate Inhalation: 0.05 ppm (R260)
Chronic Inhalation: 0.02 ppm (R260)
Acute Oral: 0.3 mg/kg/day (R260)
Intermediate Oral: 0.1 mg/kg/day (R260)
Chronic Oral: 0.1 mg/kg/day (R260)","Chronic exposure to chloroform causes liver and kidney damage. It has also been shown to have detrimental reproductive and developmental effects. Skin contact with large amounts of chloroform results in sores. Inhaling large amounts of chloroform can cause central nervous system and respiratory depression, and may be fatal. (R036)","Acute inhalation of chloroform causes dizziness, fatigue, and headache. (R036)",There is no known antidote for chloroform. Exposure is usually handled with symptomatic treatment. (R036),Q12809;Q9H252;Q9NS40;P98194;O75185;P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P78334;Q8N1C3;P18507;Q99928;O00591;P24046;P28476;A8MPY1;Q9UN88;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;P54710;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P03372;Q92731
13,T3D0012,2009-03-06 18:57:55 UTC,2009-08-04 21:27:26 UTC,"DDT, P,P'-",Organic Compound;Pesticide;Organochloride,"1, 1-Dichloro-2,2-bis(2,4'-dichlorophenyl)ethane1, 1-Dichloro-2-(o-chlorophenyl)-2-(p-chlorophenyl)ethane1,1'-(2,2,2,-Trichloroethylidene)bis[4-chlorobenzene]1,1'-(2,2,2-Trichloroethylidene)bis(4-chlorobenzene)1,1'-(2,2,2-trichloroethane-1,1-diyl)bis(4-chlorobenzene)1,1'-(2,2,2-trichloroethylidene)bis[4-chlorobenzene]1,1, 1-Trichloor-2,2-bis(4-chloor fenyl)-ethaan (DUTCH)1,1, 1-Trichlor-2,2-bis(4-chlor-phenyl)-aethan (German)1,1, 1-Trichloro-2,2-bis(p-chlorophenyl)ethane1,1,1-Trichloor-2,2-bis(4-chloor fenyl)-ethaan1,1,1-Trichloor-2,2-bis(4-chloor fenyl)-ethaan [Dutch]1,1,1-Trichlor-2,2-bis(4-chlor-phenyl)-aethan1,1,1-Trichlor-2,2-bis(4-chlor-phenyl)-aethan [German]1,1,1-Trichloro-2, 2-bis(4,4'-dichlorodiphenyl)ethane1,1,1-Trichloro-2, 2-di(4-chlorophenyl)ethane1,1,1-Trichloro-2,2-bis(4,4'-dichlorodiphenyl)ethane1,1,1-Trichloro-2,2-bis(4-chlorophenyl)ethane1,1,1-Trichloro-2,2-bis(4-chlorophenyl)ethane solution1,1,1-Trichloro-2,2-bis(p-chlorophenyl)ethane1,1,1-Trichloro-2,2-bis-(4'-chlorophenyl)ethane1,1,1-Trichloro-2,2-bis-(4'-chlorophenyl)ethane (DDT)1,1,1-Trichloro-2,2-di(4-chlorophenyl)-ethane1,1,1-Trichloro-2,2-di(4-chlorophenyl)ethane1,1,1-Trichlorobis(chlorophenyl)ethane1,1,1-Tricloro-2, 2-bis(4-cloro-fenil)-etano (ITALIAN)1,1,1-Tricloro-2,2-bis(4-cloro-fenil)-etano1,1,1-Tricloro-2,2-bis(4-cloro-fenil)-etano [Italian]1,1,1-Tricloro-2,2-bis(4-cloro-fenyl)-etano [Italian]1,1,1-trichloro-2-2-bis(4-chlorophenyl)ethane1,1-Bis(4-chlorophenyl)-2,2,2-trichloroethane1,1-Bis(p-chlorophenyl)-2,2,2-trichloroethane1,1-Bis-(p-chlorophenyl)-2,2,2-trichloroethane1,1-bis(p-Chlorophenyl)-2,2,2-trichIoroethane1-Chloro-4-[2,2,2-trichloro-1-(4-chlorophenyl)ethyl]benzene2,2,2-Trichloro-1,1-bis(4-chlorophenyl)ethane2,2,2-trichlorobis(4-chloroph enyl)ethane2,2,2-trichlorobis(4-chlorophenyl)ethane2,2-Bis(p-chlorophenyl)-1,1, 1-trichloroethane2,2-Bis(p-chlorophenyl)-1,1,1-trichloroethane2-(o-Chlorophenyl)-2-(p-chlorophenyl)-1,1-dichloroethane4,4'-DDT solution4,4'-Dichlorodiphenyltrichloroethane:DDTAavero-extraAgritanAnofexArkotineAzotoxAzotox M 33Azotox M-33Benzene, 1,1'-(2,2,2-trichloroethylidene)bis(4-chloro)-Benzene, 1,1'-(2,2,2-trichloroethylidene)bis(4-chloro-Benzene, 1,1'-(2,2,2-trichloroethylidene)bis[4-chloro-Benzene, {1,1'-(2,2,2-trichloroethylidene)bis[4-chloro-}BenzochlorylBis(p-chlorophenyl)-2,2,2-trichloroetha neBis(p-chlorophenyl)-2,2,2-trichloroethaneBosan supraBovidermolCaswell No. 308ChlofenotanChlorophenothanChlorophenothaneChlorophenothanumChlorophenothanum technicumChlorophenotoxumChlorphenotaneChlorphenothanChlorphenotoxumCitoxClofenotanClofenotaneClofenotane (inn)Clofenotane techniqueClofenotano [inn-spanish]Clofenotanum [inn-latin]D.d.t. techniqueDDTDDT (dot)DDT (van)DDT 50 WPDDT [bsi:iso]DDT and metabolitesDDT(p,p')DDT, p,p'-De de taneDedeloDeovalDetoxDetox (pesticide)DetoxanDibovanDibovinDichlorodiphenyltrichlorethaneDichlorodiphenyltrichloroethaneDichlorodiphenyltrichloroethane (DDT)DicophaneDicophanerDidigamDidimacDiphenyltrichloroethaneDnsbpDodatDykolEstonateEthane, 1,1,1-Trichloro-2,2-bis(p-chlorophenyl)-Ethane, 1,1,1-trichloro-2, 2-bis(4-chlorophenyl)-Ethane, 1,1,1-trichloro-2, 2-bis(p-chlorophenyl)-Ethane, 1,1,1-trichloro-2,2-bis(4-chlorophenyl)-Ethane, 2-(o-chlorophenyl)-2-(p-chlorophenyl)-1,1-dichloro-GenitoxGesafidGesaponGesarexGesarolGeusaponGuesaponGuesarolGyronHavero-extraHilditIvoranIxodexKlorfenoton [swedish pharmacopoeia]KopsolMicro ddt 75MutoxanMutoxinNeocidNeocid (van)NeocidolNeocidol (solid)Neocidol, solidOMS 0016 [French]P',p'-DDTP'-zeidane [france]P, p'-DDTP,p'-DDTP,p'-dichlorodiphenyltrichloroethaneP,p'-dichlorodiphenyltrichloroethane (DDT)P,p'-dichlorodiphenyltrichloromethylmethaneP,p-DDTPEB1Para,para'-DDTParachlorocidumPe ntechPentachlorinPentechPenticidePenticidumPpzeidanRCRA waste no. U061Rcra waste number U061RukseamSantobaneTafidexTbisc-ethaneTech DDTTrichloro-2,2-bis(p-chlorophenyl)ethaneTrichlorobis(4'-chlorophenyl)ethaneTrichlorobis(4-chlorophenyl)ethaneWLN: GXGGYR dg&r DGZeidaneZerdaneZithiolp,p'-DDT~p,p' -Dichloro-1,1-diphenyl-2,2,2-trichloroethanep,p'-DDT~p,p'-Dichloro-1,1-diphenyl-2,2,2-trichloroethane","DDT, P,P'- is an isomer of dichlorodiphenyltrichloroethane, an organochlorine insecticide. It is the major component of commercial mixtures of DDT. DDT was once a widely used pesticide, but today its agricultural use has been banned worldwide due to its toxicity and tendency to bioaccumulate. However, it still has limited use in disease vector control. (R152)",,50-29-3,3036,,C04623,"",16130,CPD-1125,,D003634,"DDT, P,P'-",381,,,,"InChI=1/C14H9Cl5/c15-11-5-1-9(2-6-11)13(14(17,18)19)10-3-7-12(16)8-4-10/h1-8,13H","1-chloro-4-[2,2,2-trichloro-1-(4-chlorophenyl)ethyl]benzene",http://www.biospider.ca/saved_files/mol/6e2f153e2cb92fd8f53569df27010e68_1237933606.mol,C1=CC(=CC=C1C(C2=CC=C(C=C2)Cl)C(Cl)(Cl)Cl)Cl,C1=CC(=CC=C1C(C2=CC=C(C=C2)Cl)C(Cl)(Cl)Cl)Cl,C14H9Cl5,351.914690,White solid.,108.5 °C,"","","5.5e-06 mg/mL at 25 °C [YALKOWSKY,SH & DANNENFELSER,RM (1992)]","","","",Ingestion (R153),"Cytochrome P450 2B6 (Q16678) 
Cytochrome P450 3A4 (P08684) 
Cytochrome P450 3A5 (P20815) 
Cytochrome P450 3A7 (P24462) 
Cytochrome P450 3A43 (Q9HB55)
(R153)","DDT toxicity occurs via at least four mechanisms, possibly all functioning simultaneously. DDT reduces potassium transport across the membrane. DDT inhibits the inactivation of voltaged-gated sodium channels. The channels activate (open) normally but are inactivated (closed) slowly, thus interfering with the active transport of sodium out of the nerve axon during repolarization and resulting in a state of hyperexcitability. DDT inhibits neuronal adenosine triphosphatases (ATPases), particularly Na+K+-ATPase, and Ca2+-ATPase which play vital roles in neuronal repolarization. DDT also inhibits the ability of calmodulin, a calcium mediator in nerves, to transport calcium ions that are essential for the release of neurotransmitters. All these inhibited functions reduce the rate of depolarization and increase the sensitivity of neurons to small stimuli that would not elicit a response in a fully depolarized neuron. DDT is also believed to adversely affect the reproductive system by mimicking endogenous hormones and binding to the estrogen and adrogen receptors. (R029, R153)","DDT is absorbed in the stomach and intestine, after which it enters the lymphatic system and is carried throughout the body and incorporated into fatty tissues. Metabolism of DDT occurs mainly via cytochrome P-450 enzymes in the liver and kidney, where it undergoes reductive dechlorination to DDD (dichlorodiphenyldichloroethane) and DDE (dichlorodiphenyldichloroethylene). These compounds are further degraded into additional metabolites, mainly DDA (bis(p-chlorophenyl) acetic acid), which are excreted in the urine. (R153)","LD50: 87 mg/kg (Acute oral, Rat) (R275) 
LD50: 1931 mg/kg (Acute dermal, Rat) (R275) 
LD50: 1500 mg/kg (Acute subcutaneous, Rat) (R275)","","2B, possibly carcinogenic to humans. (R264)",DDT is used as a pesticide and in disease vector control. (R152),"Acute Oral: 0.0005 mg/kg/day (R260)
Intermediate Oral: 0.0005 mg/kg/day (R260)","Exposure to DDT causes loss of weight and anorexia. DDT poisoning affects CNS function in humans, but pathologic changes are observed in the liver and reproductive organs. Hypertrophy of hepatocytes and subcellular organelles such as mitochondria, proliferation of smooth endoplasmic reticulum, centrolobular necrosis after exposure to high concentrations, and an increase in the incidence of hepatic tumors have been noted.
(R029)","Acute signs of DDT poisoning include paresthesia after oral ingestion. Studies have shown that a mammal poisoned with DDT-type agents displays periodic persistent tremoring and/or convulsive seizures that are suggestive of repetitive discharges in neurons. These repetitive tremors and seizures can be initiated by tactile and auditory stimuli.
(R029)","Treatment of DDT exposure should be primarily directed towards decontamination and supportive care, as there is no specific antidote. The use of gastric lavage and activated charcoal for large ingestions may be effective. (R274)",P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P54710;P98194;O75185;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;P62158;P03372;Q92731;P10275;Q9UL51;Q9Y3Q4;O60741;Q9P1Z3 ;P35498;Q9Y5Y9;Q9UI33;Q99250;Q9NY46;P35499;Q01118;Q9UQD0;Q14524;Q15858;Q07699;O60939;Q9NY72;Q8IWT1;P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P78334;Q8N1C3;P18507;Q99928;O00591;P24046;P28476;A8MPY1;Q9UN88
14,T3D0013,2009-03-06 18:57:55 UTC,2009-08-11 15:56:26 UTC,Aroclor 1254,Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 2,2',3,3',4-pentachloro-2,2',3,3',4'-Pentachlorobiphenyl2,2',3,3',4-Pentachloro-1,1'-biphenyl2,2',3,3',4-pentachlorobiphenyl2,2',3,4,5-PENTACHLOROBIPHENYL2,3,4,2',3'-PentachlorobiphenylArclor1254Arochlor 1254Aroclor 1254Aroclor-1254Chlorierte biphenyle, chlorgehalt 54% [German]Chlorodiphenyl (54% Chlorine)Chlorodiphenyl (54% Cl)Clorodifenili, cloro 54% [Italian]Diphenyle chlore, 54% de chlore [French]PCBPCB's (54% Cl)PCBs (54%Cl)Polychlorinated biphenyl (aroclor 1254)Polychlorobiphenyls (54% chlorine)chlorodiphenyl, 54% chlorinepolychlorinated biphenyl 1254","Aroclor 1254 is a commercial mixture of PCBs with an average chlorine content of 54%. It is composed of mainly pentachlorobiphenyls (71.44%) and hexachlorobuphenyls (21.97%) and also includes mono-, bi-, tri, tetra-, hexa, and nonachlorinated homologs. Polychlorinated biphenyls (PCBs) are a group of 209 synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. PCBs were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate in the environment and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,11097-69-1,40470,,"","",25520,"",,D020111,Aroclor 1254,101,,,http://en.wikipedia.org/wiki/Polychlorinated_biphenyl,InChI=1/C12H5Cl5/c13-8-3-1-2-6(10(8)15)7-4-5-9(14)12(17)11(7)16/h1-5H,"1,2,3-trichloro-4-(2,3-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C(=C1)Cl)Cl)C2=C(C(=C(C=C2)Cl)Cl)Cl,C1=CC(=C(C(=C1)Cl)Cl)C2=C(C(=C(C=C2)Cl)Cl)Cl,C12H5Cl5,323.883390,Oily liquids or solids that are colorless to light yellow. ,Boiling Pt : 365-390 oC,365-390 °C,"","4.3e-05 mg/mL at 20 °C [YALKOWSKY,SH & DANNENFELSER,RM (1992)]","","","","Oral
Inhalation 
Dermal 
(R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose tissue, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R264)
LD50: 358 mg/kg (Intravenous, Rat) (R264)
LD50: 880 mg/kg (Intraperitoneal, Rat) (R264)","","2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refrigerators) produced before 1977. PCBs may contaminate the air and water near hazardouc waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 µg/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P53396;P35869;P49888;P03372;P11684;P20711;P07101;Q92731
15,T3D0014,2009-03-06 18:57:55 UTC,2009-08-11 15:56:25 UTC,Aroclor 1260,Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 2,2',3,3',4,4'-hexachloro-2,2',3,3',4,4'-HEXACHLOROBIPHENYL2,2',3,3',4,4'-Hexachloro-1,1'-biphenyl2,3,4,2',3',4'-HexachlorobiphenylAROCHLOR 1260 (9CI) (CHEMICALMIXTURE)Arochlor 1260Aroclor 1260Chlorodiphenyl (60% Cl)Clophen A 60Phenoclor DP6Polychlorinated biphenyl (aroclor 1260)polychlorinated biphenyl 1260","Aroclor 1260 is a commercial mixture of PCBs with an average chlorine content of 60%. It is composed of mainly pentachlorobiphenyls (43.35%) and hexachlorobuphenyls (38.54%) and also includes mono-, bi-, tri, tetra-, hexa-, octa- and nonachlorinated homologs. Polychlorinated biphenyls (PCBs) are a group of 209 synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. PCBs were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate in the environment and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,11096-82-5,38018,,"","","","",,C026987,Aroclor 1260,,,,,InChI=1/C12H4Cl6/c13-7-3-1-5(9(15)11(7)17)6-2-4-8(14)12(18)10(6)16/h1-4H,"1,2,3-trichloro-4-(2,3,4-trichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C(=C1C2=C(C(=C(C=C2)Cl)Cl)Cl)Cl)Cl)Cl,C1=CC(=C(C(=C1C2=C(C(=C(C=C2)Cl)Cl)Cl)Cl)Cl)Cl,C12H4Cl6,357.844420,Oily liquids or solids that are colorless to light yellow. ,Boiling Pt : 385-420 oC,385-420 °C,"","1.44e-05 mg/mL at 20 °C [YALKOWSKY,SH & DANNENFELSER,RM (1992)]","","","","Oral 
Inhalation 
Dermal 
(R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1315 mg/kg (Oral, Rat) (R263)","","2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refrigerators) produced before 1977. PCBs may contaminate the air and water near hazardouc waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 µg/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P35869;P49888;P03372;P11684;P20711;Q92731;P07101
16,T3D0015,2009-03-06 18:57:55 UTC,2009-08-04 21:27:26 UTC,"Dibenzo[a,h]anthracene",Organic Compound;Industrial By-product/Pollutant;Aromatic Hydrocarbon;Polycyclic Aromatic Hydrocarbon,"1,2,5, 6-Dibenzanthraceen (DUTCH)1,2,5,6-Dibenzanthraceen1,2,5,6-Dibenzanthraceen [Dutch]1,2,5,6-Dibenzanthracene1,2,5,6-dibenzanthracene, ion(1+)1,2,5,6-dibenzanthracene, ion(1-)1,2:5, 6-Dibenzanthracene1,2:5, {6-Dibenz[a]anthracene}1,2:5,6-Benzanthracene1,2:5,6-Dibenz(a)anthracene1,2:5,6-Dibenz[a]anthracene1,2:5,6-Dibenzanthracene1,2:5,6-DibenzoanthraceneBCR138_FLUKABenz[a,h]anthraceneBenzo[k]tetrapheneDB(a,h)aDBADB[a,h]aDba (van)Dibenz(a,h)anthraceneDibenz(a,h)anthracene [polycyclic aromatic hydrocarbons]Dibenz(a,h)antraceneDibenz[a,h]anthracene solutionDibenz[a,h]antraceneDibenza[a,h]-anthraceneDibenzathraceneDibenzo(a,h)anthraceneDibenzo(a,h)anthracene [polycyclic aromatic compounds]Dibenzo[a,h]anthraceneRCRA waste no. U063Rcra waste number U063WLN: L G6 D6 B666Jdibenzo[a,h]anthracene (ACD/Name 4.0){DB[a,h]a}{dibenz[a,h]anthracene} ( ){dibenz[a,h]antracene}{dibenzo[a,h]anthracene}","Dibenzo(a,h)anthracene is one of over 100 different polycyclic aromatic hydrocarbons (PAHs). PAHs are chemicals that are formed during the incomplete burning organic substances, such as fossil fuels. They are usually found as a mixture containing two or more of these compounds. (R028)",,53-70-3,5889,,C14325,"",35299,"",,C026486,"Dibenzo[a,h]anthracene",412,,,,InChI=1/C22H14/c1-3-7-19-15(5-1)9-11-17-14-22-18(13-21(17)19)12-10-16-6-2-4-8-20(16)22/h1-14H,"naphtho[1,2-b]phenanthrene",http://www.biospider.ca/saved_files/mol/ef0f4dd40e5e96c3bc4b7744529f39e4_1237934004.mol,C1=CC=C2C(=C1)C=CC3=CC4=C(C=CC5=CC=CC=C54)C=C32,C1=CC=C2C(=C1)C=CC3=CC4=C(C=CC5=CC=CC=C54)C=C32,C22H14,278.109550,Colorless solid.,269.5 °C,"","","2.49e-06 mg/mL at 25 °C [HASSETT,JJ et al. (1980)]","","","","Oral 
Inhalation
(R028)","Serum albumin (P02768) 
Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 1B1 (Q16678) 
(R060)","The ability of PAH's to bind to blood proteins such as albumin allows them to be transported throughout the body. Many PAH's induce the expression of cytochrome P450 enzymes, especially CYP1A1, CYP1A2, and CYP1B1, by binding to the aryl hydrocarbon receptor or glycine N-methyltransferase protein. These enzymes metabolize PAH's into their toxic intermediates. The reactive metabolites of PAHs (epoxide intermediates, dihydrodiols, phenols, quinones, and their various combinations) covalently bind to DNA and other cellular macromolecules, initiating mutagenesis and carcinogenesis. The main carcinogenic metabolite of benzo(a)pyrene is the diol-epoxide trans-9,10-epoxy-7,8-dihydrodiol. (R028, R060, R068, R073)","PAH metabolism occurs in all tissues, usually by cytochrome P-450 and its associated enzymes. PAHs are metabolized into reactive intermediates, which include epoxide intermediates, dihydrodiols, phenols, quinones, and their various combinations. The phenols, quinones, and dihydrodiols can all be conjugated to glucuronides and sulfate esters; the quinones also form glutathione conjugates. (R028)","","","2A, probably carcinogenic to humans. (R264)","PAHs are released into the environment via the combustion of fossil fuels, coke oven emissions and vehicle exhausts, as well as naturally from forest fires and volcanic eruptions. PAHs from these sources may contaminate nearly water systems. They are also found in coal tar and charbroiled food. (R028)","","PAHs are carcinogens and have been associated with the increased risk of skin, respiratory tract, bladder, stomach, and kidney cancers. They may also cause reproductive effects and depress the immune system. (R028)","Acute exposure to PAHs causes irritation and inflammation of the skin and lung tissue. (R034)
",There is no known antidote for PAHs. Exposure is usually handled with symptomatic treatment. (R028),P35869;Q14749;DNA
17,T3D0016,2009-03-06 18:57:55 UTC,2009-08-04 21:27:27 UTC,Trichloroethylene,Organic Compound;Solvent;Organochloride;Anesthetic,"1,1,1-Trichloroethylene1,1,2-Trichloroethene1,1,2-Trichloroethylene1,1-Dichloro-2-chloroethylene1,2,2-Trichloroethylene1-Chloro-2,2-dichloroethyleneAcetylene trichlorideAlgylenAltene DGAnamenthBenzinolBlacosolvBlancosolvC2HCl3Caswell No. 876CecoleneChlorilenChloryleaChlorylenChorylenCircosolvCrawhaspolDensi nfluatDensinfluatDisparit bDistillex DS2Dow-triDukeronEthene, 1,1,2-trichloro-Ethene, trichloro-Ethinyl trichlorideEthylene trichlorideEthylene, trichloro-Fleck-flipFlock flipFluateGemalgeneGermalgeneInChI=1/C2HCl3/c3-1-2(4)5/h1LanadinLethurinNarcogenNarkogenNarkosoidNialkPerm-a-chlorPerm-a-clorPetzinolPhilexRCRA waste no. U228Rcra waste number U228TCETRITce (chlorohydrocarbon)ThrethylenThrethyleneTrethyleneTri-cleneTri-plusTri-plus mTriadTrialTriasolTric hloroetheneTrichlooretheenTrichlooretheen [dutch]Trichloorethyleen, triTrichloorethyleen, tri [dutch]TrichloraethenTrichloraethen [german]TrichloraethylenTrichloraethylen, triTrichloraethylen, tri [german]TrichloraethylenumTrichloraethylenum pro narcosiTrichloranTrichlorathaneTrichlorenTrichloretheneTrichlorethyleneTrichlorethylene, triTrichlorethylene, tri [french]TrichlorethylenumTrichloride, ethinylTrichloroetheneTrichloroethylene (iupac)Trichloroethylene (tce)Trichloroethylene (with epichlorohydrin)Trichloroethylene (without epichlorohydrin)Trichloroethylene [UN1710] [Poison]Trichloroethylene [inn]TrichloroethylenumTrichloroethylenum [inn-latin]TrichlorotheneTricieneTricloreteneTricloretene [italian]TricloroetileneTricloroetilene [dcit]Tricloroetilene [italian]Tricloroetileno [inn-spanish]TrieleneTrielinTrielinaTrielina [italian]TrielineTrik loneTrikloneTriklone nTrilenTrileneTrilene TE-141TrilineTrimarTriolVestrolVitranWestrosol","Trichloroethylene is a chemical compound produced from ethylene. It was originally used as an anaethetic before its toxicity was recognized. Today it is mainly used as an industrial solvent, especially for removing grease from metal parts. (R038)",,79-01-6,6575,,C06790,"",16602,TRICHLOROETHENE,,D014241,Trichloroethylene,1414,,,http://en.wikipedia.org/wiki/Trichloroethylene,InChI=1/C2HCl3/c3-1-2(4)5/h1H,"1,1,2-trichloroethene",http://www.biospider.ca/saved_files/mol/03985eadfa2d7ee21bf0ff3ab7533afe_1237934111.mol,C(=C(Cl)Cl)Cl,C(=C(Cl)Cl)Cl,C2HCl3,129.914380,Colorless liquid.,-84.7 °C,"","","1.28 mg/mL at 25 °C [HORVATH,AL et al. (1999)]","","","","Oral 
Inhalation 
Dermal
(R038)","Glutathione S-transferase P (P09211) 
Glutathione S-transferase Mu 1 (P09488) 
Glutathione S-transferase A1 (P08263) 
Glutathione S-transferase theta-2 (P30712) 
Glutathione S-transferase Mu 4 (Q03013) 
Glutathione S-transferase theta-1 (P30711) 
Glutathione S-transferase A4 (O15217) 
Glutathione S-transferase A2 (P09210) 
Glutathione S-transferase A3 (Q16772) 
Glutathione S-transferase Mu 3 (P21266) 
Glutathione S-transferase omega-1 (P78417) 
Glutathione S-transferase kappa 1 (Q9Y2Q3) 
Glutathione S-transferase Mu 2 (P28161) 
Glutathione S-transferase omega-2 (Q9H4Y5) 
Glutathione S-transferase A5 (Q7RTV2) 
Glutathione S-transferase Mu 5 (P46439) 
Glutathione S-transferase theta-4 (A8MPT4) 
Maleylacetoacetate isomerase (O43708) 
Microsomal glutathione S-transferase 1 (P10620) 
Microsomal glutathione S-transferase 2 (Q99735) 
Microsomal glutathione S-transferase 3 (O14880) 
Cytochrome P450 2E1 (P05181) 
(R111)","The toxic and carcinogenic effects of trichloroethylene are believed to be caused mainly by its metabolites, including trichloroacetic acid, dichloroacetic acid, and chloral hydrate. The nephrotoxicity and nephrocarcinogenicity of TRI have been attributed to glutathione conjunction, which forms reactive, sulfur-containing metabolites. Dichloroacetic acid is known to inhibit pyruvate dehydrogenase kinase, while chloral hydrate inhibits alcohol dehydrogenase. Studies in rodents have shown that neurotoxic effects may be caused by trichloroethylene's incorporation into brain membranes or ability to alter the fatty acid pattern of brain phospholipids and amino acids. One of the mechanisms of trichloroethylene's carcinogenicity is believed to be the peroxisome proliferation induced by its metabolites. (R038, R040, R111)","Trichloroethylene is absorbed into the bloodstream and rapidly distributed throughout the body. Some is metabolized via cytochrome P-450 enzymes and the glutathione-conjugation pathway into metabolites such as trichloroacetic acid and trichloroethanol, which are excreted primarily in the urine. However, most trichoroethylene is exhaled unchanged or as carbon dioxide. (R039)","LD50: 2402 mg/kg (Oral, Mouse) (R276)
LD50: 20001 mg/kg (Dermal, Rabbit) (R276)
LD50: 3222 mg/kg (Tntraperitoneal, Mouse) (R276)",3 to 5 mg/kg for an adult human. (R270),"2A, probably carcinogenic to humans. (R264)","Trichloroethylene is mainly used as an industrial solvent, particularily to remove grease from metal parts. It is also an ingredient in adhesives, paint removers, typewriter correction fluids, and spot removers. Exposure may result from contact with contaminated water. (R038)","Acute Inhalation: 2 ppm (R260)
Intermediate Inhalation: 0.1 ppm (R260)
Acute Oral: 0.2 mg/kg/day (R260)","Chronic inhalation or ingestion of tricholoethylene causes nerve, kidney, and liver damage, impaired immune system function, impaired fetal development in pregnant women, and possibly death. It has also been linked to both kidney and liver cancer. (R038)","Inhalation of trichloroethylene causes headaches, lung irritation, dizziness, poor coordination, and difficulty concentrating, while ingestion results in nausea. Larger amounts may cause unconciousness and impaired heart function. Skin contact often results in rashes. (R038)",There is no known antidote for trichloroethylene. Exposure is usually handled with symptomatic treatment. (R039),Q15118;Q15119;P07327;P00325;P00326;P40394;P11766;P08319;P28332;Q15120;Q16654;P98194;O75185;P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P78334;Q8N1C3;P18507;Q99928;O00591;P24046;P28476;A8MPY1;Q9UN88;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;P54710;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P03372;Q92731
18,T3D0017,2009-03-06 18:57:55 UTC,2009-08-04 21:27:27 UTC,Dieldrin,Organic Compound;Pesticide;Organochloride,":dieldrinAldrin epoxideAlvitAlvit 55Caswell No. 333Compd. 497Compound 497DeildrinDieldrenDieldrexDieldrinDieldrin [NA2761] [Poison]Dieldrin [ban:inn]Dieldrin [bsi:iso]Dieldrin [inn:ban]Dieldrina [inn-spanish]DieldrineDieldrine (french)Dieldrine [french]Dieldrine [inn-french]Dieldrine [iso-french]Dieldrinum [inn-latin]DieldriteDieldrixDielmothDildrinDorytoxExo-dieldrinHEODHeod [bsi:iso]Hexachloroepoxyoctahydro-endo,exo-dimethanonaphthaleneIlloxolInsecticide No. 497InsectlackKombi-albertanLatka 497 [Czech]Moth snub dMurdielOctaloxOxraloxPanoram D-31QuintoxRCRA waste no. P037RCRA waste number P037Red shieldShelltoxTermitoxTermitoxrm [BDH]","Dieldrin is a chlorinated hydrocarbon used as an insecticide, either by itself or as a component of the closely related insectide aldrin. As dieldrin is neurotoxin and tends to bioaccumulate, its use is now banned in most parts of the world. (R154)",,60-57-1,60963,,C13718,"",34696,1-AMINO-PROPAN-2-OL,,D004026,Dieldrin,459,,,,"InChI=1/C12H8Cl6O/c13-8-9(14)11(16)5-3-1-2(6-7(3)19-6)4(5)10(8,15)12(11,17)18/h2-7H,1H2/t2-,3+,4?,5?,6?,7?,10-,11-/m1/s1","",http://www.biospider.ca/saved_files/mol/fcc828e49aa333ab9e7724ae0a19238b_1237934240.mol,C1[C@@H]2C3C([C@H]1C4C2O4)[C@]5(C(=C([C@]3(C5(Cl)Cl)Cl)Cl)Cl)Cl,C1C2C3C(C1C4C2O4)C5(C(=C(C3(C5(Cl)Cl)Cl)Cl)Cl)Cl,C12H8Cl6O,377.870630,White powder.,175.5 °C,"","","0.000195 mg/mL at 25 °C [BIGGAR,JW & RIGGS,RI (1974)]","","","","Oral 
Inhalation 
Dermal
(R155)","Epoxide hydrolase 1 (P07099) 
Epoxide hydrolase 2 (P34913)
(R155)","Dieldrin antagonizes the action of the neurotransmitter gamma-aminobutyric acid (GABA) acting at the GABA-A receptors, effectively blocking the GABA-induced uptake of chloride ions. Dieldrin also inhibits Na+ K+ ATPase and Ca2+ and Mg2+ ATPase which are essential for the transport of calcium across membranes. This results in the accumulation of intracellular free calcium ions, which promotes release of neurotransmitters from storage vesicles, the subsequent depolarization of adjacent neurons, and the propagation of stimuli throughout the CNS. This results in hyperexcitation and generalized seizures. Dieldrin also binds to alpha-synuclein, leading to the formation of intracellular fibrils. (R029, R155)","Dieldrin is absorbed throught the gastrointestinal tract, lungs and skin. Following absorption, dieldrin is redistributed primarily to fat via the lymphatic system. Dieldrin is metabolized by liver microsomal monooxygenases and epoxide hydratases. Its metabolites, of which the primary one is 9-hydroxydieldrin, are excreted in the faeces. (R155)","LD50: 38 mg/kg (Oral, Rat) (R263)
LD50: 56 mg/kg (Dermal, Rat) (R263)
LD50: 49 mg/kg (Subcutaneous, Rat) (R277)
LD50: 9 mg/kg (Tntravenous, Rat) (R263)
LC50: 13 mg/m3 over 4 hours (Inhalation, Rat) (R277)","","3, not classifiable as to its carcinogenicity to humans. (R264)",Dieldrin is used as an insecticide. (R155),"Intermediate Oral: 0.0001 mg/kg/day (R260)
Chronic Oral: 0.00005 mg/kg/day (R260)","Dieldrin is a neurotoxin and works by overstimulating the central nervous system. Ingestion of large amounts of dieldrin causes convulsions and death. However, chronic exposure to lower amounts of dieldrin also has adverse effects because dieldrin accumulates in the body. Dieldrin is known to damage the nervous system, liver, and immune system. (R155)","Exposure to dieldrin results in headaches, dizziness, irritability, nausea and vomiting, cardiac arrhythmias, muscular weakness, uncontrolled muscle movements, hyperexcitability, seizures and coma. (R155)","Treatment is symptomatic, aimed at controlling convulsions, coma, and respiratory depression. If ingested, gastric lavage may be performed, followed by administering activated charcoal powder. (R278)",P37840;P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P18507;Q99928;O00591;P24046;P28476;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P54710;P98194;O75185;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;P78334;Q8N1C3;A8MPY1;Q9UN88;P03372;Q92731
19,T3D0018,2009-03-06 18:57:56 UTC,2009-08-26 22:06:32 UTC,"Chromium, hexavalent",Inorganic Compound;Metal;Chromium Compound,"CR(vi)Chromium (cr(sup 6+))Chromium (hexavalent compounds)Chromium (vi)Chromium compounds, hexavalentChromium hexavalent ionChromium(6+) ionsChromium(6+)ionChromium(6+)ionsChromium(vi)Chromium(vi) cationChromium(vi) compoundsChromium(vi) compounds, n.o.sChromium(vi) compounds, n.o.s.Chromium(vi) ionsChromium, hexavalentChromium, hexavalent (CR(vi))Chromium, ion (Cr 6+)Chromium, ion(Cr6+)Hexavalent chromiumchromium(6+)chromium(6+) ion",Hexavalent chromium refers to chemical compounds that contain the element chromium in the +6 oxidation state. Chromium(VI) is more toxic than other oxidation states of the chromium atom because of its greater ability to enter cells and higher redox potential. (R042),,18540-29-9,29131,,"","",33007,"",,C074702,"Chromium, hexavalent",6409,,,,InChI=1/Cr/q+6,chromium(6+),http://www.biospider.ca/saved_files/mol/,[Cr+6],[Cr+6],[Cr]6+,"","","","","","","","","","Oral 
Inhalation 
Dermal
(R042)","Sulfate transporter (P50443) 
Sulfate anion transporter 1 (Q9H2B4)
(R041)","Hexavalent chromium's carcinogenic effects are caused by its metabolites, pentavalent and trivalent chromium. The DNA damage may be caused by hydroxyl radicals produced during reoxidation of pentavalent chromium by hydrogen peroxide molecules present in the cell. Trivalent chromium may also form complexes with peptides, proteins, and DNA, resulting in DNA-protein crosslinks, DNA strand breaks, DNA-DNA interstrand crosslinks, chromium-DNA adducts, chromosomal aberrations and alterations in cellular signaling pathways. It has been shown to induce carcinogenesis by overstimulating cellular regulatory pathways and increasing peroxide levels by activating certain mitogen-activated protein kinases. It can also cause transcriptional repression by cross-linking histone deacetylase 1-DNA methyltransferase 1 complexes to CYP1A1 promoter chromatin, inhibiting histone modification. Chromium may increase its own toxicity by modifying metal regulatory transcription factor 1, causing the inhibition of zinc-induced metallothionein transcription. (R041, R042, R075, R076, R077)","Chromium is absorbed from oral, inhalation, or dermal exposure and distributes to nearly all tissues, with the highest concentrations found in kidney and liver. Bone is also a major storage site and may contribute to long-term retention. Hexavalent chromium's similarity to sulfate and chromate allow it to be transported into cells via sulfate transport mechanisms. Inside the cell, hexavalent chromium is reduced first to pentavalent chromium, then to trivalent chromium by many substances including ascorbate, glutathione, and nicotinamide adenine dinucleotide. Chromium is almost entirely excreted with the urine. (R041, R042)","",1 to 3 grams for an adult human. (R331),"1, carcinogenic to humans. (R264)","Hexavalent chromium is used for chrome plating, dyes and pigments, leather tanning, and wood preserving. (R041)","Intermediate Oral: 0.005 mg/kg/day (R260)
Chronic Oral: 0.001 mg/kg/day (R260)",Hexavalent chromium is a known carcinogen. Chronic inhalation especially has been linked to lung cancer. Hexavalent chromium has also been know to cause reproductive and developmental defects. (R041),"Breathing hexavalent chromium can cause irritation to the lining of the nose, nose ulcers, runny nose, and breathing problems, such as asthma, cough, shortness of breath, or wheezing. Ingestion of hexavalent chromium causes irritation and ulcers in the stomach and small intestine, as well as anemia. Skin contact can cause skin ulcers. (R042)","There is no known antidote for chromium poisoning. Exposure is usually handled with symptomatic treatment. (R042)
",P28482;P27361;Q13547;Q14872;DNA
20,T3D0019,2009-03-06 18:57:56 UTC,2009-08-26 22:10:46 UTC,"Phosphorus, white",Inorganic Compound;Non-Metal,"Hittorf's phosphorusOligostim Phosphore - Tab 6dhPekana - phosphorusPhosphate-novartisPhosphorousPhosphorus 4ch - 30chPhosphorus Drops C6-C1000Phosphorus Gtte 4ch-30chPhosphorus Liquid (S No. 11)Phosphorus Pwr 6xPhosphorus Tri-Iodatus 3ch - 30chPhosphorus flavusPhosphorus homaccordPhosphorus, redPhosphorus-30Phosphorus-Injeel S (12d,30d,200d,1000d/1.1ml)Red phosphorusTonimine liqViolet phosphorusWhite phosphorus","White phosphorus is an allotrope of elemental phosphorus. It does not occur naturally, but is manufactured from phosphate rocks. Since it is a smoke-producing and incendiary agent, it has many military applications, especially in smokescreens, bombs, artillery, and mortars. It is also used by industry to produce phosphoric acid and other chemicals for use in fertilizers, food additives, and cleaning compounds. (R156, R157)",,7723-14-0,5462309,,C06262,"168470
602079
606656",28659,"",,D010758,"Phosphorus, white",6567,,,http://en.wikipedia.org/wiki/Phosphorus,InChI=1/P,phosphorus,http://www.biospider.ca/saved_files/mol/,[P],[P],P,30.973760,White solid that becomes yellow when exposed to light.,44.1 °C,"","",0.0033 mg/mL at 15 oC [KIRK-OTHMER; on-line (2005)],"","","","Oral 
Inhalation 
Dermal
(R156)","Parathyroid hormone (P01270) 
Tuberoinfundibular peptide of 39 residues (Q96A98) 
Fibroblast growth factor 23 (Q9GZV9) 
(R207)","Exposure to white phosphorus has been shown to damage the rough endoplasmic reticulum and cause a disaggregation of polyribosomes. This damage results in impairment of protein synthesis, in particular, a decrease in the synthesis of the apolipoprotein portion of very low density lipoproteins (VLDL), which are required for the transport of triglycerides. This causes an accumulation of triglycerides in the liver, resulting in steatosis and fibrosis. White phosphorus also damages the mitochondia, impairing a cell’s ability to produce ATP and resulting in necrosis. The mitochondrial damage may also inhibit fatty acid oxidation, which could result in an accumulation of fat in the organs. Excess phosphorus decreases the absorption of intercellular calcified cartilage matrix by osteoclasts in the metaphyseal region of growing bones, decreasing the rate of growth of long bones. It may also enhance deposition of calcium by activating sodium-dependent phosphate transporter 1, bone morphogenic proteins 2 and 4, leptin, endogenous 1,25 dihydroxy vitamin D, vascular calcification activating factor, and measures of oxidative stress. (R156, R208)","Phosphorus may be absorbed from ingestion, inhalation, or skin contact and is widely distributed throughout the body, especially in the liver, kidney, blood, spleen, and brain. Since white phosphorus is highly reactive in the presence of oxygen, it is likely rapidly converted to its oxidation products prior to absorption into the body. Little is known about the metabolism of white phosphorus in the body, although the oxo acids of phophorus are known to be found in the bloodstream. Phosphorus in the body is regulated by parathyroid hormone, calcitriol, and fibroblast growth factor 23. (R156, R207)","",50 mg for an adult human. (R270),,"White phosphorus is used in many military applications, especially in smokescreens, bombs, artillery, and mortars. It is also used by industry to produce phosphoric acid and other chemicals for use in fertilizers, food additives, and cleaning compounds. (R156)","Acute Inhalation: 0.02 mg/m3 (R260) 
Intermediate Oral: 0.0002 mg/kg/day (R260)","Exposure to white phosphorus may cause liver, heart, or kidney damage. It can also result in death. Breathing white phosphorus for long periods may cause a condition known as ""phossy jaw"", which involves poor wound healing of the mouth and breakdown of the jaw bone. Anemia and leukopenia in people chronically exposed to airborne white phosphorus. (R156)","Breathing white phosphorus for short periods may cause coughing and irritation of the throat and lungs. Eating or drinking small amounts of white phosphorus may cause stomach cramps, or drowsiness. (R156)","Ingestion of white phosphorus can be treated with gastric lavage. Otherwise, treatment is mainly symptomatic. (R156)",P41159;Q8WUM9
21,T3D0020,2009-03-06 18:57:56 UTC,2009-08-04 21:27:27 UTC,Chlordane,Organic Compound;Pesticide;Organochloride,"«gamma»-chlordan«gamma»-chlordane.gamma.-chlordan1,3,4,7,8,9,10,10-octachlorotricyclo[5.2.1.0(2,6)]dec-8-ene1068 Steral:chlordaneAlpha-, gamma-chlordaneAlpha-chlordanAlpha-chlordaneAspon-chlordaneBELTC orodaneC-chlordaneCHLORDANE (TECHNICAL GRADE) (SEE ALSO 57-74-9)Caswell No. 174Caswell No. 174EChloordaanChloordaan (dutch)Chloordaan [dutch]Chlor kilChlor killChlordanChlordaneChlordane (alpha and gamma isomers)Chlordane (analytical grade)Chlordane (avg cis-,trans-)Chlordane (technical grade)Chlordane (technical mixture and metabolites)Chlordane (technical mixture)Chlordane (trans)Chlordane , purChlordane, alpha & gamma isomersChlordane, liquidChlordane, liquid (dot)Chlordane, technicalChlordane, technical gradeChlordane, technically gradeChlordane-technicalChlorindanChlorodaneChlorotoxChlortoxCis-chlordaneCis-photochlordaneClordanClordan (italian)Clordan [italian]ClordanoCompound kCompound k (fda)CorodaneCortilan-neuDichlorochlordeneDow-klorDowchlorGold crestIntoxIntox (insecticide)Intox 8Kilex lindaneKypchlorLatka 1068 [Czech]NiranOcta-klorOctach lorohexahydromethanoindeneOctachlorOctachlordaneOctachloro-4, 7-methanohydroindaneOctachloro-4,7-methanohydroindaneOctachloro-4,7-methanotetrahydroindaneOctachlorodihydrodicyclopentadieneOctachlorohexahydromethanoindeneOindaneOktaterrOrtho-klorPhotochlordaneRCRA waste no. U036Rcra waste number U036Shell sd-5532StarchlorSteraskinSydaneSyndaneSynklorT-chlordaneTat Chlor 4Technical chlordaneTermexTermi-dedTopichlor 20TopiclorTopiclor 20ToxichlorTrans-chlordanTrans-chlordaneUnexan-koederVelsicol 1068WLN: L C555 A IUTJ AG AG BG DG EG HG IG JG","Chlordane is a manufactured chemical that was used as a pesticide in the United States from 1948 to 1988. Chlordane occurs in two isomers, called cis-chlordane (alpha-chlordane) and trans-chlordane (gamma-chlordane). (R158)",,57-74-9,5993,,C14176,"",34623,1-AMINO-PROPAN-2-OL,,,Chlordane,271,,,,"InChI=1/C10H6Cl8/c11-3-1-2-4(5(3)12)9(16)7(14)6(13)8(2,15)10(9,17)18/h2-5H,1H2/t2?,3?,4?,5?,8-,9+/m0/s1","",http://www.biospider.ca/saved_files/mol/9fb6a8b186ea70832d9f1e9a67b18bf4_1237934546.mol,C1C2C(C(C1Cl)Cl)C3(C(=C(C2(C3(Cl)Cl)Cl)Cl)Cl)Cl,C1C2C(C(C1Cl)Cl)C3(C(=C(C2(C3(Cl)Cl)Cl)Cl)Cl)Cl,C10H6Cl8,405.797770,Colorless to amber liquid.,106 °C,"","","5.6e-05 mg/mL at 25 °C [SANBORN,JR et al. (1976)]","","","","Oral 
Inhalation
(R259)","Glutathione S-transferase P (P09211) 
Glutathione S-transferase Mu 1 (P09488) 
Glutathione S-transferase A1 (P08263) 
Glutathione S-transferase theta-2 (P30712) 
Glutathione S-transferase Mu 4 (Q03013) 
Glutathione S-transferase theta-1 (P30711) 
Glutathione S-transferase A4 (O15217) 
Glutathione S-transferase A2 (P09210) 
Glutathione S-transferase A3 (Q16772) 
Glutathione S-transferase Mu 3 (P21266) 
Glutathione S-transferase omega-1 (P78417) 
Glutathione S-transferase kappa 1 (Q9Y2Q3) 
Glutathione S-transferase Mu 2 (P28161) 
Glutathione S-transferase omega-2 (Q9H4Y5) 
Glutathione S-transferase A5 (Q7RTV2) 
Glutathione S-transferase Mu 5 (P46439) 
Glutathione S-transferase theta-4 (A8MPT4) 
Maleylacetoacetate isomerase (O43708) 
Microsomal glutathione S-transferase 1 (P10620) 
Microsomal glutathione S-transferase 2 (Q99735) 
Microsomal glutathione S-transferase 3 (O14880) 
(R159)","Chlordane is believed to bind irreversibly to DNA, leading to cell death or altered cellular function. It also affects transcription by antagonizing estrogen-related receptors. Chlordane induces hepatic cytochrome P-450, causing a large increase in the volume of the smooth endoplasmic reticulum, which results in hepatocellular enlargement and hypertrophy. Chlordane has also been shown to bind and activate retinoic acid receptor, causing various developmental defects, and inhibit alkaline phosphatases in hepatic and renal tissues. (R159, R162, R163, R205, R206)","Chlordane is highly lipophilic and is thus easily absorbed by ingestion, inhalation, and dermal exposure, then stored mainly in the fat. Chlordane is metabolized mainly in the liver and kidney. Metabolism is slow, and is believed to occur by multiple pathways involving cytochrome P-450 enzymes, glutathione-S-transferase type enzymes, and microsomal mixed-function oxidase systems. The metabolites are generally less toxic and include chlordene chlorohydrin, monohydroxylated dihydrochlordene, and oxychlordane. They are excreted in the urine and faeces. (R159)","LD50: 200 mg/kg (Oral, Rat) (R261)
LD50: 343 mg/kg (Intraperitoneal, Rat) (R261)
LD50: 10 mg/kg (Intravenous, Mouse) (R263)
LD50: 780 mg/kg (Dermal, Rat) (R263)
LC50: 100 mg/m3 over 4 hours (Inhalation, Cat) (R263)",100 mg/kg for an adult human. (R265),"2B, possibly carcinogenic to humans. (R264)",Chlordane was used as a pesticide. (R158),"Intermediate Inhalation: 0.0002 mg/m3 (R260)
Chronic Inhalation: 0.00002 mg/m3 (R260)
Acute Oral: 0.001 mg/kg/day (R260)
Intermediate Oral: 0.0006 mg/kg/day (R260)
Chronic Oral: 0.0006 mg/kg/day (R260)","Chlordane is a central nervous system stimulant, and can also damage the digestive system and the liver. Large doses have been known to cause convulsions, respiratory failure, and death. Chlordane is also known to have adverse reproductive and developmental effects. (R159)","Ingestion and inhalation of chlordane cause headaches, irritability, confusion, weakness, vision problems, vomiting, stomach cramps, diarrhea, and jaundice. (R159)","Treatment is symptomatic. It is aimed at controlling convulsions, coma, and respiratory depression. Gastric lavage, followed by the administration of activated charcoal, may be performed following ingestion. (R282)",P11474;O95718;P62508;P10826;P13631;P20813;P08684;Q9HB55;P20815;P24462;P05186;DNA;P98194;O75185;P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P78334;Q8N1C3;P18507;Q99928;O00591;P24046;P28476;A8MPY1;Q9UN88;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;P54710;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P03372;Q92731
22,T3D0021,2009-03-06 18:57:56 UTC,2009-08-04 21:27:27 UTC,"DDE, P,P'-",Organic Compound;Pesticide;Organochloride,"1, 1-Bis(p-chlorophenyl)-2,2-dichloroethylene1, {1'-(Dichloroethenylidene)bis[4-chlorobenzene]}1,1'-(2,2-dichloroethene-1,1-diyl)bis(4-chlorobenzene)1,1'-(Dichloroethenylidene)bis(4-chlorobenzene)1,1'-(Dichloroethenylidene)bis[4-chlorobenzene]1,1'-(Dichlorovinylidene)bis(chlorobenzene)1,1'-Bis(chlorophenyl)-2,2-dichloroethylene1,1-BIS(CHLOROPHENYL)-2,2-DICHLOROETHYLENE1,1-Bis(p-chlorophenyl)-2,2-dichloroethylene1,1-Dichloro-2, 2-bis(p-chlorophenyl)ethene1,1-Dichloro-2, 2-bis(p-chlorophenyl)ethylene1,1-Dichloro-2, 2-di(p-chlorophenyl)ethylene1,1-Dichloro-2,2-Bis(p-chlorophenyl)ethylene1,1-Dichloro-2,2-bis(4'-chlorophenyl)ethylene1,1-Dichloro-2,2-bis(4'-chlorophenyl)ethylene (DDE)1,1-Dichloro-2,2-bis(4-chlorophenyl)ethene1,1-Dichloro-2,2-bis(4-chlorophenyl)ethene solution1,1-Dichloro-2,2-bis(p-chlorophenyl)ethene1,1-Dichloro-2,2-bis(para-chlorophenyl) ethylene1,1-Dichloro-2,2-bis[4-chlorophenyl]ethylene1,1-Dichloro-2,2-di(p-chlorophenyl)ethylene1,1-dichloro-2,2-bis(4-chlorophenyl)ethylene1-Chloro-4-[2,2-dichloro-1-(4-chlorophenyl)vinyl]benzene1-chloro-4-[2,2-dichloro-1-(4-chlorophenyl)ethenyl]benzene2, 2-Bis(4-chlorophenyl)-1,1-dichloroethylene2, 2-Bis(p-chlorophenyl)-1,1-dichloroethylene2,2-Bis(4-chlorophenyl)-1,1-dichloroethene2,2-Bis(4-chlorophenyl)-1,1-dichloroethylene2,2-Bis(chlorophenyl)-1,1-dichloroethylene2,2-Bis(p-chlorophenyl)-1,1-dichloroethylene2,2-bis(p-chlorophenyl)-1,1-dichloroethene4,4'-DDE solution4,4'-DDE-Ring-UL-14C4,4'-DDEe4,4';-DDE solutionBenzene, 1,1'-(dichloroethenylidene)bis(4-chloro-Benzene, 1,1'-(dichloroethenylidene)bis(4-chloro- (9CI)Benzene, 1,1'-(dichloroethenylidene)bis(4-chloro-)Benzene, 1,1'-(dichloroethenylidene)bis(chloro-Benzene, 1,1'-(dichloroethenylidene)bis*4-chloro-Benzene, 1,1'-(dichloroethenylidene)bis[4-chloro-Benzene, {1,1'-(dichloroethenylidene)bis[4-chloro-}DDEDDT dehydrochlorideDDXDde (van)Dde(p,p')Dde, p,p'-Dichlorodiphenyl dichloroetheneDichlorodiphenyl dichloroethyleneDichlorodiphenyldichloroethyleneDichloroethylene, dichlorodiphenylEthylene, 1,1-dichloro-2, 2-bis(p-chlorophenyl)-Ethylene, 1,1-dichloro-2,2-bis(p-chlorophenyl)-Ethylene, 2,2-bis(chlorophenyl)-1,1-dichloro-P, p'-(dichlorodiphenyl)dichloroethyleneP,p' -ddeP,p'-(dichlorodiphenyl)dichloroethyleneP,p'-:ddeP,p'-dde (p,p'-dichlorodiphenyldichloroethylene)P,p'-dde-p, p'-DDT mixtureP,p'-dde-p,p'-DDT mixtureP,p'-dichlorodiphenoldichloroethyleneP,p'-dichlorodiphenyl dichloroethyleneP,p'-dichlorodiphenyldic hloroethylene (dde)P,p'-dichlorodiphenyldichloroethyleneP,p'-dichlorodiphenyldichloroethylene (dde)P,p-ddeP,p-dichlorodiphenyldichloroethyleneP,p[-ddePara,para'-ddeWLN: gyguyr DG&r DGp,p'-(Dichlorodiphenyl)-2,2-dichloroethylenep,p'-DDE-ring-UL-14C","DDE, P,P'- is an isomer of dichlorodiphenyldichloroethylene, an organochlorine insecticide. It is one of the components of commercial mixtures of DDT. DDT was once a widely used pesticide, but today its agricultural use has been banned worldwide due to its toxicity and tendency to bioaccumulate. However, it still has limited use in disease vector control. (R152)",,72-55-9,3035,,C04596,"",16598,PRO,,D003633,"DDE, P,P'-",380,,,,InChI=1/C14H8Cl4/c15-11-5-1-9(2-6-11)13(14(17)18)10-3-7-12(16)8-4-10/h1-8H,"1-chloro-4-[2,2-dichloro-1-(4-chlorophenyl)ethenyl]benzene",http://www.biospider.ca/saved_files/mol/21d0537ca007dd5dd6f5e92c6f7d79a0_1237934638.mol,C1=CC(=CC=C1C(=C(Cl)Cl)C2=CC=C(C=C2)Cl)Cl,C1=CC(=CC=C1C(=C(Cl)Cl)C2=CC=C(C=C2)Cl)Cl,C14H8Cl4,315.938010,"",89 °C,"","","4e-05 mg/mL at 25 °C [YALKOWSKY,SH & DANNENFELSER,RM (1992)]","","","",Ingestion (R153),"Cytochrome P450 2B6 (Q16678) 
Cytochrome P450 3A4 (P08684) 
Cytochrome P450 3A5 (P20815) 
Cytochrome P450 3A7 (P24462) 
Cytochrome P450 3A43 (Q9HB55)
(R153)","DDE toxicity occurs via at least four mechanisms, possibly all functioning simultaneously. DDE reduces potassium transport across the membrane. DDE inhibits the inactivation of voltaged-gated sodium channels. The channels activate (open) normally but are inactivated (closed) slowly, thus interfering with the active transport of sodium out of the nerve axon during repolarization and resulting in a state of hyperexcitability. DDE inhibits neuronal adenosine triphosphatases (ATPases), particularly Na+K+-ATPase, and Ca2+-ATPase which play vital roles in neuronal repolarization. DDE also inhibits the ability of calmodulin, a calcium mediator in nerves, to transport calcium ions that are essential for the release of neurotransmitters. All these inhibited functions reduce the rate of depolarization and increase the sensitivity of neurons to small stimuli that would not elicit a response in a fully depolarized neuron. DDE is also believed to adversely affect the reproductive system by mimicking endogenous hormones and binding to the estrogen and adrogen receptors. (R029, R153)","DDE is absorbed in the stomach and intestine, after which it enters the lymphatic system and is carried throughout the body and incorporated into fatty tissues. Metabolism of DDE occurs mainly via cytochrome P-450 enzymes in the liver and kidney. Its metabolites, mainly DDA (bis(p-chlorophenyl) acetic acid), are excreted in the urine. (R153)","","","2B, possibly carcinogenic to humans. (R264)","DDE is found in DDT, which is used as a pesticide and in disease vector control. (R152)","","Exposure to DDT causes loss of weight and anorexia. DDT poisoning affects CNS function in humans, but pathologic changes are observed in the liver and reproductive organs. Hypertrophy of hepatocytes and subcellular organelles such as mitochondria, proliferation of smooth endoplasmic reticulum, centrolobular necrosis after exposure to high concentrations, and an increase in the incidence of hepatic tumors have been noted. (R029)",Acute signs of DDT poisoning include paresthesia after oral ingestion. Studies have shown that a mammal poisoned with DDT-type agents displays periodic persistent tremoring and/or convulsive seizures that are suggestive of repetitive discharges in neurons. These repetitive tremors and seizures can be initiated by tactile and auditory stimuli. (R029),"Treatment of DDT exposure should be primarily directed towards decontamination and supportive care, as there is no specific antidote. The use of gastric lavage and activated charcoal for large ingestions may be effective. (R274)",P10275;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P54710;P98194;O75185;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;P62158;P03372;Q92731;Q9UL51;Q9Y3Q4;O60741;Q9P1Z3 ;P35498;Q9Y5Y9;Q9UI33;Q99250;Q9NY46;P35499;Q14524;Q01118;Q9UQD0;Q15858;Q07699;O60939;Q9NY72;Q8IWT1;P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P78334;Q8N1C3;P18507;Q99928;O00591;P24046;P28476;A8MPY1;Q9UN88
23,T3D0022,2009-03-06 18:57:56 UTC,2009-08-04 21:27:28 UTC,Hexachlorobutadiene,Organic Compound;Solvent;Organochloride,"1, 3-Butadiene, 1,1,2,3,4,4-hexachloro-1,1,2,3,4, 4-Hexachloro-1,3-butadiene1,1,2,3,4,4-Hexachloro-1,3-butadiene1,1,2,3,4,4-Hexachloro-buta-1,3-diene1,1,2,3,4,4-hexachloro-1,3-butadiene (ACD/Name 4.0)1,1,2,3,4,4-hexachlorobuta-1,3-diene1,3-Butadiene, hexachloro-1,3-HexachlorobutadieneButadiene, hexachloro-Dolen-purHCBHCBDHEXACHLOROBUTADIENE13Hexachlor-1,3-butadienHexachlor-1,3-butadien (CZECH)Hexachlor-1,3-butadien [Czech]HexachlorbutadieneHexachloro-1,3-butadieneHexachlorobuta-1,3-dieneHexachlorobutadieneHexachlorobutadiene [UN2279] [Poison]Hexachlorobutadiene-(1,3)Perchloro-1,3-butadienePerchlorob utadienePerchlorobutadieneRCRA waste no. U128Rcra waste number U128WLN: gyguygyguygg","Hexachlorobutadiene is a man-made chemical primarily produced as a by-product in the production of carbon tetrachloride and tetrachloroethene. It is also used to make rubber compounds, lubricants, in gyroscopes, as a heat transfer liquid, as a hydraulic fluid, and as a solvent.
(R165, R166)",,87-68-3,6901,,C11091,"","",BUTADIENE,,C001335,Hexachlorobutadiene,692,,,,InChI=1/C4Cl6/c5-1(3(7)8)2(6)4(9)10,"1,1,2,3,4,4-hexachlorobuta-1,3-diene",http://www.biospider.ca/saved_files/mol/aa0ebae15ab6917077cfc7681d7b44f6_1237934773.mol,C(=C(Cl)Cl)(C(=C(Cl)Cl)Cl)Cl,C(=C(Cl)Cl)(C(=C(Cl)Cl)Cl)Cl,C4Cl6,257.813120,Colorless liquid.,-21 °C,"","","0.0032 mg/mL at 25 °C [BANERJEE,S et al. (1980)]","","","","Oral 
Inhalation 
Dermal
(R166)","Glutathione S-transferase P (P09211) 
Glutathione S-transferase Mu 1 (P09488) 
Glutathione S-transferase A1 (P08263) 
Glutathione S-transferase theta-2 (P30712) 
Glutathione S-transferase Mu 4 (Q03013) 
Glutathione S-transferase theta-1 (P30711) 
Glutathione S-transferase A4 (O15217) 
Glutathione S-transferase A2 (P09210) 
Glutathione S-transferase A3 (Q16772) 
Glutathione S-transferase Mu 3 (P21266) 
Glutathione S-transferase omega-1 (P78417) 
Glutathione S-transferase kappa 1 (Q9Y2Q3) 
Glutathione S-transferase Mu 2 (P28161) 
Glutathione S-transferase omega-2 (Q9H4Y5) 
Glutathione S-transferase A5 (Q7RTV2) 
Glutathione S-transferase Mu 5 (P46439) 
Glutathione S-transferase theta-4 (A8MPT4) 
Maleylacetoacetate isomerase (O43708) 
Microsomal glutathione S-transferase 1 (P10620) 
Microsomal glutathione S-transferase 2 (Q99735) 
Microsomal glutathione S-transferase 3 (O14880) 
Kynurenine--oxoglutarate transaminase 1 (Q16773) 
Kynurenine--oxoglutarate transaminase 3 (Q6YP21) 
Gamma-glutamyltranspeptidase 1 (P19440) 
Gamma-glutamyltranspeptidase 2 (P36268) 
Putative gamma-glutamyltranspeptidase 3 (A6NGU5) 
Gamma-glutamyltransferase 5 (P36269) 
Gamma-glutamyltransferase 6 (Q6P531) 
Gamma-glutamyltransferase 7 (Q9UJ14) 
(R166)","It is believed that intermediates produced by modification of the S- 1,1,2,3,4-pentachlorodienyl cysteine derivative metabolite by gamma-glutamyltransferase are responsible for the observed effects on the proximal tubules of the nephrons. These metabolites uncouple oxidative phosphorylation, preventing the generation of ATP, and also inhibit cytochrome c-cytochrome oxidase activity and electron transport. The carcinogenic properties of hexachlorobutadiene are proposed to result from binding of the sulfenic acid degradation product or a thioketene intermediate to cellular DNA. The binding of hexachlorobutadiene to alpha 2u-globulin is believed to be an important factor in its nephrotoxicity. (R166, R167)","After absorption, most of the hexachlorobutadiene is carried to the liver, where it is metabolized by a glutathione-mediated pathway. It is initially bioactivated to S-glutathione conjugates which may later be metabolized further by beta-lyases and other enzymes. Hexachlorobutadiene and its metabolites preferentially distribute to the kidney, liver, adipose deposits, and possibly the brain. Metabolites are eventually excreted in the urine and faeces. (R166)","LD50: 90 mg/kg (Oral, Rat) (R263) 
LD50: 175 mg/kg (Intraperitoneal, Rat) (R263) 
LD50: 1211 mg/kg (Dermal, Rabbit) (R263)","","3, not classifiable as to its carcinogenicity to humans. (R264)","Hexachlorobutadiene is primarily produced as a by-product in the production of carbon tetrachloride and tetrachloroethene. It is also used to make rubber compounds, lubricants, in gyroscopes, as a heat transfer liquid, as a hydraulic fluid, and as a solvent. (R166)",Intermediate Oral: 0.0002 mg/kg/day (R260),"Hexachlorobutadiene is damaging to the liver and kidney, and may result in fatty liver degeneration, epithelial necrotizing nephritis, central nervous system depression and cyanosis.
(R165, R166)",Inhalation of hexachlorobutadiene causes nasal irritation and difficulty breathing. (R166),"As there is no antidote for hexachlorobutadiene, exposure is usually treated symptomatically. (R166)",P05090;DNA;P98194;O75185;P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P78334;Q8N1C3;P18507;Q99928;O00591;P24046;P28476;A8MPY1;Q9UN88;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;P54710;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P03372;Q92731
25,T3D0024,2009-03-06 18:57:56 UTC,2009-08-04 21:27:28 UTC,Aldrin,Organic Compound;Pesticide;Organochloride,"AldocitAldrexAldrex 30Aldrex 30 E.C.Aldrex 40Aldrin dustAldrin mixture, DRY (dot)Aldrin mixture, liquid (dot)Aldrin, cast solid (dot)Aldrin, liquid [NA2762] [Poison]Aldrin, solid [NA2761] [Poison]Aldrin-rAldrineAldrine [french]Aldrine(french)AldriteAldronAldrosolAlgranAltoxCaswell No. 012Compound 118DrinoxHHDNHHDN [bsi:iso]HHPNHexachlorohexahydro-endo, exo-dimethanonaphthaleneHexachlorohexahydro-endo,exo-dimethanonaphthaleneHexachlorohexahydro-endo-exo-dimethanonaphthaleneKortofinLatka 118 [Czech]MuraldOctaleneOctalene (van)RCRA waste no. P004RCRA waste number P004SeedrinSoilgrinTatuzinhoTipula","Aldrin is a chlorinated hydrocarbon used as an insecticide. Once in the insect, aldrin is oxidized into dieldrin, a neurotoxin. Due to the toxicity and ability of bioaccumulate of dieldrin, the use of aldrin is now banned in most parts of the world. (R279)",,309-00-2,61103,,C07552,"",25520,"",,D000452,Aldrin,41,,,http://en.wikipedia.org/wiki/Aldrin,"InChI=1/C12H8Cl6/c13-8-9(14)11(16)7-5-2-1-4(3-5)6(7)10(8,15)12(11,17)18/h1-2,4-7H,3H2/t4-,5-,6-,7+,10-,11-/m0/s1","",http://www.biospider.ca/saved_files/mol/96090e949eb1d88e27a59938a5746397_1237934973.mol,C1[C@@H]2C=C[C@@H]1[C@@H]3[C@H]2[C@@]4(C(=C([C@@]3(C4(Cl)Cl)Cl)Cl)Cl)Cl,C1C2C=CC1C3C2C4(C(=C(C3(C4(Cl)Cl)Cl)Cl)Cl)Cl,C12H8Cl6,361.875720,White powder.,104 °C,"","","1.7e-05 mg/mL at 25 °C [YALKOWSKY,SH & DANNENFELSER,RM (1992)]","","","","Oral 
Inhalation 
Dermal
(R155)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 1B1 (Q16678) 
Epoxide hydrolase 1 (P07099) 
Epoxide hydrolase 2 (P34913) 
(R155)","Aldrin antagonizes the action of the neurotransmitter gamma-aminobutyric acid (GABA) acting at the GABA-A receptors, effectively blocking the GABA-induced uptake of chloride ions. Aldrin also inhibits Na+ K+ ATPase and Ca2+ and Mg2+ ATPase which are essential for the transport of calcium across membranes. This results in the accumulation of intracellular free calcium ions, which promotes release of neurotransmitters from storage vesicles, the subsequent depolarization of adjacent neurons, and the propagation of stimuli throughout the CNS. This results in hyperexcitation and generalized seizures. (R029, R155)
","Aldrin is absorbed throught the gastrointestinal tract, lungs and skin. Following absorption, aldrin is redistributed primarily to fat via the lymphatic system. Once in the body, aldrin is readily converted to dieldrin, primarily in the liver by mixed-function oxidases of the cytochrome P-450 system, and to a lesser extent in the lung and skin. Aldrin may also be epoxidized to dieldrin by a prostaglandin synthetase-mediated pathway inextrahepatic tissues. Dieldrin is metabolized by liver microsomal monooxygenases and epoxide hydratases. Its metabolites, of which the primary one is 9-hydroxydieldrin, are excreted in the faeces. (R155)","LD50: 39 mg/kg (Oral, Rat) (R276)
LD50: 98 mg/kg (Dermal, Rat) (R276)
LD50: 150 mg/kg (Intraperitoneal, Rat) (R273)
LD50: 21 mg/kg (Intravenous, Mouse) (R273)",5 to 7 grams for an adult human. (R281),"3, not classifiable as to its carcinogenicity to humans. (R264)",Aldrin is used as an insecticide. (R279),"Acute Oral: 0.002 mg/kg/day (R260)
Chronic Oral: 0.00003 mg/kg/day (R260)","Aldrin is a neurotoxin and works by overstimulating the central nervous system. Ingestion of large amounts of aldrin causes convulsions and death. However, chronic exposure to lower amounts of aldrin also has adverse affects because it is oxidized to dieldrin, which accumulates in the body. Dieldrin is known to damage the nervous system, liver, and immune system. (R155)","Exposure to aldrin results in headaches, dizziness, irritability, nausea and vomiting, cardiac arrhythmias, muscular weakness, uncontrolled muscle movements, hyperexcitability, seizures and coma. (R155)","Treatment is symptomatic, aimed at controlling convulsions, coma, and respiratory depression. If ingested, gastric lavage may be performed, followed by administering activated charcoal powder. (R280)",P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P18507;Q99928;O00591;P24046;P28476;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P54710;P98194;O75185;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;Q8N1C3;A8MPY1;Q9UN88;P78334;P03372;Q92731
26,T3D0025,2009-03-06 18:57:56 UTC,2009-08-14 20:44:13 UTC,"DDD, P,P'-",Organic Compound;Pesticide;Organochloride,"(dichlorodiphenyl)dichloroethane1, 1-Bis(4-chlorophenyl)-2,2-dichloroethane1, 1-Bis(p-chlorophenyl)-2,2-dichloroethane1,1'-(2,2-dichloroethane-1,1-diyl)bis(4-chlorobenzene)1,1'-(2,2-dichloroethylidene)bis[4-chlorobenzene]1,1,1-Trichloro-2,2-bis(p-chlorophenyl)ethane1,1-Bis(4-chlorophenyl)-2,2-dichloroethane1,1-Bis(p-Chlorophenyl)-2,2-dichloroethane1,1-Dichloor-2, 2-bis(4-chloor fenyl)-ethaan (DUTCH)1,1-Dichloor-2,2-bis(4-chloor fenyl)-ethaan1,1-Dichloor-2,2-bis(4-chloor fenyl)-ethaan [Dutch]1,1-Dichlor-2, 2-bis(4-chlor-phenyl)-aethan (GERMAN)1,1-Dichlor-2,2-bis(4-chlor-phenyl)-aethan1,1-Dichlor-2,2-bis(4-chlor-phenyl)-aethan [German]1,1-Dichloro-2, 2-bis(4-chlorophenyl)-ethane (FRENCH)1,1-Dichloro-2, 2-bis(4-chlorophenyl)ethane1,1-Dichloro-2, 2-bis(p-chlorophenyl)ethane1,1-Dichloro-2, 2-di(4-chlorophenyl)ethane1,1-Dichloro-2,2-bis(4'-chlorophenyl)ethane1,1-Dichloro-2,2-bis(4'-chlorophenyl)ethane (DDD)1,1-Dichloro-2,2-bis(4-chlorophenyl)-ethane1,1-Dichloro-2,2-bis(4-chlorophenyl)-ethane [French]1,1-Dichloro-2,2-bis(4-chlorophenyl)ethane1,1-Dichloro-2,2-bis(p-chlorophenyl)ethane1,1-Dichloro-2,2-bis(parachlorophenyl)ethane1,1-Dichloro-2,2-di(4-chlorophenyl)ethane1,1-Dicloro-2, 2-bis(4-cloro-fenil)-etano (ITALIAN)1,1-Dicloro-2,2-bis(4-cloro-fenil)-etano1,1-Dicloro-2,2-bis(4-cloro-fenil)-etano [Italian]1-Chloro-4-[2,2-dichloro-1-(4-chlorophenyl)ethyl]benzene2,2-Bis(4-chlorophenyl)-1,1-dichloroethane2,2-Bis(p-chlorophenyl)-1, 1-dichloroethane2,2-Bis(p-chlorophenyl)-1,1-dichloroethane2,2-bis-(4-chlorophenyl)-1,1-dichloroethane4,4'-DDD solutionBenzene, 1,1'-(2,2-dichloroethylidene)bis(4-chloro-Benzene, 1,1'-(2,2-dichloroethylidene)bis(4-chloro- (9CI)Benzene, 1,1'-(2,2-dichloroethylidene)bis(4-chloro-)Benzene, 1,1'-(2,2-dichloroethylidene)bis*4-chloro-Benzene, 1,1'-(2,2-dichloroethylidene)bis[4-chloro-Benzene, {1,1'-(2,2-dichloroethylidene)bis[4-chloro-}Caswell No. 307DDDDDD(p,p')DDD, p,p'-Dichloro-2,2-bis(p-chlorophenyl)ethaneDichlorodiphenyl dichloroethaneDichlorodiphenyldichloroethaneDileneEthane, 1, 1-dichloro-2,2-bis(p-chlorophenyl)-Ethane, 1,1-dichloro-2,2-bis(p-chlorophenyl)-P, p'-(dichlorodiphenyl)dichloroethaneP,p'-(dichlorodiphenyl)dichloroethaneP,p'-DDDP,p'-dichlorodip henyl dichloroethaneP,p'-dichlorodiphenyl dichloroethaneP,p'-dichlorodiphenyldichloroethaneP,p'-dichlorodiphenyldichloroethane (DDD)P,p'-tdeP,p-DDDP,p[-DDDRCRA waste no. U060RH othaneRcra waste number U060RhothaneRhothane d-3RothaneTDETetrachlorodiphenylethaneWLN: GYGYR dg&r DGp,p'-Dichlorodiphenyl-2,2-dichloroethylene","DDD, P,P'- is an isomer of dichlorodiphenyldichloroethane, an organochlorine insecticide. It is a component of commercial mixtures of DDT. DDT was once a widely used pesticide, but today its agricultural use has been banned worldwide due to its toxicity and tendency to bioaccumulate. However, it still has limited use in disease vector control. (R152)",,72-54-8,6294,,C06636,"",27841,CPD-8985,,D003632,"DDD, P,P'-",379,,,,"InChI=1/C14H10Cl4/c15-11-5-1-9(2-6-11)13(14(17)18)10-3-7-12(16)8-4-10/h1-8,13-14H","1-chloro-4-[2,2-dichloro-1-(4-chlorophenyl)ethyl]benzene",http://www.biospider.ca/saved_files/mol/8da495de62454c8796eb7c3ac8b1aef6_1237935050.mol,C1=CC(=CC=C1C(C2=CC=C(C=C2)Cl)C(Cl)Cl)Cl,C1=CC(=CC=C1C(C2=CC=C(C=C2)Cl)C(Cl)Cl)Cl,C14H10Cl4,317.953660,White solid.,109.5 °C,"","","9e-05 mg/mL at 25 °C [BIGGAR,JW & RIGGS,RI (1974)]","","","",Ingestion (R153),"Cytochrome P450 2B6 (Q16678) 
Cytochrome P450 3A4 (P08684) 
Cytochrome P450 3A5 (P20815) 
Cytochrome P450 3A7 (P24462) 
Cytochrome P450 3A43 (Q9HB55)
(R153)","DDD toxicity occurs via at least four mechanisms, possibly all functioning simultaneously. DDD reduces potassium transport across the membrane. DDD inhibits the inactivation of voltaged-gated sodium channels. The channels activate (open) normally but are inactivated (closed) slowly, thus interfering with the active transport of sodium out of the nerve axon during repolarization and resulting in a state of hyperexcitability. DDD inhibits neuronal adenosine triphosphatases (ATPases), particularly Na+K+-ATPase, and Ca2+-ATPase which play vital roles in neuronal repolarization. DDD also inhibits the ability of calmodulin, a calcium mediator in nerves, to transport calcium ions that are essential for the release of neurotransmitters. All these inhibited functions reduce the rate of depolarization and increase the sensitivity of neurons to small stimuli that would not elicit a response in a fully depolarized neuron. DDD is also believed to adversely affect the reproductive system by mimicking endogenous hormones and binding to the estrogen and adrogen receptors. (R029, R153)","DDD is absorbed in the stomach and intestine, after which it enters the lymphatic system and is carried throughout the body and incorporated into fatty tissues. Metabolism of DDD occurs mainly via cytochrome P-450 enzymes in the liver and kidney. Its metabolites, mainly DDA (bis(p-chlorophenyl) acetic acid), are excreted in the urine. (R153)","LD50: 113 mg/kg (Oral, Rat) (R270)",5 g/kg for an adult human. (R270),"2B, possibly carcinogenic to humans. (R264)","DDD is found in DDT, which is used as a pesticide and in disease vector control. (R152)","","DDT has been shown to cause mild anemia. Exposure to DDT causes loss of weight and anorexia. DDT poisoning affects CNS function in humans, but pathologic changes are observed in the liver and reproductive organs. Hypertrophy of hepatocytes and subcellular organelles such as mitochondria, proliferation of smooth endoplasmic reticulum, centrolobular necrosis after exposure to high concentrations, and an increase in the incidence of hepatic tumors have been noted. (R029)",DDT exposure causes ataxia and abnormal stepping. Acute signs of DDT poisoning include paresthesia after oral ingestion. Studies have shown that a mammal poisoned with DDT-type agents displays periodic persistent tremoring and/or convulsive seizures that are suggestive of repetitive discharges in neurons. These repetitive tremors and seizures can be initiated by tactile and auditory stimuli. (R029),"Treatment of DDT exposure should be primarily directed towards decontamination and supportive care, as there is no specific antidote. The use of gastric lavage and activated charcoal for large ingestions may be effective. (R274)",P10275;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P54710;P98194;O75185;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;P62158;P03372;Q92731;Q9UL51;Q9Y3Q4;O60741;Q9P1Z3 ;P35498;Q9Y5Y9;Q9UI33;Q99250;Q9NY46;P35499;Q14524;Q01118;Q9UQD0;Q15858;Q07699;O60939;Q9NY72;Q8IWT1;P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P78334;Q8N1C3;P18507;Q99928;O00591;P24046;P28476;A8MPY1;Q9UN88
27,T3D0026,2009-03-06 18:57:56 UTC,2009-08-04 21:27:28 UTC,Benzidine,Organic Compound;Aromatic Hydrocarbon;Amine,"(1,1'-Biphenyl)-4,4'-diamine1,1'-Biphenyl-4,4'-Diamine4'-Amino[1,1'-biphenyl]-4-ylamine4'-amino[1,1'-biphenyl]-4-ylamine (ACD/Name 4.0)4, 4'-Biphenylenediamine4,4'-Bianiline4,4'-Biphenyldiamine4,4'-Biphenylenediamine4,4'-Diamino-1,1'-biphenyl4,4'-Diaminobiphenyl4,4'-Diaminodiphenyl4,4'-Diphenylenediamine531-85-1 (DIHYDROCHLORIDE)B1883_SIGMAB3503_SIGMABENZIDINE (SEE ALSO BENZIDINEDIHYDROCHLORIDE 531-85-1)BIPHENYL,4,4'-DIAMINOBensidineBenzidinBenzidin (czech)Benzidin [czech]BenzidinaBenzidina (italian)Benzidina [italian]Benzidine (and its salts)Benzidine [UN1885] [Poison]Benzidine baseBenzidine dihydrochlorideBenzioineBenzydynaBenzydyna (polish)Benzydyna [polish]Biphenyl, 4,4'-diamino-Biphenyl,4, 4'-diamino-Biphenyl,4,4'-diamino-Fast corinth base bP,p'-bianilineP,p'-diaminobiphenylP,p'-dianilineP,p-bianilineP-benzidineP-diaminodiphenylRCRA waste no. U021Rcra waste number U021WLN: ZR dr DZ[1,1'-Biphenyl]-4,4'-diamine[1,1'-biphenyl]-4,4'-diamine (ACD/Name 4.0)biphenyl -4,4'-ylenediaminebiphenyl-4,4'-diamine{[1,} 1'-Biphenyl\]-4,4'-diamine","Benzidine is a manufactured chemical that does not occur naturally. In the environment, benzidine is found either as an organic base or as a salt. Benzidine was used to produce dyes for cloth, paper, and leather, but is no longer produced or used commerically due to its carcinogenicity. (R168)",,92-87-5,7111,,C16444,"","","",,C029876,Benzidine,139,,,http://en.wikipedia.org/wiki/Benzidine,"InChI=1/C12H12N2/c13-11-5-1-9(2-6-11)10-3-7-12(14)8-4-10/h1-8H,13-14H2",4-(4-aminophenyl)aniline,http://www.biospider.ca/saved_files/mol/189a471e89900596b1fee30ba5e8fe9f_1237935133.mol,C1=CC(=CC=C1C2=CC=C(C=C2)N)N,C1=CC(=CC=C1C2=CC=C(C=C2)N)N,C12H12N2,184.100050,White solid.,120 °C,"","","0.322 mg/mL at 25 °C [YALKOWSKY,SH & DANNENFELSER,RM (1992)]","","","","Oral 
Inhalation 
Dermal
(R168)","Prostaglandin G/H synthase 1 (P23219) 
Choline O-acetyltransferase (P28329) 
Carnitine O-acetyltransferase (P43155) 
Arylamine N-acetyltransferase 1 (P18440) 
Arylamine N-acetyltransferase 2 (P11245) 
Arachidonate 5-lipoxygenase (P09917) 
Arachidonate 12-lipoxygenase, 12S-type (P18054) 
Arachidonate 12-lipoxygenase, 12R type (O75342) 
Arachidonate 15-lipoxygenase (P16050) 
Arachidonate 15-lipoxygenase type II (O15296) 
Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
(R168, R169, R170, R171)","N-acetylated benzidine metabolites are believed to form adducts with nucleic acids. Carcinogenesis is initiated when they are activated by peroxidation by prostaglandin H synthetase, oxidation by cytochrome P-450, or O-esterification by O-acetyltransferase or N,O-acetyltransferase. Benzidine has also been shown to bind to RNA and hemoglobin. (R168, R169)","Benzidine is absorpted following inhalation, oral, and dermal routes of exposure. Metabolism involves multiple and complex enzymatic pathways, including cytochrome P-450 and flavin monooxygenase systems, peroxidation by prostaglandin H synthase, and oxidation by lipoxygenases. The main reactions involved are N-acetylation, N-oxidation, and N-glucuronidation. Benzidine and its metabolites are excreted in the urine and faeces. (R168)","LD50: 309 mg/kg (Oral, Rat) (R263) 
LD50: 110 mg/kg (Intraperitoneal, Mouse) (R263)","","1, carcinogenic to humans. (R264)","Benzidine was used to produce dyes for cloth, paper, and leather. (R168)","","Benzidine is a known human carcinogen, most often associated with cancer of the urinary bladder. If benzidine comes in contact with skin it may cause a skin allergy. Liver, kidney, immune, and neurological effects have also been observed in animals exposed to benzidine. (R168)","","",P69905;P68871;P02042;P02100;P69891;P69892;Q6B0K9;P09105;P02008;DNA
28,T3D0027,2009-03-06 18:57:56 UTC,2009-08-11 15:56:26 UTC,Aroclor 1248,Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 3,3',5,5'-tetrachloro-1,1'-Biphenyl, 3,3',5,5'-tetrachloro- (9CI)3,3',5,5'-TETRACHLOROBIPHENYL3,3',5,5'-Tetrachlorodiphenyl3,3',5,5'-tetrachloro-1,1'-biphenyl3,5,3',5'-TetrachlorobiphenylAroclor 1248Biphenyl, 3,3',5,5'-tetrachloro-Biphenyl, 3,3',5,5'-tetrachloro- (8CI)Kanechlor 400Kaneclor 400Polychlorinated biphenyl (kanechlor 400)","Aroclor 1248 is a commercial mixture of PCBs with an average chlorine content of 48%. It is composed of mono- to heptachlorinated homologs. Polychlorinated biphenyls (PCBs) are a group of 209 synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. PCBs were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate in the environment and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,12672-29-6,36400,,"","","","",,C028617,Aroclor 1248,6366,,,,InChI=1/C12H6Cl4/c13-9-1-7(2-10(14)5-9)8-3-11(15)6-12(16)4-8/h1-6H,"1,3-dichloro-5-(3,5-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=C(C=C(C=C1Cl)Cl)C2=CC(=CC(=C2)Cl)Cl,C1=C(C=C(C=C1Cl)Cl)C2=CC(=CC(=C2)Cl)Cl,C12H6Cl4,289.922360,Oily liquids or solids that are colorless to light yellow. ,Boiling Pt : 340-375 °C,"","","0.0001 mg/mL at 20 °C [YALKOWSKY,SH & DANNENFELSER,RM (1992)]","","","","Oral
Inhalation
Dermal 
(R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are transported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 11 g/kg (Oral, Rat) (R263)","","2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refrigerators) produced before 1977. PCBs may contaminate the air and water near hazardouc waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 µg/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptoms can be done. Acute inhalation can be treated by administering oxygen. (R012)",P35869;P49888;P03372;P11684;Q92731;P07101;P20711
29,T3D0028,2009-03-06 18:57:57 UTC,2009-08-26 22:19:50 UTC,Cyanide,Organic Compound;Cyanide Compound;Nitrile,"151-50-8 (POTASSIUM)CN(-)CN-CYNCarbon nitride ionCarbon nitride ion (CN(sup 1-))Carbon nitride ion (cn1-)Chuck norrisiumCyanide (CN(sup 1-))Cyanide (anion)Cyanide (cn1-)Cyanide anionCyanide ionCyanide ionsCyanide standard for icCyanide with potassium saltCyanide(1-)Cyanide(1-) ionCyanide, freeCyanoCyanureCyanure [french]Hydrocyanic acid, ion(1-)Hydrocyanic acid, ion(1-)-IsocyanideNMENitrile anionPotassium cyanidePotassium cyanide - zinc cyanide solutionPrussiateRCRA waste no. P030Rcra waste number P030Zyanidnitridocarbonate(1-)","Certain bacteria, fungi, and algae can produce cyanide, and cyanide is found in a number of foods and plants. Cyanides also occur naturally as part of sugars or other naturally-occurring compounds. (R172)",,57-12-5,5975,,C00177,"",17514,CPD-1074,,,Cyanide,6413,,,http://en.wikipedia.org/wiki/Cyanide,InChI=1/CN/c1-2/q-1,cyanide,http://www.biospider.ca/saved_files/mol/b6f626f0c38d65a6275e7599cb7dd60a_1237935336.mol,[C-]#N,[C-]#N,[CN]-,26.003071,"","","","","","","","","Oral 
Inhalation 
Dermal
(R172)","Thiosulfate sulfurtransferase (Q16762) 
3-mercaptopyruvate sulfurtransferase (P25325) 
(R172)","Cyanide is an inhibitor of cytochrome c oxidase in the fourth complex of the electron transport chain (found in the membrane of the mitochondria of eukaryotic cells). It complexes with the ferric iron atom in this enzyme. The binding of cyanide to this cytochrome prevents transport of electrons from cytochrome c oxidase to oxygen. As a result, the electron transport chain is disrupted and the cell can no longer aerobically produce ATP for energy. Tissues that mainly depend on aerobic respiration, such as the central nervous system and the heart, are particularly affected. Cyanide is also known to produce some of its toxic effects by binding to catalase, glutathione peroxidase, methemoglobin, hydroxocobalamin, phosphatase, tyrosinase, ascorbic acid oxidase, xanthine oxidase, succinic dehydrogenase, and Cu/Zn superoxide dismutase. Cyanide binds to the ferric ion of methemoglobin to form inactive cyanmethemoglobin. (R173)","Cyanide is rapidly absorbed through oral, inhalation, and dermal routes and distributed throughout the body. Cyanide is mainly metabolized into thiocyanate by either rhodanese or 3-mercaptopyruvate sulfur transferase. Cyanide metabolites are excreted in the urine. (R172)","",200 to 300 mg for an adult human (cyanide salts). (R383),,"Cyanide compounds are used in electroplating, metallurgy, organic chemicals production, photographic developing, manufacture of plastics, fumigation of ships, and some mining processes. (R172)","","Exposure to high levels of cyanide for a short time harms the brain and heart and can even cause coma, seizures, apnea, cardiac arrest and death. Chronic inhalation of cyanide causes breathing difficulties, chest pain, vomiting, blood changes, headaches, and enlargement of the thyroid gland. Skin contact with cyanide salts can irritate and produce sores. (R172, R173)","Cyanide poisoning is identified by rapid, deep breathing and shortness of breath, general weakness, giddiness, headaches, vertigo, confusion, convulsions/seizures and eventually loss of consciousness. (R172, R173)","Antidotes to cyanide poisoning include hydroxocobalamin and sodium nitrite, which release the cyanide from the cytochrome system, and rhodanase, which is an enzyme occurring naturally in mammals that combines serum cyanide with thiosulfate, producing comparatively harmless thiocyanate. Oxygen therapy can also be administered. (R173)",P00395;P00403;P00414;P13073;P20674;P10606;P12074;Q02221;P14854;P09669;P24310;P14406;P24311;P15954;P10176;P04040;P07203;P18283;P22352;P36969;O75715;P59796;P14679;Q6YFQ2;Q96KJ9;Q8TF08;Q7Z4L0;Q96SL4;P00441;P05186;P10696;Q99643;O14521;P31040;P21912;P00390;O60397;Q8TED1 ;P08294
30,T3D0029,2009-03-06 18:57:57 UTC,2009-08-11 15:56:25 UTC,Aroclor 1242,Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 2,2',4,4'-tetrachloro-2,2',4,4'-Tetrachlorobiphenyl2,2',4,4'-Tetrachlorodiphenyl2,2',4,4'-tetrachloro-1,1'-biphenyl2,4,2',4'-TetrachlorobiphenylAroclor 1242Biphenyl, 2,2',4,4'-tetrachloro-Chlorierte biphenyle, chlorgehalt 42% [German]Chlorodiphenyl (42% Cl)Chlorodiphenyl (42% chlorine)Chlorodiphenyl, 42% chlorineClorodifenili, cloro 42% [Italian]Diphenyle chlore, 42% de chlore [French]Gechloreerdedifenyl [dutch]Polychlorinated biphenyl (aroclor 1242)Polychlorobiphenyls (42% chlorine)aroclor-1242","Aroclor 1242 is a commercial mixture of PCBs with an average chlorine content of 41.5%. It is composed of mono- to hexachlorinated homologs. Polychlorinated biphenyls (PCBs) are a group of 209 synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. PCBs were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate in the environment and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,53469-21-9,17097,,"","","","",,C027423,Aroclor 1242,,,,,InChI=1/C12H6Cl4/c13-7-1-3-9(11(15)5-7)10-4-2-8(14)6-12(10)16/h1-6H,"2,4-dichloro-1-(2,4-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C=C1Cl)Cl)C2=C(C=C(C=C2)Cl)Cl,C1=CC(=C(C=C1Cl)Cl)C2=C(C=C(C=C2)Cl)Cl,C12H6Cl4,289.922360,Oily liquids or solids that are colorless to light yellow. ,"","","","0.000277 mg/mL at 20 °C [YALKOWSKY,SH & DANNENFELSER,RM (1992)]","","","","Oral
Inhalation
Dermal 
(R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are transported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 4250 mg/kg (Oral, Rat) (R263)","","2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refrigerators) produced before 1977. PCBs may contaminate the air and water near hazardouc waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 µg/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P35869;P49888;P03372;P11684;P20711;P07101;Q92731
32,T3D0031,2009-03-06 18:57:57 UTC,2009-08-04 21:27:29 UTC,Toxaphene,Organic Compound;Pesticide;Organochloride,CamphechlorToxaphene,"Toxaphene is an insecticide containing over 670 chemicals. It was once widenly used, but it is now banned in most areas due to its toxicity and tendency to bioaccumulate in the environment. (R183)",,8001-35-2,5284469,,C15470,"","","",,D014112,Toxaphene,1399,,,,"InChI=1/C10H8Cl8/c1-4-7(2-11,3-12)9(16)6(14)5(13)8(4,15)10(9,17)18/h5-6H,1-3H2","1,2,3,4,7,7-hexachloro-6,6-bis(chloromethyl)-5-methylidenebicyclo[2.2.1]heptane",http://www.biospider.ca/saved_files/mol/,C=C1C(C2(C(C(C1(C2(Cl)Cl)Cl)Cl)Cl)Cl)(CCl)CCl,C=C1C(C2(C(C(C1(C2(Cl)Cl)Cl)Cl)Cl)Cl)(CCl)CCl,C10H8Cl8,407.813420,Yellow solid.,77 °C,"","","0.00055 mg/mL at 20 °C [MURPHY,TJ et al. (1987)]","","","","Oral 
Inhalation
(R183)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (Q16678) 
Cytochrome P450 3A4 (P08684) 
Cytochrome P450 3A5 (P20815) 
Cytochrome P450 3A7 (P24462) 
Cytochrome P450 3A43 (Q9HB55)
(R183)","The main effects of toxaphene are believed to be caused by the over stimulation of the central nervous system. The stimulation is proposed to be the result of the noncompetitive inhibition of gamma-aminobutyric acid-dependent chloride ion channels by various components of toxaphene and its metabolites. Components of toxaphene have also been shown to inhibit sodium/potassium-transporting ATPases, calcium transporting ATPases, adenylate cyclase, and acetylcholinesterase, affecting the nervous system by increasing neuron sensitivity. Toxaphene also activates the estrogen receptors, causing estrogenic effects. (R183, R184, R185, R215)","Toxaphene is absorbed through the intestines and lungs, then distributed mainly to fat tissues. Due to the complex composition of toxaphene, it requires various metabolic pathways to degrade, which involve dechlorination, dehydrodechlorination, and oxidation. Metabolism occurs primarily by hepatic mixed-function oxidases, and metabolites are excreted in the urine and faeces. (R183)","LD50: 50 mg/kg (Oral, Rat) (R283) 
LD50: 600 mg/kg (Dermal, Rat) (R283)",2 to 7 grams for an adult human. (183),"2B, possibly carcinogenic to humans. (R264)",Toxaphene was used as an insecticide. (R183) ,"Acute Oral: 0.005 mg/kg/day (R260)
Intermediate Oral: 0.001 mg/kg/day (R260)","Ingesting or inhaling toxaphene has been shown to cause damage to the lungs, nervous system, kidneys, liver, adrenal glands, and immune system. It is also known to cause developmental defects. (R183)","","",P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P18507;Q99928;O00591;P24046;P28476;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P54710;P03372;Q92731;Q8N1C3;A8MPY1;Q9UN88;P98194;O75185;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;Q08828;Q96PN6;Q08462;O60266;Q8NFM4;O95622;O43306;P51828;P40145;O60503;P22303;P78334
33,T3D0032,2009-03-06 18:57:57 UTC,2009-08-04 21:27:29 UTC,"Hexachlorocyclohexane, gamma-",Organic Compound;Pesticide;Organochloride,"«gamma»-BHC«gamma»-HCH«gamma»-benzene hexachloride«gamma»-hexachloran«gamma»-hexachlorane«gamma»-hexachlorobenzene«gamma»-hexachlorocyclohexane«gamma»-lindane«gamma»1,2,3,4,5,6-Hexachlorocyclohexane(1R,2R,3R,4R,5S,6S)-1,2,3,4,5,6-hexachlorocyclohexane(1R,2R,3S,4S,5S,6S)-1,2,3,4,5,6-hexachlorocyclohexane(1r,2R,3S,4r,5R,6S)-1,2,3,4,5,6-hexachlorocyclohexane(1r,2R,3S,4s,5R,6S)-1,2,3,4,5,6-hexachlorocyclohexane(1r,2c,3c,4t,5c,6t)-1,2,3,4,5,6-hexachlorocyclohexane(1r,2c,3t,4t,5c,6t)-1,2,3,4,5,6-hexachlorocyclohexane(1r,2r,3r,4r,5r,6r)-1,2,3,4,5,6-hexachlorocyclohexane(1s,2R,3R,4s,5S,6S)-1,2,3,4,5,6-hexachlorocyclohexane1,2,3,4,5,6-«gamma»-Hexachlorocyclohexane1,2,3,4,5,6-Hexachlorocyclohexane1,2,3,4,5,6-Hexachlorocyclohexane («gamma»)1,2,3,4,5,6-Hexachlorocyclohexane (all stereo isomers)1,2,3,4,5,6-Hexachlorocyclohexane (mixture of isomers)1,2,3,4,5,6-Hexachlorocyclohexane gamma isomer1,2,3,4,5,6-Hexachlorocyclohexane, gamma-isomer1,2,3,4,5,6-hexachlorocyclohexane, alpha isomer1a,2a,3b,4a,5b,6b-hexachlorocyclohexane1a,2b,3a,4b,5a,6b-hexachlorocyclohexaneAalindanAficideAgrocideAgrocide IIIAgrocide WPAgronexitAlpha- BHCAlpha-BHCAlpha-HCHAlpha-HCH [hexachlorocyclohexanes]Alpha-HCH solutionAlpha-benzene hexachlorideAlpha-benzenehexachlorideAlpha-hexachloranAlpha-hexachloraneAlpha-hexachlorocyclohexaneAlpha-hexachlorocyclohexanesAlpha-lindaneAm eisenatodAmeisenatodAmeisenmittel merckAmeisentodAparasinAphtiriaAphtitriaAplidalArbitexArcotal sAtlas stewardBBHBCHBHCBHC (alpha-, beta-, gamma-)BHC (insecticide)BHC insecticideBHC or HCHBHC(«gamma»)Ben-hexBenhexachlorBenhexolBentox 10BenzanexBenzene hexachlorideBenzene hexachloride (ambiguous)Benzene hexachloride, «gamma»Benzene hexachloride, all isomersBenzene hexachloride-alpha-isomerBenzene hexachloride-gamma isomerBenzene hexachloride-gamma-isomerBenzene-1,2,3,4,5,6-hexachloride ((Ambiguous)Benzene-cis-hexachlorideBenzene-trans-hexachlorideBenzenehexachloride, mixed isomersBenzenehexachloride-alpha-isomerBenzexBeta-BHCBeta-HCHBeta-HCH [hexachlorocyclohexanes]Beta-HCH solutionBeta-benzene hexachlorideBeta-hexac hlorocyclohexaneBeta-hexachloranBeta-hexachlorobenzeneBeta-hexachlorocyclohexaneBeta-hexachlorocyclohexanesBeta-isomerBeta-lindaneBexolBorer sprayCPD with unspecified stereochemistryCaswell No. 079Caswell No. 527CelanexChinoin brand of lindaneChloreseneCodechineCyclohexane, 1,2,3,4,5,6-hexachloro-Cyclohexane, 1,2,3,4,5,6-hexachloro-, «gamma»-Cyclohexane, 1,2,3,4,5,6-hexachloro-, (mixed isomers)Cyclohexane, 1,2,3,4,5,6-hexachloro-, alpha-Cyclohexane, 1,2,3,4,5,6-hexachloro-, alpha-isomerCyclohexane, 1,2,3,4,5,6-hexachloro-, beta-isomerCyclohexane, 1,2,3,4,5,6-hexachloro-, delta-Cyclohexane, 1,2,3,4,5,6-hexachloro-, delta-isomerCyclohexane, 1,2,3,4,5,6-hexachloro-, gamma-Cyclohexane, 1,2,3,4,5,6-hexachloro-, gamma-isomerCyclohexane, beta-1,2,3,4,5,6-hexachloro-Cyclohexane, delta-1,2,3,4,5,6-hexachloro-DBHDelitexDelta-BHCDelta-HCHDelta-benzene hexachlorideDelta-benzenehexachlorideDelta-hexachlorocyclohexaneDelta-lindaneDetmol extractDetmol-extraktDevoranDol granuleDolmixDrill tox-spezial aglukonDrilltox-spezial aglukonEntomoxanEpsilon HCHEpsilon-HCHEpsilon-hexachlorocyclohexaneEso dermEsodermExagamaFenoform forteForlinForst-nexenFumite lindaneGallogamaGamacarbatoxGamacidGamacideGamacide 20GamaphexGameneGamisoGamma 666Gamma BHCGamma benzene hexachlorideGamma hexachlorGamma hexachlorocyclohexaneGamma-666Gamma-:hexachlorocyclohexaneGamma-BHCGamma-BHC (lindane)Gamma-BHC benhexachlorGamma-BHC dustGamma-HCHGamma-HCH [hexachlorocyclohexanes]Gamma-HCH dustGamma-HCH or gamma-BHCGamma-benzene hexachlorideGamma-benzenehexachlorideGamma-benzohexachlorideGamma-colGamma-hexachloraneGamma-hexachlorcyclohexanumGamma-hexachlorobenzeneGamma-hexachlorocyclohexaneGamma-linda neGamma-lindaneGamma-mean 400Gamma666GammahexaGammahexaneGammalinGammalin 20GammasanGammaterrGammexGammexaneGammopazGamtoxGeobilanGexaneGybenH.c.hHCCHCCHHCHHCH (alpha)HCH (beta)HCH [bsi]HCH [iso]HCH, technical grade [hexachlorocyclohexanes]HEXAHGIHeclotoxHecoltoxHexablancHexachlorHexachloranHexachloraneHexachlorcyclohexanHexachlorcyclohexan [german]Hexachloride, benzeneHexachloride, gamma-benzeneHexachlorocyclohexaneHexachlorocyclohexane (all isomers)Hexachlorocyclohexane (mixed isomers)Hexachlorocyclohexane (mixture)Hexachlorocyclohexane (technical grade)Hexachlorocyclohexane, alpha-Hexachlorocyclohexane, beta-Hexachlorocyclohexane, delta-Hexachlorocyclohexane, gamma isomerHexachlorocyclohexane, gamma-Hexachlorocyclohexane, gamma-isomerHexachlorocyclohexane, technicalHexachlorocyclohexane, technical gradeHexachlorocyclohexane,«gamma»-isomerHexachlorocyclohexane-alphaHexachlorocyclohexane-betaHexachlorocyclohexanesHexachlorzyklohexanHexamulHexapoudreHexatoxHexavermHexcidumHexicideHexit Shampoo 1.0%Hexit lotionHexyclanHilbeec hHilbeechHortexInexitInfectopharm brand of lindaneInsecticide, BHCIsatoxIsot oxIsotoxJacutinKokotineKwellKwell-rLacco hi linLasochronLatka 666 [Czech]LendineLentoxLidenalLindaforLindagamLindagrainLindagranoxLindaloLindam ulLindamulLindane (benzene hexachloroide-gamma isomer)Lindane (g-BHC)Lindane (gamma-HCH)Lindane [hexachlorocyclohexanes]Lindane [usan:inn:ban]Lindano [inn-spanish]Lindanum [inn-latin]LindapoudreLindaterraLindatoxLindexLindosepLintoxLinvurLorexaneMglawik lMilbol 49Mixture nameMszycolMurfume grain store smokeNeo-scabicidolNew kotolNexen FBNexen-FBNexi t-starkNexitNexit-starkNexol-eNicochloranNovigamNoviganOmnitoxOvadziakOwadziakPLKPMS lindanePMS-lindanePS71_SUPELCOPedraczakPflanzolPharmascience brand of lindanePms-Lindane Lot 1%Pms-Lindane Shp 1%PmslindaneQuelladaRCRA waste no. U129RCRA waste number U129Sang gammaSang-«gamma»ScabecidScabeneScabene lotionScabisanSilvanolSpritz-rapidinSpritzlindaneSpruehpflanzolStiefel brand of lindaneStreunexSubmarT-HCHTBHTechnical HCHTechnical hexachlorocyclohexaneTetocidTrans-alpha-benzenehexachlorideTri-6Trives-tVerindal ultraVitonagrisol g-20agrocide 2agrocide 6gagrocide 7alpha-1,2,3,4,5,6-Hexachlorocyclohexanebeta-1,2,3,4,5,6-Hexachlorocyclohexanedelta-(Aeeeee)-1,2,3,4,5,6-hexachlorocyclohexanedelta-1,2,3,4,5,6-Hexachlorocyclohexanedetox 25g-1,2,3,4,5,6-Hexachlorocyclohexanegamma-1,2,3,4,5,6-Hexachlorocyclohexanegeolin g 3hungaria l7","Hexachlorocyclohexane, Gamma- is one of eight isoforms of the commercially manufactured chemical hexachlorocyclohexane. It is used as an insecticide on fruit, vegetables, and forest crops and is also available as a prescription (lotion, cream, or shampoo) to treat head and body lice, and scabies. (R186)",,58-89-9,727,,C06988,"",32888,GAMMA-HCH,,D001556,"Hexachlorocyclohexane, gamma-",695,,,http://en.wikipedia.org/wiki/Lindane,"InChI=1/C6H6Cl6/c7-1-2(8)4(10)6(12)5(11)3(1)9/h1-6H/t1-,2-,3+,4+,5-,6-","1,2,3,4,5,6-hexachlorocyclohexane",http://www.biospider.ca/saved_files/mol/7f0d48cdd4a476e9de202b4063e18374_1237935760.mol,C1(C(C(C(C(C1Cl)Cl)Cl)Cl)Cl)Cl,C1(C(C(C(C(C1Cl)Cl)Cl)Cl)Cl)Cl,C6H6Cl6,287.860070,White solid or colorless vapor.,112.5 °C,"","","0.0073 mg/mL at 25 °C [RICHARDSON,LT & MILLER,DM (1960)]","","","","Oral 
Inhalation 
Dermal
(R186)","Cytochrome P450 2E1 (P05181) 
Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
(R186)","Hexachlorocyclohexane is a neurotoxin that interferes with GABA neurotransmitter function by interacting with the GABA-A receptor-chloride channel complex at the picrotoxin binding site, causing over stimulation of the central nervous system. It is also believed to inhibit sodium/potassium-transporting ATPases and be an endocrine disruptor. In the liver, hexachlorocyclohexane is thought to cause oxidative stress by interfering with hepatic oxidative capacity and glutathione metabolism, increasing lipid metabolism, and inhibiting magnesium ATPase activity. Hexachlorocyclohexane may also inhibit gap junction and intercellular communication, leading to uncontrolled cell growth and tumor promotion. (R186, R187, R188)","Hexachlorocyclohexane is absorbed through the skin, lungs, and intestines, then distributed mainly to the adipose tissue but also to the brain, kidney, muscle, and blood. Metabolism occurs via dechlorination, dehydrogenation, dehydrochlorination, and hydroxylation by hepatic cytochrome P-450 enzymes. The main metabolites are polychlorophenols and 1,2,4-trichlorocyclohexane-4,5-epoxide, which are excreted in the urine. (R186)","LD50: 76 mg/kg (Oral, Rat) (R263)
LD50: 50 mg/kg (Dermal, Rabbit) (R263)
LD50: 125 mg/kg (Intraperitoneal, Mouse) (R263)",28 g for an adult human. (R270),"2B, possibly carcinogenic to humans. (R264)","Hexachlorocyclohexane is used as an insecticide on fruit, vegetables, and forest crops and is also available as a prescription (lotion, cream, or shampoo) to treat head and body lice, and scabies. (R186)","Acute Oral: 0.003 mg/kg/day (R260)
Intermediate Oral: 0.00001 mg/kg/day (R260)","Exposure to large amounts of hexachlorocyclohexane can harm the nervous system, producing a range of symptoms from headache and dizziness to seizures, convulsions and more rarely death. Hexachlorocyclohexane is known to damage the liver, kidneys, and immune system, as well as cause blood disorders and reproductive and developmental defects. Hexachlorocyclohexane is also potentially carcinogenic. (R186, R187)","Exposure to large amounts of hexachlorocyclohexane can harm the nervous system, producing a range of symptoms from headache and dizziness to seizures, convulsions and more rarely death. (R187)","Hexachlorocyclohexane poisoning is treated symptomatically. Gastric lavage, followed by the administration of activated charcoal, may be performed upon ingestion. (R284)",P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P18507;Q99928;O00591;P24046;P28476;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P54710;P62508;P10275;P06401;Q8N1C3;A8MPY1;Q9UN88;P78334;P98194;O75185;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;P03372;Q92731
34,T3D0033,2009-03-06 18:57:57 UTC,2009-08-04 21:27:29 UTC,Tetrachloroethylene,Organic Compound;Solvent;Organochloride,"1,1,2, 2-Tetrachloroethylene1,1,2,2-Tetrachloroethene1,1,2,2-Tetrachloroethylene1,1,2,2-tetrachloroethylene (ACD/Name 4.0)AnkilostinAntisal 1Antisol 1Carbon bichlorideCarbon dichlorideCaswell No. 827CzterochloroetylenCzterochloroetylen [polish]Czterochloroetylen(polish)DidakeneDilatin PTDistillex DS4Dow-perDowperEthene, tetrachloro-Ethylene tetrachlorideEthylene, tetrachloro-Fedal-unNEMANema (van)Nema, veterinaryPCEPERPERCPERKPerawi nPerawinPerchloorethyleen, perPerchloorethyleen, per [dutch]Perchloorethyleen, per(dutch)PerchlorPerchloraethylen, perPerchloraethylen, per [german]Perchloraethylen, per(german)PerchlorethylenePerchlorethylene, perPerchlorethylene, per [french]Perchlorethylene, per(french)PerchloroethylenePerclenePerclene TGPerclene dPercloroetilenePercloroetilene [italian]Percloroetilene(italian)PercosolvPercosolvePerklonePersecRCRA waste no. U210Rcra waste number U210TCETetlenTetracapTetrachlooretheenTetrachlooretheen [dutch]Tetrachlooretheen(dutch)TetrachloraethenTetrachloraethen [german]Tetrachloraethen(german)TetrachlorethyleneTetrachloroetheneTetrachloroethylene (iupac)Tetrachloroethylene [UN1897] [Poison]TetracloroeteneTetracloroetene [italian]Tetracloroetene(italian)TetraguerTetralenoTetralexTetravecTetrochloroethaneTetroguerTetropilWLN: gyguygg","Tetrachloroethylene is a manufactured chlorocarbon. It is widely used for dry cleaning of fabrics and for metal-degreasing. It is also used to make other chemicals and is used in some consumer products, such as paint strippers and spot removers. (R198)",,127-18-4,31373,,C06789,"",17300,TETRACHLOROETHENE,,D013750,Tetrachloroethylene,1350,,,http://en.wikipedia.org/wiki/Tetrachloroethylene,InChI=1/C2Cl4/c3-1(4)2(5)6,"1,1,2,2-tetrachloroethene",http://www.biospider.ca/saved_files/mol/d357c496b520067b32e79974ca525b1d_1237935959.mol,C(=C(Cl)Cl)(Cl)Cl,C(=C(Cl)Cl)(Cl)Cl,C2Cl4,163.875410,Colorless liquid.,-22.3 °C,"","","0.206 mg/mL at 25 °C [HORVATH,AL et al. (1999)]","","","","Oral 
Inhalation 
Dermal
(R198)","Glutathione S-transferase P (P09211) 
Glutathione S-transferase Mu 1 (P09488) 
Glutathione S-transferase A1 (P08263) 
Glutathione S-transferase theta-2 (P30712) 
Glutathione S-transferase Mu 4 (Q03013) 
Glutathione S-transferase theta-1 (P30711) 
Glutathione S-transferase A4 (O15217) 
Glutathione S-transferase A2 (P09210) 
Glutathione S-transferase A3 (Q16772) 
Glutathione S-transferase Mu 3 (P21266) 
Glutathione S-transferase omega-1 (P78417) 
Glutathione S-transferase kappa 1 (Q9Y2Q3) 
Glutathione S-transferase Mu 2 (P28161) 
Glutathione S-transferase omega-2 (Q9H4Y5) 
Glutathione S-transferase A5 (Q7RTV2) 
Glutathione S-transferase Mu 5 (P46439) 
Glutathione S-transferase theta-4 (A8MPT4) 
Maleylacetoacetate isomerase (O43708) 
Microsomal glutathione S-transferase 1 (P10620) 
Microsomal glutathione S-transferase 2 (Q99735) 
Microsomal glutathione S-transferase 3 (O14880) 
Cytochrome P450 2B6 (P20813) 
(R198)","Tetrachloroethylene is believed to affect the central nervous system by altering the fatty acid pattern of brain phospholipids and amino acids, or being incorporated into brain membranes, which may alter neural conduction velocity. Tetrachloroethylene's liver toxicity is caused mainly by its metabolite, trichloroacetic acid (TCA), which induces hepatocellular peroxisomes, causing DNA damage and leading to liver cancer. It is also thought to interfere specifically with energy-dependent hepatic transport functions by inhibiting cell membrane ATPases and decreasing hepatocyte ATP levels. (R198, R199)","Tetrachloroethylene is readily absorbed following inhalation, oral, and dermal exposure. Once tetrachloroethylene is absorbed, its relatively high lipophilicity results in distribution to
fatty tissue. Some tetrachloroethylene is metabolized to trichloroacetic acid (TCA) by cytochrome P-450 enzymes and the glutathione-conjugation pathway, then excreted in the urine. The remaining unmetabolized tetrachloroethylene is exhaled. (R198)","LD50: 3835 mg/kg (Oral, Rat) (R198)
LD50: 4678 mg/kg (Intraperitoneal, Rat) (R276)",2857 mg/kg for an adult human. (R261),"2A, probably carcinogenic to humans. (R264)","Tetrachloroethylene is used for dry cleaning of fabrics and for metal-degreasing. It is also used to make other chemicals and is used in some consumer products, such as paint strippers and spot removers. (R198)","Acute Inhalation: 2 ppm (R260)
Intermediate Inhalation: 0.1 ppm (R260)
Acute Oral: 0.2 mg/kg/day (R260)","Tetrachloroethylene is a central nervous system depressant. It is also known to cause liver and kidney damage, and is a probably carcinogen. (R198)","Exposure to high concentrations of tetrachloroethylene can cause dizziness, headache, sleepiness, confusion, nausea, difficulty in speaking and walking, unconsciousness, and death. Irritation may result from repeated or extended skin contact with it. (R198)","Tetrachloroethylene has no known antidote, and exposure is usually treated symptomatically. (R198)",P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P54710;P98194;O75185;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P78334;Q8N1C3;P18507;Q99928;O00591;P24046;P28476;A8MPY1;Q9UN88;P03372;Q92731
35,T3D0034,2009-03-06 18:57:57 UTC,2009-08-04 21:27:29 UTC,Heptachlor,Organic Compound;Pesticide;Organochloride,"1,4,5,6,7,8,8-Heptachlorotetrahydro-4,7-methanoindene3,4,5,6,7,8,8-Heptachlorodicyclopentadiene3,4,5,6,7,8,8a-Heptachlorodicyclopentadiene3-Chlorochlordene:heptachlorAaheptaAgroceresArbinex 30TNBasaklorCaswell No. 474Dicyclopentadiene, 3,4,5,6,7,8, 8a-heptachloro-Dicyclopentadiene, 3,4,5,6,7,8,8a-heptachloro-DrinoxDrinox H-34EptacloroEptacloro (italian)Eptacloro [italian]GPKHGold Crest H-60, TermideHeptaHepta klorHeptachloorHeptachloor (dutch)Heptachloor [dutch]Heptachlor (technical grade)Heptachlor [bsi:iso]Heptachlor and metabolitesHeptachlor solutionHeptachloraneHeptachloreHeptachlore (french)Heptachlore [french]Heptachlore [iso-french]Heptachlorotetrahydro-4, 7-methanoindeneHeptachlorotetrahydro-4,7-methanoindeneHeptagranHeptagranoxHeptaklorHeptamakHeptamulHeptasolHeptoxLatka 104Latka 104 [Czech]RCRA waste no. P059Rcra waste number P059RhodiachlorSoleptaxTechnical heptachlorTetrahydroVelsicol 104Velsicol heptachlorWLN: L C555 A DU IUTJ AG AG BG FG HG IG JGalpha-Dicyclopentadiene, 3,4,5,6,7,8,8A-heptachloro-","Heptachlor is a manufactured cyclodiene organochlorine insecticide. As it is a persistant organic pollutant, heptachlor use is banned or limited in most areas. (R218, R219)",,76-44-8,3589,,C14185,"",34785,"",,D006533,Heptachlor,688,,,http://en.wikipedia.org/wiki/Heptachlor,"InChI=1/C10H5Cl7/c11-4-2-1-3-5(4)9(15)7(13)6(12)8(3,14)10(9,16)17/h1-5H/t3?,4?,5?,8-,9+/m0/s1","",http://www.biospider.ca/saved_files/mol/0e8f92fceca5c9b8e144bebbc110e8ef_1237936085.mol,C1=CC(C2C1C3(C(=C(C2(C3(Cl)Cl)Cl)Cl)Cl)Cl)Cl,C1=CC(C2C1C3(C(=C(C2(C3(Cl)Cl)Cl)Cl)Cl)Cl)Cl,C10H5Cl7,369.821090,White or tan powder.,95.5 °C,,,"0.00018 mg/mL at 25 °C [BIGGAR,JW & RIGGS,RI (1974)]",,,,"Oral 
Inhalation 
Dermal
(R218)","Alkaline phosphatase (P05186) 
Cytochrome P450 19A1 (P11511) 
Cytochrome P450 19A2 (P05177) 
(R218)","Heptachlor is a central nervous system stimulant. It non-competitively blocks neurotransmitter action at gamma-amino butyric acid receptors, resulting in overstimulation of the nervous system. Heptachlor is also believed to exert carcinogenic effects by activating key kinases in signalling pathways and inhibiting apoptosis. (R218, R220, R221)","Heptachlor is readily absorbed by the skin, lungs and gastrointestinal tract. It is readily metabolized by liver microsomes into heptachlor epoxide, its most persistent and toxic metabolite, which is mainly stored in adipose tissue. Heptachlor epoxide is excreted in the urine and faeces. (R218)","LC50: 150 mg/kg over 4 hours (Inhalation, Cat) (R285)
LD50: 500-2000 mg/kg (Dermal, Rabbit) (R285)
LD50: 80-90 mg/kg (Oral, Rabbit) (R285)
LD50: 27 mg/kg (Intraperitoneal, Rat) (R285)",,"2B, possibly carcinogenic to humans. (R264)","Heptachlor was originally widely produced as an insecticide, but is now used only in fire ant control in underground transformers. (R218)","Acute Oral: 0.0006 mg/kg/day (R260)
Intermediate Oral: 0.0001 mg/kg/day (R260)","Exposure to heptachlor may cause damage to your liver, nervous system, and immune system. (R218)","Heptachlor poisoning may cause convulsions, vomiting, seizures, confusion, incoordination, excitability, coma, hypotension, and respiratory failure. (R218)","Treatment is symptomatic and is aimed at controlling convulsions, coma, and respiratory depression. (R218)
",P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;Q8N1C3;P18507;Q99928;O00591;P24046;P28476;A8MPY1;Q9UN88;P78334;P98194;O75185;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;P54710;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P03372;Q92731
36,T3D0035,2009-03-06 18:57:57 UTC,2009-08-11 14:27:43 UTC,"1,2-Dibromoethane",Organic Compound;Pesticide;Gasoline Additive/Component;Organochloride,"α,β-dibromoethane.alpha.,.beta.-dibromoethane1,2 Dibromoethane1,2,Dibromoethane1,2-DIBROMO TETRADEUTERO ETHANE1,2-Dibromaethan1,2-Dibromaethan [German]1,2-Dibromoetano1,2-Dibromoetano [Italian]1,2-Dibromoethane1,2-Dibromoethane solution1,2-Dibromoethane(Ethylene bromide)1,2-Dibromomethane1,2-Dibroomethaan1,2-Dibroomethaan [Dutch]1,2-Ethylene dibromide1,2-dibromoethane (EDB)AadibroomAethylenbromidAethylenbromid [german]Alpha,beta-dibromoethaneAlpha,omega-dibromoethaneBromide, ethyleneBromofumeBromuro di etileBromuro di etile [italian]CH2BrCH2BrCaswell No. 439CelmideDBEDibromide, ethyleneDibromides, ethyleneDibromoet haneDibromoethaneDibromoethane, 1,2-DibromoethyleneDibromure d'ethyleneDibromure d'ethylene [french]Dibromure d'ethylene [iso-french]DowfumeDowfume 40Dowfume W 85Dowfume W-100Dowfume W-8Dowfume W-85Dowfume W-90Dowfume W85Dowfume edbDwubromoetanDwubromoetan [polish]E-d-beeEDBEdabromEthylene bromideEthylene dibromideEthylene dibromide [UN1605] [Poison]Ethylene dibromide [bsi:iso]Ethylene dibromidesFumo-gasGarden dowfumeGlycol bromideGlycol dibromideIscobrome dKopfumeNefisNephisPestmasterPestmaster edb-85RCRA waste no. U067Rcra waste number U067SYM dibromoethaneSYM-dibromoethaneSanhyuumSoilbromSoilbrom 90ECSoilbrom-100Soilbrom-40Soilbrom-85Soilbrom-90Soilbrom-90ecSoilbrome-85SoilfumeUnifume","1,2-Dibromoethane is a mainly synthetic chemical that also occurs in small amounts naturally in the ocean. It was once widely used as an additive in leaded gasoline and a pesticide, however, today it's use is restricted to only certain pesticides and dye preparations. (R222)",,106-93-4,7839,,C11088,"",28534,CPD-8985,,D015946,"1,2-Dibromoethane",418,,,,InChI=1/C2H4Br2/c3-1-2-4/h1-2H2,"1,2-dibromoethane",http://www.biospider.ca/saved_files/mol/a39d3bb4b587630d5698bc9eb983ca6b_1237936224.mol,C(CBr)Br,C(CBr)Br,C2H4Br2,185.867980,Colorless liquid.,9.9 °C,,,"3.91 mg/mL at 25 °C [HORVATH,AL et al. (1999)]",,,,"Oral 
Inhalation 
Dermal
(R222)","Glutathione S-transferase P (P09211) 
Glutathione S-transferase Mu 1 (P09488) 
Glutathione S-transferase A1 (P08263) 
Glutathione S-transferase theta-2 (P30712) 
Glutathione S-transferase Mu 4 (Q03013) 
Glutathione S-transferase theta-1 (P30711) 
Glutathione S-transferase A4 (O15217) 
Glutathione S-transferase A2 (P09210) 
Glutathione S-transferase A3 (Q16772) 
Glutathione S-transferase Mu 3 (P21266) 
Glutathione S-transferase omega-1 (P78417) 
Glutathione S-transferase kappa 1 (Q9Y2Q3) 
Glutathione S-transferase Mu 2 (P28161) 
Glutathione S-transferase omega-2 (Q9H4Y5) 
Glutathione S-transferase A5 (Q7RTV2) 
Glutathione S-transferase Mu 5 (P46439) 
Glutathione S-transferase theta-4 (A8MPT4) 
Maleylacetoacetate isomerase (O43708) 
Microsomal glutathione S-transferase 1 (P10620) 
Microsomal glutathione S-transferase 2 (Q99735) 
Microsomal glutathione S-transferase 3 (O14880) 
Cytochrome P450 2E1 (P05181) 
(R222)","The metabolite 2-bromoacetaldehyde produces liver damage by binding to cellular proteins. S-(2-bromoethyl)glutathione, another metabolite, exerts genotoxic and carcinogenic effects by binding to DNA. Antispermatogenic effects of 1,2-dibromoethanes metabolites may be caused by their covalent binding to thiol groups of nucleoproteins in nuclei of spermatozoa. Such adduct formation interferes with DNA, causing improper packing of the chromatin. (R222)","1,2-Dibromoethane is rapidly absorbed by ingestion, inhalation, and dermal routes, then distributed mainly to the kidneys, liver, and spleen. It can be metabolized by either the cytochrome P-450 system or the glutathione  S-transferase system. Many of the metabolites are toxic, and include 2-bromoacetaldehyde and S-(2-bromoethyl)glutathione. These metabolites may be further broken down and excreted in the urine. (R222)","LD50: 108 mg/kg (Oral, Rat) (R263)
LD50: 300 mg/kg (Dermal, Rat) (R263) 
LD50: 220 mg/kg (Intraperitoneal, Mouse) (R263) 
LC50: 14300 mg/m3 over 30 mins (Inhalation, Rat) (R263)","","2A, probably carcinogenic to humans. (R264)","1,2-Dibromoethane was once widely used as an additive in leaded gasoline and a pesticide, however, today it's use is restricted to only certain pesticides (treatment of logs for termites and beetles, control of moths in beehives) and dye preparations. (R222)",,"Long term exposure can result in liver, kidney, and reproductive system damage. 1,2-Dibromoethane is also known to have adverse effects on the brain. (R222)","Redness and inflammation, including skin blisters and mouth and stomach ulcers, can occur if large amounts of 1,2-dibromoethaneare are swallowed. Breathing high levels may cause depression and collapse. (R222)","",P02768;DNA;P03372;Q92731
37,T3D0036,2009-03-06 18:57:58 UTC,2009-08-04 21:27:30 UTC,"Hexachlorocyclohexane, beta-",Organic Compound;Pesticide;Organochloride,"β,1,2,3,4,5,6-Hexachlorocyclohexaneβ-BHCβ-HCHβ-benzene hexachlorideβ-hexachlorocyclohexaneβ-lindane(1R,2R,3R,4R,5S,6S)-1,2,3,4,5,6-hexachlorocyclohexane(1R,2R,3S,4S,5S,6S)-1,2,3,4,5,6-hexachlorocyclohexane(1r,2R,3S,4r,5R,6S)-1,2,3,4,5,6-hexachlorocyclohexane(1r,2R,3S,4s,5R,6S)-1,2,3,4,5,6-hexachlorocyclohexane(1r,2c,3c,4t,5c,6t)-1,2,3,4,5,6-hexachlorocyclohexane(1r,2c,3t,4t,5c,6t)-1,2,3,4,5,6-hexachlorocyclohexane(1r,2r,3r,4r,5r,6r)-1,2,3,4,5,6-hexachlorocyclohexane(1s,2R,3R,4s,5S,6S)-1,2,3,4,5,6-hexachlorocyclohexane1,2,3,4,5,6-Hexachlorocyclohexane1,2,3,4,5,6-Hexachlorocyclohexane (all stereo isomers)1,2,3,4,5,6-Hexachlorocyclohexane (mixture of isomers)1,2,3,4,5,6-Hexachlorocyclohexane gamma isomer1,2,3,4,5,6-Hexachlorocyclohexane, gamma-isomer1,2,3,4,5,6-hexachlorocyclohexane, alpha isomer1a,2a,3b,4a,5b,6b-hexachlorocyclohexane1a,2b,3a,4b,5a,6b-hexachlorocyclohexaneAalindanAficideAgrocideAgrocide IIIAgrocide WPAgronexitAlpha- BHCAlpha-BHCAlpha-HCHAlpha-HCH [hexachlorocyclohexanes]Alpha-HCH solutionAlpha-benzene hexachlorideAlpha-benzenehexachlorideAlpha-hexachloranAlpha-hexachloraneAlpha-hexachlorocyclohexaneAlpha-hexachlorocyclohexanesAlpha-lindaneAm eisenatodAmeisenatodAmeisenmittel merckAmeisentodAparasinAphtiriaAphtitriaAplidalArbitexArcotal sBBHBCHBHCBHC βBHC (alpha-, beta-, gamma-)BHC (insecticide)BHC insecticideBHC or HCHBHC-β isomerBen-hexBenhexachlorBenhexolBenzanexBenzene hexachlorideBenzene hexachloride (ambiguous)Benzene hexachloride, all isomersBenzene hexachloride-alpha-isomerBenzene hexachloride-gamma isomerBenzene hexachloride-gamma-isomerBenzene-1,2,3,4,5,6-hexachloride ((Ambiguous)Benzene-cis-hexachlorideBenzene-trans-hexachlorideBenzenehexachloride, mixed isomersBenzenehexachloride-alpha-isomerBenzexBeta-BHCBeta-HCHBeta-HCH [hexachlorocyclohexanes]Beta-HCH solutionBeta-benzene hexachlorideBeta-hexac hlorocyclohexaneBeta-hexachloranBeta-hexachlorobenzeneBeta-hexachlorocyclohexaneBeta-hexachlorocyclohexanesBeta-isomerBeta-lindaneBexolBorer sprayCPD with unspecified stereochemistryCaswell No. 079Caswell No. 527CelanexChinoin brand of lindaneChloreseneCodechineCyclohexane, β-1,2,3,4,5,6-hexachloro-Cyclohexane, 1,2,3,4,5,6-hexachloro-Cyclohexane, 1,2,3,4,5,6-hexachloro-, β-Cyclohexane, 1,2,3,4,5,6-hexachloro-, β-isomerCyclohexane, 1,2,3,4,5,6-hexachloro-, (mixed isomers)Cyclohexane, 1,2,3,4,5,6-hexachloro-, alpha-Cyclohexane, 1,2,3,4,5,6-hexachloro-, alpha-isomerCyclohexane, 1,2,3,4,5,6-hexachloro-, beta-isomerCyclohexane, 1,2,3,4,5,6-hexachloro-, delta-Cyclohexane, 1,2,3,4,5,6-hexachloro-, delta-isomerCyclohexane, 1,2,3,4,5,6-hexachloro-, gamma-Cyclohexane, 1,2,3,4,5,6-hexachloro-, gamma-isomerCyclohexane, 1,2,3,4,5,6-hexachloro-, trans-Cyclohexane, beta-1,2,3,4,5,6-hexachloro-Cyclohexane, delta-1,2,3,4,5,6-hexachloro-DBHDelitexDelta-BHCDelta-HCHDelta-benzene hexachlorideDelta-benzenehexachlorideDelta-hexachlorocyclohexaneDelta-lindaneDetmol extractDetmol-extraktDevoranDol granuleDolmixDrill tox-spezial aglukonDrilltox-spezial aglukonEntomoxanEpsilon HCHEpsilon-HCHEpsilon-benzenehexachlorideEpsilon-hexachlorocyclohexaneEso dermEsodermExagamaFenoform forteForlinForst-nexenGallogamaGamacarbatoxGamacidGamacideGamacide 20GamaphexGameneGamisoGamma 666Gamma BHCGamma benzene hexachlorideGamma hexachlorGamma hexachlorocyclohexaneGamma-666Gamma-:hexachlorocyclohexaneGamma-BHCGamma-BHC (lindane)Gamma-BHC benhexachlorGamma-HCHGamma-HCH [hexachlorocyclohexanes]Gamma-HCH or gamma-BHCGamma-benzene hexachlorideGamma-benzenehexachlorideGamma-benzohexachlorideGamma-colGamma-hexachloraneGamma-hexachlorcyclohexanumGamma-hexachlorobenzeneGamma-hexachlorocyclohexaneGamma-linda neGamma-lindaneGamma-mean 400Gamma666GammahexaGammahexaneGammalinGammaterrGammexGammexaneGammopazGamtoxGeobilanGexaneGybenH.c.hHC βHCCHCCHHCHHCH (alpha)HCH (beta)HCH [bsi]HCH [iso]HCH, technical grade [hexachlorocyclohexanes]HCH-βHEXAHGIHeclotoxHecoltoxHexablancHexachlorHexachloranHexachloraneHexachlorcyclohexanHexachlorcyclohexan [german]Hexachloride, benzeneHexachloride, gamma-benzeneHexachlorocyclohexaneHexachlorocyclohexane (all isomers)Hexachlorocyclohexane (mixed isomers)Hexachlorocyclohexane (mixture)Hexachlorocyclohexane (technical grade)Hexachlorocyclohexane, alpha-Hexachlorocyclohexane, beta-Hexachlorocyclohexane, delta-Hexachlorocyclohexane, gamma isomerHexachlorocyclohexane, gamma-Hexachlorocyclohexane, gamma-isomerHexachlorocyclohexane, technicalHexachlorocyclohexane, technical gradeHexachlorocyclohexane-alphaHexachlorocyclohexane-betaHexachlorocyclohexanesHexachlorzyklohexanHexamulHexapoudreHexatoxHexavermHexcidumHexicideHexit Shampoo 1.0%Hexit lotionHexyclanHilbeec hHilbeechHortexInexitInfectopharm brand of lindaneInsecticide, BHCIsatoxIsot oxIsotoxJacutinKokotineKwellKwell-rLacco hi linLasochronLatka 666 [Czech]LendineLentoxLidenalLindaforLindagamLindagrainLindagranoxLindaloLindam ulLindamulLindane (benzene hexachloroide-gamma isomer)Lindane (gamma-HCH)Lindane [hexachlorocyclohexanes]Lindane [usan:inn:ban]Lindano [inn-spanish]Lindanum [inn-latin]LindapoudreLindaterraLindatoxLindexLindosepLintoxLinvurLorexaneMglawik lMixture nameMszycolNeo-scabicidolNexen FBNexen-FBNexi t-starkNexitNexit-starkNexol-eNicochloranNovigamNoviganOmnitoxOvadziakOwadziakPLKPMS lindanePMS-lindanePS71_SUPELCOPedraczakPflanzolPharmascience brand of lindanePms-Lindane Lot 1%Pms-Lindane Shp 1%PmslindaneQuelladaRCRA waste no. U129RCRA waste number U129Sang gammaScabecidScabeneScabisanSilvanolSpritz-rapidinSpritzlindaneSpruehpflanzolStiefel brand of lindaneStreunexSubmarT-HCHTBHTRI-6Technical HCHTechnical hexachlorocyclohexaneTetocidTrans-α-benzenehexachlorideTrans-alpha-benzenehexachlorideTrives-tVerindal ultraVitonagrisol g-20agrocide 2agrocide 6gagrocide 7alpha-1,2,3,4,5,6-Hexachlorocyclohexanebentox 10beta-1,2,3,4,5,6-Hexachlorocyclohexanedelta-(Aeeeee)-1,2,3,4,5,6-hexachlorocyclohexanedelta-1,2,3,4,5,6-Hexachlorocyclohexanedetox 25gamma-1,2,3,4,5,6-Hexachlorocyclohexanegammalin 20geolin g 3hungaria l7milbol 49","Hexachlorocyclohexane, Beta- is one of eight isoforms of the commercially manufactured chemical hexachlorocyclohexane. It is used as an insecticide on fruit, vegetables, and forest crops and is also available as a prescription (lotion, cream, or shampoo) to treat head and body lice, and scabies. (R186)",,319-85-7,727,,C06988,"",32888,GAMMA-HCH,,C023888,"Hexachlorocyclohexane, beta-",694,,,http://en.wikipedia.org/wiki/Lindane,"InChI=1/C6H6Cl6/c7-1-2(8)4(10)6(12)5(11)3(1)9/h1-6H/t1-,2-,3+,4+,5-,6-","1,2,3,4,5,6-hexachlorocyclohexane",http://www.biospider.ca/saved_files/mol/65658d076507b5695b0cd4f4890dd2d9_1237936377.mol,C1(C(C(C(C(C1Cl)Cl)Cl)Cl)Cl)Cl,C1(C(C(C(C(C1Cl)Cl)Cl)Cl)Cl)Cl,C6H6Cl6,287.860070,White solid or colorless vapor.,314.5 °C,"","","0.00024 mg/mL at 25 °C [WEIL,L et al. (1974)]","","","","Oral 
Inhalation 
Dermal
(R186)","Cytochrome P450 2E1 (P05181) 
Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
(R186)","Hexachlorocyclohexane is a neurotoxin that interferes with GABA neurotransmitter function by interacting with the GABA-A receptor-chloride channel complex at the picrotoxin binding site, causing over stimulation of the central nervous system. It is also believed to inhibit sodium/potassium-transporting ATPases and be an endocrine disruptor. In the liver, hexachlorocyclohexane is thought to cause oxidative stress by interfering with hepatic oxidative capacity and glutathione metabolism, increasing lipid metabolism, and inhibiting magnesium ATPase activity. Hexachlorocyclohexane may also inhibit gap junction and intercellular communication, leading to uncontrolled cell growth and tumor promotion. (R186, R187, R188)","Hexachlorocyclohexane is absorbed through the skin, lungs, and intestines, then distributed mainly to the adipose tissue but also to the brain, kidney, muscle, and blood. Metabolism occurs via dechlorination, dehydrogenation, dehydrochlorination, and hydroxylation by hepatic cytochrome P-450 enzymes. The main metabolites are polychlorophenols and 1,2,4-trichlorocyclohexane-4,5-epoxide, which are excreted in the urine. (R186)","LD50: 6 g/kg (Oral, Rat) (R261)","","2B, possibly carcinogenic to humans. (R264)","Hexachlorocyclohexane is used as an insecticide on fruit, vegetables, and forest crops and is also available as a prescription (lotion, cream, or shampoo) to treat head and body lice, and scabies. (R186)","Acute Oral: 0.05 mg/kg/day (R260)
Intermediate Oral: 0.0006 mg/kg/day (R260)","Exposure to large amounts of hexachlorocyclohexane can harm the nervous system, producing a range of symptoms from headache and dizziness to seizures, convulsions and more rarely death. Hexachlorocyclohexane is known to damage the liver, kidneys, and immune system, as well as cause blood disorders and reproductive and developmental defects. Hexachlorocyclohexane is also potentially carcinogenic. (R186, R187)","Exposure to large amounts of hexachlorocyclohexane can harm the nervous system, producing a range of symptoms from headache and dizziness to seizures, convulsions and more rarely death. (R187)","Hexachlorocyclohexane poisoning is treated symptomatically. Gastric lavage, followed by the administration of activated charcoal, may be performed upon ingestion. (R284)",P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P18507;Q99928;O00591;P24046;P28476;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P54710;P62508;P10275;P06401;Q8N1C3;A8MPY1;Q9UN88;P78334;P98194;O75185;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;P03372;Q92731
38,T3D0037,2009-03-06 18:57:58 UTC,2009-08-04 21:27:30 UTC,Acrolein,Organic Compound;Industrial Precursor/Intermediate;Aldehyde,"2 Propenal2-Propen-1-one2-Propenal (Acrylaldehyde)2-Propenal, homopolymer2-Propenaldehyde4S8501_SUPELCOAcquiniteAcraldehydeAcraldehydeacroleinaAcraldehydeacroleina [italian]Acraldehydeacroleina(italian)AcroleinAcrolein, inhibitedAcrolein, inhibited [UN1092] [Poison]AcroleinaAcroleina [italian]AcroleineAcroleine [dutch, french]Acroleine(dutch, french)AcrylaldehydAcrylaldehyd [german]Acrylaldehyd(german)AcrylaldehydeAcrylic aldehydeAcrylic aldehyde, inhibitedAkroleinAkrolein [czech]Akrolein(czech)AkroleinaAkroleina [polish]Akroleina(polish)Aldehyde acryliqueAldehyde acrylique [french]Aldehyde acrylique(french)Aldehyde, acrylicAldehyde, allylAldehyde, ethyleneAldeide acrilicaAldeide acrilica [italian]Aldeide acrilica(italian)Allyl aldehydeAqualinAqualineBiocideCH2=CHCHOCaswell No. 009CroleanEthylene aldehydeInChI=1/C3H4O/c1-2-3-4/h2-3H,1HMagnacideMagnacide hMagnacide h and bPapitePolyacroleinProp-2-en-1-alPropenalPropenal [czech]Propenal, inhibitedPropenaldehydePropylene aldehydeRCRA waste no. P003Rcra waste number P003SlimicideTrans-acroleinWLN: VH1U1acrylaldehyde (ACD/Name 4.0)prop-2-en -1-alprop-2-enal","Acrolein is the simplest unsaturated aldehyde. It is produced widely via the oxidation of propene but is most often immediately reacted with other products due to its instability and toxicity. Acrolein is used as a pesticide to control algae, weeds, bacteria, and mollusks. It is also used to make other chemicals. Small amounts of acrolein can be formed when trees, tobacco, other plants, gasoline, and oil are burned. (R224, R225)",,107-02-8,7847,,C01471,"",15368,T-2-NONENAL-CMPD,,D000171,Acrolein,24,,,,"InChI=1/C3H4O/c1-2-3-4/h2-3H,1H2",prop-2-enal,http://www.biospider.ca/saved_files/mol/a80cc764c13f68840dcad28b61b11c34_1237936595.mol,C=CC=O,C=CC=O,C3H4O,56.026220,,-87.7 °C,,,"212 mg/mL at 25 °C [SEIDELL,A (1941)]",,,,"Oral 
Inhalation 
Dermal
(R224)",,"Acrolein rapidly and irreversibly binds to lysine moieties and sulfhydryl groups found on many cellular molecules forming thiol ethers. By this mechanism acrolein can bind to messenger compounds to produce direct cytotoxic effects or secondary effects from interrupted cell signaling pathways. Perturbation of inflammatory responses in bronchial epithelial cells was demonstrated by direct action of acrolein on the inhibitor of nuclear factor kappa-B (IκB) kinase, which inhibits activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) transcription factor and suppresses interleukin 8 (IL-8) production. Rapid binding of acrolein to neural receptors in the corneal and nasal mucosa results in rapid depolarization of the associated neurons to produce ocular and nasal irritation. Acrolein also binds rapidly to glutathione, which may be inhibitory to the enzyme glutathione peroxidase and result in a lower level of cellular protection against oxygen radical toxicity. Further, the adduction of glutathione generates GS-propionaldehyde, which produces oxygen and possibly hydroxy radicals via cytosolic aldehyde dehydrogenase. Acrolein inhibits thioredoxin and thioredoxin reductase, which disrupts the cellular thiol redox balance necessary for cell survival. It interferes with normal reverse cholesterol transport by high density lipoprotein (HDL) by modifying specific sites in apolipoprotein A-I. Acrolein also inhibits aldehyde dehydrogenases and activates the transient receptor potential cation channel. (R224, R226, R227, R228)","Acrolein can be absorbed though oral, inhalation, or dermal routes. In the liver and kidneys, acrolein forms conjugates with glutathione, cysteine, N-acetylcysteine, and/or thioredoxin. Acrolein can also be transformed into acrylic acid by liver cytosol or microsomes, or it can be oxidized to glycidaldehyde by lung or liver microsomes. Acrolein metabolites are excreted in the urine. (R224)","LC50: 130 ppm over 30 minutes (Inhalation, Rat) (R286) 
LD50: 562 mg/kg (Dermal, Rabbit) (R287) 
LD50: 46 mg/kg (Oral, Rat) (R287) 
LD50: 30 mg/kg (Subcutaneous, Rat) (R287)",10 ppm for an adult human. (R270),"3, not classifiable as to its carcinogenicity to humans. (R264)","Acrolein is used as a pesticide to control algae, weeds, bacteria, and mollusks. It is also used to make other chemicals, such as polyester resin, polyurethane, propylene glycol, acrylic acid, acrylonitrile, and glycerol. Small amounts of acrolein can be formed when trees, tobacco, other plants, gasoline, and oil are burned. (R224)","Acute Inhalation: 0.003 ppm (R260)
Intermediate Inhalation: 0.00004 ppm (R260)
Intermediate Oral: 2 mg/kg/day (R260)","Acrolein is a severe pulmonary irritant and lachrymatory agent. Breathing large amounts of acrolein damages the lungs and could cause death. (R224, R225)","Ingestion of acrolein causes stomach irritation, vomiting, stomach ulcers and bleeding. Breathing acrolein may cause eye watering, burning of the nose and throat and a decreased breathing rate. (R224)","",O15111;O14920;Q14164;P10599;Q99757;Q16881;Q9NNW7;Q86VQ6;P02647;P47895;P51648;P30838;P00352;O94788;P43353;P48448;P30837;O75891;Q3SY69;O75762;P51649;Q9Y6K9
39,T3D0038,2009-03-06 18:57:58 UTC,2009-08-04 21:27:30 UTC,Disulfoton,Organic Compound;Pesticide;Organophosphate,"Caswell No. 341Di-systonDi-syston gDimazDisiptonDisulfatonDisulfoton [bsi:iso]Disulfoton mixtureDisyston FE-10DisystoxDithiodemetonDithiosystoxDutionEkatin TDEkatineEthyl thiometonEthylthiodemetonEthylthiometon bFruminFrumin alFrumin gGlebofosInsyst-dM 74 (Pesticide)M-74 (Pesticide)O,O-Diaethyl-S-(2-aethylthio-aethyl)-dithiophosphatO,O-Diaethyl-S-(3-thia-pentyl)-dithiophosphatO,O-Diaethyl-S-(3-thia-pentyl)-dithiophosphat [German]O,O-Diethyl 2-ethylthioethyl phosphorodithioateO,O-Diethyl S-(2-(ethylthio)ethyl) dithiophosphateO,O-Diethyl S-(2-(ethylthio)ethyl)phosphorodithioateO,O-Diethyl S-(2-eththioethyl) phosphorodithioateO,O-Diethyl S-(2-eththioethyl) thiothionophosphateO,O-Diethyl S-(2-ethylmercaptoethyl) dithiophosphateO,O-Diethyl S-2-(ethylthio)ethyl phosphorodithioateO,O-Diethyl S-[2-(Ethylthio)ethyl] dithiophosphateO,O-Diethyl S-[2-(ethylthio)ethyl] phosphorodithioateO,O-Diethyl-S-(2-ethylthio-ethyl)-dithiofosfaatO,O-Diethyl-S-(2-ethylthio-ethyl)-dithiofosfaat [Dutch]O,O-Dietil-S-(2-etiltio-etil)-ditiofosfatoO,O-Dietil-S-(2-etiltio-etil)-ditiofosfato [Italian]O,O-Ethyl S-2(ethylthio)ethyl phosphorodithioateO,O-diethyl 2-(ethylthio)ethyl dithiophosphateO,o-diethyl-s-ethylmercapto-ethyl dithiophosphatePS652_SUPELCORCRA waste no. P039Rcra waste number P039S-[2-(ethylsulfanyl)ethyl] O,O-dimethyl dithiophosphateSolvigranSolvirexThiodemetonThiodemetronVUagT 1-4o,o-Diethyl S-[2-(ethylsulfanyl)ethyl] dithiophosphate",Disulfoton is a manufactured organophosphate used as a pesticide. It is used mainly in agriculture to protect field and vegetable crops. (R230),,298-04-4,3118,,"","",38661,"",,D004222,Disulfoton,1916,,,http://en.wikipedia.org/wiki/Disulfoton,"InChI=1/C8H19O2PS3/c1-4-9-11(12,10-5-2)14-8-7-13-6-3/h4-8H2,1-3H3",diethoxy-(2-ethylsulfanylethylsulfanyl)-sulfanylidene-$l^{5}-phosphane,http://www.biospider.ca/saved_files/mol/,CCOP(=S)(OCC)SCCSCC,CCOP(=S)(OCC)SCCSCC,C8H19O2PS3,274.028480,Colorless (pure) or dark yellow (technical grade) oil.,-25 °C,,,"0.0163 mg/mL at 20 °C [BOWMAN,BT & SANS,WW (1983A)]",,,,"Oral 
Inhalation 
Dermal
(R230)","Cytochrome P450 1A2 (P05177) 
Cytochrome P450 3A4 (P08684) 
Cytochrome P450 2B6 (P20813) 
Cytochrome P450 2C9 (P11712) 
Cytochrome P450 2C18 (P33260) 
Cytochrome P450 2C19 (P33261) 
Cytochrome P450 2D6 (P10635) 
Dimethylaniline monooxygenase [N-oxide-forming] 1 (Q01740) 
(R231)","The toxic metabolites of disulfoton, mainly disulfoton sulfoxide, disulfoton sulfone, demeton S-sulfoxide and demeton S-sulfone, inhibit acetylcholinesterase in nervous tissue. The inhibition of acetylcholinesterase results in the accumulation of acetylcholine at the muscarinic and nicotinic cholinergic receptors of nerve synapses, which causes an overstimulation of cholinergic nerves and effector organs. Prolonged exposure to disulfoton results in diminished cholinergic signs as tolerance develops, likely as a result of reduced density of muscarinic receptor binding sites. (R230)","Disulfoton is lipophilic and easily absorbed by oral, inhalation, and dermal routes, then distributed primarily to the liver and in smaller quantities to the kidney, fat, skin, muscle, brain, and other organs. In the liver, cytochrome
P-450 monooxygenase and flavin adenine dinucleotide monooxygenase metabolize disulfoton into its toxic intermediates, which include disulfoton sulfoxide, disulfoton sulfone, demeton S-sulfoxide and demeton S-sulfone. The active metabolites ultimately undergo hydrolysis to more polar metabolites that are not toxic and are excreted in the urine. (R230)","LD50: 25 mg/kg (Dermal, Rat) (R289) 
LD50: 6.8 mg/kg (Oral, Rat) (R289) 
LD50: 9.4 mg/kg (Intraperitoneal, Rat) (R289)",,,"Disulfoton is used mainly in agriculture to protect field and vegetable crops, as well as some fruit and nut crops. It may also be used in smaller quantities on home and garden plants and for mosquito control in swamps. (R230)","Acute Inhalation: 0.006 mg/m3 (R260)
Intermediate Inhalation: 0.0002 mg/m3 (R260)
Acute Oral: 0.001 mg/kg/day (R260)
Intermediate Oral: 0.00009 mg/kg/day (R260)
Chronic Oral: 0.00006 mg/kg/day (R260)","Disulfoton mainly causes harmful effects to the nervous system, such as narrowing of the pupils, vomiting, diarrhea, drooling, difficulty in breathing, tremors, convulsions, and even death. Chronic ingestion of disulfoton may affect the eyes and cause nearsightedness. Disulfoton is also believed to cause developmental problems. (R230)","Depending on the amount of disulfoton that enters the body, effects on the nervous system, such as narrowing of the pupils, vomiting, diarrhea, drooling, difficulty in breathing, tremors, convulsions, and even death may occur. Skin contact with disulfoton may cause weakness and fatigue. (R230)","Treatment for disulfoton poisoning is symptomatic and may include ventilatory support, emesis, or the administration of atropine sulfate and pralidoxime chloride. (R288)",P22303
40,T3D0039,2009-03-06 18:57:58 UTC,2009-08-04 21:27:30 UTC,Benzo[a]anthracene,Organic Compound;Industrial By-product/Pollutant;Aromatic Hydrocarbon;Polycyclic Aromatic Hydrocarbon,"1, 2-Benzanthracene1, 2-Benzoanthracene1,2-Benz(a)anthracene1,2-Benz[a]anthracene1,2-Benzanthracene1,2-Benzanthrazen1,2-Benzanthrazen (GERMAN)1,2-Benzanthrazen [German]1,2-Benzanthrene1,2-Benzoanthracene2,3-Benzophenanthrene2,3-BenzphenanthreneAmbap123B2209_ALDRICHBABCR271_FLUKABenz(a)anthraceneBenz(a)anthracene [polycyclic aromatic compounds]Benz(a)anthracene [polycyclic aromatic hydrocarbons]Benz[a]anthracene solutionBenzanthraceneBenzanthreneBenzo(a)anthraceneBenzo(b)phenanthreneBenzo[a]anthraceneBenzo[a]phenanthreneBenzo[b]phenanthreneBenzoanthraceneNaphthanthraceneRCRA waste no. U018Rcra waste number U018TetrapheneWLN: L D6 B666Jbenzo[a]anthracene (ACD/Name 4.0){1,2-Benz[a]anthracene}{benz[a]anthracene}{benzo[a]anthracene}{benzo[a]phenanthrene}{benzo[b]phenanthrene}","Benzo[a]anthracene is one of over 100 different polycyclic aromatic hydrocarbons (PAHs). PAHs are chemicals that are formed during the incomplete burning organic substances, such as fossil fuels. They are usually found as a mixture containing two or more of these compounds.
",,56-55-3,5954,,C14317,"",51348,"",,C030935,Benzo[a]anthracene,6379,,,,InChI=1/C18H12/c1-2-7-15-12-18-16(11-14(15)6-1)10-9-13-5-3-4-8-17(13)18/h1-12H,benzo[a]anthracene,http://www.biospider.ca/saved_files/mol/a0f2931127023486473cfba9301de731_1237936795.mol,C1=CC=C2C(=C1)C=CC3=CC4=CC=CC=C4C=C32,C1=CC=C2C(=C1)C=CC3=CC4=CC=CC=C4C=C32,C18H12,228.093900,Yellow-blue solid.,84 °C,"","","9.4e-06 mg/mL at 25 °C [MAY,WE et al. (1978)]","","","","Oral 
Inhalation 
(R028)","Serum albumin (P02768) 
Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 1B1 (Q16678) 
(R060)","The ability of PAH's to bind to blood proteins such as albumin allows them to be transported throughout the body. Many PAH's induce the expression of cytochrome P450 enzymes, especially CYP1A1, CYP1A2, and CYP1B1, by binding to the aryl hydrocarbon receptor or glycine N-methyltransferase protein. These enzymes metabolize PAH's into their toxic intermediates. The reactive metabolites of PAHs (epoxide intermediates, dihydrodiols, phenols, quinones, and their various combinations) covalently bind to DNA and other cellular macromolecules, initiating mutagenesis and carcinogenesis. (R028, R060, R068, R073)","PAH metabolism occurs in all tissues, usually by cytochrome P-450 and its associated enzymes. PAHs are metabolized into reactive intermediates, which include epoxide intermediates, dihydrodiols, phenols, quinones, and their various combinations. The phenols, quinones, and dihydrodiols can all be conjugated to glucuronides and sulfate esters; the quinones also form glutathione conjugates. (R028)","","","2B, possibly carcinogenic to humans. (R264)","PAHs are released into the environment via the combustion of fossil fuels, coke oven emissions and vehicle exhausts, as well as naturally from forest fires and volcanic eruptions. PAHs from these sources may contaminate nearly water systems. They are also found in coal tar and charbroiled food. (R028)","","PAHs are carcinogens and have been associated with the increased risk of skin, respiratory tract, bladder, stomach, and kidney cancers. They may also cause reproductive effects and depress the immune system. (R028)","Acute exposure to PAHs causes irritation and inflammation of the skin and lung tissue. (R034)
",There is no known antidote for PAHs. Exposure is usually handled with symptomatic treatment. (R028),P35869;Q14749;DNA
41,T3D0040,2009-03-06 18:57:58 UTC,2009-08-04 21:27:30 UTC,"3,3'-Dichlorobenzidine",Organic Compound;Industrial Precursor/Intermediate;Aromatic Hydrocarbon;Amine;Organochloride,"(1,1'-Biphenyl)-4,4'-diamine, 3,3'-dichloro-3, 3'-Dichlorobenzidine3,3 Dichlorobenzidine3,3' Dichlorobenzidine3,3'-Dichlorbenzidin3,3'-Dichlorbenzidin (CZECH)3,3'-Dichlorbenzidin [Czech]3,3'-Dichloro-(1,1'-biphenyl)-4,4'-diamine3,3'-Dichloro-4, 4'-diaminodiphenyl3,3'-Dichloro-4,4'-biphenyldiamine3,3'-Dichloro-4,4'-diamino(1,1-biphenyl)3,3'-Dichloro-4,4'-diaminobiphenyl3,3'-Dichloro-4,4'-diaminodiphenyl3,3'-Dichloro-p,p'-bianiline3,3'-Dichlorobenzidin [Czech]3,3'-Dichlorobenzidina3,3'-Dichlorobenzidina (spanish)3,3'-Dichlorobenzidina [Spanish]3,3'-Dichlorobenzidine3,3'-Dichlorobenzidine base3,3'-Dichlorobiphenyl-4,4'-diamine3,3'-dichloro[1,1'-biphenyl]-4,4'-diamine (ACD/Name 4.0)3,3'-dichlorobiphenyl-4,4'-ylenediamine3,3-Dichloro-[1,1]-biphenyl-4,4-diamine3,3-Dichlorobenzidine4 ,4'-diamino-3,3'-dichlorobiphenyl4'-Amino-3,3'-dichloro(1,1'-biphenyl)-4-ylamine4'-Amino-3,3'-dichloro[1,1'-biphenyl]-4-ylamine4, 4'-Diamino-3,3'-dichlorobiphenyl4,4'-Diamino-3, 3'-dichlorodiphenyl4,4'-Diamino-3,3'-dichlorobiphenyl4,4'-Diamino-3,3'-dichlorodiphenylBenzidine, 3,3'-dichloro-Curithane C 126Curithane C126DCBDichlorobenzidineDichlorobenzidine baseDichlorobenzidine, 3,3'-O,o'-dichlorobenzidineOrtho,ortho'-dichlorobenzidineRCRA waste no. U073Rcra waste number U073WLN: ZR bg DR dz CG{[1,1'-Biphenyl]-4,4'-diamine,} 3, 3'-dichloro-","3,3'-Dichlorobenzidine is a manufactured chemical used in pigments for printing inks, textiles, plastics and enamels, paint, leather, and rubber. (R232)",,91-94-1,7070,,"","",25520,CPD-801,,D015101,"3,3'-Dichlorobenzidine",435,,,,"InChI=1/C12H10Cl2N2/c13-9-5-7(1-3-11(9)15)8-2-4-12(16)10(14)6-8/h1-6H,15-16H2",4-(4-amino-3-chlorophenyl)-2-chloroaniline,http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C=C1C2=CC(=C(C=C2)N)Cl)Cl)N,C1=CC(=C(C=C1C2=CC(=C(C=C2)N)Cl)Cl)N,C12H10Cl2N2,252.022100,Gray to purple crystalline solid.,132-133 °C,,,"0.0031 mg/mL at 25 °C [BANERJEE,S et al. (1980)]",,,,"Oral 
Inhalation 
Dermal
(R232)","Arylamine N-acetyltransferase 1 (P18440) 
Arylamine N-acetyltransferase 2 (P11245) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 4B1 (P13584) 
(R232)","3,3’-Dichlorobenzidine's mechanism of toxicity derives mainly from the adduction of DNA by its metabolites. The formation of nitroso derivatives during metabolism, yielding a sulfinic acid amide with hemoglobin in erythrocytes, is suggested to be a mechanism for this adduct formation. 3,3’-Dichlorobenzidine can act on the aryl hydrocarbon receptor to induce the activity of cytochrome p-450 enzymes, which metabolize 3,3’-dichlorobenzidine, along with other polyhalogenated aromatics, into their toxic intermediates. (R232, R233, R234)","3,3'-Dichlorobenzidine is absorbed via ingestion, inhalation, and dermal routes. The major path of metabolism is believed to be N-acetylation via hepatic N-acetyltransferases, producing metabolites such as N-acetyl-3,3’-dichlorobenzidine and N,N-diacetyl-3,3’-dichlorobenzidine. 3,3'-Dichlorobenzidine may also be activated to toxic intermediates by certain cytochrome P-450 monooxygenases. Metabolites are excreted primarily in urine and to a lesser extent in faeces. (R232)","LD50: 8 g/kg (Dermal, Rat) (R290) 
LD50: 3.82 g/kg (Oral, Rat) (R290)",,"2B, possibly carcinogenic to humans. (R264)","3,3'-Dichlorobenzidine is used in pigments for printing inks, textiles, plastics and enamels, paint, leather, and rubber. (R232)",,"The salt form of 3,3'-dichlorobenzidine may cause sore throat, respiratory infections, stomach upset, headache, dizziness, caustic burns, and dermatitis. 3,3'-Dichlorobenzidine is also believed to be a possible carcinogen. (R232)","The salt form of 3,3'-dichlorobenzidine may cause sore throat, respiratory infections, stomach upset, headache, dizziness, caustic burns, and dermatitis. (R232)","Treatment for 3,3'-dichlorobenzidine poisoning is usually supportive. (R232)",P69905;P68871;P02042;P02100;P69891;P69892;Q6B0K9;P09105;P02008;P35869;DNA;P98194;O75185;P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P78334;Q8N1C3;P18507;Q99928;O00591;P24046;P28476;A8MPY1;Q9UN88;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;P54710;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P03372;Q92731
42,T3D0041,2009-03-06 18:57:58 UTC,2009-08-04 21:27:31 UTC,Endrin,Organic Compound;Pesticide;Organochloride,":endrinAldrinCaswell No. 423Compd. 269Compound 269EN 57 (VAN)EndrexEndricolEndrin 1.6 ECEndrin 20 ECEndrin and metabolitesEndrin isomerEndrin mixtureEndrineEndrine (french)Endrine [french]Experimental Insecticide 269Hexachloroepoxyoctahydro-endo, endo-dimethanonaphthaleneHexachloroepoxyoctahydro-endo,endo-dimethanonaphthaleneHexachloroepoxyoctahydro-endo,endo-dimethanonapthaleneHexadrinLatka 269Latka 269 [Czech]MendrinNendrinOktanexRCRA waste no. D013RCRA waste no. P051Rcra waste number P051SD 3419 IlloxolStardrinStardrin 20experimental insecticide no. 269","Endrin is a chlorinated hydrocarbon used as an insecticide on cotton, maize, and rice. It also acts as an avicide and rodenticide. Due to its toxicity and tendency to bioaccumulate, its use is now banned in most parts of the world. (R190)",,72-20-8,12358480,,"","",25520,DIHYDROKAEMPFEROL-CMPD,,D004732,Endrin,572,,,http://en.wikipedia.org/wiki/Endrin,"InChI=1/C12H8Cl6O/c13-8-9(14)11(16)5-3-1-2(6-7(3)19-6)4(5)10(8,15)12(11,17)18/h2-7H,1H2/t2-,3?,4-,5+,6-,7+,10-,11+/m1/s1","","",C1[C@@H]2[C@@H]3[C@H]([C@H]1[C@H]4[C@@H]2O4)[C@@]5(C(=C([C@]3(C5(Cl)Cl)Cl)Cl)Cl)Cl,C1C2C3C(C1C4C2O4)C5(C(=C(C3(C5(Cl)Cl)Cl)Cl)Cl)Cl,C12H8Cl6O,377.870630,White solid.,226-230 °C,"","","0.00025 mg/mL at 25 °C [BIGGAR,JW & RIGGS,RI (1974)]","","","","Oral
(R190)","","Endrin antagonizes the action of the neurotransmitter gamma-aminobutyric acid (GABA) acting at the GABA-A receptors, effectively blocking the GABA-induced uptake of chloride ions and causing hyperexcitability of the central nervous system. Endrin also inhibits Na+ K+ ATPase and Ca2+ and Mg2+ ATPase which are essential for the transport of calcium across membranes. This results in the accumulation of intracellular free calcium ions, which promotes release of neurotransmitters from storage vesicles, the subsequent depolarization of adjacent neurons, and the propagation of stimuli throughout the central nervous system. Endrin also causes increased lipid peroxidation, decreased membrane fluidity, and DNA damage in hepatocytes, but the exact mechanism is unknown. (R029, R191)","Endrin is absorbed orally and distributed primarily to the fat and skin. The major biotransformation
product is anti-l 2-hydroxyendrin and the corresponding sulfate, as well as glucuronide metabolites. Anti- and syn-12-hydroxyendrin and 12-ketoendrin are the main toxic metabolites of endrin. Endrin and its metabolites are excreted in urine and feces. (R191)","LD50: 3 mg/kg (Oral, Rat) (R263) 
LD50: 12 mg/kg (Dermal, Rat) (R263)","","3, not classifiable as to its carcinogenicity to humans. (R264)",Endrin is used as a pesticide. (R190),"Intermediate Oral: 0.002 mg/kg/day (R260)
Chronic Oral: 0.0003 mg/kg/day (R260)","Endrin poisoning affects primarily the nerve system. Exposure causes various harmful effects including hyperexcitability, severe central nervous system damage, and death. Endrin is also believed to cause birth defects. (R029, R191)","Symptoms that may result from endrin poisoning are headaches, dizziness, nervousness, confusion, nausea, vomiting, and convulsions. (R191)","Treatment is symptomatic, aimed at controlling convulsions, coma, and respiratory depression. If ingested, gastric lavage may be performed, followed by administering activated charcoal powder. (R291)",P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P18507;Q99928;O00591;P24046;P28476;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P54710;P98194;O75185;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;Q8N1C3;A8MPY1;Q9UN88;P78334;P03372;Q92731
43,T3D0042,2009-03-06 18:57:58 UTC,2009-08-27 18:07:31 UTC,Beryllium,Inorganic Compound;Metal;Beryllium Compound,"BEBENBERYLLIUM, 99%BerilioBeryllium [beryllium and certain beryllium compounds]Beryllium and beryllium compoundsBeryllium and certain beryllium compoundsBeryllium and compoundsBeryllium atomBeryllium atomic absorption standard solutionBeryllium compounds, n.o.s. [UN1566] [Poison]Beryllium dustBeryllium elementBeryllium metalBeryllium metal [beryllium and beryllium compounds]Beryllium metallicBeryllium metallicumBeryllium powderBeryllium, elementalBeryllium, metal powderBeryllium, powder [UN1567] [Poison]Beryllium, ultra high purityBeryllium-9GluciniumGlucinumRCRA waste no. P015Rcra waste number P015beryllium(0)","Beryllium is a lightweight alkaline earth metal with the atomic number 4. It is a relatively rare element found naturally only combined with other elements in minerals. It is primarily used as a hardening agent in alloys, and is also an ideal aerospace material due to its high melting point and temperature stability. (R078)",,7440-41-7,5460467,,C16460,"108730
142858
181000",30501,CPD0-1230,,D001608,Beryllium,6383,,,http://en.wikipedia.org/wiki/Beryllium,InChI=1/Be.2H,beryllium,http://www.biospider.ca/saved_files/mol/99b48a7d5f413e1e435ea801dacfa11b_1237937083.mol,[Be++],[Be++],[Be]2+,9.012180,Grey metallic solid.,1300 °C,"","","","","","",Inhalation (R078),"Transthyretin (P02766)
Ferritin light chain (P02792)
Ferritin heavy chain (P02794)
Ferritin, mitochondrial (Q8N4E7)
Ferritin heavy polypeptide-like 17 (Q9BXU8)
Putative ferritin heavy polypeptide-like 19 (P0C7X4)
(R079)","Once in the body, beryllium acts as a hapten and interacts with human leucocyte antigen (HLA) DP presenting cells in the lungs, becoming physically associated with a major histocompatability (MHC) class II molecule. This MHC class II-beryllium-peptide complex is recognized by the T lymphocyte receptor, triggering CD4+ T lymphocyte activation and proliferation. The resulting inflammatory response is a cell-mediated process orchestrated by cytokines and results in the formation of (usually pulmonary) granulomas. Beryllium's toxicity may be controlled by the iron-storage protein ferritin, which sequesters beryllium by binding it and preventing it from interacting with other enzymes. (R079, R083, R235)","Beryllium is absorbed mainly through the lungs, where it enters the bloodstream and is transported throughout the body by binding to prealbumins and γ-globulins. Beryllium accumulates in lung tissue and the skeleton. It is excreted mainly in the urine. (R079)","","","1, carcinogenic to humans. (R264)","Beryllium is purified for use in nuclear weapons and reactors, aircraft and space vehicle structures, instruments, x-ray machines, and mirrors. Beryllium ores are used to make speciality ceramics for electrical and high-technology applications. Beryllium is often found in alloys which are used in automobiles, computers, sports equipment, and dental bridges. (R078)",Chronic Oral: 0.002 mg/kg/day (R260),"Acute inhalation of a high level of beryllium can results in a pneumonia-like condition called acute beryllium disease. Chronic inhalation of beryllium can caused an inflammatory reaction in the respiratory system called chronic beryllium disease. Chronic beryllium disease may result in anorexia and weight loss, as well as right side heart enlargement and heart disease in advanced cases. Chronic exposure can also increase the risk of lung cancer. Skin contact with beryllium results in contact dermatitus.
(R078, R079)","Chronic beryllium disease causes fatigue, weakness, difficulty breathing, and a persistent dry cough.
(R078, R079)","Chronic beryllium disease is treated with immunosuppressive medicines, usually of the glucocorticoid class. (R078)",P20036;P13763;P04440
44,T3D0043,2009-03-06 18:57:58 UTC,2009-08-04 21:27:31 UTC,"Hexachlorocyclohexane, delta-",Organic Compound;Pesticide;Organochloride,"α, 2α,3α,4α,6β)-«delta»,1,2,3,4,5,6-Hexachlorocyclohexane«delta»-BHC«delta»-HCH«delta»-benzene hexachloride«delta»-hexachlorocyclohexane(1R,2R,3R,4R,5S,6S)-1,2,3,4,5,6-hexachlorocyclohexane(1R,2R,3S,4S,5S,6S)-1,2,3,4,5,6-hexachlorocyclohexane(1r,2R,3S,4r,5R,6S)-1,2,3,4,5,6-hexachlorocyclohexane(1r,2R,3S,4s,5R,6S)-1,2,3,4,5,6-hexachlorocyclohexane(1r,2c,3c,4t,5c,6t)-1,2,3,4,5,6-hexachlorocyclohexane(1r,2c,3t,4t,5c,6t)-1,2,3,4,5,6-hexachlorocyclohexane(1r,2r,3r,4r,5r,6r)-1,2,3,4,5,6-hexachlorocyclohexane(1s,2R,3R,4s,5S,6S)-1,2,3,4,5,6-hexachlorocyclohexane1,2,3,4,5,6-Hexachlorocyclohexane1,2,3,4,5,6-Hexachlorocyclohexane (all stereo isomers)1,2,3,4,5,6-Hexachlorocyclohexane (mixture of isomers)1,2,3,4,5,6-Hexachlorocyclohexane gamma isomer1,2,3,4,5,6-Hexachlorocyclohexane, gamma-isomer1,2,3,4,5,6-Hexachlorohexane(β-bhc)1,2,3,4,5,6-hexachlorocyclohexane (ACD/Name 4.0)1,2,3,4,5,6-hexachlorocyclohexane, alpha isomer1a,2a,3b,4a,5b,6b-hexachlorocyclohexane1a,2b,3a,4b,5a,6b-hexachlorocyclohexaneAalindanAficideAgrocideAgrocide IIIAgrocide WPAgronexitAlpha- BHCAlpha-BHCAlpha-HCHAlpha-HCH [hexachlorocyclohexanes]Alpha-HCH solutionAlpha-benzene hexachlorideAlpha-benzenehexachlorideAlpha-hexachloranAlpha-hexachloraneAlpha-hexachlorocyclohexaneAlpha-hexachlorocyclohexanesAlpha-lindaneAm eisenatodAmeisenatodAmeisenmittel merckAmeisentodAparasinAphtiriaAphtitriaAplidalArbitexArcotal sBBHBCHBHCBHC «delta»BHC (alpha-, beta-, gamma-)BHC (insecticide)BHC insecticideBHC or HCHBHC-«delta» isomerBen-hexBenhexachlorBenhexolBenzanexBenzene hexachlorideBenzene hexachloride (ambiguous)Benzene hexachloride, all isomersBenzene hexachloride-alpha-isomerBenzene hexachloride-gamma isomerBenzene hexachloride-gamma-isomerBenzene-1,2,3,4,5,6-hexachloride ((Ambiguous)Benzene-cis-hexachlorideBenzene-trans-hexachlorideBenzenehexachloride, mixed isomersBenzenehexachloride-alpha-isomerBenzexBeta-BHCBeta-HCHBeta-HCH [hexachlorocyclohexanes]Beta-HCH solutionBeta-benzene hexachlorideBeta-hexac hlorocyclohexaneBeta-hexachloranBeta-hexachlorobenzeneBeta-hexachlorocyclohexaneBeta-hexachlorocyclohexanesBeta-isomerBeta-lindaneBexolBorer sprayCPD with unspecified stereochemistryCaswell No. 079Caswell No. 527CelanexChinoin brand of lindaneChloreseneCodechineCyclohexane, «delta»,1,2,3,4,5,6-hexachloro-Cyclohexane, 1,2,3,4,5,6-hexachloro-Cyclohexane, 1,2,3,4,5,6-hexachloro-, «delta»-Cyclohexane, 1,2,3,4,5,6-hexachloro-, (mixed isomers)Cyclohexane, 1,2,3,4,5,6-hexachloro-, alpha-Cyclohexane, 1,2,3,4,5,6-hexachloro-, alpha-isomerCyclohexane, 1,2,3,4,5,6-hexachloro-, beta-isomerCyclohexane, 1,2,3,4,5,6-hexachloro-, delta-Cyclohexane, 1,2,3,4,5,6-hexachloro-, delta-isomerCyclohexane, 1,2,3,4,5,6-hexachloro-, gamma-Cyclohexane, 1,2,3,4,5,6-hexachloro-, gamma-isomerCyclohexane, beta-1,2,3,4,5,6-hexachloro-Cyclohexane, delta-1,2,3,4,5,6-hexachloro-DBHDelitexDelta-BHCDelta-HCHDelta-benzene hexachlorideDelta-benzenehexachlorideDelta-hexachlorocyclohexaneDelta-lindaneDetmol extractDetmol-extraktDevoranDol granuleDolmixDrill tox-spezial aglukonDrilltox-spezial aglukonEntomoxanEpsilon HCHEpsilon-HCHEpsilon-benzenehexachlorideEpsilon-hexachlorocyclohexaneEso dermEsodermExagamaFenoform forteForlinForst-nexenG-BHC-«delta»GallogamaGamacarbatoxGamacidGamacideGamacide 20GamaphexGameneGamisoGamma 666Gamma BHCGamma benzene hexachlorideGamma hexachlorGamma hexachlorocyclohexaneGamma-666Gamma-:hexachlorocyclohexaneGamma-BHCGamma-BHC (lindane)Gamma-BHC benhexachlorGamma-HCHGamma-HCH [hexachlorocyclohexanes]Gamma-HCH or gamma-BHCGamma-benzene hexachlorideGamma-benzenehexachlorideGamma-benzohexachlorideGamma-colGamma-hexachloraneGamma-hexachlorcyclohexanumGamma-hexachlorobenzeneGamma-hexachlorocyclohexaneGamma-linda neGamma-lindaneGamma-mean 400Gamma666GammahexaGammahexaneGammalinGammaterrGammexGammexaneGammopazGamtoxGeobilanGexaneGybenH.c.hHCCHCCHHCHHCH (alpha)HCH (beta)HCH [bsi]HCH [iso]HCH, technical grade [hexachlorocyclohexanes]HCH-«delta»HCH-dHEXAHGIHeclotoxHecoltoxHexablancHexachlorHexachloranHexachloraneHexachlorcyclohexanHexachlorcyclohexan [german]Hexachloride, benzeneHexachloride, gamma-benzeneHexachlorocyclohexaneHexachlorocyclohexane (all isomers)Hexachlorocyclohexane (mixed isomers)Hexachlorocyclohexane (mixture)Hexachlorocyclohexane (technical grade)Hexachlorocyclohexane, alpha-Hexachlorocyclohexane, beta-Hexachlorocyclohexane, delta-Hexachlorocyclohexane, gamma isomerHexachlorocyclohexane, gamma-Hexachlorocyclohexane, gamma-isomerHexachlorocyclohexane, technicalHexachlorocyclohexane, technical gradeHexachlorocyclohexane-alphaHexachlorocyclohexane-betaHexachlorocyclohexanesHexachlorzyklohexanHexamulHexapoudreHexatoxHexavermHexcidumHexicideHexit Shampoo 1.0%Hexit lotionHexyclanHilbeec hHilbeechHortexInexitInfectopharm brand of lindaneInsecticide, BHCIsatoxIsot oxIsotoxJacutinKokotineKwellKwell-rLacco hi linLasochronLatka 666 [Czech]LendineLentoxLidenalLindaforLindagamLindagrainLindagranoxLindaloLindam ulLindamulLindane (benzene hexachloroide-gamma isomer)Lindane (gamma-HCH)Lindane [hexachlorocyclohexanes]Lindane [usan:inn:ban]Lindano [inn-spanish]Lindanum [inn-latin]LindapoudreLindaterraLindatoxLindexLindosepLintoxLinvurLorexaneMglawik lMixture nameMszycolNeo-scabicidolNexen FBNexen-FBNexi t-starkNexitNexit-starkNexol-eNicochloranNovigamNoviganOmnitoxOvadziakOwadziakPLKPMS lindanePMS-lindanePedraczakPflanzolPharmascience brand of lindanePms-Lindane Lot 1%Pms-Lindane Shp 1%PmslindaneQuelladaRCRA waste no. U129RCRA waste number U129Sang gammaScabecidScabeneScabisanSilvanolSpritz-rapidinSpritzlindaneSpruehpflanzolStiefel brand of lindaneStreunexSubmarT-HCHTBHTechnical HCHTechnical hexachlorocyclohexaneTetocidTrans-alpha-benzenehexachlorideTri-6Trives-tVerindal ultraVitonagrisol g-20agrocide 2agrocide 6gagrocide 7alpha-1,2,3,4,5,6-Hexachlorocyclohexanebentox 10beta-1,2,3,4,5,6-Hexachlorocyclohexanedelta-(Aeeeee)-1,2,3,4,5,6-hexachlorocyclohexanedelta-1,2,3,4,5,6-Hexachlorocyclohexanedetox 25gamma-1,2,3,4,5,6-Hexachlorocyclohexanegammalin 20geolin g 3hungaria l7milbol 49","Hexachlorocyclohexane, Delta- is one of eight isoforms of the commercially manufactured chemical hexachlorocyclohexane. It is used as an insecticide on fruit, vegetables, and forest crops and is also available as a prescription (lotion, cream, or shampoo) to treat head and body lice, and scabies. (R186)",,319-86-8,727,,C06988,"",39095,GAMMA-HCH,,C086916,"Hexachlorocyclohexane, delta-",6461,,,http://en.wikipedia.org/wiki/Lindane,"InChI=1/C6H6Cl6/c7-1-2(8)4(10)6(12)5(11)3(1)9/h1-6H/t1-,2-,3+,4+,5-,6-","1,2,3,4,5,6-hexachlorocyclohexane",http://www.biospider.ca/saved_files/mol/c2706d5bd005a4d880d476ee6f38b212_1237937200.mol,C1(C(C(C(C(C1Cl)Cl)Cl)Cl)Cl)Cl,C1(C(C(C(C(C1Cl)Cl)Cl)Cl)Cl)Cl,C6H6Cl6,287.860070,White solid or colorless vapor.,141.5 °C,"","","0.01 mg/mL at 20 °C [SHIU,WY et al.(1990)]","","","","Oral 
Inhalation 
Dermal
(R186)","Cytochrome P450 2E1 (P05181) 
Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
(R186)","Hexachlorocyclohexane is a neurotoxin that interferes with GABA neurotransmitter function by interacting with the GABA-A receptor-chloride channel complex at the picrotoxin binding site, causing over stimulation of the central nervous system. It is also believed to inhibit sodium/potassium-transporting ATPases and be an endocrine disruptor. In the liver, hexachlorocyclohexane is thought to cause oxidative stress by interfering with hepatic oxidative capacity and glutathione metabolism, increasing lipid metabolism, and inhibiting magnesium ATPase activity. Hexachlorocyclohexane may also inhibit gap junction and intercellular communication, leading to uncontrolled cell growth and tumor promotion. (R186, R187, R188)","Hexachlorocyclohexane is absorbed through the skin, lungs, and intestines, then distributed mainly to the adipose tissue but also to the brain, kidney, muscle, and blood. Metabolism occurs via dechlorination, dehydrogenation, dehydrochlorination, and hydroxylation by hepatic cytochrome P-450 enzymes. The main metabolites are polychlorophenols and 1,2,4-trichlorocyclohexane-4,5-epoxide, which are excreted in the urine. (R186)","LD50: 1000 mg/kg (Oral, Rat) (R261)","","2B, possibly carcinogenic to humans. (R264)","Hexachlorocyclohexane is used as an insecticide on fruit, vegetables, and forest crops and is also available as a prescription (lotion, cream, or shampoo) to treat head and body lice, and scabies. (R186)","","Exposure to large amounts of hexachlorocyclohexane can harm the nervous system, producing a range of symptoms from headache and dizziness to seizures, convulsions and more rarely death. Hexachlorocyclohexane is known to damage the liver, kidneys, and immune system, as well as cause blood disorders and reproductive and developmental defects. Hexachlorocyclohexane is also potentially carcinogenic. (R186, R187)","Exposure to large amounts of hexachlorocyclohexane can harm the nervous system, producing a range of symptoms from headache and dizziness to seizures, convulsions and more rarely death. (R187)","Hexachlorocyclohexane poisoning is treated symptomatically. Gastric lavage, followed by the administration of activated charcoal, may be performed upon ingestion. (R284)",P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P18507;Q99928;O00591;P24046;P28476;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P54710;P62508;P10275;P06401;Q8N1C3;A8MPY1;Q9UN88;P78334;P98194;O75185;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;P03372;Q92731
45,T3D0044,2009-03-06 18:57:58 UTC,2009-08-04 21:27:31 UTC,"1,2-Dibromo-3-chloropropane",Organic Compound;Pesticide;Organochloride;Organobromide,"1, 2-Dibrom-3-chlor-propan (GERMAN)1, 2-Dibromo-3-cloro-propano (ITALIAN)1,2-Dibrom-3-chlor-propan1,2-Dibrom-3-chlor-propan [German]1,2-Dibromo-3-chloropropane1,2-Dibromo-3-cloro-propano1,2-Dibromo-3-cloro-propano [Italian]1,2-Dibromochloropropane1,2-Dibroom-3-chloorpropaan1,2-Dibroom-3-chloorpropaan (DUTCH)1,2-Dibroom-3-chloorpropaan [Dutch]1,2-dibromo-3-chloropropane (ACD/Name 4.0)1,2-dibromo-3-chloropropane (DBCP)1,3-Dibromo-3-chloropropane1-Chloro-2,3-dibromopropane2,3-Dibromo-1-chloropropane3-Chloro-1,2-dibromopropaneBBCPC3H5Br2ClCBCPCaswell No. 287ClCH2CHBrCH2BrDBCPDibromchlorpropanDibromchlorpropan (german)Dibromchlorpropan [german]Dibromo-3-chloropropane, 1,2- (DBCP)DibromochloropropaneDibromochloropropane [UN2872] [Poison]Durham Nematicode EM 17.1Fumag onFumagonFumazon 86FumazoneFumazone 86Fumazone 86eGro-tone nematode granularInChI=1/C3H5Br2Cl/c4-1-3(5)2-6/h3H,1-2HNemabromNemafumeNemagonNemagon 20Nemagon 206Nemagon 20GNemagon 90Nemagon soil fumigantNemagoneNemanaxNemanexNemapazNemasetNematocideNematocide EM 12.1Nematocide EM 15.1Nematocide Solution EM 17.1NematoxNemazonOxy DBCPPropane, 1,2-dibromo-3-chloro- ( )Propane, 1-chloro-2,3-dibromo-Propane, dibromochloro-RCRA waste no. U066RCRA waste number U066WLN: G1YE1E","1,2-Dibromo-3-chloropropane is a manufactured chemical and the active ingredient in the nematicide Nemagon, also known as Fumazone. Nemagon is a soil fumigant formerly used in agriculture but banned to most areas today. (R237)",,96-12-8,7280,,C14336,"","",BETA-AMINOPROPIONITRILE,,C007318,"1,2-Dibromo-3-chloropropane",416,,,,"InChI=1/C3H5Br2Cl/c4-1-3(5)2-6/h3H,1-2H2","1,2-dibromo-3-chloropropane",http://www.biospider.ca/saved_files/mol/a10a668ea6a04adebfcfa2a0bc0413c6_1237937373.mol,C(C(CBr)Br)Cl,C(C(CBr)Br)Cl,C3H5Br2Cl,233.844650,Colorless liquid.,6 °C,,,"1.23 mg/mL at 20 °C [MUNNECKE,DE & VANGUNDY,SD (1979)]",,,,Oral Inhalation Dermal (R236),"Glutathione S-transferase P (P09211) 
Glutathione S-transferase Mu 1 (P09488) 
Glutathione S-transferase A1 (P08263) 
Glutathione S-transferase theta-2 (P30712) 
Glutathione S-transferase Mu 4 (Q03013) 
Glutathione S-transferase theta-1 (P30711) 
Glutathione S-transferase A4 (O15217) 
Glutathione S-transferase A2 (P09210) 
Glutathione S-transferase A3 (Q16772) 
Glutathione S-transferase Mu 3 (P21266) 
Glutathione S-transferase omega-1 (P78417) 
Glutathione S-transferase kappa 1 (Q9Y2Q3) 
Glutathione S-transferase Mu 2 (P28161) 
Glutathione S-transferase omega-2 (Q9H4Y5) 
Glutathione S-transferase A5 (Q7RTV2) 
Glutathione S-transferase Mu 5 (P46439) 
Glutathione S-transferase theta-4 (A8MPT4) 
Maleylacetoacetate isomerase (O43708) 
Microsomal glutathione S-transferase 1 (P10620) 
Microsomal glutathione S-transferase 2 (Q99735) 
Microsomal glutathione S-transferase 3 (O14880) 
(R236)","The initial metabolism of 1,2-dibromo-3-chloropropane to reactive epoxide metabolites that bind to DNA and other macromolecules may be responsible for its hepatotoxicity and nephrotoxicity. The mechanism of 1,2-dibromo-3-chloropropane's testicular toxicity is believed to be due to either the inhibition of sperm carbohydrate metabolism, probably at the step of nicotinamide adenine dinucleotide (NADH) dehydrogenase activity in the mitochondrial electron transport chain, or drect DNA damage caused by its metabolites. (R236, R238)","1,2-Dibromo-3-chloropropane is absorbed via oral, inhalation, and dermal routes. It accumulates mainly in the kidney, liver, and adipose tissues. 1,2-Dibromo-3-chloropropane is intially converted to epoxy derivatives, which are
further hydrolyzed and debrominated. Glutathione (GSH) conjugation of epoxide intermediates in the liver is believed to produce precursors to toxic intermediates. The metabolites are excreted mainly in the urine. (R236)","LD50: 100 mg/kg (Oral, Rabbit) (R292)
LC50: 1480 mg/m3 over 1 hour (Inhalation, Rat) (R292)","","2B, possibly carcinogenic to humans. (R264)","1,2-Dibromo-3-chloropropane is the active ingredient in the nematicide Nemagon, also known as Fumazone. Nemagon is a soil fumigant formerly used in agriculture. (R236)","Intermediate Inhalation: 0.0002 ppm (R260)
Intermediate Oral: 0.002 mg/kg/day (R260)","Breathing high levels of 1,2-dibromo-3-chloropropane causes reproductive damage, including reduced sperm counts, birth defects, and infertility. It may also damage the stomach, liver, kidneys, brain, spleen, blood, and lungs, and cause skin and eye damage from direct contact. (R236)","Symptoms of 1,2-dibromo-3-chloropropane exposure include headaches, nausea, lightheadedness, and weakness. (R236)","",P49821;P19404;P56181;O75306;O75489;O43181;O43920;O75380;O75251;O00217;P28331;P03886;P03891;P03897;P03905;P03901;P03915;P03923;DNA;P98194;O75185;P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P78334;Q8N1C3;P18507;Q99928;O00591;P24046;P28476;A8MPY1;Q9UN88;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;P54710;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P03372;Q92731
46,T3D0045,2009-03-06 18:57:58 UTC,2009-08-04 21:27:31 UTC,Pentachlorophenol,Organic Compound;Pesticide;Aromatic Hydrocarbon;Organochloride,"1-Hydroxy-2,3,4,5,6-pentachlorobenzene1-Hydroxypentachlorobenzene2, 3,4,5,6-Pentachlorophenol2,3,4,5,6-PENTACHLOROPHENOL, TECHNICAL GRADE2,3,4,5,6-Pentachlorophenol2,3,4,5,6-Pentachlorophenol (Dowicide EC-7)2,3,4,5,6-pentachlorophenol (ACD/Name 4.0)AcutoxCaswell No. 641Chem-pentaChem-tolChlonChlorophenCryptogil oilCryptogil olDow pentachlorophenol dp-2 antimicrobialDowcide 7Dowicide 7Dowicide 7 AntimicrobialDowicide ec-7Dowicide gDura treet IIDura-treetDurotoxEP 30 (pesticide)ForepenForpen-50 Wood PreservativeFungifenGlazd pentaGrundier arbezolLauxt olLauxtolLauxtol aLiropremOntrack we herbicideOrtho triox liquid vegetation killerOsmoplasticOsmose wood preserving compoundP2604_ALDRICHPCIPCPPCP (pesticide)PCP, pentaPKHFPS7_SUPELCOPenchlorolPenchlorolsantophen 20PentaPenta WRPenta concentratePenta readyPenta-kilPentachloorfenolPentachloorfenol (dutch)Pentachloorfenol [dutch]Pentachloro-phenolPentachlorofenolPentachlorophenatePentachlorophenate, sodiumPentachlorophenolPentachlorophenol [UN3155] [Poison]Pentachlorophenol [bsi:iso]Pentachlorophenol purePentachlorophenol solutionPentachlorophenol, dowicide ec-7Pentachlorophenol, dp-2Pentachlorophenol, purifiedPentachlorophenol, technicalPentachlorphenolPentachlorphenol (german)Pentachlorphenol [german]PentaclorofenoloPentaclorofenolo (italian)Pentaclorofenolo [italian]PentaconPentasolPenwarPeratoxPermacidePermagardPermasanPermatoxPermatox pentaPermitePhenol, pentachloro-, purePol nuPol-nuPole topper fluidPrevenolPreventol pPriltoxRCRA waste no. U242Rcra waste number U242SantobriteSantophenSantophen 20SinituhoSodium pentachlorophenateTerm-I-trolThompson's wood fixWLN: QR bg CG dg eg FGWatershed wood preservativeWeed and brush killerWeedoneWitophen pWoodtreat apentachlorophenol dp-2permatox dp-2","Pentachlorophenol (PCP) is a manufactured substance which is a restricted use pesticide and is used industrially as a wood preservative for utility poles, railroad ties, and wharf pilings. It can be found in two forms: PCP itself or as the sodium salt of PCP, which dissolves easily in water. (R239, R240)",,87-86-5,992,,C02575,"",17642,CPD-10489,,D010416,Pentachlorophenol,1132,,,,InChI=1/C6HCl5O/c7-1-2(8)4(10)6(12)5(11)3(1)9/h12H,"2,3,4,5,6-pentachlorophenol",http://www.biospider.ca/saved_files/mol/3b400c5c6dcbd4b3200900962ecb7998_1237937502.mol,C1(=C(C(=C(C(=C1Cl)Cl)Cl)Cl)Cl)O,C1(=C(C(=C(C(=C1Cl)Cl)Cl)Cl)Cl)O,C6HCl5O,263.847000,Colorless (pure) or dark gray to brown (inpure) solid.,174 °C,,,"0.014 mg/mL at 25 °C [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral 
Inhalation 
Dermal
(R239)","UDP-glucuronosyltransferase 1-1 (P22309) 
UDP-glucuronosyltransferase 1-4 (P22310) 
Sulfotransferase 1A1 (P50225) 
Sulfotransferase 1A2 (P50226) 
Sulfotransferase 1A3/1A4 (P50224) 
Cytochrome P450 3A4 (P08684) 
Cytochrome P450 3A7 (P24462) 
(R239)","Pentachlorophenol is believed to exert its toxic effects by uncoupling mitochondrial oxidative phosphorylation, thereby causing accelerated aerobic metabolism and increased heat production. This results from pentachlorophenol binding to liver mitochondrial proteins and inducing conformational changes in enzymes involved in oxidative phosphorylation. Pentachlorophenol can also bind to cell membranes, causing changes in the hydrogen ion permeability of the membrane lipid matrix and disrupting membrane structure and function. Pentachlorophenol causes adverse effects on thyroid homeostasis, decreasing serum thyroxine by competing for serum protein thyroxine binding sites. Pentachlorophenol also competes with thyroxine for uptake into cerebrospinal fluid at the T4 binding site of transthyretin. Pentachlorophenol inhibits mitochondrial ATP-ase activity, preventing the the formation of ATP and the release of energy to the cell from the breakdown of ATP to ADP. Pentachlorophenol metabolites, especially quinones and semiquinones, may damage DNA by forming adducts. (R239, R244)","Pentachlorophenol is efficiently absorbed following inhalation, oral, and dermal exposure, then binds to plasma proteins and is distributed to the liver, lungs, kidneys, blood, fat tissues, and brain. Extensive plasma protein binding of pentachlorophenol may account for its low degree of metabolism. Metabolism of pentachlorophenol occurs in the liver, and the major pathways are conjugation to form the glucuronide and oxidative dechlorination to form tetrachlorohydroquinone (TCHQ). Pentachlorophenol and its metabolites are excreted mainly in the urine. (R239)","LD50: 27 mg/kg (Oral, Rat) (R293)
LD50: 96 mg/kg (Dermal, Rat) (R293)
LD50: 56 mg/kg (Intraperitoneal, Rat) (R293)
LD50: 58 mg/kg (Subcutaneous, Rat) (R293)",,,"Pentachlorophenol is a restricted use pesticide and is used industrially as a wood preservative for utility poles, railroad ties, and wharf pilings. (R239)","Acute Oral: 0.005 mg/kg/day (R260)
Intermediate Oral: 0.001 mg/kg/day (R260)
Chronic Oral: 0.001 mg/kg/day (R260)","Exposure to high levels of pentachlorophenol can cause the cells in the body to produce excess heat. The body temperature can increase to dangerous levels, causing injury to various organs and tissues, and even death. HIgh doses of pentachlorophenol may also cause damage to the immune system, liver, thyroid, kidneys, blood, lungs, nervous system, gastrointestional tract, and reproductive system. (R239)","Exposure to high levels of pentachlorophenol can cause the cells in the body to produce excess heat, resulting in a very high fever, profuse sweating, and difficulty breathing. Contact with pentachlorophenol, particularly in the form of vapor can irritate the skin, eyes, and mouth. (R239, R240)","As pentachlorophenol has no specific antidote, treatment is mainly symptomatic and may include respiratory assistance and administering IV fluids. (R294)",P50225;P50226;P50224;P22303;P02766;P43155;P28329;Q7L5N7;P05543;Q8NF37;P54710;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P20648;P54707;P51164;Q9UN42;P98194;O75185;P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P78334;Q8N1C3;P18507;Q99928;O00591;P24046;P28476;A8MPY1;Q9UN88;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;P03372;Q92731
47,T3D0046,2009-03-06 18:57:59 UTC,2009-08-04 21:27:31 UTC,Heptachlor epoxide,Organic Compound;Pesticide;Organochloride,β-heptachlorepoxideEpoxyheptachlorHCEHeptachlore epoxideVelsicol 53-CS-17,"Heptachlor epoxide is a chemical produced when heptachlor is broken down by bacteria and animals. Heptachlor is a manufactured cyclodiene organochlorine insecticide. As it is a persistant organic pollutant, heptachlor use is banned or limited in most areas. The epoxide is more likely to be found in the environment than heptachlor. (R218, R219)",,1024-57-3,13930,,C14327,"",25520,"",,D006534,Heptachlor epoxide,6458,,,,"InChI=1/C10H5Cl7O/c11-3-1-2(4-5(3)18-4)9(15)7(13)6(12)8(1,14)10(9,16)17/h1-5H","",http://www.biospider.ca/saved_files/mol/ae168fae18dbf6eb3c48e1156bc224ca_1237937675.mol,C12C(C(C3C1O3)Cl)C4(C(=C(C2(C4(Cl)Cl)Cl)Cl)Cl)Cl,C12C(C(C3C1O3)Cl)C4(C(=C(C2(C4(Cl)Cl)Cl)Cl)Cl)Cl,C10H5Cl7O,385.816010,,160 °C,,,"0.0002 mg/mL at 25 °C [BIGGAR,JW & RIGGS,RI (1974)]",,,,"Oral 
Inhalation 
Dermal
(R218)",,"Heptachlor epoxide is a central nervous system stimulant. It non-competitively blocks neurotransmitter action at gamma-amino butyric acid receptors, resulting in overstimulation of the nervous system. Heptachlor epoxide is also believed to exert carcinogenic effects by activating key kinases in signalling pathways and inhibiting apoptosis. (R218, R220, R221)","Heptachlor epoxide is readily absorbed by the skin, lungs and gastrointestinal tract and excreted in the urine and faeces. (R218)",,,"2B, possibly carcinogenic to humans. (R264)","Heptachlor epoxide is a chemical produced when heptachlor is broken down by bacteria and animals. Heptachlor was originally widely produced as an insecticide, but is now used only in fire ant control in underground transformers. (R218)",,"Exposure to heptachlor epoxide may cause damage to liver, nervous system, and immune system. (R218)","Heptachlor epoxide poisoning may cause convulsions, vomiting, seizures, confusion, incoordination, excitability, coma, hypotension, and respiratory failure. (R218)","Treatment is symptomatic and is aimed at controlling convulsions, coma, and respiratory depression. (R218) ",P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;Q8N1C3;P18507;Q99928;O00591;P24046;P28476;A8MPY1;Q9UN88;P78334;P98194;O75185;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;P54710;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P03372;Q92731
48,T3D0047,2009-03-06 18:57:59 UTC,2009-08-04 21:27:32 UTC,Carbon tetrachloride,Organic Compound;Solvent;Reagent;Organochloride,"BenzenoformBenzinoformCC m0CCl4CTCarbon chlorideCarbon chloride (CCl4)Carbon tetCarbon tetrachloride [UN1846] [Poison]Carbon tetrachloride [bsi:iso]CarbonaCarboneum chloratumCarbontetrachlorideCaswell No. 164Chlorid uhlicityChlorid uhlicity [czech]Czterochlorek weglaCzterochlorek wegla (polish)Czterochlorek wegla [polish]FasciolinFlukoidsFreon 10HSDB 53Halon 104KatharinKohlenstofftetrachloridMethane tetrachlorideMethane, tetrachloro-NecatorinaNecatorinePerchloromethanePhenoxinR 10 (Refrigerant)RCRA waste no. U211Rcra waste number U211Refrigerant R10SeretinTetraTetrachloorkoolstofTetrachloorkoolstof (dutch)Tetrachloorkoolstof [dutch]TetrachloormetaanTetrachloride, carbonTetrachloridocarbonTetrachlorkohlenstoffTetrachlorkohlenstoff, tetraTetrachlorkohlenstoff, tetra (german)Tetrachlorkohlenstoff, tetra [german]TetrachlormethanTetrachlormethan (german)Tetrachlormethan [german]TetrachlorocarbonTetrachlorom ethaneTetrachloromethaneTetrachlorure de carboneTetrachlorure de carbone (french)Tetrachlorure de carbone [french]Tetrachlorure de carbone [iso-french]TetraclorometanoTetraclorometano (italian)Tetraclorometano [italian]Tetracloruro di carbonioTetracloruro di carbonio (italian)Tetracloruro di carbonio [italian]TetrafinolTetraformTetraform (van)TetrasolThawpitUnivermVermoestricidWLN: GXGGGtetrachloromethane (ACD/Name 4.0)","Carbon tetrachloride manufactured chemical used as a reagent in synthetic chemistry and formerly in fire extinguishers, as a precursor to refrigerants, and as a cleaning agent. It is a colourless liquid with a ""sweet"" smell that can be detected at low levels. (R200)",,56-23-5,5943,,C07561,"",27385,CPD-842,,D002251,Carbon tetrachloride,253,,,http://en.wikipedia.org/wiki/Carbon tetrachloride,"InChI=1/CCl4/c2-1(3,4)5",tetrachloromethane,http://www.biospider.ca/saved_files/mol/323ea2aecf6ce9d14b90ac8631190fdd_1237937770.mol,C(Cl)(Cl)(Cl)Cl,C(Cl)(Cl)(Cl)Cl,CCl4,151.875410,Clear liquid.,-23 °C,,,"0.793 mg/mL at 25 °C [HORVATH,AL (1982)]",,,,"Oral 
Inhalation 
Dermal
(R245)","Cytochrome P450 2E1 (P05181)
(R245)","Unmetabolized carbon tetrachloride, depresses the central nervous system. All other toxic effects of carbon tetrachloride are related to its biotransformation via cytochrome P-450 enzymes, specifically CYP2E1. Metabolism of carbon tetrachloride by CYP2E1 may result in the destruction of the enzyme during the metabolic process, either by direct attack of radicals on the cytochrome(s) or highly localized lipid peroxidation resulting in detachment of P-450 proteins from the microsomal membranes. Reactive metabolites of carbon tetrachloride causes hepatic damage via haloalkylation of cellular macromolecules and lipid peroxidation. Carbon tetrachloride also perturbs the intracellular calcium homeostasis. Increased cytosolic levels of calcium may result from an influx of extracellular calcium caused by plasma membrane damage and decreased intracellular calcium sequestering. Higher levels of calcium activate enzymes such as proteases, which hydrolyze proteins in neighboring cells, leading to a progression of the lesion. Carbon tetrachloride's carcinogenicity is likely the result of certain reactive metabolites that bind to nuclear proteins, lipids, and DNA. (R029, R245)","Carbon tetrachloride is absorbed readily from the gastrointestinal and respiratory tracts, and more slowly through the skin. It is distributed to all major organs, with highest concentrations in the fat, liver, bone marrow, adrenals, blood, brain, spinal cord, and kidney. Once carbon tetrachloride is absorbed, it is metabolized by cytochrome P-450 enzymes, with the production of the trichloromethyl radical. Aerobically, metabolism of the trichloromethyl radical can eventually form phosgene. Anaerobically, the radical can undergo reactions to form chloroform, hexachloroethane, or carbon monoxide. Carbon tetrachloride is excreted primarily in exhaled air and in the feces, with relatively minimal amounts in the urine. (R245)","LD50: 2800 mg/kg (Oral, Rat) (R286)",1700 to 1800 mg/kg for an adult human. (R293),"2B, possibly carcinogenic to humans. (R264)","Carbon tetrachloride was used in the production of refrigeration fluid and propellants for aerosol cans, as a pesticide, as a cleaning fluid and degreasing agent, in fire extinguishers, and in spot removers. (R245)","Intermediate Inhalation: 0.03 ppm (R260)
Chronic Inhalation: 0.03 ppm (R260)
Acute Oral: 0.02 mg/kg/day (R260)
Intermediate Oral: 0.007 mg/kg/day (R260)","High exposure to carbon tetrachloride can cause liver, kidney, and central nervous system damage. Single cell necrosis, which is evident after 5h to 6h after dosing, progresses to maximal centrilobular necrosis within 24h to 48h. Cellular regeneration is maximal 36h to 48h after dosing. The rate and extent of tissue repair are important determinants of the ultimate outcome of liver injury. In severe cases, coma and even death may occur. (R029, R245)","Carbon tetrachloride exposure causes headaches, dizziness, sleepiness, nausea, and vomiting. (R245)","",P05181;DNA;P98194;O75185;P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P78334;Q8N1C3;P18507;Q99928;O00591;P24046;P28476;A8MPY1;Q9UN88;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;P54710;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P03372;Q92731
49,T3D0048,2009-03-06 18:57:59 UTC,2009-08-25 19:55:47 UTC,Aroclor 1221,Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"","Aroclor 1221 is a commercial mixture of PCBs with an average chlorine content of 21%. It is composed of mainly monochlorobiphenyls (60.06%), and also includes bi-, tri, tetra-, and pentachlorinated homologs. Polychlorinated biphenyls (PCBs) are a group of 209 synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. PCBs were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate in the environment and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,11104-28-2,"",,"","","","",,C032739,Aroclor 1221,,,,,"","",http://www.biospider.ca/saved_files/mol/,"",Clc1ccc(c(Cl)c1Cl)-c1ccc(Cl)c(Cl)c1Cl,"","",Clear oil.,Boiling Pt : 290-325 oC,275–320 °C,1.18 g/cm3,"0.015 mg/mL at 25 °C [MABEY,WR et al. (1981)]","",141–150 °C,6.7x10-3 mmHg at 25 °C,"Oral 
Inhalation 
Dermal 
(R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 3980 mg/kg (Oral, Rat) (R263)","","2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refrigerators) produced before 1977. PCBs may contaminate the air and water near hazardouc waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 µg/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P35869;P49888;P03372;P11684;P20711;Q92731;P07101
50,T3D0049,2009-03-06 18:57:59 UTC,2009-08-27 18:13:26 UTC,Cobalt,Inorganic Compound;Metal;Cobalt Compound,"AquacatCOCOBALT, POWDER, 99.9%Cobalt Oligosol Liq 0.45mg/2mlCobalt atomic absorption standard solutionCobalt icp/DCP standard solutionCobalt solutionCobalt standard for icCobalt(II) nitrate solutionCobalt-59Cobalt-liqCobaltum Dps 4ch-30chCobaltum metallicumCobaltum muriaticumCobaltum nitricumCobatope-57Coblatum nitricumKobaltOligostim Cobalt - Tab 6dhRaney-cobaltSuper cobalt","Cobalt is a metallic element with the atomic number 27. It is found naturally in rocks, soil, water, plants, and animals, and is mainly used to produce alloys and pigments. In small amounts cobalt is an essential element for life, as it is part of vitamin B12. However, excess exposure is known to exhibit toxic effects. Cobalt also exists in the toxic radioactive form Cobalt-60. (R084, R085)",,7440-48-4,104730,,C00175,"",27638,COBALT-FACTOR-III,,D003035,Cobalt,7202,,,http://en.wikipedia.org/wiki/Cobalt,InChI=1/Co,cobalt,http://www.biospider.ca/saved_files/mol/f04380b9728cd63a8000ec42753a3f28_1237937947.mol,[Co++],[Co++],[Co]2+,58.933189,Grey metallic solid.,1495 °C,"","","","","","","Inhalation 
Oral 
Dermal 
Radiation
(R084)",Serum albumin (P02768) (R087),"Cobalt is believed to exhibit its toxicity through a oxidant-based and free radical-based processes. It produces oxygen radicals and may be oxidized to ionic cobalt, causing increased lipid peroxidation, DNA damage, and inducing certain enzymes that lead to cell apoptosis. Cobalt has also been shown to block inorganic calcium channels, possibly impairing neurotransmission. Cobalt can also chelate lipoic acids, impairing oxidation of pyruvate or fatty acids. In addition, cobalt may inhibit DNA repair by interacting with zinc finger DNA repair proteins, and has also been shown to inhibit heme synthesis and glucose metabolism. Cobalt may activate specific helper T-lymphocyte cells and interact directly with immunologic proteins, such as antibodies (IgA and IgE) or Fc receptors, resulting in immunosensitization. Radioactive cobalt damages DNA, RNA, and lipids through ionizing events. (R084)","Cobalt is absorbed though the lungs, gastrointestinal tract, and skin. Since it is a component of the vitamin B12 (cyanocobalamin), it is distributed to most tissues of the body. It is transported in the blood, often bound to albumin, with the highest levels being found in the liver and kidney. Cobalt is excreted mainly in the urine and faeces. (R084)","LD50: 6170 mg/kg (Oral, Rat) (R293)
LD50: 100 mg/kg (Intraperitoneal, Rat) (R293)",1 to 2 mg/m3 for an adult human. (R270),"2B, possibly carcinogenic to humans. (R264)","Cobalt is used to produce alloys used in the manufacture of aircraft engines, magnets, grinding and cutting tools, artificial hip and knee joints. Cobalt compounds are also used to color glass, ceramics and paints, and used as a drier for porcelain enamel and paints. Radioactive cobalt is used for commercial and medical purposes, such as for sterilizing medical equipment and consumer products, radiation therapy for treating cancer patients, manufacturing plastics, and irradiating food. (R084)","Chronic Inhalation: 0.0001 mg/m3 (R260) 
Intermediate Oral: 0.01 mg/kg/day (R260) 
Acute Radiation: 4 mSv (R260) 
Chronic Radiation: 1 mSv/yr (R260)","Exposure to high amount of cobalt can cause heart, lung, kidney, and liver damage. Skin contact is known to result in contact dermatitus. Cobalt may also have mutagenic and carcinogenic effects. Exposure to cobalt radiation causes cell damage and can lead to severe burns and death at high doses. (R084, R085)","Exposure to cobalt radiation may cause acute radiation syndrome, which is characterized by nausea, vomiting, diarrhea, bleeding, and possibly coma. (R084)",Treatment of cobalt poisoning is symptomatic. (R084),P00915;P00918;P22748;Q13936;P01854;P01877;P01876;P23025;P09874;P22557;P13196;Q06432;Q9Y698;O60359;Q9UBN1;Q9UF02;Q9BXT2;P62955;Q8WXS5;Q8WXS4;P54289;Q9NY47;Q8IZS8;Q7Z3S7;Q01668;O60840;Q13698;Q02641;Q08289;P54284;O00305;Q00975;O00555;Q15878;DNA
51,T3D0050,2009-03-06 18:57:59 UTC,2009-08-04 21:27:32 UTC,"DDT, O,P'-",Organic Compound;Pesticide;Organochloride,"(-)-o,p'-DDT1,1,1-Trichloro-2-(o-chlorophenyl)-2-(p-chlorophenyl)ethane1-Chloro-2-(2,2,2-trichloro-1-(4-chlorophenyl)ethyl)benzene1-Chloro-2-[2,2,2-trichloro-1-(4-chlorophenyl)ethyl]benzene2, 2-Bis(o,p-chlorophenyl)-1,1,1-trichloroethane2,2,2,o,p'-Pentachloroethylidenebisbenzene2,2-Bis(o,p-chlorophenyl)-1,1,1-trichloroethane2-(2-Chlorophenyl)-2-(4-chlorophenyl)-1,1,1-trichloroethaneDDT, o,p'-DDT-o,p'O,p'-DDTO,p'-DDT, (r)-isomerO,p-DDTOrtho,para'-DDTWLN: GXGGYR bg&r DG","DDT, O,P'- is an isomer of dichlorodiphenyltrichloroethane, an organochlorine insecticide. It is the major component of commercial mixtures of DDT. DDT was once a widely used pesticide, but today its agricultural use has been banned worldwide due to its toxicity and tendency to bioaccumulate. However, it still has limited use in disease vector control. (R152)",,789-02-6,13089,,C14187,"","","",,C016340,"DDT, O,P'-",,,,,"InChI=1/C14H9Cl5/c15-10-7-5-9(6-8-10)13(14(17,18)19)11-3-1-2-4-12(11)16/h1-8,13H","1-chloro-4-[2,2,2-trichloro-1-(2-chlorophenyl)ethyl]benzene",http://www.biospider.ca/saved_files/mol/bf01e91fed3a7484274264f2c2932b4a_1237938184.mol,C1=CC=C(C(=C1)C(C2=CC=C(C=C2)Cl)C(Cl)(Cl)Cl)Cl,C1=CC=C(C(=C1)C(C2=CC=C(C=C2)Cl)C(Cl)(Cl)Cl)Cl,C14H9Cl5,351.914690,White solid.,"","","","8.5e-05 mg/mL at 25 °C [YALKOWSKY,SH & DANNENFELSER,RM (1992)]","","","",Ingestion (R153),"Cytochrome P450 2B6 (Q16678) 
Cytochrome P450 3A4 (P08684) 
Cytochrome P450 3A5 (P20815) 
Cytochrome P450 3A7 (P24462) 
Cytochrome P450 3A43 (Q9HB55)
(R153)","DDT toxicity occurs via at least four mechanisms, possibly all functioning simultaneously. DDT reduces potassium transport across the membrane. DDT inhibits inactivation of the porous channels through which sodium ions pass. The channels activate (open) normally but are inactivated (closed) slowly, thus interfering with the active transport of sodium out of the nerve axon during repolarization, causing a state of hyperexcitability. DDT inhibits neuronal adenosine triphosphatases (ATPases), particularly Na+K+-ATPase, and Ca2+-ATPase which play vital roles in neuronal repolarization. DDT also inhibits the ability of calmodulin, a calcium mediator in nerves, to transport calcium ions that are essential for the release of neurotransmitters. All these inhibited functions reduce the rate of depolarization and increase the sensitivity of neurons to small stimuli that would not elicit a response in a fully depolarized neuron. DDT is also believed to adversely affect the reproductive system by mimicking endogenous hormones and binding to the estrogen and adrogen receptors. (R029, R153)","DDT is absorbed in the stomach and intestine, after which it enters the lymphatic system and is carried throughout the body and incorporated into fatty tissues. Metabolism of DDT occurs mainly via cytochrome P-450 enzymes in the liver and kidney, where it undergoes reductive dechlorination to DDD (dichlorodiphenyldichloroethane) and DDE (dichlorodiphenyldichloroethylene). These compounds are further degraded into additional metabolites, mainly DDA (bis(p-chlorophenyl) acetic acid), which are excreted in the urine. (R153)","LD50: 87 mg/kg (Oral, Rat) (R275)
LD50: 1931 mg/kg (Dermal, Rat) (R275) 
LD50: 1500 mg/kg (Subcutaneous, Rat) (R275)","","2B, possibly carcinogenic to humans. (R264)",DDT is used as a pesticide and in disease vector control. (R152),"","Exposure to DDT causes loss of weight and anorexia. DDT poisoning affects CNS function in humans, but pathologic changes are observed in the liver and reproductive organs. Hypertrophy of hepatocytes and subcellular organelles such as mitochondria, proliferation of smooth endoplasmic reticulum, centrolobular necrosis after exposure to high concentrations, and an increase in the incidence of hepatic tumors have been noted.
(R029)","Acute signs of DDT poisoning include paresthesia after oral ingestion. Studies have shown that a mammal poisoned with DDT-type agents displays periodic persistent tremoring and/or convulsive seizures that are suggestive of repetitive discharges in neurons. These repetitive tremors and seizures can be initiated by tactile and auditory stimuli.
(R029)","Treatment of DDT exposure should be primarily directed towards decontamination and supportive care, as there is no specific antidote. The use of gastric lavage and activated charcoal for large ingestions may be effective. (R274)",P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P54710;P98194;O75185;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;P62158;P03372;Q92731;P10275;Q9UL51;Q9Y3Q4;O60741;Q9P1Z3 ;P35498;Q9Y5Y9;Q9UI33;Q99250;Q9NY46;P35499;Q14524;Q01118;Q9UQD0;Q15858;Q07699;O60939;Q9NY72;Q8IWT1;P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P78334;Q8N1C3;P18507;Q99928;O00591;P24046;P28476;A8MPY1;Q9UN88
52,T3D0051,2009-03-06 18:57:59 UTC,2009-08-11 15:56:24 UTC,Aroclor 1016,Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 3,3',5-trichloro-3,3',5-TRICHLOROBIPHENYLArochlor 1016Aroclor 1016Chlorodiphenyl (41% Cl)Polychlorinated biphenyl (aroclor 1016)","Aroclor 1016 is a commercial mixture of PCBs with an average chlorine content of 41.5%. It is composed of mainly trichlorobiphenyls (54.67%), and also includes mono-, bi-, tetra-, and pentachlorinated homologs. Polychlorinated biphenyls (PCBs) are a group of 209 synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. PCBs were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate in the environment and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,12674-11-2,38037,,"","","","",,C027386,Aroclor 1016,99,,,,InChI=1/C12H7Cl3/c13-10-3-1-2-8(4-10)9-5-11(14)7-12(15)6-9/h1-7H,"1,3-dichloro-5-(3-chlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=CC(=C1)Cl)C2=CC(=CC(=C2)Cl)Cl,Clc1cccc(c1)-c1cc(Cl)cc(Cl)c1,C12H7Cl3,255.961330,Clear oil.,"",325–356 °C ,1.37 g/cm3,"0.00042 mg/mL at 25 °C [MABEY,WR et al. (1981)]","",170 °C,4x10-4 mmHg at 25 °C,"Oral 
Inhalation 
Dermal 
(R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are transported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 2300 mg/kg (Acute oral, Rat) (R263)","","2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refrigerators) produced before 1977. PCBs may contaminate the air and water near hazardouc waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 µg/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P35869;P49888;P03372;P11684;P20711;Q92731;P07101
53,T3D0052,2009-03-06 18:57:59 UTC,2009-08-25 15:53:56 UTC,Di-n-butyl phthalate,Organic Compound;Plasticizer;Aromatic Hydrocarbon;Phthalate,"1,2-Benzenedicarboxylic acid, dibutyl esterAraldite 502BUFABenzene-o-dicarboxylic acid di-n-butyl esterBenzene-o-dicarboxylic acid, di-n-butyl esterBenzenedicarboxylic acid, dibutyl esterButyl phthalateCaswell No. 292Celluflex DPBDBPDBP (ester)Di n butyl phthalateDi-n-butyl phthalateDi-n-butyl phthalate (dbup)Di-n-butylester kyseliny ftalove [czech]Di-n-butylorthophthalateDibutyl 1, 2-benzenedicarboxylateDibutyl 1,2-benzenedicarboxylateDibutyl ester of 1,2-benzenedicarboxylic acidDibutyl o-phthalateDibutyl phthalatedDibutyl-1,2-benzenedicarboxylateDibutyl-o-phthalateDibutyll phthalateDibutylphthatlateElaolErgoplast FDBErsoplast fdaGenoplast bHatcol DBPHexaplas m/bKodaflex DBPMorflex 240N-butyl phthalateN-butylphthalateO-benzenedicarboxylic acid, dibutyl esterOrtho-dibutyl phthalatePalatinol DBPPalatinol cPhthalate, butylPhthalate, di-n-butylPhthalate, dibutylPhthalate, dibutyl-Phthalic acid di-n-butyl esterPhthalic acid dibutyl esterPhthalic acid, dibutyl esterPolycizer DBPRC plasticizer DBPRCRA waste no. U069RCRA waste number U069Staflex DBPUniflex DBPUnimoll DBUniplex 150WLN: 4OVR BVO2Witcizer 300dibutyl phthalate (ACD/Name 4.0)","Di-n-butyl phthalate is a manufactured chemical that is added to plastics, paint, glue, hair spray, and other household products. It is commonly found in the environment, and most people are exposed to low levels in the air, water, and food. However, it is believed to have relativel low toxicity. (R258)",,84-74-2,3026,,"","",25520,"",,D003993,Di-n-butyl phthalate,1740,,,http://en.wikipedia.org/wiki/Dibutyl phthalate,"InChI=1/C16H22O4/c1-3-5-11-19-15(17)13-9-7-8-10-14(13)16(18)20-12-6-4-2/h7-10H,3-6,11-12H2,1-2H3","dibutyl benzene-1,2-dicarboxylate",http://www.biospider.ca/saved_files/mol/,CCCCOC(=O)C1=CC=CC=C1C(=O)OCCCC,CCCCOC(=O)c1ccccc1C(=O)OCCCC,C16H22O4,278.151810,Colorless oily liquid.,-35 °C,,,"0.0112 mg/mL at 25 °C [HOWARD,PH et al. (1985)]",,,,"Oral 
Inhalation 
Dermal
(R258)","UDP-glucuronosyltransferase 1-1 (P22309) 
UDP-glucuronosyltransferase 1-3 (P35503) 
UDP-glucuronosyltransferase 1-4 (P22310) 
UDP-glucuronosyltransferase 1-5 (P35504) 
UDP-glucuronosyltransferase 1-6 (P19224) 
UDP-glucuronosyltransferase 1-7 (Q9HAW7) 
UDP-glucuronosyltransferase 1-8 (Q9HAW9) 
UDP-glucuronosyltransferase 1-9 (O60656) 
UDP-glucuronosyltransferase 1-10 (Q9HAW8) 
UDP-glucuronosyltransferase 2A1 (Q9Y4X1) 
UDP-glucuronosyltransferase 2A3 (Q6UWM9) 
UDP-glucuronosyltransferase 2B4 (P06133) 
UDP-glucuronosyltransferase 2B7 (P16662) 
UDP-glucuronosyltransferase 2B10 (P36537) 
UDP-glucuronosyltransferase 2B11 (O75310) 
UDP-glucuronosyltransferase 2B15 (P54855) 
UDP-glucuronosyltransferase 2B17 (O75795) 
UDP-glucuronosyltransferase 2B28 (Q9BY64) 
UDP-glucuronosyltransferase 3A1 (Q6NUS8) 
UDP-glucuronosyltransferase 3A2 (Q3SY77) 
(R258)","The most characteristic effect of di-n-butyl phthalate is testicular atrophy. Di-n-butyl phthalate exposure causes both the release of iron from hemoglobin and/or transferrin in the liver and spleen, and the subsequent depletion of iron in the blood and testes. The decreased amount of available iron results in a decrease in succinate dehydrogenase activity in the Sertoli cells. This results in disturbances in the energy transfer system between Sertoli cells and germ cells, which is required for the differentiation of male germ cells and their progression through the seminiferous epithelium and release as mature spermatozoa. Di-n-butyl phthalate may also exhibit weak estrogenic activity. It has been shown to exhibit toxic effects in liver mitochondria by uncoupling energy-linked processes and inhibiting succinate dehydrogenase. (R258, R259)","Di-n-butyl phthalate is absorbed via oral, inhalation, and dermal routes. It is rapidly distributed and cleared from the body. Metabolism of di-n-butyl phthalate proceeds mainly by nonspecific esterases in the gastrointestinal tract, which hydrolyze of one butyl ester bond to yield mono-n-butyl phthalate, the primary toxic metabolite. Mono-n-butyl phthalate is conjugated with glucuronic acid via glucuronosyltransferase and excreted in the urine. (R258)","LD50: 3050 mg/kg (Acute intraperitoneal, Rat) (R261)
LD50: 720 mg/kg (Acute intravenous, Mouse) (R261)
LD50: 5289 mg/kg (Acute oral, Mouse) (R261)
LC50: 25 g/m3 over 2 hours (Inhalation, Mouse) (R261)",,,"Di-n-butyl phthalate is used to make plastics more flexible and is also in carpet backings, paints, glue, insect repellents, hair spray, nail polish, and rocket fuel. (R258)","","Adverse effects from di-n-butyl phthalate exposure have not yet been reported in humans. However, animals studies have shown that di-n-butyl phthalate can affect reproductive ability by decreasing sperm count and causing birth defects. (R258)",Skin contact with di-n-butyl phthalate may cause mild irritation. (R258),"",Q99643;O14521;P31040;P21912;Q07869;P37231
54,T3D0053,2009-03-06 18:57:59 UTC,2009-08-27 18:15:19 UTC,Nickel,Inorganic Compound;Metal;Nickel Compound,"16-08 NickelAlcan 756Carbonyl nickel powderDextrin, nickel complexFibrexFibrex pMalleable nickelMetallic nickelNINI 0901-S (harshaw)NICKEL, POWDER, 99.9%, 100 MESHNICKEL, SPONGE, 99.999%Ni(+)Ni+Niccolum Liquid (S#1155)-LiqNiccolum carbonicumNiccolum metallicumNiccolum sulfuricumNichelNichel [italian]Nickel 200Nickel 201Nickel 204Nickel 205Nickel 207Nickel 211Nickel 212Nickel 213Nickel 222Nickel 223Nickel 229Nickel 270Nickel [nickel and certain nickel compounds]Nickel [nickel and nickel compounds]Nickel catalystNickel cationNickel compoundsNickel liquidNickel metal and insoluble compoundsNickel particlesNickel spongeNickel(I) cationNickel, dextrin complexesNickel, elementalNickel, elemental/metalNickel, ion (Ni1+)Nickel, metalNickel, metal and insoluble compoundsNickel, metal, soluble, insoluble, and inorganicNickel, soluble compoundsNickel, soluble saltsNiquelRaney alloyRaney nickelnickel(1+)nickel(1+) ion","Nickel is a chemical compound with the atomic number 28. It is found abundantly in nature in laterite ore minerals, such as limonite, garnierite, and pentlandite. Pure nickel is mainly used to make alloys, which are found in items such as coins, jewelry, valves and heat exchangers. Nickel compounds are used for nickel plating, to color ceramics, to make some batteries, and as catalysts. Nickel also has a biological role, and is found in certain enzymes, including urease, hydrogenase, methylcoenzyme M reductase, and carbon monoxide dehydrogenase. (R097, R098)",,7440-02-0,935,,C00291,"",28112,CPD-7425,,D009532,Nickel,946,,,http://en.wikipedia.org/wiki/Nickel,InChI=1/Ni,nickel,http://www.biospider.ca/saved_files/mol/5bbad61751e56b5639ef7332d0782944_1237938546.mol,[Ni++],[Ni++],[Ni]2+,57.935341,Silvery-white metallic solid. ,1455 °C,"","","","","","","Oral 
Inhalation 
Dermal
(R098)","Serum albumin (P02768) 
Alpha-2-macroglobulin (P01023) 
(R098)","Nickel is known to substitute for other essential elements in certain enzmes, such as calcineurin. It is genotoxic, and some nickel compounds have been shown to promote cell proliferation. Nickel has a high affinity for chromatin proteins, particularly histones and protamines. The complexing of nickel ions with heterochromatin results in a number of alterations including condensation, DNA hypermethylation, gene silencing, and inhibition of histone acetylation, which have been shown to disturb gene expression. Nickel has also been shown to alter several transcription factors, including hypoxia-inducible transcription factor, activating transcription factor, and NF-KB transcription factor. There is also evidence that nickel ions inhibit DNA repair, either by directly inhibiting DNA repair enzymes or competing with zinc ions for binding to zinc-finger DNA binding proteins, resulting in structural changes in DNA that prevent repair enzymes from binding. Nickel ions can also complex with a number of cellular ligands including amino acids, peptides, and proteins resulting in the generation of oxygen radicals, which induce base damage, DNA strand breaks, and DNA protein crosslinks. (R098, R100)","Nickel is absorbed mainly through the lungs and gastrointestinal tract. Once in the body it enters the bloodstream, where it binds to albumin, L-histidine, and α2-macroglobulin. Nickel tends to accumulate in the lungs, thyroid, kidney, heart, and liver. Absorbed nickel is excreted in the urine, whereas unabsorbed nickel is excreted in the faeces. (R098)","LD50: 250 mg/kg (Intraperionteal, Rat) (R293)","","1, carcinogenic to humans (compounds) and 2B, possibly carcinogenic to humans (metal, alloys). (R264)","Pure nickel is mainly used to make alloys, which are found in items such as coins, jewelry, valves and heat exchangers. Nickel compounds are used for nickel plating, to color ceramics, to make some batteries, and as catalysts. (R098)","Intermediate Inhalation: 0.0002 mg/m3 (R260)
Chronic Inhalation: 0.00009 mg/m3 (R260)","The most common harmful health effect of nickel in humans is an allergic reaction. This usually manifests as a skin rash, although some people experience asthma attacks. Long term inhahation of nickel causes chronic bronchitis and reduced lung function, as well as damage to the naval cavity. Ingestion of excess nickel results in damage to the stomach, blood, liver, kidneys, and immune system, as well as having adverse effects on reproduction and development. (R098)","Symptoms of nickel poisoning include headache, nausea, vomiting, dizziness, irritability, and difficulty sleeping, followed by chest pains, sweating, rapid heart beat, and a dry cough. (R099)",Excess exposure to nickel is usually handled by preventing further exposure and symptomatic treatment. Nickel poisoning may also be treated using chelation therapy with sodium diethyldithiocarbamate. (R099),P63098;P62805;P68431;Q16695;P84243;P04554;Q71DI3;Q96LZ3;Q08209;P16298;P48454;Q9NNZ6;P04553;P07305;Q02539;P16403;P16402;P10412;P16401;Q8IZA3;P22492;Q92522;Q75WM6;P0C0S8;Q96QV6;P04908;Q93077;P20671;Q96KK5;Q99878;Q6FI13;Q8IUE6;Q16777;Q7L7L0;P0C5Y9;P0C5Z0;Q9BTM1;Q71UI9;P16104;P0C0S5;Q96A08;P33778;P62807;P58876;Q93079;P06899;O60814;Q99880;Q99879;Q99877;P23527;Q16778;Q5QNW6;Q8N257;P0C1H6;P57053;Q7Z2G1;Q6NXT2;P49450;Q99525;Q6DN03	;Q6DRA6;Q96Q83;O75164;Q96KS0;Q9Y4C1;Q9GZT9;Q9H6Z9;Q6NS38
55,T3D0054,2009-03-06 18:57:59 UTC,2009-08-04 21:27:33 UTC,Endosulfan,Organic Compound;Pesticide;Organochloride,":endosulfanAlpha-endosulfanAlpha-endosulfan solutionBenzoepinBeositCaswell No. 420ChlorthiepinChlortiepinCrisulfanCyclodanDevisulfanDevisulphanEndocelEndosalfan and metabolitesEndosolEndosulfan 35 ECEndosulfan 35ECEndosulfan IEndosulfan I (alpha)Endosulfan IIEndosulfan [ansi:bsi:iso]Endosulfan and metabolitesEndosulfan solutionEndosulfan, technical gradeEndosulphanEndotafEnsureGoldenleaf tobacco sprayHexachlorohexahydromethano 2,4,3-benzodioxathiepin-3-oxideHildaHildanInsectopheneKop-thiodanMalixNiagara 5,462PFF Thiodan 4EPS81_SUPELCOPhaserRCRA waste no. P050RCRA waste number P050RasayansulfanSialanThiforThimulThiodanThiodan 35Thiodan 4E Insecticide LiquidThiodan 4ECThiodan 4EC InsecticideThiodan 50 WPThiodan 50 WP InsecticideThiodan dust insecticideThiodan rophenThioforThiomulThionateThionexThiosulfanThiosulfan tionelThiotoxThiotox (insecticide)TionelTionexTiovelbenzo[e][1,3,2]dioxathiepin-3-oxideniagra 5462","Endosulfan is a organochlorine insecticide and acaricide. It is used to control insects on food and non-food crops and also as a wood preservative. Due to its toxicity and tendency to bioaccumulate, the use of endosulfan is banned in many areas. (R192, R193)",,115-29-7,3224,,C11090,"",4791,"",,D004726,Endosulfan,571,,,http://en.wikipedia.org/wiki/Endosulfan,"InChI=1/C9H6Cl6O3S/c10-5-6(11)8(13)4-2-18-19(16)17-1-3(4)7(5,12)9(8,14)15/h3-4H,1-2H2","",http://www.biospider.ca/saved_files/mol/0f50ae532aabe091bd574050087954ad_1237938772.mol,C1C2C(COS(=O)O1)C3(C(=C(C2(C3(Cl)Cl)Cl)Cl)Cl)Cl,C1C2C(COS(=O)O1)C3(C(=C(C2(C3(Cl)Cl)Cl)Cl)Cl)Cl,C9H6Cl6O3S,403.816880,Cream- to brown-colored solid.,106 °C,"","","0.000325 mg/mL at 22 °C [TOMLIN,C (1994)]","","","","Oral 
Inhalation 
Dermal
(R194)","Cytochrome P450 2B6 (P20813) 
Cytochrome P450 3A4 (P08684) 
Cytochrome P450 3A5 (P20815) 
(R196)","Endosulfan antagonizes the action of the neurotransmitter gamma-aminobutyric acid (GABA) acting at the GABA-A receptors, effectively blocking the GABA-induced uptake of chloride ions. Endosulfan also inhibits Na+ K+ ATPase and Ca2+ and Mg2+ ATPase which are essential for the transport of calcium across membranes. This results in the accumulation of intracellular free calcium ions, which promotes release of neurotransmitters from storage vesicles, the subsequent depolarization of adjacent neurons, and the propagation of stimuli throughout the CNS. This results in hyperexcitation and generalized seizures. Endosulfan is also an endocrine disruptor and acts as an agonist at the progesterone receptor and estrogen receptors. (R029, R193, R194, R195, R312)","Endosulfan is absorbed by inhalation, oral, and dermal routes of exposure. It accumulates mainly in the liver, kidney, and brain, and is metabolized to polar and nonpolar metabolites by cytochrome P-450 enzymes. Endosulfan and its metabolites, which include sulfate, diol, α-hydroxyether, lactone, and ether derivatives of endosulfan, are excreted in the urine and faeces. (R194)","LD50: 18 mg/kg (Oral, Rat) (R263) 
LD50: 34 mg/kg (Dermal, Rat) (R263) 
LD50: 8 mg/kg (Intraperitoneal, Rat) (R263) 
LD50: 360 mg/kg (Subcutaneous, Rabbit) (R263) 
LC50: 80 mg/m3 over 4 hours (Inhalation, Rat) 
(R263)",50 to 500 mg/kg for an adult human. (R310),,"Endosulfan is used as an insecticide, acaricide, and in wood preservatives. (R194)","Intermediate Oral: 0.005 mg/kg/day (R260)
Chronic Oral: 0.002 mg/kg/day (R260)","Endosulfan is a neurotoxin and damages the central nervous system, causing effects such as intermittent muscle twitching and myoclonic jerking. Endosulfan can also damage the kidneys, testes, and liver, and may possibly affect the body's ability to fight infection. It is also an endocrine disruptor and causes reproductive and developmental damage. (R029, R193, R194)","Symptoms of endosulfan poisoning include hyperactivity, hyperreflexia, tremors, dizziness, headache, convulsions, lack of coordination, staggering, difficulty breathing, nausea and vomiting, diarrhea, and in severe cases, unconsciousness. (R029, R193, R194)","Treatment is symptomatic, aimed at controlling convulsions, coma, and respiratory depression. If ingested, gastric lavage may be performed, followed by administering activated charcoal powder. (R311)",P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P18507;Q99928;O00591;P24046;P28476;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P54710;P98194;O75185;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;P06401;P03372;Q92731;Q8N1C3;A8MPY1;Q9UN88;P78334
56,T3D0055,2009-03-06 18:58:00 UTC,2009-08-04 21:27:33 UTC,Endosulfan sulfate,Organic Compound;Pesticide;Organochloride,"5-Norbornene-2,3-dimethanol, 1,4,5,6,7,7-hexachoro-, cyclicEndosulfan sulfate solutionEndosulfan sulphateEndosulphan sulphatePS813_SUPELCOThiodan sulfate","Endosulfan sulfate is one of the primary metabolites of endosulfan. Endosulfan is a organochlorine insecticide and acaricide. It is used to control insects on food and non-food crops and also as a wood preservative. Due to its toxicity and tendency to bioaccumulate, the use of endosulfan is banned in many areas. (R192, R193)",,1031-07-8,13940,,"","","","",,,Endosulfan sulfate,7979,,,http://en.wikipedia.org/wiki/Endosulfan sulfate,"InChI=1/C9H6Cl6O4S/c10-5-6(11)8(13)4-2-19-20(16,17)18-1-3(4)7(5,12)9(8,14)15/h3-4H,1-2H2","",http://www.biospider.ca/saved_files/mol/,C1C2C(COS(=O)(=O)O1)C3(C(=C(C2(C3(Cl)Cl)Cl)Cl)Cl)Cl,C1C2C(COS(=O)(=O)O1)C3(C(=C(C2(C3(Cl)Cl)Cl)Cl)Cl)Cl,C9H6Cl6O4S,419.811800,"",181-182 °C,"","","0.00048 mg/mL at 20 °C [SHIU,WY et al. (1990)]","","","",Oral Inhalation Dermal (R194),"Cytochrome P450 2B6 (P20813)
Cytochrome P450 3A4 (P08684)
Cytochrome P450 3A5 (P20815)
(R196)","Endosulfan sulfate antagonizes the action of the neurotransmitter gamma-aminobutyric acid (GABA) acting at the GABA-A receptors, effectively blocking the GABA-induced uptake of chloride ions. Endosulfan sulfate also inhibits Na+ K+ ATPase and Ca2+ and Mg2+ ATPase which are essential for the transport of calcium across membranes. This results in the accumulation of intracellular free calcium ions, which promotes release of neurotransmitters from storage vesicles, the subsequent depolarization of adjacent neurons, and the propagation of stimuli throughout the CNS. This results in hyperexcitation and generalized seizures. Endosulfan sulfate is also an endocrine disruptor and acts as an agonist at the progesterone receptor and estrogen receptors. (R029, R193, R194, R195, R312)","Endosulfan and its metabolites, which include sulfate, diol, α-hydroxyether, lactone, and ether derivatives of endosulfan, are excreted in the urine and faeces. (R194)","","",,"Endosulfan is used as an insecticide, acaricide, and in wood preservatives. (R194)","","Endosulfan is a neurotoxin and damages the central nervous system, causing effects such as intermittent muscle twitching and myoclonic jerking. Endosulfan can also damage the kidneys, testes, and liver, and may possibly affect the body's ability to fight infection. It is also an endocrine disruptor and causes reproductive and developmental damage. (R029, R193, R194)","Symptoms of endosulfan poisoning include hyperactivity, hyperreflexia, tremors, dizziness, headache, convulsions, lack of coordination, staggering, difficulty breathing, nausea and vomiting, diarrhea, and in severe cases, unconsciousness. (R029, R193, R194)","Treatment is symptomatic, aimed at controlling convulsions, coma, and respiratory depression. If ingested, gastric lavage may be performed, followed by administering activated charcoal powder. (R311)",P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P18507;Q99928;O00591;P24046;P28476;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P54710;P98194;O75185;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;P06401;P03372;Q92731;Q8N1C3;A8MPY1;Q9UN88;P78334
57,T3D0056,2009-03-06 18:58:00 UTC,2009-08-04 21:27:33 UTC,Diazinon,Organic Compound;Pesticide;Organophosphate,"Agridin 60Alfa-toxAntigalAntigal (van)AntlakBassadinonBasudinBasudin 10 GBasudin 5GBasudin sBazudenBazudinBazudineCaswell No. 342CiazinonCompassCompass (insecticide)Cooper's flystrike powderDacutoxDassitoxDazzelDelzinonDi aterr-fosDiagranDianonDiaterr-fosDiazajetDiazideDiazinonDiazinon AG 500Diazinon [ansi:bsi:iso]Diazinon liquidDiazinon solutionDiazitolDiazolDicidDiethyl 2-isopropyl-4-met hyl-6-pyrimidyl thionophosphateDiethyl 2-isopropyl-4-methyl-6-pyrimidyl thionophosphateDiethyl dimpylatumDimpilato [inn-spanish]DimpylatDimpylateDimpylate [inn]DimpylatumDimpylatum [inn-latin]DipofeneDisonexDizictolDiziktolDizinilDizinonDrawizonDyzolEktobandExodinExodin (van)FL ytrolFezudinFlytrolGalesanGarden toxGardentoxIsopropylmethylpyrimidyl diethyl thiophosphateKFM blowfly dressingKayazinonKayazolKleen-dokKnox Out 2FMKnox outKnox out yellow jacket contorlKnox-outMeodinonNedcidolNemacurNeocidolNeocidol (oil)Neocidol veterinary powderNeodinonNeotsidolNipsanNucidolO, O-Diethyl 2-isopropyl-4-methylpyrimidyl-6-thiophosphateO,O-Diethyl 2-isopropyl-4-methylpyrimidyl-6-thiophosphateO,O-Diethyl-O-(2-isopropyl-4-methylpyrimidyl)thiophosphateOleodiazinonOptimizerPS90_SUPELCORoot guardSarolexSpectracideSpectracide 25ECSrolexTerminatorWLN: T6N CNJ BY1 & 1 DOPS & O2 & O2 F1","Diazinon is the common name of O,O-diethyl-O-(2-isopropyl-6-methyl-pyrimidine-4-yl)phosphorothioate, a synthetic organophosphorus pesticide. It was formerly used as the active ingredient in household and garden products used to control pests such as flies, fleas, and cockroaches. Its use is now restricted to agricultural purposes and is used mainly on fruit and vegetable field crops. (R313, R314)",,333-41-5,3017,,C14324,"",34682,"",,D003976,Diazinon,411,,,,"InChI=1/C12H21N2O3PS/c1-6-15-18(19,16-7-2)17-11-8-10(5)13-12(14-11)9(3)4/h8-9H,6-7H2,1-5H3",diethoxy-(6-methyl-2-propan-2-ylpyrimidin-4-yl)oxy-sulfanylidene-$l^{5}-phosphane,http://www.biospider.ca/saved_files/mol/c12db59cc8ceae89d7774321f4cfd011_1237939067.mol,CCOP(=S)(OCC)OC1=NC(=NC(=C1)C)C(C)C,CCOP(=S)(OCC)OC1=NC(=NC(=C1)C)C(C)C,C12H21N2O3PS,304.101050,Colorless oil (pure) or pale to dark brown liquid (technical).,< 25 °C,,,"0.04 mg/mL at 25 °C [SHAROM,MS et al. (1980A)]",,,,"Oral
Inhalation
Dermal
(R313)","Cytochrome P450 2C19 (P33261) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Cytochrome P450 3A4 (P08684)
Cytochrome P450 3A5 (P20815)
Cytochrome P450 2D6 (P10635)
Serum paraoxonase/arylesterase 1 (P27169) 
Liver carboxylesterase 1 (P23141) 
Carboxylesterase 3 (Q6UWW8)","Diazoxon the main toxic intermediate of diazinon, inhibits acetylcholinesterase in the central and peripheral nervous system. This results in the accumulation of acetylcholine, causing excessive stimulation of cholinergic fibers in the postganglionic parasympathetic nerve endings, neuromuscular junctions of the skeletal muscles, and cells of the central nervous system that results in hyperpolarization and receptor desensitization. This produces muscarinic, nicotinic, and CNS effects. Death is usually due to depression of the neurons in the brainstem, resulting in loss of respiratory drive and paralysis of the respiratory muscles, and/or cardiac failure. Diazinon cytotoxicity involves glutathione-modulated generation of reactive oxygen species, causing oxidative stress. (R313)","Diazinon is absorbed via ingestion, inhalation, and dermal routes. It is rapidly metabolized and does not accumulate significantly in body tissues. Diazinon is metabolized by cytochrome P-450 enzymes, mainly CYP2C19, which initially oxidize it to the intermediate phosphooxythiran. Phosphooxythiran may undergo spontaneous desulfuration to form diazoxon, the main toxic intermediate. Alternatively, phosphooxythiran may be deactivated via hydrolysis, desulfuration, and deoxygenation to form metabolites 2-isopropyl4- methyl-6-hydroxypyrimidine (IMHP), diethylthiophosphate (DETP), and DEP, all of which are excreted in the urine. Detoxification of diazoxon to IMHP and DEP occurs via hydrolysis catalyzed by hepatic and extrahepatic A-esterases and B-esterases. (R313)","LD50: 66 mg/kg (Oral, Rat) (R263)
LD50: 180 mg/kg (Dermal, Rat) (R263)
LD50: 65 mg/kg (Intraperitoneal, Rat) (R263)
LD50: 58 mg/kg (Subcutaneous, Mouse) (R263)
LD50: 180 mg/kg (Intravenous, Mouse) (R263)
",25 g for an adult human. (R316),,"Diazinon is used as an insecticide in agriculture, mainly on fruit and vegetable field crops. (R313)","Intermediate Inhalation: 0.01 mg/m3 (R260)
Acute Oral: 0.006 mg/kg/day (R260)
Intermediate Oral: 0.002 mg/kg/day (R260)
Chronic Oral: 0.0007 mg/kg/day (R260)",Diazinon affects mainly the nervous system. Exposure to high concentrations may results in coma and possibly death. (R313),"The symptoms associated with diazinon poisoning in humans include weakness, headaches, tightness in the chest, blurred vision, nonreactive pinpoint pupils, excessive salivation, difficulty breathing, sweating, nausea, vomiting, diarrhea, abdominal cramps, and slurred speech. (R314)",Diazinon poisoning may be treated with the antidote atropine and/or certain oximes. Artificial respiration may be needed. (R315),P22303;Q63HM1
58,T3D0057,2009-03-06 18:58:00 UTC,2009-08-04 21:27:33 UTC,"Endosulfan, alpha",Organic Compound;Pesticide;Organochloride,"&alpha;-endosulfan&alpha;-thiodanA-endosulfan-alphaAlpha-benzoepinAlpha-endosulfanAlpha-thiodanBeta-thionexEndosulfanEndosulfan &alpha;Endosulfan 1Endosulfan aEndosulfan, alpha","Endosulfan, Alpha is the stabler of two stereoisomers of endosulfan. Endosulfan is a organochlorine insecticide and acaricide. It is used to control insects on food and non-food crops and also as a wood preservative. Due to its toxicity and tendency to bioaccumulate, the use of endosulfan is banned in many areas. (R192, R193)",,959-98-8,6433227,,"","",25520,"",,,"Endosulfan, alpha",8139,,,,"InChI=1/C9H6Cl6O3S/c10-5-6(11)8(13)4-2-18-19(16)17-1-3(4)7(5,12)9(8,14)15/h3-4H,1-2H2/t3-,4+,7-,8?,19?/m1/s1","",http://www.biospider.ca/saved_files/mol/,C1[C@H]2[C@@H](COS(=O)O1)[C@]3(C(=C(C2(C3(Cl)Cl)Cl)Cl)Cl)Cl,C1C2C(COS(=O)O1)C3(C(=C(C2(C3(Cl)Cl)Cl)Cl)Cl)Cl,C9H6Cl6O3S,403.816880,Cream- to brown-colored solid.,"","","","0.00051 mg/mL at 20 °C [BOWMAN,BT & SANS,WW (1983)]","","","",Oral Inhalation Dermal (R194),"Cytochrome P450 2B6 (P20813)
Cytochrome P450 3A4 (P08684)
Cytochrome P450 3A5 (P20815)
(R196)","Endosulfan antagonizes the action of the neurotransmitter gamma-aminobutyric acid (GABA) acting at the GABA-A receptors, effectively blocking the GABA-induced uptake of chloride ions. Endosulfan also inhibits Na+ K+ ATPase and Ca2+ and Mg2+ ATPase which are essential for the transport of calcium across membranes. This results in the accumulation of intracellular free calcium ions, which promotes release of neurotransmitters from storage vesicles, the subsequent depolarization of adjacent neurons, and the propagation of stimuli throughout the CNS. This results in hyperexcitation and generalized seizures. Endosulfan is also an endocrine disruptor and acts as an agonist at the progesterone receptor and estrogen receptors. (R029, R193, R194, R195, R312)","Endosulfan is absorbed by inhalation, oral, and dermal routes of exposure. It accumulates mainly in the liver, kidney, and brain, and is metabolized to polar and nonpolar metabolites by cytochrome P-450 enzymes. Endosulfan and its metabolites, which include sulfate, diol, α-hydroxyether, lactone, and ether derivatives of endosulfan, are excreted in the urine and faeces. (R194)","LD50: 18 mg/kg (Oral, Rat) (R263) 
LD50: 34 mg/kg (Dermal, Rat) (R263) 
LD50: 8 mg/kg (Intraperitoneal, Rat) (R263) 
LD50: 360 mg/kg (Subcutaneous, Rabbit) (R263) 
LC50: 80 mg/m3 over 4 hours (Inhalation, Rat) 
(R263)",50 to 500 mg/kg for an adult human. (R310),,"Endosulfan is used as an insecticide, acaricide, and in wood preservatives. (R194)",Intermediate Oral: 0.005 mg/kg/day (R260) Chronic Oral: 0.002 mg/kg/day (R260),"Endosulfan is a neurotoxin and damages the central nervous system, causing effects such as intermittent muscle twitching and myoclonic jerking. Endosulfan can also damage the kidneys, testes, and liver, and may possibly affect the body's ability to fight infection. It is also an endocrine disruptor and causes reproductive and developmental damage. (R029, R193, R194)","Symptoms of endosulfan poisoning include hyperactivity, hyperreflexia, tremors, dizziness, headache, convulsions, lack of coordination, staggering, difficulty breathing, nausea and vomiting, diarrhea, and in severe cases, unconsciousness. (R029, R193, R194)","Treatment is symptomatic, aimed at controlling convulsions, coma, and respiratory depression. If ingested, gastric lavage may be performed, followed by administering activated charcoal powder. (R311)",P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P18507;Q99928;O00591;P24046;P28476;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P54710;P98194;O75185;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;P06401;P03372;Q92731;Q8N1C3;A8MPY1;Q9UN88;P78334
59,T3D0058,2009-03-06 18:58:00 UTC,2009-08-04 21:27:33 UTC,Xylene,Organic Compound;Solvent;Aromatic Hydrocarbon,"1,3-Dimethylbenzene, benzylated1,3-Dimethylbenzol1,3-Xylene1,3-dimethylbenzene2,4-Xylene3-xyleneBENZENE,1,3-DIMETHYLBenzene, 1,3-dimethyl-Benzene, 1,3-dimethyl-, benzylatedBenzene, m-dimethyl-M-dimethylbenzeneM-methyltolueneM-xyleneM-xylene, benzylatedM-xylenesM-xylolMeta-xyleneSantosol 150WLN: 1R C1Xylene, m-Xylene, m-isomerXylene, mixed isomersXylenesm-Xylene [UN1307] [Flammable liquid]","Xylene refers to the mixture of its three aromatic hydrocarbon isomers: meta-xylene, ortho-xylene, and para-xylene. It occurs naturally in petroleum and coal tar, and is major component of gasoline and fuel oil. Xylene is used mainly as a solvent and in the printing, rubber, and leather industries. (R029, R319)",,1330-20-7,7929,,"","",27338,CPD-1125,,,Xylene,1479,,,,"InChI=1/C8H10/c1-7-4-3-5-8(2)6-7/h3-6H,1-2H3","1,3-dimethylbenzene",http://www.biospider.ca/saved_files/mol/,CC1=CC(=CC=C1)C,CC1=CC(=CC=C1)C,C8H10,106.078250,Colorless liquid.,Boiling Pt : 138.5 oC,138.5 °C,,"0.106 mg/mL at 25 °C [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral
Inhalation
Dermal
(R319)","Serum albumin (P02768)
Cytochrome P450 2E1 (P05181) 
Cytochrome P450 1A2 (P05177) 
(R319)","In the blood, xylene is bound to serum proteins and accumulates primarily in the adipose tissue. The lipophilic effects of xylene, which dissolve lipid membranes, is responsible for the irritant effects on eyes, mucous membranes and skin. In addition, the lipophilicity of xylene is responsible for its narcotic and anaesthetic properties, which are similar for the three isomers. The mechanism of is anesthetic function probably relates to intercalation of the chemical into neuronal cell membranes, changing membrane properties that affect transmission of nerve impulses. The mechanism could be either by a disruption of the lipid environment in which membrane proteins function or by direct interaction with the hydrophobic/hydrophilic conformation of proteins in the neuronal membrane. Acute-duration oral or intermediate-duration inhalation exposures to high concentrations of xylene may result in death of cochlear hair cells and hearing loss. Experiments suggest that renal toxicity of xylene may be related to its metabolism by CYP2E1, which generates the production of oxidative intermediates and subsequent necrosis. Nephrotoxicity from xylene may involve induction of apoptosis through the activation of mitochondrial caspase-9 and caspase-3. (N009)","Xylenes are well absorbed by the inhalation and oral routes. Approximately 60% of inspired xylene is retained and approximately 90% of ingested xylene is absorbed. Absorption also occurs by the dermal route, but to a much lesser extent than by the inhalation and oral routes. Following absorption, xylene is rapidly distributed throughout the body by way of the systemic circulation. In the blood, it is primarily bound to serum proteins and accumulates primarily in adipose tissue. Xylene is primarily metabolized by oxidation of a methyl group and conjugation with glycine to yield the methylhippuric acid, whicih is the primary metabolite excreted in urine. Aromatic hydroxylation of xylene to xylenol occurs to only a limited extent in humans. Less than 2% of an absorbed dose is excreted in the urine as xylenol. Other minor metabolites found in urine include methylbenzyl alcohol and glucuronic acid conjugates of the oxidized xylene. In humans, hepatic microsomal CYP2E1 is the primary enzyme involved with the metabolism of xylene to methylbenzylalcohol, the dominant pathway leading to the formation of methylhippuric acid isomers. Unmetabolized xylene can be exhalated or also excreted in urine. (N009) ","LD50: 1590 mg/kg (Oral, Rat) (R276)
LC50: 6350 ppm over 4 hours (Inhalation, Rat) (R286)
LD50: 1548 mg/kg (Intraperitoneal, Mouse) (R293)
LD50: 1700 mg/kg (Subcutaneous, Rat) (R293)",50 and 500 mg/kg for an adult human. (R321),"3, not classifiable as to its carcinogenicity to humans. (R264)","Xylene mainly affects the nervous system. Exposure may cause delayed reaction time, impaired short-term memory, and changes in one’s sense of balance. High levels of exposure can result in coma, respiratory depression and death from cerebral anoxia. Xylene may also damage the liver, kidney, and lungs. Effects on fetal body weight and delay of skeletal ossification can occur in pregnant women. (N009, R319, R320) ","Acute Inhalation: 2 ppm (R260)
Intermediate Inhalation: 0.6 ppm (R260)
Chronic Inhalation: 0.05 ppm (R260)
Acute Oral: 1 mg/kg/day (R260)
Intermediate Oral: 0.4 mg/kg/day (R260)
Chronic Oral: 0.2 mg/kg/day (R260)","Xylene mainly affects the nervous system. Exposure may cause delayed reaction time, impaired short-term memory, and changes in one’s sense of balance. High levels of exposure can result in coma, respiratory depression and death from cerebral anoxia. Xylene may also damage the liver, kidney, and lungs. Effects on fetal body weight and delay of skeletal ossification can occur in pregnant women. (N009, R319, R320) ","Dizziness, drowsiness, headache, and nausea can follow ihnalation and ingestion exposure. Burning sensations and abdominal pain can also result from ingestion. Dry skin, redness, and pain can result from dermal and eye exposure depending on the route of exposure. Conjunctivitis, dermatitis, irritation to respiratory tract, dyspnea, anorexia, vomiting, fatigue, vertigo, incoordination, irritation, gangrene and anemia can also follow xylene poisoning. (N010)","Gastric lavage is generally NOT indicated following oral exposure, as it is likely to increase the risk of aspiration. Activated charcoal may induce vomiting and increase pulmonary aspiration risk, and is generally NOT indicated. It should be limited to rare situations when there is a toxic coingestant. Following inhalation exposure, move patient to fresh air. Monitor for respiratory distress, if cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with inhaled beta2 agonist and oral or parenteral corticosteroids. The development of pulmonary edema from extreme vapor inhalation may be delayed up to 72 hours. If symptomatic, obtain chest x-ray, if severe, monitor arterial blood gases or pulse oximetry. Supplemental oxygen, PEEP, or CPAP may be necessary. Do not administer excessive fluids. Irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes in case of eye exposure. Following dermal exposure, remove contaminated clothing and wash exposed area thoroughly with soap and water. A physician may need to examine the area if irritation or pain persists. (R264) ",P05181;P13584
60,T3D0059,2009-03-06 18:58:00 UTC,2009-08-04 21:27:34 UTC,"Chlordane, cis-",Organic Compound;Pesticide;Organochloride,"&alpha;-chlordan&alpha;-chlordaneAlpha-chlordaneChlordan, cis-Chlordane cisCis-chlordan","cis-Chlordane, also known as alpha-chlordane, is one of two isomers of chlordane. Chlordane is a manufactured chemical that was used as a pesticide in the United States from 1948 to 1988. (R158)",,5103-71-9,12303035,,"","",39068,"",,,"Chlordane, cis-",,,,,"InChI=1/C10H6Cl8/c11-3-1-2-4(5(3)12)9(16)7(14)6(13)8(2,15)10(9,17)18/h2-5H,1H2/t2?,3-,4-,5-,8+,9-/m1/s1","",http://www.biospider.ca/saved_files/mol/,C1[C@@H]2[C@H]([C@@H]([C@@H]1Cl)Cl)[C@]3(C(=C([C@@]2(C3(Cl)Cl)Cl)Cl)Cl)Cl,C1C2C(C(C1Cl)Cl)C3(C(=C(C2(C3(Cl)Cl)Cl)Cl)Cl)Cl,C10H6Cl8,405.797770,Colorless to amber liquid.,"",,,"5.6e-05 mg/mL at 25 °C [MABEY,WR et al. (1981)]",,,,Oral Inhalation (R259),Glutathione S-transferase P (P09211) Glutathione S-transferase Mu 1 (P09488) Glutathione S-transferase A1 (P08263) Glutathione S-transferase theta-2 (P30712) Glutathione S-transferase Mu 4 (Q03013) Glutathione S-transferase theta-1 (P30711) Glutathione S-transferase A4 (O15217) Glutathione S-transferase A2 (P09210) Glutathione S-transferase A3 (Q16772) Glutathione S-transferase Mu 3 (P21266) Glutathione S-transferase omega-1 (P78417) Glutathione S-transferase kappa 1 (Q9Y2Q3) Glutathione S-transferase Mu 2 (P28161) Glutathione S-transferase omega-2 (Q9H4Y5) Glutathione S-transferase A5 (Q7RTV2) Glutathione S-transferase Mu 5 (P46439) Glutathione S-transferase theta-4 (A8MPT4) Maleylacetoacetate isomerase (O43708) Microsomal glutathione S-transferase 1 (P10620) Microsomal glutathione S-transferase 2 (Q99735) Microsomal glutathione S-transferase 3 (O14880) (R159),"Chlordane is believed to bind irreversibly to DNA, leading to cell death or altered cellular function. It also affects transcription by antagonizing estrogen-related receptors. Chlordane induces hepatic cytochrome P-450, causing a large increase in the volume of the smooth endoplasmic reticulum, which results in hepatocellular enlargement and hypertrophy. Chlordane has also been shown to bind and activate retinoic acid receptor, causing various developmental defects, and inhibit alkaline phosphatases in hepatic and renal tissues. (R159, R162, R163, R205, R206)","Chlordane is highly lipophilic and is thus easily absorbed by ingestion, inhalation, and dermal exposure, then stored mainly in the fat. Chlordane is metabolized mainly in the liver and kidney. Metabolism is slow, and is believed to occur by multiple pathways involving cytochrome P-450 enzymes, glutathione-S-transferase type enzymes, and microsomal mixed-function oxidase systems. The metabolites are generally less toxic and include chlordene chlorohydrin, monohydroxylated dihydrochlordene, and oxychlordane. They are excreted in the urine and faeces. (R159)","LD50: 200 mg/kg (Oral, Rat) (R261) LD50: 343 mg/kg (Intraperitoneal, Rat) (R261) LD50: 10 mg/kg (Intravenous, Mouse) (R263) LD50: 780 mg/kg (Dermal, Rat) (R263) LC50: 100 mg/m3 over 4 hours (Inhalation, Cat) (R263)",100 mg/kg for an adult human. (R265),"2B, possibly carcinogenic to humans. (R264)",Chlordane was used as a pesticide. (R158),Intermediate Inhalation: 0.0002 mg/m3 (R260) Chronic Inhalation: 0.00002 mg/m3 (R260) Acute Oral: 0.001 mg/kg/day (R260) Intermediate Oral: 0.0006 mg/kg/day (R260) Chronic Oral: 0.0006 mg/kg/day (R260),"Chlordane is a central nervous system stimulant, and can also damage the digestive system and the liver. Large doses have been known to cause convulsions, respiratory failure, and death. Chlordane is also known to have adverse reproductive and developmental effects. (R159)","Ingestion and inhalation of chlordane cause headaches, irritability, confusion, weakness, vision problems, vomiting, stomach cramps, diarrhea, and jaundice. (R159)","Treatment is symptomatic. It is aimed at controlling convulsions, coma, and respiratory depression. Gastric lavage, followed by the administration of activated charcoal, may be performed following ingestion. (R282)",P05186;P20813;P08684;Q9HB55;P20815;P24462;P62508;P10826;P13631;P11474;O95718;DNA;P03372;Q92731
61,T3D0060,2009-03-06 18:58:00 UTC,2009-08-04 21:27:34 UTC,Dibromochloropropane,Organic Compound;Pesticide;Organochloride;Organobromide,"1,2-DIBROMO-3-CHLOROPROPANE1,2-Dibrom-3-chlor-propan1,2-Dibrom-3-chlor-propan [German]1,2-Dibromo-3-chloropropane (DBCP)1,2-Dibromo-3-cloro-propano1,2-Dibromo-3-cloro-propano [Italian]1,2-Dibromochloropropane1,2-Dibroom-3-chloorpropaan1,2-Dibroom-3-chloorpropaan [Dutch]1,3-Dibromo-3-chloropropane1-Chloro-2,3-dibromopropane2,3-Dibromo-1-chloropropane3-Chloro-1,2-dibromopropaneBBCPC3H5Br2ClCBCPCaswell No. 287DBCPDibromchlorpropanDibromchlorpropan [german]Dibromo-3-chloropropane, 1,2- (DBCP)DibromochloropropaneDibromochloropropane [UN2872] [Poison]Durham Nematicode EM 17.1Fumag onFumagonFumazon 86FumazoneFumazone 86Fumazone 86EGro-tone nematode granularInChI=1/C3H5Br2Cl/c4-1-3(5)2-6/h3H,1-2HNemabromNemafumeNemagonNemagon 20Nemagon 206Nemagon 20GNemagon 90Nemagon soil fumigantNemagoneNemanaxNemanexNemapazNemasetNematocideNematocide EM 12.1Nematocide EM 15.1Nematocide Solution EM 17.1NematoxNemazonOxy DBCPPropane, 1,2-dibromo-3-chloro-Propane, 1-chloro-2,3-dibromo-Propane, dibromochloro-RCRA waste no. U066RCRA waste number U066WLN: G1YE1E","Dibromochloropropane is a manufactured chemical and the active ingredient in the nematicide Nemagon, also known as Fumazone. Nemagon is a soil fumigant formerly used in agriculture but banned to most areas today. (R237)",,67708-83-2,7280,,"","","","",,,Dibromochloropropane,,,,,"InChI=1/C3H5Br2Cl/c4-1-3(5)2-6/h3H,1-2H2","1,2-dibromo-3-chloropropane",http://www.biospider.ca/saved_files/mol/,C(C(CBr)Br)Cl,C(C(CBr)Br)Cl,C3H5Br2Cl,233.844650,Colorless liquid.,"",,,"",,,,Oral Inhalation Dermal (R236),Glutathione S-transferase P (P09211) Glutathione S-transferase Mu 1 (P09488) Glutathione S-transferase A1 (P08263) Glutathione S-transferase theta-2 (P30712) Glutathione S-transferase Mu 4 (Q03013) Glutathione S-transferase theta-1 (P30711) Glutathione S-transferase A4 (O15217) Glutathione S-transferase A2 (P09210) Glutathione S-transferase A3 (Q16772) Glutathione S-transferase Mu 3 (P21266) Glutathione S-transferase omega-1 (P78417) Glutathione S-transferase kappa 1 (Q9Y2Q3) Glutathione S-transferase Mu 2 (P28161) Glutathione S-transferase omega-2 (Q9H4Y5) Glutathione S-transferase A5 (Q7RTV2) Glutathione S-transferase Mu 5 (P46439) Glutathione S-transferase theta-4 (A8MPT4) Maleylacetoacetate isomerase (O43708) Microsomal glutathione S-transferase 1 (P10620) Microsomal glutathione S-transferase 2 (Q99735) Microsomal glutathione S-transferase 3 (O14880) (R236),"The initial metabolism of dibromochloropropane to reactive epoxide metabolites that bind to DNA and other macromolecules may be responsible for its hepatotoxicity and nephrotoxicity. The mechanism of dibromochloropropane's testicular toxicity is believed to be due to either the inhibition of sperm carbohydrate metabolism, probably at the step of nicotinamide adenine dinucleotide (NADH) dehydrogenase activity in the mitochondrial electron transport chain, or direct DNA damage caused by its metabolites. (R236, R238)","Dibromochloropropane  is absorbed via oral, inhalation, and dermal routes. It accumulates mainly in the kidney, liver, and adipose tissues. Dibromochloropropane  is initially converted to epoxy derivatives, which are further hydrolyzed and debrominated. Glutathione (GSH) conjugation of epoxide intermediates in the liver is believed to produce precursors to toxic intermediates. The metabolites are excreted mainly in the urine. (R236)","LD50: 100 mg/kg (Oral, Rabbit) (R292) LC50: 1480 mg/m3 over 1 hour (Inhalation, Rat) (R292)",,"2B, possibly carcinogenic to humans. (R264)","Dibromochloropropane is the active ingredient in the nematicide Nemagon, also known as Fumazone. Nemagon is a soil fumigant formerly used in agriculture. (R236)",Intermediate Inhalation: 0.0002 ppm (R260) Intermediate Oral: 0.002 mg/kg/day (R260),"Breathing high levels of dibromochloropropane causes reproductive damage, including reduced sperm counts, birth defects, and infertility. It may also damage the stomach, liver, kidneys, brain, spleen, blood, and lungs, and cause skin and eye damage from direct contact. (R236)","Symptoms of dibromochloropropane exposure include headaches, nausea, lightheadedness, and weakness. (R236)","",P03886;P49821;P19404;P56181;O75306;O75489;O43181;O43920;O75380;O75251;O00217;P28331;P03891;P03897;P03905;P03901;P03915;P03923;P03372;Q92731
62,T3D0061,2009-03-06 18:58:00 UTC,2009-08-04 21:27:34 UTC,Methoxychlor,Organic Compound;Pesticide;Aromatic Hydrocarbon;Organochloride,"1, 1-Bis(p-methoxyphenyl)-2,2,2-trichloroethane1,1'-(2,2, 2-Trichloroethylidene)bis(4-methoxybenzene)1,1'-(2,2,2-Trichloroethylidene)-bis[4-methoxybenzene]1,1'-(2,2,2-Trichloroethylidene)bis(4-methoxybenzene)1,1'-(2,2,2-trichloroethane-1,1-diyl)bis(4-methoxybenzene)1,1,1-Trichlor-2,2-bis(4-methoxy-phenyl)-aethan1,1,1-Trichlor-2,2-bis(4-methoxy-phenyl)-aethan [German]1,1,1-Trichloro-2, 2-bis(p-anisyl)ethane1,1,1-Trichloro-2, 2-bis(p-methoxyphenyl)ethane1,1,1-Trichloro-2, 2-di(4-methoxyphenyl)ethane1,1,1-Trichloro-2,2-bis(4-methoxyphenyl)ethane1,1,1-Trichloro-2,2-bis(p-anisyl)ethane1,1,1-Trichloro-2,2-bis(p-methoxyphenyl)ethane1,1,1-Trichloro-2,2-bis-(p-methoxyphenyl)ethane1,1,1-Trichloro-2,2-di(4-methoxyphenyl)ethane1,1-Bis(p-methoxyphenyl)-2,2,2-trichloroethane2, 2-Di(p-methoxyphenyl)-1,1,1-trichloroethane2,2,2-Trichloro-1,1-bis(4-methoxyphenyl)ethane2,2,2-t richloro-1,1-bis(4-methoxyphenyl)ethane2,2-Bis (p-methoxyphenol)-1,1,1-trichloroethane2,2-Bis(4-methoxyphenyl)-1,1,1-trichloroethane2,2-Bis(p-anisyl)-1, 1,1-trichloroethane2,2-Bis(p-anisyl)-1,1,1-trichloroethane2,2-Bis(p-methoxyphenyl)-1,1, 1-trichloroethane2,2-Bis(p-methoxyphenyl)-1,1,1-trichloroethane2,2-Di(p-anisyl)-1,1,1-trichloroethane2,2-Di(p-methoxyphenyl)-1,1,1-trichloroethane2,2-Di-(p-methoxyphenyl)-1,1,1-trichloroethane2,2-Di-p-anisyl-1,1,1-trichloroethane4,4-(2,2,2-Trichloroethylidene)dianisoleBenzene, 1,1'-(2,2, {2-trichloroethylidene)bis[4-methoxy-}Benzene, 1,1'-(2,2,2-trichloroethylidene)bis(4-methoxy)-Benzene, 1,1'-(2,2,2-trichloroethylidene)bis(4-methoxy-Benzene, 1,1'-(2,2,2-trichloroethylidene)bis*4-methoxy-Benzene, 1,1'-(2,2,2-trichloroethylidene)bis[4-methoxy-Bis(p-anisyl)-1,1,1-trichloroethaneBis(p-methoxyphenyl)-1,1,1-trichloroethaneCaswell No. 550ChemformChemform methoxychlorDMDTDMDTOMS 466Di(p-methoxyphenyl) trichloromethyl methaneDi(p-methoxyphenyl)trichloromethyl methaneDianisyl trichloroethaneDianisyltrichlorethaneDianisyltrichloroethaneDimethox ydiphenyltrichloroethaneDimethoxy-DDTDimethoxy-DTDimethoxydiphenyltrichloroethaneDouble-m ecEthane, 1,1,1-trichloro-2, 2-bis(p-methoxyphenyl)-Ethane, 1,1,1-trichloro-2,2-bis(p-methoxyphenyl)-Ethane, 2,2-bis(p-anisyl)-1,1, 1-trichloro-Ethane, 2,2-bis(p-anisyl)-1,1,1-trichloro-Flo pro mcseed protectantHigalmetoxKid pest project (methoxychlor) (see also methoxychlor)M1501_SIGMAMaralateMarlateMarlate 2-mr emulsifiable insecticideMarlate 300 flowableMarlate 400 flowable concentrateMarlate 50 WPMarlate methoxychlor insecticideMaxieMeoclMethoxcideMethoxoMethoxy DDTMethoxy-DDTMethoxychlor (see also kid pest project (methoxychlor))Methoxychlor 2 ecMethoxychlor [95%]Methoxychlor [bsi:iso]Methoxychlor solutionMethoxychlor, technicalMethoxychloreMethoxychlore [iso-french]MetoksychlorMetoksychlor (polish)Metoksychlor [polish]MetoxMezox kMoxieP, p'-methoxychlorP,p'-(dimethoxydiphenyl)trichloroethaneP,p'-DMDTP,p'-dimethoxydiphenyltrichl oroethaneP,p'-dimethoxydiphenyltrichloroethaneP,p'-dwumetoksydwufenylotrojchloroetanP,p'-dwumetoksydwufenylotrojchloroetan [polish]P,p'-methoxychlorPS83_SUPELCOPmethoxychlorPrentoxPubertal methoxychlor studyRCRA waste no. U247Rcra waste number U247Trichloroethane, dianisylWLN: GXGGYR DO1&R DO1","Methoxychlor is a manufactured organochlorine used as an insecticide against flies, mosquitoes, cockroaches, chiggers, and a wide variety of other insects. It is used on agricultural crops and livestock, and in animal feed, barns, grain storage bins, home garden, and on pets. (R323)",,72-43-5,4115,,C11043,"",6842,"",,D008731,Methoxychlor,843,,,http://en.wikipedia.org/wiki/Methoxychlor,"InChI=1/C16H15Cl3O2/c1-20-13-7-3-11(4-8-13)15(16(17,18)19)12-5-9-14(21-2)10-6-12/h3-10,15H,1-2H3","1-methoxy-4-[2,2,2-trichloro-1-(4-methoxyphenyl)ethyl]benzene",http://www.biospider.ca/saved_files/mol/7746a23d35985d02f53c003f52640ed5_1237939613.mol,COC1=CC=C(C=C1)C(C2=CC=C(C=C2)OC)C(Cl)(Cl)Cl,COC1=CC=C(C=C1)C(C2=CC=C(C=C2)OC)C(Cl)(Cl)Cl,C16H15Cl3O2,344.013760,Pale-yellow powder.,87 °C,"","","0.0001 mg/mL at 25 °C [RICHARDSON,LT & MILLER,DM (1960)]","","","",Oral Dermal (R323),"Cytochrome P450 2C19 (P33261) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2A6 (P11509) 
Cytochrome P450 2C9 (P11712) 
Cytochrome P450 2B6 (P20813)
Cytochrome P450 2D6 (P10635)
Cytochrome P450 2E1 (P05181) 
Cytochrome P450 3A4 (P08684)
(R323)","Certain mono- and bis-hydroxy metabolites of methoxychlor, especially 2,2-bis(p-hydroxyphenyl)-1,1, 1-trichloroethane (HPTE), act as estrogen analogues. HPTE is an estrogen receptor alpha agonist, and also acts as an antagonist at the estrogen receptor beta and androgen receptor. This affects protein synthesis, which is believed to cause many of methoxychlor's estrogenic effects, such as decreased fertility. As methoxychlor is also a structural analogue of DDT, it is believed to have the same neurotoxic effects. This includes preventing the deactivation of the sodium gate after neuron activation and membrane depolarization, resulting in hyperexcitability of the nerve. Like DDT, methoxychlor may also inhibit neuronal adenosine triphosphatases (ATPases), particularly Na+K+-ATPase and Ca2+-ATPase, which play vital roles in neuronal repolarization. This contributes to the reduced rate of depolarization and increases the sensitivity of neurons to small stimuli that would not elicit a response in a fully depolarized neuron. (R029, R325)","Methoxychlor is well absorbed by the gastrointestinal tract and to a lesser extent by the skin. Once in the bloodstream, methoxychlor appears to distribute to most tissues of the body, with highest levels usually found in fat. Methoxychlor is metabolized rapidly by cytochrome P450 enzymes in the liver, undergoing demethylation to form phenolic derivatives, with dechlorination and dehydrochlorination reactions occurring to a lesser extent. The metabolites of methoxychlor are excreted mainly in the faeces. (R323)","LD50: 3460 mg/kg (Oral, Rat) (R323)",6400 mg/kg for an adult human. (R324),"3, not classifiable as to its carcinogenicity to humans. (R264)","Methoxychlor is used as an insecticide against flies, mosquitoes, cockroaches, chiggers, and a wide variety of other insects. It is used on agricultural crops and livestock, and in animal feed, barns, grain storage bins, home garden, and on pets. (R323)",Intermediate Oral: 0.005 mg/kg/day (R260),"Animal studies show that methoxychlor may affect the reproductive system, causing harm to the ovaries, uterus, and mating cycle in females, and the testes and prostate in males, as well as decreased fertility in both sexes. Methoxychlor exposure may also cause EEG pattern changes. (R029. R323)","High levels of methoxychlor may cause fatigue, lethargy, tremors, convulsions and seizures. (R029, R323)","",P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P54710;P98194;O75185;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;Q9UL51;Q9Y3Q4;O60741;Q9P1Z3 ;P35498;Q9Y5Y9;Q9UI33;Q99250;Q9NY46;P35499;Q14524;Q01118;Q9UQD0;Q15858;Q07699;O60939;Q9NY72;Q8IWT1;P03372;Q92731;P10275
63,T3D0062,2009-03-06 18:58:00 UTC,2009-08-04 21:27:34 UTC,Benzo[k]fluoranthene,Organic Compound;Industrial By-product/Pollutant;Aromatic Hydrocarbon;Polycyclic Aromatic Hydrocarbon,"11,12-Benzo(k)fluoranthene11,12-Benzofluoranthene2,3,1',8'-Binaphthylene8,9-Benzfluoranthene8,9-BenzofluorantheneBCR048R_FLUKABenzo(k)fluorantheneBenzo(k)fluoranthene [polycyclic aromatic compounds]Benzo(k)fluoranthene [polycyclic aromatic hydrocarbons]Benzo[k]fluoranthene solutionDibenzo(b,JK)fluoreneDibenzo[b,JK]fluorene","Benzo[k]fluoranthene is one of over 100 different polycyclic aromatic hydrocarbons (PAHs). PAHs are chemicals that are formed during the incomplete burning organic substances, such as fossil fuels. They are usually found as a mixture containing two or more of these compounds. (R028)",,207-08-9,9158,,C14321,"","","",,C022921,Benzo[k]fluoranthene,6382,,,,InChI=1/C20H12/c1-2-6-15-12-19-17-10-4-8-13-7-3-9-16(20(13)17)18(19)11-14(15)5-1/h1-12H,benzo[k]fluoranthene,http://www.biospider.ca/saved_files/mol/bed80d15f6dcdf373924c10de2d78ec4_1237939736.mol,C1=CC=C2C=C3C4=CC=CC5=C4C(=CC=C5)C3=CC2=C1,C1=CC=C2C=C3C4=CC=CC5=C4C(=CC=C5)C3=CC2=C1,C20H12,252.093900,Pale yellow solid.,217 °C,"","","8e-07 mg/mL at 25 °C [PEARLMAN,RS et al. (1984)]","","","",Oral Inhalation (R028),Serum albumin (P02768) Cytochrome P450 1A1 (P04798) Cytochrome P450 1A2 (P05177) Cytochrome P450 1B1 (Q16678) (R060),"The ability of PAH's to bind to blood proteins such as albumin allows them to be transported throughout the body. Many PAH's induce the expression of cytochrome P450 enzymes, especially CYP1A1, CYP1A2, and CYP1B1, by binding to the aryl hydrocarbon receptor or glycine N-methyltransferase protein. These enzymes metabolize PAH's into their toxic intermediates. The reactive metabolites of PAHs (epoxide intermediates, dihydrodiols, phenols, quinones, and their various combinations) covalently bind to DNA and other cellular macromolecules, initiating mutagenesis and carcinogenesis. (R028, R060, R068, R073) ","PAH metabolism occurs in all tissues, usually by cytochrome P-450 and its associated enzymes. PAHs are metabolized into reactive intermediates, which include epoxide intermediates, dihydrodiols, phenols, quinones, and their various combinations. The phenols, quinones, and dihydrodiols can all be conjugated to glucuronides and sulfate esters; the quinones also form glutathione conjugates. (R028)","","","2B, possibly carcinogenic to humans. (R264)","PAHs are released into the environment via the combustion of fossil fuels, coke oven emissions and vehicle exhausts, as well as naturally from forest fires and volcanic eruptions. PAHs from these sources may contaminate nearly water systems. They are also found in coal tar and charbroiled food. (R028)","","PAHs are carcinogens and have been associated with the increased risk of skin, respiratory tract, bladder, stomach, and kidney cancers. They may also cause reproductive effects and depress the immune system. (R028)","Acute exposure to PAHs causes irritation and inflammation of the skin and lung tissue. (R034)
",There is no known antidote for PAHs. Exposure is usually handled with symptomatic treatment. (R028),P35869;Q14749;DNA
64,T3D0063,2009-03-06 18:58:00 UTC,2009-08-04 21:27:34 UTC,Endrin ketone,Organic Compound;Pesticide;Organochloride,&laquo;delta&raquo;-Keto 153&laquo;delta&raquo;-ketoendrinDelta-ketoendrinEndrin-ketone solutiondelta-Keto 153,"Endrin ketone is the chemical produced when endrin is exposed to light. Endrin is a chlorinated hydrocarbon used as an insecticide on cotton, maize, and rice. It also acts as an avicide and rodenticide. Due to its toxicity and tendency to bioaccumulate, its use is now banned in most parts of the world. (R190)",,53494-70-5,62060,,"","","","",,,Endrin ketone,,,,,"InChI=1/C12H8Cl6O/c13-8-9(14)6-2-1-3(7(6)19)4-5(2)11(9,16)12(17,18)10(4,8)15/h2-6,8H,1H2","",http://www.biospider.ca/saved_files/mol/,C1C2C3C4C1C(=O)C2C5(C3(C(C4(C5Cl)Cl)(Cl)Cl)Cl)Cl,C1C2C3C4C1C(=O)C2C5(C3(C(C4(C5Cl)Cl)(Cl)Cl)Cl)Cl,C12H8Cl6O,377.870630,,"",,,"",,,,Oral (R190),,"Endrin antagonizes the action of the neurotransmitter gamma-aminobutyric acid (GABA) acting at the GABA-A receptors, effectively blocking the GABA-induced uptake of chloride ions and causing hyperexcitability of the central nervous system. Endrin also inhibits Na+ K+ ATPase and Ca2+ and Mg2+ ATPase which are essential for the transport of calcium across membranes. This results in the accumulation of intracellular free calcium ions, which promotes release of neurotransmitters from storage vesicles, the subsequent depolarization of adjacent neurons, and the propagation of stimuli throughout the central nervous system. Endrin also causes increased lipid peroxidation, decreased membrane fluidity, and DNA damage in hepatocytes, but the exact mechanism is unknown. (R029, R191)","Endrin is absorbed orally and distributed primarily to the fat and skin. The major biotransformation product is anti-l 2-hydroxyendrin and the corresponding sulfate, as well as glucuronide metabolites. Anti- and syn-12-hydroxyendrin and 12-ketoendrin are the main toxic metabolites of endrin. Endrin and its metabolites are excreted in urine and feces. (R191)",,,,Endrin is used as a pesticide. (R190),,"Endrin poisoning affects primarily the nerve system. Exposure causes various harmful effects including hyperexcitability, severe central nervous system damage, and death. Endrin is also believed to cause birth defects. (R029, R191)","Symptoms that may result from endrin poisoning are headaches, dizziness, nervousness, confusion, nausea, vomiting, and convulsions. (R191)","Treatment is symptomatic, aimed at controlling convulsions, coma, and respiratory depression. If ingested, gastric lavage may be performed, followed by administering activated charcoal powder. (R291)",P98194;O75185;P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P78334;Q8N1C3;P18507;Q99928;O00591;P24046;P28476;A8MPY1;Q9UN88;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;P54710;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P03372;Q92731
65,T3D0064,2009-03-06 18:58:01 UTC,2009-08-04 21:27:34 UTC,"Chlordane, trans-",Organic Compound;Pesticide;Organochloride,"&beta;-chlordan&beta;-chlordaneBeta-chlordaneChlordan, trans-Chlordane &laquo;gamma&raquo; (trans)Chlordane transTrans-&laquo;gamma&raquo;-chlordaneTrans-chlordanTrans-gamma-chlordane","Trans-chlordane, also known as gamma-chlordane, is one of two isomers of chlordane. Chlordane is a manufactured chemical that was used as a pesticide in the United States from 1948 to 1988. (R158)",,5103-74-2,12303036,,"","",39069,"",,,"Chlordane, trans-",,,,,"InChI=1/C10H6Cl8/c11-3-1-2-4(5(3)12)9(16)7(14)6(13)8(2,15)10(9,17)18/h2-5H,1H2/t2?,3-,4+,5+,8-,9+/m0/s1","",http://www.biospider.ca/saved_files/mol/,C1[C@@H]2[C@H]([C@@H]([C@H]1Cl)Cl)[C@]3(C(=C([C@@]2(C3(Cl)Cl)Cl)Cl)Cl)Cl,C1C2C(C(C1Cl)Cl)C3(C(=C(C2(C3(Cl)Cl)Cl)Cl)Cl)Cl,C10H6Cl8,405.797770,Colorless to amber liquid.,"",,,"5.6e-05 mg/mL at 25 °C [MABEY,WR et al. (1981)]",,,,Oral Inhalation (R259),Glutathione S-transferase P (P09211) Glutathione S-transferase Mu 1 (P09488) Glutathione S-transferase A1 (P08263) Glutathione S-transferase theta-2 (P30712) Glutathione S-transferase Mu 4 (Q03013) Glutathione S-transferase theta-1 (P30711) Glutathione S-transferase A4 (O15217) Glutathione S-transferase A2 (P09210) Glutathione S-transferase A3 (Q16772) Glutathione S-transferase Mu 3 (P21266) Glutathione S-transferase omega-1 (P78417) Glutathione S-transferase kappa 1 (Q9Y2Q3) Glutathione S-transferase Mu 2 (P28161) Glutathione S-transferase omega-2 (Q9H4Y5) Glutathione S-transferase A5 (Q7RTV2) Glutathione S-transferase Mu 5 (P46439) Glutathione S-transferase theta-4 (A8MPT4) Maleylacetoacetate isomerase (O43708) Microsomal glutathione S-transferase 1 (P10620) Microsomal glutathione S-transferase 2 (Q99735) Microsomal glutathione S-transferase 3 (O14880) (R159),"Chlordane is believed to bind irreversibly to DNA, leading to cell death or altered cellular function. It also affects transcription by antagonizing estrogen-related receptors. Chlordane induces hepatic cytochrome P-450, causing a large increase in the volume of the smooth endoplasmic reticulum, which results in hepatocellular enlargement and hypertrophy. Chlordane has also been shown to bind and activate retinoic acid receptor, causing various developmental defects, and inhibit alkaline phosphatases in hepatic and renal tissues. (R159, R162, R163, R205, R206)","Chlordane is highly lipophilic and is thus easily absorbed by ingestion, inhalation, and dermal exposure, then stored mainly in the fat. Chlordane is metabolized mainly in the liver and kidney. Metabolism is slow, and is believed to occur by multiple pathways involving cytochrome P-450 enzymes, glutathione-S-transferase type enzymes, and microsomal mixed-function oxidase systems. The metabolites are generally less toxic and include chlordene chlorohydrin, monohydroxylated dihydrochlordene, and oxychlordane. They are excreted in the urine and faeces. (R159)","LD50: 200 mg/kg (Oral, Rat) (R261) LD50: 343 mg/kg (Intraperitoneal, Rat) (R261) LD50: 10 mg/kg (Intravenous, Mouse) (R263) LD50: 780 mg/kg (Dermal, Rat) (R263) LC50: 100 mg/m3 over 4 hours (Inhalation, Cat) (R263)",100 mg/kg for an adult human. (R265),"2B, possibly carcinogenic to humans. (R264)",Chlordane was used as a pesticide. (R158),Intermediate Inhalation: 0.0002 mg/m3 (R260) Chronic Inhalation: 0.00002 mg/m3 (R260) Acute Oral: 0.001 mg/kg/day (R260) Intermediate Oral: 0.0006 mg/kg/day (R260) Chronic Oral: 0.0006 mg/kg/day (R260),"Chlordane is a central nervous system stimulant, and can also damage the digestive system and the liver. Large doses have been shown to cause convulsions, respiratory failure, and death. Chlordane is also known to have adverse reproductive and developmental effects. (R159)","Ingestion and inhalation of chlordane cause headaches, irritability, confusion, weakness, vision problems, vomiting, stomach cramps, diarrhea, and jaundice. (R159)","Treatment is symptomatic. It is aimed at controlling convulsions, coma, and respiratory depression. Gastric lavage, followed by the administration of activated charcoal, may be performed following ingestion. (R282)",P05186;P20813;P08684;Q9HB55;P20815;P24462;P62508;P10826;P13631;P11474;O95718;DNA;P03372;Q92731
66,T3D0065,2009-03-06 18:58:01 UTC,2009-08-04 21:27:35 UTC,Chromium(VI) oxide,Inorganic Compound;Chromium Compound,"Amperit 704.0Anadonis greenAnhydride chromiqueAnhydride chromique [french]Anidride cromicaAnidride cromica [italian]C-grun [german]C.I. Pigment Green 17CI Pigment Green 17Casalis greenChrom(vi)-oxidChromeChrome (trioxyde de) [french]Chrome Green F 3Chrome bronzeChrome greenChrome ocherChrome ochreChrome oxideChrome oxide (Cr2O3)Chrome oxide green BXChrome oxide green GN-mChrome oxide green GPChromiaChromia (CrO3)Chromic (vi) acidChromic acidChromic acid greenChromic acid mixtureChromic acid on Amberlyst A-26Chromic acid, chromium saltChromic acid, polymer-supportedChromic acid, solidChromic acid,chromic(vi)acidChromic acid,solidChromic anhydrideChromic oxideChromic oxide [chromium and chromium compounds]Chromic trioxideChromic(vi) acidChromicum acidumChromium Oxide X1134Chromium Tab 500mcgChromium anhydrideChromium oxideChromium oxide (Cr2O3)Chromium oxide (Cr4O12)Chromium oxide (Cr8O12)Chromium oxide (CrO3)Chromium oxide greenChromium oxide greensChromium oxide hydrateChromium oxide pigmentChromium oxide tetrahydrateChromium sesquioxideChromium trioxide (chemical mixture study)Chromium trioxide [chromium and chromium compounds]Chromium trioxide, anhydrous [UN1463] [Oxidizer]Chromium trioxide, sinteredChromium(3+) oxideChromium(3+) trioxideChromium(6+) trioxideChromium(6+)trioxidChromium(III) oxideChromium(III) oxide (2:3)Chromium(III) sesquioxideChromium(VI) oxide (1:3)Chromium(vi) oxideChromium(vi) trioxideChromosulfuric acidChromous trioxideChromsaeureanhydridChromsaeureanhydrid [german]ChromtrioxidChromtrioxid [german]ChroomtrioxydeChroomtrioxyde [dutch]ChroomzuuranhydrideChroomzuuranhydride [dutch]Cosmetic hydrophobic Green 9409Cosmetic micro blend chrome oxide 9229CrO3Cromo(triossido di)Cromo(triossido di) [italian]Dichromium trioxideDichromium trioxide [ban]Green chrome oxideGreen chromic oxideGreen chromium oxideGreen cinnabarGreen oxide of chromiumGreen oxide of chromium OC-31Green rougeKromex U 1Leaf greenLevanox green gaMonochromium oxideMonochromium trioxideOKhP1Oil greenOxide of chromiumPigment green 17Puratronic chromium trioxidePure Chromium Oxide Green 59Red oxide of chromiumSintered chromium trioxideTrioxochromiumTrioxyde de chrome[CrO3]chromium oxide, 51Cr-labeledchromium(6+) oxide",Chromium(VI) oxide is a chemical compound of hexavalent chromium. It is used mainly in electroplating. Hexavalent chromium is more toxic than other oxidation states of the chromium atom because of its greater ability to enter cells and higher redox potential. (R116),,1333-82-0,14915,,"","",48240,"",,C028801,Chromium(VI) oxide,8144,,,http://en.wikipedia.org/wiki/Chromium trioxide,InChI=1/Cr.3O,trioxochromium,http://www.biospider.ca/saved_files/mol/,O=[Cr](=O)=O,O=[Cr](=O)=O,CrO3,99.925260,Dark red-brown solid.,197 °C,"","","","","","",Oral Inhalation Dermal (R042),Sulfate transporter (P50443) Sulfate anion transporter 1 (Q9H2B4) (R041),"Hexavalent chromium's carcinogenic effects are caused by its metabolites, pentavalent and trivalent chromium. The DNA damage may be caused by hydroxyl radicals produced during reoxidation of pentavalent chromium by hydrogen peroxide molecules present in the cell. Trivalent chromium may also form complexes with peptides, proteins, and DNA, resulting in DNA-protein crosslinks, DNA strand breaks, DNA-DNA interstrand crosslinks, chromium-DNA adducts, chromosomal aberrations and alterations in cellular signaling pathways. It has been shown to induce carcinogenesis by overstimulating cellular regulatory pathways and increasing peroxide levels by activating certain mitogen-activated protein kinases. It can also cause transcriptional repression by cross-linking histone deacetylase 1-DNA methyltransferase 1 complexes to CYP1A1 promoter chromatin, inhibiting histone modification. Chromium may increase its own toxicity by modifying metal regulatory transcription factor 1, causing the inhibition of zinc-induced metallothionein transcription. (R041, R042, R075, R076, R077)","Chromium is absorbed from oral, inhalation, or dermal exposure and distributes to nearly all tissues, with the highest concentrations found in kidney and liver. Bone is also a major storage site and may contribute to long-term retention. Hexavalent chromium's similarity to sulfate and chromate allow it to be transported into cells via sulfate transport mechanisms. Inside the cell, hexavalent chromium is reduced first to pentavalent chromium, then to trivalent chromium by many substances including ascorbate, glutathione, and nicotinamide adenine dinucleotide. Chromium is almost entirely excreted with the urine. (R041, R042)","LD50: 80 mg/kg (Oral, Rat) (R263)
LD50: 14 mg/kg (Intraperitoneal, Mouse) (R263)
",1 to 3 grams for an adult human. (R331),"1, carcinogenic to humans. (R264)",Chromium(VI) oxide is used mainly in electroplating. (R116),"Intermediate Oral: 0.005 mg/kg/day (R260)
Chronic Oral: 0.001 mg/kg/day (R260)",Hexavalent chromium is a known carcinogen. Chronic inhalation especially has been linked to lung cancer. Hexavalent chromium has also been known to cause reproductive and developmental defects. (R041),"Breathing hexavalent chromium can cause irritation to the lining of the nose, nose ulcers, runny nose, and breathing problems, such as asthma, cough, shortness of breath, or wheezing. Ingestion of hexavalent chromium causes irritation and ulcers in the stomach and small intestine, as well as anemia. Skin contact can cause skin ulcers. (R042)",There is no known antidote for chromium poisoning. Exposure is usually handled with symptomatic treatment. (R042),P28482;P27361;Q13547;Q14872;DNA
67,T3D0066,2009-03-06 18:58:01 UTC,2009-08-04 21:27:35 UTC,Methane,Organic Compound;Fuel;Industrial Precursor/Intermediate,"AG 3 (Adsorbent)AG 5 (Adsorbent)ART 2Acetylene blackActicarboneActivated carbonActivated charcoalAdsorbitAerodag gAk (adsorbent)Alkanes, C1-2Amoco PX 21Animal bone charcoalAnthrasorbAqua nucharAquadagAroflowArogenArotoneArovelArrowAtj-sAtj-s graphiteAtlanticBAUBiogasBlack 140Black Kosmos 33Black leadBlack pearlsC.I. Pigment Black 10C.I. Pigment Black 6C.I. Pigment Black 7CF 8 (Carbon)CHCI Pigment black 7CLF IICUZ 3CWN 2Calcotone blackCancarbCanesorbCanlubCarbeneCarbodisCarbolacCarbolac 1CarbometCarbonCarbon blackCarbon black BV and vCarbon black, acetyleneCarbon black, channelCarbon black, furnaceCarbon black, lampCarbon black, thermalCarbon, activatedCarbon, activated [UN1362] [Spontaneously combustible]Carbon, amorphousCarbon, colloidalCarbon, vitreousCarbon-12CarboneCarboniumCarbonoCarbopol Z 4Carbopol extraCarbopol mCarbopol z extraCarbosieveCarbosorbit rCarbyneCaswell No. 161CecarbonCeylon black leadChannel blackChar, from refuse burnerCharcoalCharcoal, activatedCharcoal, except activatedCoke powderColgon BPLColgon PCB 12X30Colgon PCB-dCollocarbColumbia LCKColumbia carbonConductexConductex 900ContinexCorax aCorax pCroflexCrolacDarcoDegussaDelussa black FWDiamondDiamond-Durex oEagle germantownElectrographiteElftexEssexExcelsiorExp-fExplosion acetylene blackExplosion blackFarbrussFectoFiltrasorbFiltrasorb 200Filtrasorb 400Fire dampFlamrussFortafil 5YFurnace blackFurnalFurnexFurnex N 765Gas blackGas-furnace blackGastexGrafoilGrafoil gtaGraphiteGraphite (all forms except graphite fibers)Graphite (natural), dustGraphite (synthetic)Graphite, naturalGraphite, syntheticGraphitic acidGraphnol N 3MGrosafeHitco HMG 50HuberHumenegroHydrodarcoImpingement blackImpingement carbonsIrgalite 1104JADOKetjenblack ecKohlenstoffKorobonKosminkKosmobilKosmolakKosmosKosmothermKosmovarLamp blackLampblackMA 100 (Carbon)MPG 6MYRMagecolMarsh gasMetanexMetanoMethanMethane in gaseus stateMethanetriylMethyl hydrideMethyleneMethylidyneMicronexMiike 20Mineral carbonModulexMogulMogul lMolaccoMonarch 1300Monarch 700Natural gasNeo spectra beads agNeo-spectra IINeo-spectra mark IINeotexNiteron 55NoritNucharOil-furnace blackOu-bP 33 (carbon black)PapyexPeach blackPelikan C 11/1431aPelletexPermablak 663PhilblackPhilblack N 550Philblack N 765Philblack oPigment black 6Pigment black 7PlumbagoPlumbago (graphite)PrintexPrintex 60Pyro-Carb 406RavenRaven 30Raven 420Raven 500RebonexRegalRegal 300Regal 330Regal 400RRegal 600Regal 99Regal SRFRegentRocol X 7119Royal spectraS 1 (Graphite)SKGSKLN 1SKTSKT (adsorbent)SchungiteSevacarbSevalShawinigan acetylene blackShell carbonShungiteSilver graphiteSpecial Black 1V & VSpecial schwarzSpheronSpheron 6StatexStatex N 550Sterling MTSterling N 765Sterling NSSterling SO 1Stove blackSuchar 681Super-carbovarSuper-spectraSuperbaSupersorbon S 1Supersorbon ivSwedish black leadSwine FLY ashTetrahydridocarbonTherma-atomic blackThermal acetylene blackThermal blackThermatomicThermaxThermblackTinoliteToka Black 4500Toka Black 5500Toka Black 8500UNKUcar 38Vitreous carbonWatercarbWhetleriteWitcarb 940hydridocarbon(3.)hydridocarbon(3.) (quartet)r 50 (refrigerant)","Methane is is the simplest alkane and also the major component of natural gas, about 87% by volume. Though it is biologically inactive and thus of limited toxicity, methane is highly flammable, potentially explosive, and an asphyxiant. Methane is also a relatively potent greenhouse gas, with a high global warming potential. (R332, R333)",,74-82-8,297,,C01438,"250650
609236",16183,CH4,,D008697,Methane,3261,,,http://en.wikipedia.org/wiki/Methane,InChI=1/CH4/h1H4,methane,http://www.biospider.ca/saved_files/mol/4e6981acbe4de608da1c46e5483fc182_1237940113.mol,C,C,CH4,16.031300,Colorless gas.,-182.4 °C,,,"0.022 mg/mL at 25 °C [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,Inhalation (R333),,"Methane is an asphyxiant and displaces oxygen in enclosed spaces. At high enough concentrations, oxygen depletion may cause asphyxiation. Low concentrations of surrounding oxygen results in deficient oxygen to the organs, compounded by increased oxygen exhalation during respiration. This results in generalized hypoxia and possibly death. (R332, R335)",Methane is biologically inactive. (R333),"LC50: 326 gm/m3 over 2 hours (Inhalation, Mouse) (R334)",,,"Methane is the major component of natural gas, which is found in geological deposits known as natural gas fields and used as vehicle fuel in its compressed form. Methane may be burned to produce electricity and is often piped into homes for domestic heating and cooking purposes. Methane is also used in industrial processes to produce chemicals such as hydrogen, methanol, acetic acid, and acetic anhydride. (R332)",,"Methane is an asphyxiant and displaces oxygen in enclosed spaces. At high enough concentrations, oxygen depletion may cause asphyxiation, resulting in generalized hypoxia and possibly death. (R332, R333)","Symptoms of methane asphyxiation include nausea, vomiting, difficulty breathing, irregular heartbeat, headache, drowsiness, fatigue, dizziness, disorientation, mood swings, tingling sensation, loss of coordination,
suffocation, convulsions, unconsciousness, coma, and possibly death. (R334)","Asphyxiation should be treated by moving the affected person to an uncontaminated area, then giving artificial respiration and administering oxygen, if necessary. (R334)",""
68,T3D0067,2009-03-06 18:58:01 UTC,2009-08-04 21:27:35 UTC,"Endosulfan, beta",Organic Compound;Pesticide;Organochloride,"&beta;-endosulfan&beta;-thiodanAlpha-thionexB-endosulfan-betaBeta-benzoepinBeta-endosulfanBeta-thiodanEndosulfan 2Endosulfan bEndosulfan, betaEndosulfan-&beta;General weed killer","Endosulfan, Beta is one of two stereoisomers of endosulfan. Endosulfan is an organochlorine insecticide and acaricide. It is used to control insects on food and non-food crops and as a wood preservative. Due to its toxicity and tendency to bioaccumulate, the use of endosulfan is banned in many areas. (R192, R193)",,33213-65-9,6434141,,"","",25520,"",,,"Endosulfan, beta",8145,,,,"InChI=1/C9H6Cl6O3S/c10-5-6(11)8(13)4-2-18-19(16)17-1-3(4)7(5,12)9(8,14)15/h3-4H,1-2H2/t3-,4+,7-,8?,19?/m0/s1","",http://www.biospider.ca/saved_files/mol/,C1[C@@H]2[C@H](COS(=O)O1)[C@@]3(C(=C(C2(C3(Cl)Cl)Cl)Cl)Cl)Cl,C1C2C(COS(=O)O1)C3(C(=C(C2(C3(Cl)Cl)Cl)Cl)Cl)Cl,C9H6Cl6O3S,403.816880,Cream- to brown-colored solid.,"","","","0.00045 mg/mL at 20 °C [BOWMAN,BT & SANS,WW (1983)]","","","",Oral Inhalation Dermal (R194),Cytochrome P450 2B6 (P20813) Cytochrome P450 3A4 (P08684) Cytochrome P450 3A5 (P20815) (R196),"Endosulfan antagonizes the action of the neurotransmitter gamma-aminobutyric acid (GABA) acting at the GABA-A receptors, effectively blocking the GABA-induced uptake of chloride ions. Endosulfan also inhibits Na+ K+ ATPase and Ca2+ and Mg2+ ATPase which are essential for the transport of calcium across membranes. This results in the accumulation of intracellular free calcium ions, which promotes release of neurotransmitters from storage vesicles, the subsequent depolarization of adjacent neurons, and the propagation of stimuli throughout the CNS. This results in hyperexcitation and generalized seizures. Endosulfan is also an endocrine disruptor and acts as an agonist at the progesterone receptor and estrogen receptors. (R029, R193, R194, R195, R312)","Endosulfan is absorbed by inhalation, oral, and dermal routes of exposure. It accumulates mainly in the liver, kidney, and brain, and is metabolized to polar and nonpolar metabolites by cytochrome P-450 enzymes. Endosulfan and its metabolites, which include sulfate, diol, α-hydroxyether, lactone, and ether derivatives of endosulfan, are excreted in the urine and faeces. (R194)","LD50: 18 mg/kg (Oral, Rat) (R263) LD50: 34 mg/kg (Dermal, Rat) (R263) LD50: 8 mg/kg (Intraperitoneal, Rat) (R263) LD50: 360 mg/kg (Subcutaneous, Rabbit) (R263) LC50: 80 mg/m3 over 4 hours (Inhalation, Rat) (R263)",50 to 500 mg/kg for an adult human. (R310),,"Endosulfan is used as an insecticide, acaricide, and in wood preservatives. (R194)",Intermediate Oral: 0.005 mg/kg/day (R260) Chronic Oral: 0.002 mg/kg/day (R260),"Endosulfan is a neurotoxin and damages the central nervous system, causing effects such as intermittent muscle twitching and myoclonic jerking. Endosulfan can also damage the kidneys, testes, and liver, and may possibly affect the body's ability to fight infection. It is also an endocrine disruptor and causes reproductive and developmental damage. (R029, R193, R194)","Symptoms of endosulfan poisoning include hyperactivity, hyperreflexia, tremors, dizziness, headache, convulsions, lack of coordination, staggering, difficulty breathing, nausea and vomiting, diarrhea, and in severe cases, unconsciousness. (R029, R193, R194)","Treatment is symptomatic, aimed at controlling convulsions, coma, and respiratory depression. If ingested, gastric lavage may be performed, followed by administering activated charcoal powder. (R311)",P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P18507;Q99928;O00591;P24046;P28476;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P54710;P98194;O75185;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;P06401;P03372;Q92731;Q8N1C3;A8MPY1;Q9UN88;P78334
69,T3D0068,2009-03-06 18:58:01 UTC,2009-08-25 19:57:21 UTC,Aroclor 1232,Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"","Aroclor 1232 is a commercial mixture of PCBs with an average chlorine content of 32%. It is composed of mono- to heptachlorinated homologs. Polychlorinated biphenyls (PCBs) are a group of 209 synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. PCBs were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate in the environment and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,11141-16-5,"",,"","","","",,,Aroclor 1232,,,,,"","",http://www.biospider.ca/saved_files/mol/,"",Clc1ccc(c(Cl)c1)-c1ccc(Cl)cc1Cl,"","",Clear oil.,"",290–325 °C,1.26 g/cm3,"0.00145 mg/mL at 25 °C [MABEY,WR et al. (1981)]","",152–154 °C,4.06x10-3 mmHg at 25 °C,Oral Inhalation Dermal (R012),Cytochrome P450 1A1 (P04798) Cytochrome P450 1A2 (P05177) Cytochrome P450 2B6 (P20813) Serum albumin (P02768) (R012),"The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are transported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose tissue, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 4470 mg/kg (Oral, Rat) (R263)","","2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refrigerators) produced before 1977. PCBs may contaminate the air and water near hazardouc waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 µg/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptoms can be done. Acute inhalation can be treated by administering oxygen. (R012)",P35869;P49888;P03372;P11684;P20711;Q92731;P07101
70,T3D0069,2009-03-06 18:58:01 UTC,2009-08-04 21:27:35 UTC,Endrin aldehyde,Organic Compound;Pesticide;Organochloride,Endrin aldehyde,"Endrin aldehyde is a chemical produced by the breakdown of endrin. Endrin is a chlorinated hydrocarbon used as an insecticide on cotton, maize, and rice. It also acts as an avicide and rodenticide. Due to its toxicity and tendency to bioaccumulate, its use is now banned in most parts of the world. (R190)",,7421-93-4,522524,,"","","",1-AMINO-PROPAN-2-OL,,,Endrin aldehyde,,,,,"InChI=1/C12H8Cl6O/c13-8-5-3(2-19)1-4-6(5)9(14,12(8,17)18)11(16)7(4)10(8,11)15/h2-7H,1H2","",http://www.biospider.ca/saved_files/mol/,C1C(C2C3C1C4C5(C2(C(C3(C45Cl)Cl)(Cl)Cl)Cl)Cl)C=O,C1C(C2C3C1C4C5(C2(C(C3(C45Cl)Cl)(Cl)Cl)Cl)Cl)C=O,C12H8Cl6O,377.870630,,"",,,"2.4e-05 mg/mL [SHIU,WY et al. (1990)]",,,,Oral (R190),,"Endrin antagonizes the action of the neurotransmitter gamma-aminobutyric acid (GABA) acting at the GABA-A receptors, effectively blocking the GABA-induced uptake of chloride ions and causing hyperexcitability of the central nervous system. Endrin also inhibits Na+ K+ ATPase and Ca2+ and Mg2+ ATPase which are essential for the transport of calcium across membranes. This results in the accumulation of intracellular free calcium ions, which promotes release of neurotransmitters from storage vesicles, the subsequent depolarization of adjacent neurons, and the propagation of stimuli throughout the central nervous system. Endrin also causes increased lipid peroxidation, decreased membrane fluidity, and DNA damage in hepatocytes, but the exact mechanism is unknown. (R029, R191)","Endrin is absorbed orally and distributed primarily to the fat and skin. The major biotransformation product is anti-l 2-hydroxyendrin and the corresponding sulfate, as well as glucuronide metabolites. Anti- and syn-12-hydroxyendrin and 12-ketoendrin are the main toxic metabolites of endrin. Endrin and its metabolites are excreted in urine and feces. (R191)","LD50: >500 mg/kg (Oral, Mouse) (R191)",,,Endrin is used as a pesticide. (R190),,"Endrin poisoning affects primarily the nerve system. Exposure causes various harmful effects including hyperexcitability, severe central nervous system damage, and death. Endrin is also believed to cause birth defects. (R029, R191)","Symptoms that may result from endrin poisoning are headaches, dizziness, nervousness, confusion, nausea, vomiting, and convulsions. (R191)","Treatment is symptomatic, aimed at controlling convulsions, coma, and respiratory depression. If ingested, gastric lavage may be performed, followed by administering activated charcoal powder. (R291)",P98194;O75185;P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P78334;Q8N1C3;P18507;Q99928;O00591;P24046;P28476;A8MPY1;Q9UN88;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;P54710;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P03372;Q92731
71,T3D0070,2009-03-06 18:58:01 UTC,2009-08-04 21:27:36 UTC,Benzofluoranthene,Organic Compound;Industrial By-product/Pollutant;Aromatic Hydrocarbon;Polycyclic Aromatic Hydrocarbon,"1,2-Benzfluoranthrene1,2-Benzofluoranthene1,2-benzfluorantheneBenz(a)aceanthryleneBenzo(a)fluorantheneBenzofluorantheneDibenzo(c,LM)fluorene","Benzofluoranthene is one of over 100 different polycyclic aromatic hydrocarbons (PAHs). PAHs are chemicals that are formed during the incomplete burning organic substances, such as fossil fuels. They are usually found as a mixture containing two or more of these compounds. (R028)",,56832-73-6,9146,,"","","","",,,Benzofluoranthene,,,,,InChI=1/C20H12/c1-2-8-15-13(6-1)12-14-7-5-11-17-16-9-3-4-10-18(16)20(15)19(14)17/h1-12H,"",http://www.biospider.ca/saved_files/mol/,C1=CC=C2C(=C1)C=C3C=CC=C4C3=C2C5=CC=CC=C54,C1=CC=C2C(=C1)C=C3C=CC=C4C3=C2C5=CC=CC=C54,C20H12,252.093900,"","","","","","","","",Oral Inhalation (R028),Serum albumin (P02768) Cytochrome P450 1A1 (P04798) Cytochrome P450 1A2 (P05177) Cytochrome P450 1B1 (Q16678) (R060),"The ability of PAH's to bind to blood proteins such as albumin allows them to be transported throughout the body. Many PAH's induce the expression of cytochrome P450 enzymes, especially CYP1A1, CYP1A2, and CYP1B1, by binding to the aryl hydrocarbon receptor or glycine N-methyltransferase protein. These enzymes metabolize PAH's into their toxic intermediates. The reactive metabolites of PAHs (epoxide intermediates, dihydrodiols, phenols, quinones, and their various combinations) covalently bind to DNA and other cellular macromolecules, initiating mutagenesis and carcinogenesis. (R028, R060, R068, R073)","PAH metabolism occurs in all tissues, usually by cytochrome P-450 and its associated enzymes. PAHs are metabolized into reactive intermediates, which include epoxide intermediates, dihydrodiols, phenols, quinones, and their various combinations. The phenols, quinones, and dihydrodiols can all be conjugated to glucuronides and sulfate esters; the quinones also form glutathione conjugates. (R028)","","",,"PAHs are released into the environment via the combustion of fossil fuels, coke oven emissions and vehicle exhausts, as well as naturally from forest fires and volcanic eruptions. PAHs from these sources may contaminate nearly water systems. They are also found in coal tar and charbroiled food. (R028)","","PAHs are carcinogens and have been associated with the increased risk of skin, respiratory tract, bladder, stomach, and kidney cancers. They may also cause reproductive effects and depress the immune system. (R028)","Acute exposure to PAHs causes irritation and inflammation of the skin and lung tissue. (R034)
",There is no known antidote for PAHs. Exposure is usually handled with symptomatic treatment. (R028),P35869;Q14749;DNA
72,T3D0071,2009-03-06 18:58:01 UTC,2009-08-04 21:27:36 UTC,Toluene,Organic Compound;Solvent;Industrial Precursor/Intermediate;Aromatic Hydrocarbon,"Antisal 1aBenzene, methylBenzene, methyl-Caswell No. 859DracylMBNMethacideMethane, phenyl-Methyl-benzeneMethylbenzeneMethylbenzene (toluene)MethylbenzolMonomethyl benzeneOctadeuterotoluenePhenyl methanePhenylmethaneRCRA waste no. U220Rcra waste number U220RetinaphthaTOLTolu-solTolueenTolueen [dutch]Tolueen(dutch)ToluenToluen [czech]Toluen(czech)Toluene (technical)Toluene [UN1294] [Flammable liquid]Tolueno [spanish]ToluolToluoloToluolo [italian]Toluolo(italian)toluene (ACD/Name 4.0)",Toluene is an aromatic hydrocarbon that occurs naturally in crude oil and in the tolu tree. It is also produced in the process of making gasoline and other fuels from crude oil and making coke from coal. (R336),,108-88-3,1140,,C01455,"",17578,CPD-616,,D014050,Toluene,1391,,,http://en.wikipedia.org/wiki/Toluene,"InChI=1/C7H8/c1-7-5-3-2-4-6-7/h2-6H,1H3",methylbenzene,http://www.biospider.ca/saved_files/mol/3d9c51c2ad3b1ec206f8eed8acaa5ff1_1237940635.mol,CC1=CC=CC=C1,CC1=CC=CC=C1,C7H8,92.062600,Colorless liquid.,-94.9 °C,,,"0.526 mg/mL at 25 °C [SANEMASA,I et al. (1982)]",,,,"Oral
Inhalation
Dermal
(R336)","Cytochrome P450 2E1 (P05181)
Cytochrome P450 2B6 (P20813)
Cytochrome P450 2C8 (P10632)
Cytochrome P450 1A2 (P05177)
Cytochrome P450 1A1 (P04798)
(R336)","Neurological effects such as central nervous system depression and narcosis is generally thought to involve reversible interactions between toluene and components of nervous system membranes or intercalation of toluene into its lipid bilayer. This may change the activities of enzymes involved in the synthesis and/or degradation of neurotransmitters or alter the binding of neurotransmitters to membrane receptors. Toluene binds to cardiac Na+ channels in the open state and unbinds either when channels move between inactivated states or from an inactivated to a closed state. The use and frequency-dependent block of Na+ by toluene might be responsible, at least in part, for its arrhythmogenic effect. (R201, R336)","Inhalation and ingestion are the primary routes of exposure, though toluene may also be absorbed through the skin. It accumulates rapidly in the brain and is subsequently deposited in other tissues according to their lipid content, with the highest levels attained in adipose tissue. The primary initial
steps in toluene metabolism is side-chain hydroxylation catalyzed predominately by the cytochrome P450 isozyme CYP2E1, followed by oxidation to benzoic acid. Most of the benzoic acid is then conjugated with glycine to form hippuric acid,
but a small portion can be conjugated with UDP-glucuronate to form the acyl-glucuronide. A very small portion of absorbed toluene can be converted by CYP1A2, CYP2B2, or CYP2E1 to ortho- or para-cresol. These metabolites are excreted in the urine, and the remaining toluene is exhaled unchanged. (R029, R336)","LD50: 5000 mg/kg (Oral, Rat) (R263)
LD50: 1332 mg/kg (Intraperitoneal, Rat) (R263) 
LD50: 1960 mg/kg (Intravenous, Rat) (R263) 
LD50: 2250 mg/kg (Subcutaneous, Mouse) (R263) 
LD50: 12,124 mg/kg (Dermal, Rabbit) (R263) 
LC50: 400 ppm over 24 hours (Inhalation, Mouse) (R263)",50 mg/kg for an adult human. (R293),"3, not classifiable as to its carcinogenicity to humans. (R264)","Toluene is used in paints, paint thinners, fingernail polish, lacquers, adhesives, and rubber and in some printing and leather tanning processes. Gasoline, which contains 5 to 7 perfect toluene by weight, is the largest source of atmospheric emissions and exposure of the general populace. (R029, R336)","Acute Inhalation: 1 ppm (R260)
Chronic Inhalation: 0.08 ppm (R260)
Acute Oral: 0.8 mg/kg/day (R260)
Intermediate Oral: 0.02 mg/kg/day (R260)","Toluene primarily targets the nervous system and severe neurotoxicity is sometimes diagnosed in persons who have abused toluene for a prolonged period. Clinical signs include abnormal electroencephalographic (EEG) activity, tremors, nystagmus, and cerebral atrophy as well as impaired hearing vision, and speech. Magnetic resonance imaging has revealed permanent changes in brain structure that corresponds to the degree of brain dysfunction. (R029)","The central nervous system is the primary target organ of toluene and other alkylbenzenes. Manifestations of exposure range from slight dizziness and headache to unconciousness, respiratory depression and death. Other symptoms include tiredness, confusion, weakness, memory loss, nausea, loss of appetite, and hearing and color vision loss. These symptoms usually disappear when exposure is stopped. (R029, R336)",Acute central nervous system effects are rapidly reversible upon cessation of exposure. (R020),Q07699;O60939;Q9NY72;Q8IWT1;Q14524;Q8TCU5;O60391;Q12879;Q13224;Q14957;O15399;Q05586;P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P78334;Q8N1C3;P18507;Q99928;O00591;P24046;P28476;A8MPY1;Q9UN88;Q15822;P43681;P30532;P36544;P17787;Q9UGM1;P30926
73,T3D0072,2009-03-06 18:58:01 UTC,2009-08-04 21:27:36 UTC,2-Hexanone,Organic Compound;Solvent;Ketone,"2-Hexanone2-Hexanone Methyl n-butyl ketoneButyl methyl ketoneHexan-2-oneHexanoneHexanone-2Ketone, butyl methylMBKMNBKMethyl butyl ketoneMethyl n-butyl ketoneN-butyl methyl ketonePropylacetonen-C4H9COCH3","2-Hexanone is an organic compound used in the past in paint and paint thinner, to make other chemical substances, and to dissolve oils and waxes. It is no longer produced or used due to its harmful health effects, but it is a waste product of industrial activities such as wood pulping, coal gasification, and oil shale operations. (R343)
",,591-78-6,11583,,"","","",2K-ADIPATE,,D008742,2-Hexanone,1960,,,,"InChI=1/C6H12O/c1-3-4-5-6(2)7/h3-5H2,1-2H3",hexan-2-one,http://www.biospider.ca/saved_files/mol/,CCCCC(C)=O,CCCCC(C)=O,C6H12O,100.088810,Colorless liquid.,-55.5 °C,,,"17.5 mg/mL at 20 °C [PAPA,AJ & SHERMAN,PDJR (1981)]",,,,"Oral
Inhalation
Dermal
(R343)",,"2-Hexanone's toxicity is believed to be caused by covalent binding of its metabolites, especially 2,5-hexanedione, with axonal components of nerve tissue and inhibition of enzymes associated with the production of energy in this tissue. 2-Hexanone and 2,5-hexanedione may also inhibit sulfhydryl-dependent enzymes such as fructose-6-phosphate kinase and glyceraldehyde-3-phosphate dehydrogenase, as well as certain creatine kinases and adenylate kinases, impairing energy metabolism and subsequently resulting in axon deterioration. In addition, 2,5-hexanedione can covalently cross-links neurofilaments, causing large axonal swellings. (R343, R344, R345)","2-Hexanone is absorbed via ingestion, inhalation, and dermal routes, then distributed widely throughout the body, with the highest levels in the liver and blood. Metabolism is likely similar to that of other aliphatic ketones, proceeding via reduction to the corresponding secondary alcohol, 2-hexanol. An alternate pathway is oxidation to the corresponding alcohol, 5-hydroxy-2-hexanone, followed by further oxidation to the diketone 2,5-hexanedione. 2-Hexanone and its metabolites are excreted via exhalation or in the urine. (R343)","LD50: 2590 mg/kg (Oral, Rat) (R261)
LD50: 4800 mg/kg (Dermal, Rabbit) (R261)
",,,"2-Hexanone was used in the past in paint and paint thinner, to make other chemical substances, and to dissolve oils and waxes. Today it is formed as a waste product resulting from industrial activities such as wood pulping, coal gasification, and oil shale operations. (R343)
",,Breathing 2-hexanone affects the nervous and reproductive systems. This may include pathologies such as peripheral neuropathy and developmental defects. (R343),"Chronic 2-hexanone exposure causes weakness, numbness, tingling in the skin of the hands and feet, irritation to the lungs, and narcosis. (R343)","",Q9UIJ7;P04406;O14556;Q01813;P17858;P08237;P12277;P17540;P06732;P12532;P54819;P00568;P27144;Q9Y6K8;Q9Y3D8;Q96M32
74,T3D0073,2009-03-06 18:58:02 UTC,2009-08-04 21:27:36 UTC,"2,3,7,8-Tetrachlorodibenzo-p-dioxin",Organic Compound;Industrial By-product/Pollutant;Chlorinated Dibenzo-p-dioxin;Aromatic Hydrocarbon;Organochloride,"2,3,6,7-Tetrachlorodibenzo-p-dioxin2,3,7,8-:tetrachlorodibenzo-p-dioxin2,3,7,8-Czterochlorodwubenzo-p-dwuoksyny2,3,7,8-Czterochlorodwubenzo-p-dwuoksyny [Polish]2,3,7,8-Tetra polychlorinated dibenzo-p-dioxin2,3,7,8-Tetrachloro(b,e)dibenzodioxin2,3,7,8-Tetrachloro(b,f)dibenzodioxin2,3,7,8-Tetrachloro-dibenzo[b,e][1,4]dioxin2,3,7,8-Tetrachlorodibenzo(b,e)(1,4)dioxan2,3,7,8-Tetrachlorodibenzo(b,e)(1,4)dioxin2,3,7,8-Tetrachlorodibenzo-1,4-Dioxin2,3,7,8-Tetrachlorodibenzo[b,e][1,4]dioxin2,3,7,8-Tetrachlorooxanthrene2,3,7,8-tetrachlorodibenzodioxin2,3,7,8-tetrachlorodibenzodioxineDibenzo(b,e)(1,4)dioxin, 2,3,7,8-tetrachloro-Dibenzo-p-dioxin, 2,3,7,8-tetrachloro-Dibenzo[b,e][1,4]dioxin, 2,3,7,8-tetrachloro-DioksynyDioksyny [polish]DioxinDioxin (herbicide contaminant)Dioxin mixtureDioxineTCDB dTCDDTcdbdTef transgenics (TCDD)Tetrachlorodibenzo-1,4-dioxinTetrachlorodibenzo-p-dioxinTetrachlorodibenzodioxinTetradioxin[3H]-TCDDdibenzo-dioxin, 2,3,7,8-tetrachlorinated","2,3,7,8-Tetrachlorodibenzo-p-dioxin is the most toxic of 75 chlorinated dibenzo-p-dioxin (CDD) congeners. CDDs are a class of manufactured chemicals that consist of dioxin skeletel structures with chlorine substituents. They are also persistent organic pollutants (POPs), thus their production is regulated in most areas. Dioxins occur as by-products from the manufacture of organochlorides, the bleaching of paper, chlorination by waste and drinking water treatment plants, municipal solid waste and industrial incinerators, and natural sources such as volcanoes and forest fires. (R346, R347)",,1746-01-6,15625,,C07557,"",28119,"",,D013749,"2,3,7,8-Tetrachlorodibenzo-p-dioxin",1346,,,,InChI=1/C12H4Cl4O2/c13-5-1-9-10(2-6(5)14)18-12-4-8(16)7(15)3-11(12)17-9/h1-4H,"2,3,7,8-tetrachlorooxanthrene",http://www.biospider.ca/saved_files/mol/c7cad842ac57cb7b2e6ef69d25f4eea4_1237940912.mol,C1=C2C(=CC(=C1Cl)Cl)OC3=CC(=C(C=C3O2)Cl)Cl,C1=C2C(=CC(=C1Cl)Cl)OC3=CC(=C(C=C3O2)Cl)Cl,C12H4Cl4O2,319.896540,Colorless solid.,305 °C,,,"2e-07 mg/mL at 25 °C [SHIU,WY et al. (1988)]",,,,"Oral 
Inhalation 
Dermal 
(R346)",,"CDDs bind to the aryl hydrocarbon (Ah) receptor and subsequently alter the transcription of several genes (oncogenes, growth factors, receptors, hormones, and drug-metabolizing enzymes). The affinity for the Ah receptor depends on the structure of the specific CDD. The change in gene expression may result from the direct interaction of the Ah receptor and its heterodimer-forming partner, the aryl hydrocarbon receptor nuclear translocator, with gene regulatory elements or the initiation of a phosphorylation/dephosphorylation cascade that subsequently activates other transcription factors. The change in transcription/translation of these genes is believed to be the cause of most of the toxic effects of CDDs. 2,3,7,8-tetrachlorodibenzo-p-dioxin's carcinogenicity is thought to be the result of its ability to alter the capacity of both exogenous and endogenous substances to damage the DNA by inducing CYP1A1- and CYP1A2-dependent drug-metabolizing enzymes. (R346)","CDDs are absorbed through oral, inhalation, and dermal routes of exposure. CDDs are carried in the plasma by serum lipids and lipoproteins, and mainly distributed in the liver and adipose tissue. CDDs are slowly metabolized to polar metabolites by the microsomal monooxygenase system. These metabolites can undergo conjugation with glucuronic acid and glutathione. They may increase the rate of their own metabolism by inducing both phase I and phase II enzymes. The major routes of excretion of CDDs are the bile and the faeces, though smaller amounts are excreted in the urine and via lactation. (R346)","LD50:201 ug/kg (Oral, Rat) (R293) 
LD50: 120 ug/kg (Intraperitoneal, Mouse) (R263) ",,"1, carcinogenic to humans. (R264) ","Dioxins occur as by-products from the manufacture of organochlorides, the bleaching of paper, chlorination by waste and drinking water treatment plants, municipal solid waste and industrial incinerators, and natural sources such as volcanoes and forest fires. (R346, R347) ","Acute Oral: 0.0002 ug/kg/day (R260) 
Intermediate Oral: 0.00002 ug/kg/day (R260) 
Chronic Oral: 0.000001 ug/kg/day (R260) ","Exposure to large amounts of CDDs causes chloracne, a severe skin disease with acne-like lesions that occur mainly on the face and upper body. CDDs may also cause liver damage and induce long-term alterations in glucose metabolism and subtle changes in hormonal levels. In addition, studies have shown that CDDs may disrupt the endocrine system and weaken the immune system, as well as cause reproductive damage and birth defects, central and peripheral nervous system pathologies, thyroid disorders, endometriosis, and diabetes. 2,3,7,8-Tetrachlorodibenzo-p-dioxin is also a known as a human carcinogen. (R346, R347)","In addition to chloracne, CDD exposure causes skin rashes, discoloration, and excessive body hair. (R346) ","Treatment of CDD exposure may include washing the area of contact, different methods of gastrointestinal decontamination, administration of intravenous fluids, or forced alkaline diuresis. (R622)",P35869;P02766
75,T3D0074,2009-03-06 18:58:02 UTC,2009-08-27 18:16:55 UTC,Zinc,Inorganic Compound;Metal;Zinc Compound,"Abrasion ontAnusol Ointment 0.5%Anusol Suppositories 10mgAnuzinc Suppositories 10mgAveeno diaper rash creamBaza protectBio statol (pour hommes)Blue powderC.I. Pigment black 16C.I. Pigment metal 6Canus li'l goat's zinc ointmentChelated Zinc Tab 10mgChelated Zinc Tab 50mgChelazome Zinc Cap 30mgCritic-aid skin pasteDR. scholl's medicated foot powderDelavilleDermagran Ii Moisturiz.Spray-Liq Top 1mg/MlDiaper-careEgozinc Ointment - 0.5%Egozinc Suppositories-10mgEgozinc Tab 220mgEmanay zinc dustFlavo-zinc lozengesFormule P-4 Ont 15%Formule P5 Ont 25%GalzinGerber diaper rash ointmentGranular zincIhle's pasteInfazinc Ont 15%JasadJohnson's diaper rash creamLead refinery vacuum zincLozenges - zinc acetateMega Zinc Tab 100mgMen Formula - Cap 5mgMerrilliteMicro ZNOligostim Zinc - Tab 6dhPascoPate D'ihle Pst 25%Penaten creamPhyto-Zinc Cap 50mgRiva-Sol Ont 0.5%Sandoz anuzincShaklee DR chewable tabletsSudocremSunblock Spf 15Triple Care Cream 10%Viscopaste Pb7 Dressing 10%Woodward's diaper rash creamZNZN(II)Zinaderm Cream 15%Zinc (Citrate) Capsule 50mgZinc (Gluconate) 100mg - TabZinc (Gluconate) 30 Mg TabletsZinc (Gluconate) 50mg TabletsZinc 15mg TabZinc 25mg Hvp Chelate - Tab 25mgZinc 25mg TabZinc 50 MgZinc 50 Mg Citrate - CapletZinc 50 TabletsZinc 50mgZinc Amino Acid Chelate Tab 10mgZinc Amino Acid Chelate Tab 15mgZinc Cap 50mgZinc Caps 30mgZinc Citrate 50mgZinc Citrate Chelate Tab 50mgZinc Citrate Tab 15mgZinc Citrate Tab 50mgZinc Cream 50gm 150mg/GmZinc Gluconate Tab 10mgZinc Gluconate Tab 50mgZinc Gluconate Tablets 50mgZinc Liquid- 15mg/5mlZinc Lozenge 23mgZinc Oligosol Liq 0.47mg/2mlZinc Onguent 20%Zinc Oxide Cream - 15%Zinc Oxide Ont 20%Zinc Srt 50mgZinc Tab 10mgZinc Tab 20mgZinc Tab 25mgZinc Tab 25mg Hvp ChelatedZinc Tab 50mgZinc Tablets 50mgZinc Vallerate Liquid (S#388)Zinc chloride in plastic containerZinc citrateZinc creamZinc dustZinc formulaZinc gluconateZinc gluconate tabZinc ionZinc ointmentZinc ointment BPZinc oral sprayZinc oxide PWRZinc oxide creamZinc powderZinc powder - zinc dust (pyrophoric)Zinc tallyZinc, ashesZinc, powder or dust, non-pyrophoricZinc, powder or dust, pyrophoricZincitrate Cap 30mgZincoderm Ointment - 40%ZincofaxZincofax extra strengthZincum 3x PwrZincum Cyanatum-Injeel Forte Liq (6d,10d,30d,200d/1.1ml)Zincum Gtte 4ch-30chZincum Met 4ch-30chZincum Metallicum Liquid (S#98)-3,6,9,12x.CmZincum Metallicum-Injeel Forte Liq (6d,12d,30d,200d/1.1ml)Zincum Phosphoratum Liquid (S#1110)-6,9x..CmZincum aceticumZincum bromatumZincum carbonicumZincum cyanatumZincum iodatumZincum metallicumZincum muriaticumZincum oxydatumZincum phosphoratumZincum picricumZincum sulfuricumZincum sulphricumZincum sulphuricumZincum valerianicumZipzoc","Zinc is a metallic element with the atomic number 30. In nature, it is principally found as the mineral sphalerite. Though excess zinc is harmful, it is an essential element for life as a cofactor for over 300 enzymes. Zinc has many commercial uses as coatings to prevent rust, in dry cell batteries, and can be mixed with other metals to produce alloys such as brass and bronze. Zinc compounds are widely used in industry to make paint, rubber, dyes, wood preservatives, and ointments. (R112, R113)
",,7440-66-6,23994,,C00038,"103600
110900
113705
121300
125270
137164
138750
150330
163729
165240
180200
184757
188840
190080
191170
191290
194470
300414
300473
314998
600140
600310
600871
600993
601487
601757
601758
602432
602575
602630
603693
604386
604485
606829
607035
607102
607818
608072
608118",30185,ZN%2b2,,D015032,Zinc,6568,,,http://en.wikipedia.org/wiki/Zinc,InChI=1/Zn,zinc,http://www.biospider.ca/saved_files/mol/2c2cbc043c430fc4d9606e97ab0b7597_1237941391.mol,[Zn++],[Zn++],[Zn]2+,63.929138,Bluish-white metallic solid.,419.5 °C,"","","","","","","Oral 
Inhalation 
Dermal
(R113)","Metallothionein-2 (P02795)
Metallothionein-1G (P13640)
Metallothionein-1H (P80294)
Metallothionein-3 (P25713)
Metallothionein-1F (P04733)
Metallothionein-1E (P04732)
Metallothionein-1X (P80297)
Metallothionein-1A (P04731)
Metallothionein-1B (P07438)
Metallothionein-1M (Q8N339)
Metallothionein-4 (P47944)
Metallothionein-1L (Q93083)
Cysteine-rich protein 1 (P50238)
Cysteine-rich protein 2 (P52943)
Cysteine-rich protein 3 (Q6Q6R5)
Serum albumin (P02768)
(R113, R128, R164)","Excessive zinc intake alters copper and iron absorption, most likely through competitive binding in intestinal mucosal cells. Stomach acid dissolves metallic zinc, producing zinc chloride, which is a corrosive product damaging the stomach lining. Metal fume fever is thought to be an immune response to inhaled zinc. (R112, R113, R128)","Zinc enters the body through the lungs, skin, and gastrointestinal tract. Intestinal absorption of zinc is controlled by zinc carrier protein CRIP and metallothioneins. Zinc is widely distributed in tissues and tissues fluids, and concentrated in the liver, gastrointestinal tract, kidney, skin, lung, brain, heart, and pancreas. Zinc binds to carbonic anhydrase in erythrocytes, and to albumin, α2-macroglobulin, and amino acids in the the plasma. Albumin and amino acid bound zinc can diffuse across tissue membranes. Zinc is excreted in the urine and faeces. (R113)","LD50: 630 mg/kg (Oral, Rat) (R351)","",,"Zinc has many commercial uses as coatings to prevent rust, in dry cell batteries, and can be mixed with other metals to produce alloys such as brass and bronze. Zinc compounds are widely used in industry to make paint, rubber, dyes, wood preservatives, and ointments. (R113)","Intermediate Oral: 0.3 mg/kg/day (R260)
Chronic Oral: 0.3 mg/kg/day (R260)","Chronic exposure to zinc causes anemia, atazia, lethargy, and decreases the level of HDL (good) cholesterol in the body. It is also believed to cause pancreatic and reproductive damages. Unbalanced levels of copper and zinc binding to Cu,Zn-superoxide dismutase have been linked to amyotrophic lateral sclerosis (ALS). (R113)
","Ingestion of large doses of zinc causes stomach cramps, nausea, and vomiting. Acute inhalation of large amounts of zinc causes metal fume fever, which is characterized by chills, fever, headache, weakness, dryness of the nose and throat, chest pain, and coughing. Dermal contact with zinc results in skin irritation. (R113)","Zinc poisoning is treated symptomatically, often by administering fluids such as water or milk, or with gastric lavage. (R113)",P00441
76,T3D0075,2009-03-06 18:58:02 UTC,2009-08-04 21:27:36 UTC,Dimethylarsinic acid,Organic Compound;Arsenic Compound,"Acide cacodyliqueAcide cacodylique (french)Acide cacodylique [french]Acide dimethylarsenique [french]Acide dimethylarsiniqueAcide dimethylarsinique (french)Acide dimethylarsinique [french]Agent blueAlkargenAnsarAnsar 138ArsanArsecodileArsine oxide, dimethylhydroxy-Arsine oxide, hydroxydimethyl-Arsine oxide, hydroxydimethyl- (8CI)Arsine oxide, hydroxydimethyl-, lithium saltArsinic acid, dimethyl-Arsinic acid, dimethyl-, lithium saltBolateBollsBolls-eyeC0125_SIGMACacodylateCacodylic acidCacodylic acid [UN1572] [Poison]Caswell No. 133ChexmateCotton aide HCDMAADilicDimethylarsenic acidDimethylarsinic acidDimethylarsinic acid (9CI)Dimethylarsinic acid [bsi:iso]Dimethylarsinic acid, lithium saltDimethylarsonic acidEraseHydroxydimethylarsine oxideKakodylsaeureKyselina kakodylovaKyselina kakodylova [czech]Lithium cacodylateLithium, [(dimethyloxoarsenio)oxy]-Me2As(=O)OHMoncidePS51_SUPELCOPhytarPhytar 138Phytar 560Phytar 600RCRA waste no. U136Rad-e-cate 25Rad-e-cate 35Rcra waste number U136SalvoSilvisarSilvisar 510Sylvicor[As(CH3)2O(OH)]dimethylarsinic acid (ACD/Name 4.0)rad-e-cat 25",Dimethylarsinic acid is an organic derivative of arsine. It may be formed from the oxidation of gaseous methylated arsines by bacteria and fungi or the transformation of inorganic arsenic compounds. It is also one of the major metabolites of arsenic. (R009),,75-60-5,2513,,C07308,"",48765,DIMETHYLARSINATE,,D002101,Dimethylarsinic acid,516,,,,"InChI=1/C2H7AsO2/c1-3(2,4)5/h1-2H3,(H,4,5)",dimethylarsinic acid,http://www.biospider.ca/saved_files/mol/acf4626704d00a020399b505aebdb480_1237941495.mol,C[As](C)(O)=O,C[As](C)(O)=O,C2H7AsO2,137.966200,Colorless solid.,195 °C,"","","2000 mg/mL at 25 °C [YALKOWSKY,SH & DANNENFELSER,RM (1992)]","","","","Oral 
Inhalation 
Dermal
(R009)","","Arsenic and its metabolites disrupt ATP production through different mechanisms. At the level of the citric acid cycle, arsenic inhibits the pyruvate dehydrogenase and uncouples the oxidative phosphorylation by competing with phosphate. This leads to inhibition of energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is increased, leading to oxidative stress due to the formation of reactive oxygen species. Arsenic's carginogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (R001, R054)",Arsenic and its metabolites are primarily excreted in the urine. (R009),"LD50: 644 mg/kg (Oral, Rat) (R263)
LD50: 720 mg/kg (Intraperitoneal, Rat) (R353)","","1, carcinogenic to humans. (R264)",Dimethylarsinic acid is used as an herbicide and pesticide. (R354),"","Arsenic poisoning can lead to death from multi-system organ failure, probably from necrotic cell death, not apoptosis. Arsenic is also a known carcinogen, especially in skin, liver, bladder and lung cancers. (R001, R055)","Exposure to lower levels of arsenic can cause nausea and vomiting, decreased production of red and white blood cells, abnormal heart rhythm, damage to blood vessels, and a sensation of “pins and needles” in hands and feet. Breathing high levels of inorganic arsenic can provoque sore throat or irritated lungs. Arsenic also affects the brain, causing neurological disturbances such as headaches, confusion, and drowsiness. (R002)","Arsenic poisoning can be treated by chelation therapy, using chelating agents such as dimercaprol, EDTA or DMSA. Charcoal tablets may also be used for less severe cases. In addition, maintaining a diet high in sulfur helps eliminate arsenic from the body. (R055)",P69905;P68871;P68032;P68133;P62736;P60709;P63261;P63267;P10515;P23025;P03372;P04150;P00390;P00738;Q14145;P09874;A6NKZ8 ;Q99867;Q9H853;P08559;P29803;P11177;O00330;Q16881;Q9NNW7;Q86VQ6;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2;Q9UJT1;Q9UJT0;P23258;Q9NRH3
77,T3D0076,2009-03-06 18:58:02 UTC,2009-08-04 21:27:37 UTC,Di(2-ethylhexyl)phthalate,Organic Compound;Plasticizer;Phthalate,"'dioctyl' phthalate1, 2-Benzenedicarboxylic acid, bis(2-ethylhexyl) ester1, 2-Benzenedicarboxylic acid, bis(ethylhexyl) ester1,2-Benzenedicarboxylic acid1,2-Benzenedicarboxylic acid bis(2-ethylhexyl) ester1,2-Benzenedicarboxylic acid bis-(1-ethylhexyl) ester1,2-Benzenedicarboxylic acid, bis(2-ethylhexyl) ester1,2-Benzenedicarboxylic acid, bis(ethylhexyl) ester1,2-Benzenedicarboxylic acid, bis-(1-ethylhexyl) ester2-Ethylhexyl phthalateBEHPBenzenedicarboxylic acid, bis(2-ethylhexyl) esterBi(2-ethylhexyl)trimellitate esterBis (2-Ethylhexyl) Phthalate (Dioctyl phthalate)Bis(2-ethylhexy) phthalateBis(2-ethylhexyl) 1, 2-benzenedicarboxylateBis(2-ethylhexyl) 1,2-benzenedicarboxylateBis(2-ethylhexyl) o-phthalateBis(2-ethylhexyl) phthalateBis(2-ethylhexyl) phthalate-ring-UL-14CBis(2-ethylhexyl)ester phthalic acidBis(ethylhexyl) phthalateBis-(2-ethylhexyl)-phthalate (DEHP)Bis-(2-ethylhexyl)ester kyseliny ftaloveBis-(2-ethylhexyl)ester kyseliny ftalove (czech)Bis-(2-ethylhexyl)ester kyseliny ftalove [Czech]Bis-2-ethyl-hexyl-phthalateBisoflex 81Bisoflex 82Bisoflex dopCaswell No. 392KCelluflex dopCompound 889DEHPDI(2-ETHYLHEXYL) PHTHALATE (SEE ALSO CAS 103-23-1)DOFDOPDi(2-Ethylhexyl phthalate)Di(2-ethylhexyl) o-phthalateDi(2-ethylhexyl) orthophthalateDi(2-ethylhexyl) phthalateDi(2-ethylhexyl)orthophthalateDi(2-ethylhexyl)phthalateDi(2-ethylhexyl)phthalate (DEHP)Di(ethylhexyl) phthalateDi-(2-ethylhexyl) phthalateDi-2 ethyl hexyl adipateDi-2-ethyl hexyl azelateDi-2-ethylhexyl phthalateDi-2-ethylhexylphthalateDi-iso-octyl phthalateDi-sec-octyl phthalateDiacizer dopDicapryl phthalateDiethylhexyl phthalateDioctyl o-benzenedicarboxylateDioctyl phthalateDioctyl phthalate (van)Dioctyl-o-benzenedicarboxylateDioctylphthalateDof [russian plasticizer]Ergoplas t fdoErgoplast fdoErgoplast fdo-sEtalonEtalon (plasticizer)Ethyl hexyl phthalateEthylhexyl phthalateEviplast 80Eviplast 81FleximelFlexol dopFlexol plasticizer dopGood-rite gp 264Hatcol dopHercoflex 260Jayflex dopKodaflex DPKodaflex dehpKodaflex dopMerrol dopMollan oMonocizer dopMorflex 310Morflex 410N-dioctyl phthalateNuoplaz dopO-benzenedicarboxylic acid, dioctyl esterOctoilOctyl PH thalateOctyl phthalateOctyl phthalate (van)Palatinol ahPalatinol dopPhthalic acid bis(2-ethylhexyl ester)Phthalic acid bis(2-ethylhexyl ester)-ring-UL-14CPhthalic acid di(2-ethylhexyl) esterPhthalic acid dioctyl esterPhthalic acid dioctyl ester (van)Phthalic acid, bis(2-ethylhexyl) esterPhthalic acid, dioctyl esterPittsburgh PX-138Plasthall dopPlasticizer 28PPlatinol ahPlatinol dopPolycizer 162Polycizer dopRC plasticizer dopRCRA waste no. U028Rcra waste number U028Reomol D 79PReomol DCPReomol dopSansocizer R 8000Sansocizer dopSconamoll dopSicol 150Staflex dopTRANSGENIC MODEL EVALUATION (DI(2-ETHYLHEXYL) PHTHALATE)Truflex dopUnion carbide flexo l 380Union carbide flexol 380Vestinol ahVinicizer 80WLN: 4Y2 & 1OVR BVO1Y4 & 2WLN: 8OVR BVO8Witcizer 312bis (2-Etheylexyl) Phthalatebis(2-ethylhexyl) phthalate (ACD/Name 4.0)bis-(2-ethylhexyl) 1,2-benzenedicar boxylatebis-(2-ethylhexyl) 1,2-benzenedicarboxylate","Di(2-ethylhexyl) phthlate (DEHP) is a manufactured chemical that is commonly added to plastics to make them flexible. DEHP exposure is generally low and not harmful, but increased exposures resulting from intravenous fluids delivered through plastic tubing or ingesting contaminated foods or water may have toxic effects. This is of particular concern since DEHP is known to leach into liquid that come in contact with DEHP containing plastic. (R355, R356)",,117-81-7,8343,,C03690,"",17747,BIS2-ETHYLHEXYLPHTHALATE,,D004051,Di(2-ethylhexyl)phthalate,617,,,http://en.wikipedia.org/wiki/Bis(2-ethylhexyl)phthalate,"InChI=1/C24H38O4/c1-5-9-13-19(7-3)17-27-23(25)21-15-11-12-16-22(21)24(26)28-18-20(8-4)14-10-6-2/h11-12,15-16,19-20H,5-10,13-14,17-18H2,1-4H3","bis(2-ethylhexyl) benzene-1,2-dicarboxylate",http://www.biospider.ca/saved_files/mol/2d6dacd9a4d0c0c9969912a38266b2c3_1237941604.mol,CCCCC(CC)COC(=O)C1=CC=CC=C1C(=O)OCC(CC)CCCC,CCCCC(CC)COC(=O)C1=CC=CC=C1C(=O)OCC(CC)CCCC,C24H38O4,390.277010,Coloress liquid.,-55 °C,,,"0.00027 mg/mL at 25 °C [DEFOE,DL et al. (1990)]",,,,Oral (R355),,"Monoethylhexylphthalate (MEHP), one of the major metabolites of DEHP, induces peroxisome proliferation by activating peroxisome proliferator activated receptors. This is believed to increase production of hydrogen peroxide by peroxisomes and enhance cell proliferation, leading to hepatotoxic and carcinogenic effects. MEHP is also believed to exhibit testicular toxicity by targeting and damaging the Sertoli cells. DEHP may act as an antiandrogen during a critical stage of reproductive tract differentiation by reducing testosterone in fetal males, hindering development. (R355, R359)","DEHP is mainly absorbed via ingestion. It is hydrolyzed in the small intestine and absorbed as monoethylhexylphthalate (MEHP) and 2-ethylhexanol, then likely distributed to the adipose tissues and kidneys. MEHP is further metabolized via numerous oxidative reactions, resulting in the formation of 30 or more metabolites, some of which can be conjugated with glucuronic acid for excretion. Oxidation of 2-ethylhexanol primarily yields 2-ethylhexanoic acid and several keto acid derivatives. Most DEHP metabolites are excreted in the urine as glucuronide conjugates, while unmetabolized DEHP is excreted in the faeces. (R355)","LD50: 33.9 g/kg (Oral, Rabbit) (R360)
LD50: 10 g/kg (Dermal, Guinea pig) (R360)
LD50: 30.7 g/kg (Intraperitoneal, Rat) (R360)",,"3, not classifiable as to its carcinogenicity to humans. (R264)","DEHP is present in plastic products such as wall coverings, tablecloths, floor tiles, furniture upholstery, shower curtains, garden hoses, swimming pool liners, rainwear, baby pants, dolls, some toys, shoes, automobile upholstery and tops, packaging film and sheets, sheathing for wire and cable, medical tubing, and blood storage bags. (R355)","Intermediate Oral: 0.1 mg/kg/day (R260)
Chronic Oral: 0.06 mg/kg/day (R260)","Chronic and/or high levels of DEHP exposure may cause reproductive and developmental damage. This includes damaged sperm, delayed sexual maturity, and deficiencies in the development of male babies. DEHP may also cause liver and kidney damage, and is potentially carcinogenic. (R355, R356)",,"",Q07869;Q03181;P37231
78,T3D0077,2009-03-06 18:58:02 UTC,2009-08-27 18:18:25 UTC,Chromium,Inorganic Compound;Metal;Chromium Compound,"Action o gCHROMIUM, POWDER, 325 MESH, 99.9%CRCR(-)Chelated Chromium 200 McgChelated Chromium 200mcgChelated Chromium Gtf 500mcg TabChelated Chromium Tab 200mcgChromChrom [german]Chromar 500mcgChromatone - Tab 100mcgChromeChrome Zme - Capsule - 200 McgChrome [french]Chromic acid and chromatesChromicum acidumChromide(-I)Chromium 200mcgChromium 200mcg TabletsChromium 400 McgChromium Caps 0.2mgChromium Chelate 500 McgChromium Gtf 200 CapChromium Gtf 200 McgChromium Gtf 200mcgChromium Gtf 500 Mcg TabletChromium Gtf 500mcgChromium Gtf Tab 500mcgChromium Tab 200mcgChromium Tab 250mcgChromium Tab 500mcgChromium anionChromium citrateChromium compoundsChromium kalisulfuricumChromium metalChromium metal [chromium and chromium compounds]Chromium(II) compoundsChromium(III) atomic absorption standard solutionChromium(III) compoundsChromium(vi) atomic absorption standard solutionChromium, elementalChromium, metalChromium, metal and chromium(III) compoundsChromium, metal and insol. saltsCromoGTF chromiumGTF chromium tabletsGtf Chromium Tab 200mcgMega Chrome T V Tab 100mcgMicro CRNubodyNubody chromium amino acid chelateOmnilife d.v.Opti Chromium (Trivalent)Caplet 200mcgQuilon l chromium complex solutionS.s. formulaT-lemonT.R. Chromium 500mcg TabletTJ yellowchromide(1-)","Chromium is a chemical element which has the symbol Cr and atomic number 24. It naturally occurs in rocks, animals, plants, and soil, and is usually mined as chromite ore. Chromium is a hard metal and is used mainly for making steel. Chromium is most toxic in its +6 oxidation state (chromium(VI)) due to its greater ability to enter cells and higher redox potential. Trivalent chromium (chromium(III)) however, is biologically necessary for sugar and lipid metabolism in humans. (R045)",,7440-47-3,23976,,C06268,271400,28073,"",,D002857,Chromium,7192,,,http://en.wikipedia.org/wiki/Chromium,InChI=1/Cr/q+3,chromium,http://www.biospider.ca/saved_files/mol/,[Cr+3],[Cr+3],[Cr]3+,51.940510,"",1900 °C,"","","","","","",Oral Inhalation Dermal (R042),Sulfate transporter (P50443) Sulfate anion transporter 1 (Q9H2B4) (R041),"Hexavalent chromium's carcinogenic effects are caused by its metabolites, pentavalent and trivalent chromium. The DNA damage may be caused by hydroxyl radicals produced during reoxidation of pentavalent chromium by hydrogen peroxide molecules present in the cell. Trivalent chromium may also form complexes with peptides, proteins, and DNA, resulting in DNA-protein crosslinks, DNA strand breaks, DNA-DNA interstrand crosslinks, chromium-DNA adducts, chromosomal aberrations and alterations in cellular signaling pathways. It has been shown to induce carcinogenesis by overstimulating cellular regulatory pathways and increasing peroxide levels by activating certain mitogen-activated protein kinases. It can also cause transcriptional repression by cross-linking histone deacetylase 1-DNA methyltransferase 1 complexes to CYP1A1 promoter chromatin, inhibiting histone modification. Chromium may increase its own toxicity by modifying metal regulatory transcription factor 1, causing the inhibition of zinc-induced metallothionein transcription. (R041, R042, R075, R076, R077)","Chromium is absorbed from oral, inhalation, or dermal exposure and distributes to nearly all tissues, with the highest concentrations found in kidney and liver. Bone is also a major storage site and may contribute to long-term retention. Hexavalent chromium's similarity to sulfate and chromate allows it to be transported into cells via sulfate transport mechanisms. Inside the cell, hexavalent chromium is reduced first to pentavalent chromium, then to trivalent chromium by different pathways including ascorbate, glutathione, and nicotinamide adenine dinucleotide. Chromium is almost entirely excreted in the urine. (R041, R042)","",1 to 3 grams of hexavalent chromium for an adult human. (R331),"1, carcinogenic to humans (hexavalent) and 3, not classifiable as to its carcinogenicity to humans (metallic, trivalent). (R264)","Elemental chromium is used mainly for making steel. Hexavalent chromium is used for chrome plating, dyes and pigments, leather tanning, and wood preserving. (R041, R045)","Intermediate Oral: 0.005 mg/kg/day (Hexavalent chromium) (R260) 
Chronic Oral: 0.001 mg/kg/day (Hexavalent chromium) (R260)",Hexavalent chromium is a known carcinogen. Chronic inhalation especially has been linked to lung cancer. Hexavalent chromium has also been shown to affect reproduction and development. (R041),"Breathing hexavalent chromium can cause irritation to the lining of the nose, nose ulcers, runny nose, and breathing problems, such as asthma, cough, shortness of breath, or wheezing. Ingestion of hexavalent chromium causes irritation and ulcers in the stomach and small intestine, as well as anemia. Skin contact can cause skin ulcers. (R042)","There is no known antidote for chromium poisoning. Exposure is usually handled with symptomatic treatment. (R042)
",P28482;P27361;Q13547;Q14872;DNA
79,T3D0078,2009-03-06 18:58:02 UTC,2009-08-04 21:27:37 UTC,Naphthalene,Organic Compound;Industrial By-product/Pollutant;Aromatic Hydrocarbon;Polycyclic Aromatic Hydrocarbon,"AlbocarbonCamphor tarCaswell No. 587DezodoratorMighty 150Mighty rd1Moth ballsMoth flakesMothballsN3145_SIGMAN7394_SIGMANPYNaftalenNaftalen (polish)Naftalen [polish]Naphtalene [iso:french]Naphtalinum 1ch-30chNaphthalene (molten)Naphthalene [bsi:iso]Naphthalene solutionNaphthalene, crudeNaphthalene, crude or refinedNaphthalene, crude or refined [UN1334] [Flammable solid]Naphthalene, moltenNaphthalene, molten [UN2304] [Flammable solid]Naphthalene, pureNaphthalene-UL-14CNaphthalinNaphthalineNaphthalinumNaphtheneNapthalene, moltenRCRA waste no. U165Rcra waste number U165Tar camphorWhite tarnaphthalene (ACD/Name 4.0)","Naphthalene is one of over 100 different polycyclic aromatic hydrocarbons (PAHs). PAHs are chemicals that are formed during the incomplete burning organic substances, such as fossil fuels. They are usually found as a mixture containing two or more of these compounds. (R028)",,91-20-3,931,,C00829,"",16482,ALPHA-NAPHTHALENEACETAMIDE,,C031721,Naphthalene,934,,,http://en.wikipedia.org/wiki/Naphthalene,InChI=1/C10H8/c1-2-6-10-8-4-3-7-9(10)5-1/h1-8H,naphthalene,http://www.biospider.ca/saved_files/mol/0d9845edc6ba001c21e5a22e5a4ba3bc_1237941900.mol,C1=CC=C2C=CC=CC2=C1,C1=CC=C2C=CC=CC2=C1,C10H8,128.062600,White crystals.,80.2 °C,"","","0.031 mg/mL at 25 °C [PEARLMAN,RS et al. (1984)]","","","",Oral Inhalation (R028),Serum albumin (P02768) Cytochrome P450 1A1 (P04798) Cytochrome P450 1A2 (P05177) Cytochrome P450 1B1 (Q16678) (R060),"PAH's are transported throughout the body after binding blood proteins such as albumin. Binding to the aryl hydrocarbon receptor or glycine N-methyltransferase induces the expression of cytochrome P450 enzymes (especially CYP1A1, CYP1A2, and CYP1B1). These cytochrome enzymes metabolize PAH's into various toxic intermediates (epoxide intermediates, dihydrodiols, phenols, quinones, and their various combinations). The reactive metabolites of PAHs covalently bind to DNA and other cellular macromolecules, initiating mutagenesis and carcinogenesis. (R028, R060, R068, R073)","PAH metabolism occurs in all tissues, usually by cytochrome P-450 and its associated enzymes. PAHs are metabolized into reactive intermediates, which include epoxide intermediates, dihydrodiols, phenols, quinones, and their various combinations. The phenols, quinones, and dihydrodiols can be conjugated to glucuronides and sulfate esters; and the quinones can form glutathione conjugates. (R028)","LD50: 490 mg/kg (Oral, Rat) (R327)
LD50: >20 g/kg (Dermal, Rabbit) (R327)
LD50: 150 mg/kg (Intraperitoneal, Mouse) (R263)
LD50: 969 mg/kg (Subcutaneous, Mouse) (R263)
LD50: 100 mg/kg (Intravenous, Mouse) (R263)","","2B, possibly carcinogenic to humans. (R264)","PAHs are released into the environment via the combustion of fossil fuels, coke oven emissions and vehicle exhausts, as well as naturally from forest fires and volcanic eruptions. PAHs from these sources may contaminate nearly water systems. They are also found in coal tar and charbroiled food. (R028)","","PAHs are carcinogens and have been associated with the increased risk of skin, respiratory tract, bladder, stomach, and kidney cancers. They may also cause reproductive effects and depress the immune system. Naphthalene also damages and destroys red blood cells, causing hemolytic anemia. (R028, R035)","Acute exposure to PAHs causes irritation and inflammation of the skin and lung tissue. Some symptoms of hemolytic anemia are fatigue, lack of appetite, restlessness, and pale skin. Exposure to large amounts of naphthalene may also cause nausea, vomiting, diarrhea, blood in the urine, and a yellow color to the skin. (R034, R035)
",There is no known antidote for PAHs. Exposure is usually handled with symptomatic treatment. (R028),P35869;Q14749;DNA
80,T3D0079,2009-03-06 18:58:02 UTC,2009-08-04 21:27:37 UTC,"1,1-Dichloroethene",Organic Compound;Organochloride,"1,1-Dichloroethene1,1-Dichloroethene (9CI)1,1-Dichloroethene homopolymer1,1-Dichloroethylene1,1-Dichloroethylene, inhibited1,1-dichloroethylene (vinylidine chloride):vinylidene chlorideAs-dichloroethyleneAsym-dichloroethyleneCH2=CCl2Chlorure de vinylideneChlorure de vinylidene [french]Ethene, 1,1-dichloro-, homopolymerEthylene, 1,1-dichloro-InChI=1/C2H2Cl2/c1-2(3)4/h1HPolyvinylidene chlorideRCRA waste no. U078Rcra waste number U078SconatexVDCVinylidene chlorideVinylidene chloride (II)Vinylidene chloride (inhibited)Vinylidene chloride(II)Vinylidene chloride, inhibitedVinylidene chloride, inhibited [UN1303] [Flammable liquid]Vinylidene chloride, monomerVinylidene dichlorideVinylidine chloride","1,1-Dichloroethene is a manufactured organochloride compound. It is used in the production of certain plastics as a comonomer in the polymerization of vinyl chloride, acrylonitrile, and acrylates. It is also used to make flame retardant coatings for fiber and carpet backings, and in piping, coating for steel pipes, and in adhesive applications. (R362, R363)",,75-35-4,6366,,C14039,"",34031,11-DCE,,C029297,"1,1-Dichloroethene",1470,,,,InChI=1/C2H2Cl2/c1-2(3)4/h1H2,"1,1-dichloroethene",http://www.biospider.ca/saved_files/mol/c686a17fd81e0a17d9050644a561eb60_1237942048.mol,C=C(Cl)Cl,C=C(Cl)Cl,C2H2Cl2,95.953360,,-122.5 °C,,,"2.42 mg/mL at 25 °C [HORVATH,AL et al. (1999)]",,,,"Oral
Inhalation
Dermal
(R362)",Cytochrome P450 2E1 (P05181) Glutathione S-transferase P (P09211) Glutathione S-transferase Mu 1 (P09488) Glutathione S-transferase A1 (P08263) Glutathione S-transferase theta-2 (P30712) Glutathione S-transferase Mu 4 (Q03013) Glutathione S-transferase theta-1 (P30711) Glutathione S-transferase A4 (O15217) Glutathione S-transferase A2 (P09210) Glutathione S-transferase A3 (Q16772) Glutathione S-transferase Mu 3 (P21266) Glutathione S-transferase omega-1 (P78417) Glutathione S-transferase kappa 1 (Q9Y2Q3) Glutathione S-transferase Mu 2 (P28161) Glutathione S-transferase omega-2 (Q9H4Y5) Glutathione S-transferase A5 (Q7RTV2) Glutathione S-transferase Mu 5 (P46439) Glutathione S-transferase theta-4 (A8MPT4) Maleylacetoacetate isomerase (O43708) Microsomal glutathione S-transferase 1 (P10620) Microsomal glutathione S-transferase 2 (Q99735) Microsomal glutathione S-transferase 3 (O14880) (R362),"1,1-Dichloroethene toxicity is caused by its reactive metabolites, which include epoxides, acyl chlorides, and halogenated aldehydes generated via oxidation by cytochrome P-450 2E1. These metabolites, especially 2,2-dichloroacetaldehyde and 2-chloroacetyl chloride, damage the liver by binding to cellular macromolecules. They also form glutathione S conjugates by the action of glutathione S-transferases located in the hepatic cytosol and microsomes. These are delivered to the kidney, where renal processing by beta-lyase and cysteine conjugate S-oxidase lead to nephrotoxic products. The metabolites are also known to damage the bronchiolar Clara cells in the lung. (R362)","1,1-Dichloroethene is absorbed via oral, inhalation, and dermal routes. It is rapidly distributed in the body, mainly to the liver and kidneys. Hepatic microsomal cytochrome P-450 enzymes metabolize 1,1-dichloroethene into its toxic metabolites, which include epoxides, acyl chlorides, and halogenated aldehydes. The main metabolites are believed to be 2,2-dichloroacetaldehyde and 2-chloroacetyl chloride. These are later detoxified by hydroxylation and conjugation with glutathione. Excretion of 1,1-dichloroethene metabolites occurs primarily in the urine and exhaled air. (R362)","LD50: 200 mg/kg (Oral, Rat) (R263)
LC50: 6350 ppm/4 hr (Inhalation, Rat) (R263)",,"3, not classifiable as to its carcinogenicity to humans. (R264)","1,1-Dichloroethene is used in the production of certain plastics as a comonomer in the polymerization of vinyl chloride, acrylonitrile, and acrylates. It is also used to make flame retardant coatings for fiber and carpet backings, and in piping, coating for steel pipes, and in adhesive applications. (R362, R263)","Intermediate Inhalation: 0.02 ppm (R260)
Chronic Oral: 0.009 mg/kg/day (R260)","1,1-Dichloroethene mainly affects the central nervous system. It may lead to sedation, inebriation, convulsions, spasms, and unconsciousness. 1,1-Dichloroethene may also damage the livers, kidneys, and lungs. (R362, R363)","1,1-Dichloroethene mainly affects the central nervous system and may lead to sedation, inebriation, convulsions, spasms, and unconsciousness. It also irritates the respiratory tract, eyes, and skin upon contact. (R362)","Treatment of 1,1-dichloroethene poisoning is mainly symptomatic. It may include respiratory assistance, gastric lavage, and/or the oral administration of activated charcoal. (R364)",P98194;O75185;P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P78334;Q8N1C3;P18507;Q99928;O00591;P24046;P28476;A8MPY1;Q9UN88;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;P54710;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P03372;Q92731
81,T3D0080,2009-03-06 18:58:02 UTC,2009-08-04 21:27:37 UTC,Methylene chloride,Organic Compound;Solvent;Organochloride,"AerotheneAerothene MMBichloride, methyleneCH2Cl2Chloride, methyleneChlorure de methyleneChlorure de methylene (french)DCMDichloride, methyleneDichloromethaneDistillex DS3DriveritFreon 30M-clean dMethane dichlorideMethane, dichloro-MethokloneMethylene bichlorideMethylene dichlorideMetylenu chlorekMetylenu chlorek (polish)NarkotilNevolinRcra waste number U080SalesthinSolaesthinSolmethinedichloromethane (ACD/Name 4.0)",Methylene chloride is a manufactured chemical used as an industrial solvent and as a paint stripper. It may also be found in some aerosol and pesticide products and is used in the manufacture of photographic film. (R366),,75-09-2,6344,,C02271,"",15767,CPD-4521,,D008752,Methylene chloride,885,,,http://en.wikipedia.org/wiki/Methylene chloride,InChI=1/CH2Cl2/c2-1-3/h1H2,dichloromethane,http://www.biospider.ca/saved_files/mol/33eb87e4915f3ae2d30a5795ab630eff_1237942200.mol,C(Cl)Cl,C(Cl)Cl,CH2Cl2,83.953360,Colorless liquid.,-95.1 °C,,,"13 mg/mL at 25 °C [HORVATH,AL (1982)]",,,,"Oral
Inhalation
Dermal
(R366)","Cytochrome P450 2E1 (P05181)
Glutathione S-transferase theta-1 (P30711)
(R366)","Methylene chloride targets the lungs, blood system, and nervous system. In the lungs its metabolites damage Clara cells. It is also metabolized into carbon monoxide, which binds to hemoglobin to produce dose-dependent increases in carboxyhemoglobin. This results in the reduced oxygen transport and neurological dysfunction characteristic of carboxyhemoglobinemia (carbon monoxide poisoning). Methylene chloride is also believed to cause neurotoxicity by interfering with signal transmission in a manner similar to general anesthetics. Certain metabolites, such as formaldehyde, may result in carcinogenic effects by causing DNA single strand breaks, DNA-protein crosslinks, and other mutations. (R029, R366)","Absorption mainly occurs via inhalation, but may also result from oral or dermal exposure. Methylene chloride is mainly distributed to the adipose tissue and liver. It may be metabolized by cytochrome P-450 2E1, which ultimately produces carbon monoxide and carbon dioxide via formyl chloride. Methylene chloride can also be metabolized by theta glutathione-S-transferase, which produces carbon dioxide via a postulated glutathione conjugate (S-chloromethyl
glutathione) and formaldehyde. Both pathways produce toxic metabolites which are excreted mainly in expired air, but also in the urine. (R029, R366)","LD50: 437 mg/kg (Intraperitoneal, Mouse) (R263)
LD50: 6460 mg/kg  (Subcutaneous, Mouse) (R263)
LD50: 1600 mg/kg (Oral, Rat) (R353)
LC50: 14400 ppm over 7 hours (Inhalation, Mouse) (R263)","357 mg/kg (oral) or 50,000 ppm (inhalation) for an adult human. (R371)","2B, possibly carcinogenic to humans. (R264)","Methylene chloride is widely used as a solvent in industrial processes, paint stripper, and degreaser. It is also used in food preparation, aerosol propellants, pesticides, and the manufacture of photographic film. (R029, R366)","Acute Inhalation: 0.6 ppm (R260)
Intermediate Inhalation: 0.3 ppm (R260)
Chronic Inhalation: 0.3 ppm (R260)
Acute Oral: 0.2 mg/kg/day (R260)
Chronic Oral: 0.06 mg/kg/day (R260)","Exposure to methylene chloride may cause optic neuropathy and hepatitis. Very high concentrations can lead to unconciousness, coma, and death. It is metabolized to carbon monoxide, potentially leading to carbon monoxide poisoning. Methylene chloride also causes liver and kidney injury, and may be a carcinogen. (R029, R367)","Breathing large amounts of methylene chloride causes dizziness, nausea, tingling or numbness of the finger and toes, loss of concentration, and reduced hand-eye coordination. Very high concentrations can lead to unconciousness, coma, and death. Skin contact with methylene chloride causes burning and redness of the skin. (R366, R367)","Treatment of methylene chloride exposure is mainly symptomatic. Ingested methylene chloride may be removed by emesis and/or gastric lavage, and activated charcoal. Hyperbaric oxygen may be used to treat the carbon monoxide poisoning that can result from inhalation of methylene chloride. (R368)",P69905;P68871;P02042;P02100;P69891;P69892;Q6B0K9;P09105;P02008;P03372;Q92731
82,T3D0081,2009-03-06 18:58:02 UTC,2009-08-25 19:58:11 UTC,Aroclor 1240,Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"","Aroclor 1240 is a commercial mixture of PCBs with an average chlorine content of 40%. Polychlorinated biphenyls (PCBs) are a group of 209 synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. PCBs were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate in the environment and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,71328-89-7,"",,"","","","",,,Aroclor 1240,,,,,"","",http://www.biospider.ca/saved_files/mol/,"",Clc1cccc(c1)-c1cc(Cl)cc(Cl)c1,"","",Oily liquids or solids that are colorless to light yellow. ,"","","","","","","",Oral Inhalation Dermal (R012),Cytochrome P450 1A1 (P04798) Cytochrome P450 1A2 (P05177) Cytochrome P450 2B6 (P20813) Serum albumin (P02768) (R012),"The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are transported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose tissue, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) 
LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)","","2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refrigerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 µg/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P35869;P49888;P03372;P11684;P20711;Q92731;P07101
83,T3D0082,2009-03-06 18:58:02 UTC,2009-08-04 21:27:38 UTC,"2,4,6-Trinitrotoluene",Organic Compound;Explosive;Reagent;Aromatic Hydrocarbon;Nitrite,"&alpha;-TNT-TNT.alpha.-TNT1-Methyl-2,4,6-trinitrobenzene1-methyl-2,4,6-trinitrotoluene2,4, 6-Trinitrotoluene2,4,6-Trinitrotolueen2,4,6-Trinitrotolueen [Dutch]2,4,6-Trinitrotolueen(DUTCH)2,4,6-Trinitrotoluene2,4,6-Trinitrotoluol2,4,6-Trinitrotoluol [German]2,4,6-Trinitrotoluol(GERMAN)2,4,6-trinitritoluene2-Methyl-1,3,5-trinitrobenzeneAlpha-TNTAlpha-trinitrotoluolBenzene, 2-methyl-1,3,5-trinitro-EntsufonGradetolS-trinitrotolueneS-trinitrotoluolSYM-trinitrotolueneSYM-trinitrotoluolSYN-trinitrotolueneTNLTNTTNT-toliteTNT-tolite [french]TNT-tolite(french)TolitToliteToluene, 2,4,6-trinitro-Toluene, 2,4,6-trinitro- (wet)TrilitTrinitrotoluenTrinitrotoluene, DRYTrinitrotoluene, DRY(dot)Trinitrotoluene, wetTrinitrotoluene, wet (dot)TrinitrotoluolTritolTritol (explosive)TritonTrojnitrotoluenTrojnitrotoluen [polish]Trojnitrotoluen(polish)TrotylTrotyl oilWLN: WNR B1 CNW ENW","Trinitrotoluene (TNT), or more specifically, 2,4,6-trinitrotoluene, is a chemical compound with the formula C6H2(NO2)3CH3. This yellow-coloured solid is a reagent (reactant) in chemistry but is best known as a useful explosive material with convenient handling properties. The explosive yield of TNT is considered the standard measure of strength of bombs and other explosives. In chemistry, TNT is used to generate charge transfer salts. (R249)",,118-96-7,8376,,C16391,"",46053,CPD-9138,,D014303,"2,4,6-Trinitrotoluene",6562,,,http://en.wikipedia.org/wiki/Trinitrotoluene,"InChI=1/C7H5N3O6/c1-4-6(9(13)14)2-5(8(11)12)3-7(4)10(15)16/h2-3H,1H3","2-methyl-1,3,5-trinitrobenzene",http://www.biospider.ca/saved_files/mol/ad39bfc3832f48efbc3ae84b7891aabc_1237942442.mol,CC1=C(C=C(C=C1[N+](=O)[O-])[N+](=O)[O-])[N+](=O)[O-],CC1=C(C=C(C=C1[N+](=O)[O-])[N+](=O)[O-])[N+](=O)[O-],C7H5N3O6,227.017830,"Pale yellow, odorless solid. Loose ""needles"" before melt-casting. A solid block after being poured into a casing. (R249)",80.1 °C,240 °C (R250),1.65 g/cm³ (R250),"0.115 mg/mL at 23 °C [PHELAN,JM & BARNETT,JL (2001)]",,,Pa at 20 °C: negligible (R250),"Oral
Inhalation
Dermal 
(R250)",,"2,4,6-Trinitrotoluene is a competitive inhibitor with respect to NADPH and a noncompetitive inhibitor with respect to L-arginine. It binds to the P450 reductase domain of the eNOS and suppresses l-citrulline formation by shunting electrons away from the normal catalytic pathway. The reduction of TNT then produces reactive oxygen species (ROS), such as superoxide (O2.−), and hydrogen peroxide (H2O2). The overproduction of superoxide is associated with oxidative stress-mediated induction of cataracts. The inhibition of the eNOS activity occurs in a concentration-dependent manner. (R296, R297)","2,4,6-Trinitrotoluene rapidly and completely enters the body through inhalation or ingestion, but more slowly through the skin. Once 2,4,6-trinitrotoluene is in the blood, it travels throughout the body to all of the organs. When it reaches the liver, it breaks down and changes into several different substances, such as 4-aminodinitrotoluene, 2-aminodinitrotoluene and 2,4-diamino-6-nitrotoluene. Most of these substances travel in the blood until they reach the kidneys. Almost all of the 2,4,6-trinitrotoluene that enters the body breaks down and leaves the body in the urine within 24 hours. (R251)",,,"3, not classifiable as to its carcinogenicity to humans. (R264)","2,4,6-Trinitrotoluene is an explosive used in military shells, bombs, and grenades, in industrial uses, and in underwater blasting. Exposure may results from drinking contaminated water that has migrated from chemical waste disposal sites, breathing contaminated air, eating contaminated foods such as fruits and vegetables, and/or eating contaminated soil. (R251)",Intermediate Oral: 0.0005 mg/kg/day (R260),"Exposition to high concentrations of 2,4,6-trinitrotoluene in air can lead to several harmful health effects, including anemia and abnormal liver function. Similar blood and liver effects, as well as spleen enlargement and other harmful effects on the immune system, have been observed in animals that ate or breathed 2,4,6-trinitrotoluene. Other effects in humans include skin irritation after prolonged skin contact, and cataract development after long-term (365 days or longer) exposure. It is not known whether 2,4,6-trinitrotoluene can cause birth defects in humans. However, male animals treated with high doses of 2,4,6-trinitrotoluene have developed serious reproductive system effects. Moreover, the EPA has determined that 2,4,6-trinitrotoluene is a possible human carcinogen. (R251)","Exposure to  2,4,6-trinitrotoluene causes headache, blue lips or finger nails, blue skin, cough, sore throat, laboured breathing, vomiting, abdominal cramps, unconsciousness. Dermal exposure may cause pain and redness at the exposed surface and yellowish staining of the skin. (R250)","In some cases, gastric lavage, activated charcoal, and emetics have been suggested as useful in reducing absorption of the general class of nitro compounds to which 2,4,6-trinitrotoluene belongs. (R251)",P29474
85,T3D0084,2009-03-06 18:58:03 UTC,2009-08-04 21:27:38 UTC,Hydrazine,Organic Compound;Industrial Precursor/Intermediate;Hydrazine,"AmerzineCatalyzed hydrazineDiamideDiamineDiazaneH2NNH2HDZHydrazinHydrazine (anhydrous)Hydrazine (hydrazine sulfate)Hydrazine baseHydrazine solutionHydrazine sulfateHydrazine, anhydrousHydrazine/hydrazine sulfateHydrazinesHydrazynaHydrazyna [polish]LevoxineNitrogen hydrideOxytreat 35RCRA waste no. U133Rcra waste number U133Scav-ox IIUltra pureZerox","Hydrazine is a colourless liquid chemical compound with an ammonia-like odor and is derived from the same industrial chemistry processes that manufacture ammonia. However, hydrazine has physical properties that are more similar to those of water. Hydrazine is highly toxic and dangerously unstable, and is usually handled as aqueous solution for safety reasons. Hydrazine is mainly used as a foaming agent in preparing polymer foams, but significant applications also include its uses as a precursor to polymerization catalysts and pharmaceuticals. Additionally, hydrazine is used in various rocket fuels and to prepare the gas precursors used in air bags. Approximately 260,000 tons are manufactured annually. (R298)",,302-01-2,9321,,C05361,"",15571,4-HYDROXYMETHYLPHENYLHYDRAZINE,,C029424,Hydrazine,713,,,http://en.wikipedia.org/wiki/Hydrazine,InChI=1/H4N2/c1-2/h1-2H2,hydrazine,http://www.biospider.ca/saved_files/mol/76938da3e33a70803205ea15d9d62a84_1237942592.mol,NN,NN,H4N2,32.037450,Colorless liquid.,2 °C,,,"1000 mg/mL [AMOORE,JE & HAUTALA,E (1983)]",,,,"Oral
Inhalation
Dermal
(R299)",,"At least two mechanisms of action have been observed. One involves the direct binding of those hydrazines with a free amino group (hydrazine and 1,1-dimethylhydrazine) to key cellular molecules. Hydrazine reacts with alpha-keto acids such as vitamin B6 to form hydrazoines compounds. By binding to keto acids and forming hydrazones, hydrazine inhibits oxygen consumption with mitochondrial substrates in vitro. A second mechanism involves the generation of reactive species such as free radical intermediates or methyldiazonium ions as a result of metabolism. (R300)","Hydrazines are likely to be more rapidly absorbed into the blood after ingestion or exposure to the skin than after inhalation. Once in the blood, they are probably carried to all the tissues of the body. Soon after exposure, the levels of hydrazines in the tissues fall since they are metabolised in several products such as acetyl-, diacetylhydrazine, pyruvate hydrazone, urea, and acyclic compound (1,4,5,6-tetrahydro-6-oxo-3-pyridazine carboxylic acid). However, these metabolites interacts with some important proteins and might be harmful to the body. Some studies showed that metabolites and unchanged hydrazine leave the body within one day. 
Small amounts can also be found in the expired air. (R300, R301)",,"LD50: 60 mg/kg (Oral, Rat)
LD50: 91 mg/kg (Dermal, Rabbit)
LC50: 570ppm/4h (Inhalation, Rat) 
(R302)","2B, possibly carcinogenic to humans. (R264)","Hydrazine is mainly used as a foaming agent in preparing polymer foams, but significant applications also include its uses as a precursor to polymerization catalysts and pharmaceuticals. Additionally, hydrazine is used in various rocket fuels and to prepare the gas precursors used in air bags. Exposure may occur from breathing contaminated air in or near a facility that makes, processes, or uses hydrazines, eating fish contaminated with hydrazines, drinking or swimming in water that has been contaminated with hydrazines, or touching soil contaminated with hydrazines, such as near some military bases or hazardous waste sites. Breathing cigarette smoke indirectly or using tobacco products may expose to small amounts of hydrazine or 1,1-dimethylhydrazine. (R300) ",Intermediate Inhalation: 0.004 ppm (R260),"Breathing hydrazines for short periods may cause coughing and irritation of the throat and lungs, convulsions, tremors, or seizures. Breathing hydrazines for long periods may cause liver and kidney damage, as well as serious effects on reproductive organs. Eating or drinking small amounts of hydrazines may cause nausea, vomiting, uncontrolled shaking, inflammation of the nerves, drowsiness, or coma. (R300)","Hydrazine may cause corrosive burning sensations, confusion, convulsions, abdominal cramps, headache, unconsciousness, vomiting, weakness, shortness of breath, or sore throat and cough, depending on the route of exposure. (R299)","Induced emesis, gastric lavage, use of saline cathartics, or activated charcoal are commonly used to decrease the gastrointestinal absorption of hydrazines. In general, these treatments are most effective when used within a few hours after oral exposure. Following dermal or ocular exposures to hydrazines, all contaminated clothing should be removed, and contacted skin should be washed immediately with soap and water. Eyes that have come in contact with hydrazines should be flushed with copious amounts of water. Contact lenses should be removed prior to flushing with water. (R300)",""
86,T3D0085,2009-03-06 18:58:03 UTC,2009-08-04 21:27:38 UTC,"1,2-Dichloroethane",Organic Compound;Solvent;Industrial Precursor/Intermediate;Organochloride,"&alpha;,&beta;-dichloroethane.alpha.,.beta.-dichloroethane1,2-Bichloroethane1,2-Dichloorethaan1,2-Dichloorethaan [Dutch]1,2-Dichlor-aethan1,2-Dichlor-aethan [German]1,2-Dichloraethan1,2-Dichlorethane1,2-Dichloroethane1,2-Dicloroetano1,2-Dicloroetano [Italian]1,2-Ethylene dichloride1,2-Ethylidene dichloride1,2-dichloroethane (ethylene dichloride)12-DICHLOROETHANE2-DichloroethaneAethylenchloridAethylenchlorid [german]AethylendichloridAlpha, beta-dichloroethaneAlpha,beta-dichloroethaneBichlorure d'ethyleneBichlorure d'ethylene [french]Borer solBrocideCH2ClCH2ClCaswell No. 440Chlorure d'ethyleneChlorure d'ethylene [french]Cloruro di etheneCloruro di ethene [italian]DCEDestruxol borer- solDestruxol borer-solDi-chlor-mulsionDichlor-mulsionDichloremulsionDichloro-1,2-ethaneDichloro-1,2-ethane [French]DichloroethaneDichloroethane, 1,2-DichloroethyleneDichlorure d'ethylene [iso-french]Dutch liquidDutch oilEDCEdc (halocarbon)Ethane dichlorideEthane, 1,2-dichloro-EthyleendichlorideEthyleendichloride [dutch]Ethylene chlorideEthylene dichloride [UN1184] [Flammable liquid]Ethylene dichloride [bsi:iso]Freon 150Glycol dichlorideHSDB 65InChI=1/C2H4Cl2/c3-1-2-4/h1-2HRCRA waste no. U077RY Dichloro-1,2-ethaneRcra waste number U077S-dichloroethaneSYM-dichloroethaneethylene dichloride, 14C-labeledethylene dichloride, 14C2-labeledethylene dichloride, 36Cl-labeledethylene dichloride, 38Cl-labeledethylene dichloride, ion (1+)","1,2-Dichloroethane is a clear, manufactured liquid that is not found naturally in the environment. It evaporates quickly at room temperature and has a pleasant smell and a sweet taste. 1,2-Dichloroethane burns with a smoky flame. It is most common used to make vinyl chloride, which is used to make a variety of plastic and vinyl products. (R303)",,107-06-2,11,,C06752,"",27789,CPD-681,,C024565,"1,2-Dichloroethane",443,,,,InChI=1/C2H4Cl2/c3-1-2-4/h1-2H2,"1,2-dichloroethane",http://www.biospider.ca/saved_files/mol/18ac57d467f05168df8122a693672393_1237942753.mol,C(CCl)Cl,C(CCl)Cl,C2H4Cl2,97.969010,Colorless liquid.,-35.5 °C,,,"8.6 mg/mL at 25 °C [HORVATH,AL et al. (1999)]",,,,"Oral
Inhalation
Dermal
(R304)",Cytochrome P450 2E1 (P05181) Glutathione S-transferase P (P09211) Glutathione S-transferase Mu 1 (P09488) Glutathione S-transferase A1 (P08263) Glutathione S-transferase theta-2 (P30712) Glutathione S-transferase Mu 4 (Q03013) Glutathione S-transferase theta-1 (P30711) Glutathione S-transferase A4 (O15217) Glutathione S-transferase A2 (P09210) Glutathione S-transferase A3 (Q16772) Glutathione S-transferase Mu 3 (P21266) Glutathione S-transferase omega-1 (P78417) Glutathione S-transferase kappa 1 (Q9Y2Q3) Glutathione S-transferase Mu 2 (P28161) Glutathione S-transferase omega-2 (Q9H4Y5) Glutathione S-transferase A5 (Q7RTV2) Glutathione S-transferase Mu 5 (P46439) Glutathione S-transferase theta-4 (A8MPT4) Maleylacetoacetate isomerase (O43708) Microsomal glutathione S-transferase 1 (P10620) Microsomal glutathione S-transferase 2 (Q99735) Microsomal glutathione S-transferase 3 (O14880) (R303),"1,2-Dichloroethane is metabolized to 2-chloroacetaldehyde, S-(2-chloroethyl)glutathione by conjugation with glutathione, and to other putative reactive intermediates capable of binding covalently to cellular macromolecules in the liver, kidney, and other tissues. The conjugation of 1,2-dichloroethane with glutathione is catalyzed primarily by glutathione S-transferases. 1,2-Dichloroethane appears to be activated to mutagenic species to a lesser extent by the hepatic microsomal cytochrome P-450 enzyme system. Reactive metabolites of 1,2-dichloroethane produced by hepatic microsomal cytochrome P-450 can bind to cellular proteins and DNA. It has been suggested that 1,2-dichloroethane-induced toxicity occurs when the biotransformation processes are saturated, thereby allowing higher levels of 1,2-dichloroethane to circulate throughout the body and conjugate with glutathione instead of being detoxified and eliminated. (R303, R305)","Due to its physical properties such as its lipophilicity, 1,2-dichloroethane is likely to be absorbed across the alveolar membranes of the lung, mucosal membranes of the gastrointestinal tract, and the skin by passive diffusion. Once in the body, it is widely distributed, with the greatest amounts accumulating in the more lipophilic tissues. The primary route of biotransformation involves conjugation with glutathione to yield nonvolatile urinary metabolites. The other route, a cytocrome P-450-mediated oxidation is responsible for the formation of chloroacetaldehyde. Metabolic saturation appears to occur sooner after oral (gavage) administration than after inhalation exposure. Following inhalation or oral exposure, elimination of 1,2-dichloroethane occurs primarily via excretion of soluble metabolites in the urine and excretion of unchanged parent compound and carbon dioxide in the expired air. (R303)",,"LD50: 680 mg/kg (Oral, Rat) (R303)
LD50: 489-413 mg/kg (Oral, Mouse) (R303)","2B, possibly carcinogenic to humans. (R264)","The most common use of 1,2-dichloroethane is in the production of vinyl chloride which is used to make a variety of plastic and vinyl products including polyvinyl chloride (PVC) pipes, furniture and automobile upholstery, wall coverings, housewares, and automobile parts. It is also used as a solvent and is added to leaded gasoline to remove lead. Exposure occurs mainly by breathing air or drinking water contaminated with 1,2-dichloroethane. Humans can be exposed to low levels of 1,2-dichloroethane through the skin or air by contact with old products made with 1,2-dichloroethane. (R303)","Chronic Inhalation: 0.6 ppm (R260)
Intermediate Oral: 0.2 mg/kg/day (R260)","Breathing or swallowing large amounts of 1,2-dichloroethane can produce nervous system disorders, kidney diseases, or lung effects. This can also lead to heart failure. Skin lesions and benign pulmonary tumors were reported in animals exposed dermally to liquid 1,2-dichloroethane. 1,2-dichloroethane can cause death from cardiac arrhythmia, bronchitis, hemorrhagic gastritis and colitis, hepatocellular damage, renal tubular necrosis and calcification, central nervous system depression, and histological changes in brain tissue after a sufficient single oral dose. (R303)","1,2-Dichloroethane exposure causes abdominal pain, coughing, dizziness, drowsiness, headache, nausea, sore throat, diarrhea, unconsciousness, and vomiting, depending on the contact surface and the intensity. Redness of the eyes or skin occurs upon contact. (R304)","Blood gases should be monitored, a good ventilation maintained, and cardiac arrhythmias observed for a minimum of 24 hours. In the event of a ventricular arrhythmia, lidocaine or beta-blockers could be administered. Serum creatinine, hepatic aminotransferase, electrolytes, and fluid balance for signs of hepatic or renal failure should be monitored. Dialysis may be helpful in the event of renal failure. Hepatic failure may be treated with fresh frozen plasma, vitamin K, low protein diet, neomycin, and lactulose. (R303)",P07237;P98194;O75185;P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P78334;Q8N1C3;P18507;Q99928;O00591;P24046;P28476;A8MPY1;Q9UN88;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;P54710;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P03372;Q92731
87,T3D0086,2009-03-06 18:58:03 UTC,2009-08-04 21:27:38 UTC,"2,4,6-Trichlorophenol",Organic Compound;Pesticide;Aromatic Hydrocarbon;Organochloride,"1,3,5-Trichloro-2-hydroxybenzene1,3,5-Trichlorophenol2, 4,6-Trichlorfenol (CZECH)2,4,6-:trichlorophenol2,4,6-Trichlorfenol2,4,6-Trichlorfenol [Czech]2,4,6-Trichloro-2-hydroxybenzene2,4,6-Trichlorophenol2,4,6-Trichlorophenol (2,4,6-TCP)2,4,6-trichlorophenol (ACD/Name 4.0)2,4,6-trichlorophenol, 14C-labeled2,4,6-trichlorophenol, Zn salt2,4,6-trichlorophenol, copper(+1) salt2,4,6-trichlorophenol, copper(+2) salt2,4,6-trichlorophenol, nickel(+2) salt2,4,6-trichlorophenol, potassium salt2,4,6-trichlorophenol, sodium saltDowcide 2SDowicide 2SOMALPS10_SUPELCOPhenachlorPhenaclorPhenol, 2,4, 6-trichloro-RCRA waste no. U231Rcra waste number U231TCPTrichloro-2-hydroxybenzeneTrichloro-2-hydroxybenzene, 2,4,6-TrichlorophenolTrichlorophenol, 2,4,6-WLN: QR bg DG FG","2,4,6-Trichlorophenol (or 2,4,6-TCP) is a chlorinated phenol that has been used as a fungicide, herbicide, insecticide, antiseptic, defoliant, and glue preservative. It is a yellow solid with a strong, sweet odour. It decomposes on heating to produce toxic and corrosive fumes including hydrogen chloride and chlorine. The technical grade of this substance may contain polychlorinated dibenzodioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), and other contaminants. It is an environmental pollutant that has been found in fresh water lakes such as the Great Lakes. (R306)",,88-06-2,6914,,C07098,"",28755,CPD-10489,,C024564,"2,4,6-Trichlorophenol",1417,,,,"InChI=1/C6H3Cl3O/c7-3-1-4(8)6(10)5(9)2-3/h1-2,10H","2,4,6-trichlorophenol",http://www.biospider.ca/saved_files/mol/f8c1ae21a1863975af8ee10e8fb7b6a7_1237942872.mol,C1=C(C=C(C(=C1Cl)O)Cl)Cl,C1=C(C=C(C(=C1Cl)O)Cl)Cl,C6H3Cl3O,195.924950,"Yellow solid with a strong, sweet odour.",69 °C,246 °C,1.675,"0.8 mg/mL at 25 °C [NEELY,WB (1984)]",,,,"Oral
Inhalation
Dermal
(R307)",,"It has been suggested that 2,4,6-TCP would interfer with mitochondrial oxidative phosphorylation and inhibit cytochrome P-450-dependent mixes-function oxidases. 2,4,6-TCP has been identified to inhibit acetylcholinesterase in humans. It also disturbs liver microsomal detoxication functions by a selective inhibition of the terminal oxygenation enzyme P-450. (R307, R309, R318)","Human studies indicate that sulfation and glucuronidation are the main metabolic pathways of 2,4,6-TCP, which is excreted in the urine as conjugated metabolites. In general, 2,4,6-TCP undergoes biotic isomerization to other trichlorophenol isomers and conjugation with glucuronic acid. Glucuronic acid accounts for approximately 80% of the conjugates detected in urine. Metabolites generated following incubation of 2,4,6-TCP are 2,6-dichloro-1,4-hydroquinone and two isomers of hydroxypentachlorodiphenyl ether. The 2,6-dichloro-1,4-semiquinone free radical was also identified. (R307)",,,"2B, possibly carcinogenic to humans. (R264)","2,4,6-Trichlorophenol has been used as a fungicide, herbicide, insecticide, antiseptic, defoliant, and glue preservative. Skin contact while treating wood with the tetrachlorophenols is the most likely route of exposure. Exposure may also occur from drinking water that has been disinfected with chlorine and breathing air contaminated by 2,4,6-trichlorophenol. (R307)","Acute Oral: 0.01 mg/kg/day (Rat) (R307) 
Intermediate oral: 0.003 mg/kg/day (Rat) (R307)","Exposure through the skin can lead to acne and mild injury of the liver. Major effects after ingestion of 2,4,6-trichlorophenol affect the liver and the immune system. Toxic manifestations include central nervous system depression followed by increased respiration, hyperthermia, a blood pressure rise, progressive euromuscular weakness, and cyanosis. (R307)","Inhalation of 2,4,6-trichlorophenol may cause coughing and sore throat. Eye or skin contact causes redness and pain at the site of contact. Convulsions, diarrhoea, dizziness, deadache, shortness of breath, vomiting, weakness, and ataxia may occur after ingestion. (R308)","",P22303;P98194;O75185;P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P78334;Q8N1C3;P18507;Q99928;O00591;P24046;P28476;A8MPY1;Q9UN88;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;P54710;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P03372;Q92731
88,T3D0087,2009-03-06 18:58:03 UTC,2009-08-04 21:27:38 UTC,"2,4-Dinitrophenol",Organic Compound;Industrial Precursor/Intermediate;Aromatic Hydrocarbon;Nitrite,"&alpha;-dinitrophenol.alpha.-dinitrophenol1'alpha-2,4-Dinitrophenol1-Hydroxy-2,4-dinitrobenzene2, 4-Dinitrofenol(DUTCH)2,4 Dinitrophenol2,4-Dinitrofenol2,4-Dinitrofenol [Dutch]2,4-Dinitrophenol-UL-14C2,4-bis(hydroxy(oxido)amino)phenol (ACD/Name 4.0)AldifenAlpha-dinitrophenolCamello mosquito coilsCaswell No. 392Chemox peCobra salts (impregna salts)DNFDNPDinitraDinitrofenoloDinitrofenolo [italian]Dinitrofenolo(italian)DinitrophenolDinitrophenolsDinofanFenoxylFenoxyl carbon nMaroxol-50NINNitro kleenupNitrophenNitrophen (van)NitropheneNitrophene (van)Osmoplastic-rOsmotox-plusPhenol, &alpha;-dinitro-Phenol, .alpha.-dinitro-Phenol, 2,4-dinitro-Phenol, alpha-dinitro-RCRA waste no. P048Rcra waste number P048Shirakiku brand mosquito coilsSolfo Black 2B SupraSolfo black BBSolfo black SBSolfo black bSolfo black gTertrosulfur PBRTertrosulfur black PBTertrosulphur PBRTertrosulphur black PBWLN: WNR bq enwnchembio.125-comp2nchembio.147-comp19","2,4-Dinitrophenol, also called DNP is a yellow solid with no known smell. It dissolves slightly in water. DNP present in water and soil as a pollutant does not easily evaporate to air. It uncouples oxidative phosphorylation by carrying protons across the mitochondrial membrane, leading to a rapid consumption of energy without generation of ATP. 2,4-DNP was used in the 1930s as a weightreduction drug, but this was discontinued in 1938 because of the many reports of adverse effects in people who used it. (R326, R328)",,51-28-5,1493,,C02496,"",918,CPD-8179,,D019297,"2,4-Dinitrophenol",532,,,"http://en.wikipedia.org/wiki/2,4-Dinitrophenol","InChI=1/C6H4N2O5/c9-6-2-1-4(7(10)11)3-5(6)8(12)13/h1-3,9H","2,4-dinitrophenol",http://www.biospider.ca/saved_files/mol/2efe377bd787f6b75cd0291f0542b73b_1237942947.mol,C1=CC(=C(C=C1[N+](=O)[O-])[N+](=O)[O-])O,C1=CC(=C(C=C1[N+](=O)[O-])[N+](=O)[O-])O,C6H4N2O5,184.012020,"Yellow, crystalline solid.",115.5 °C,,,"2.79 mg/mL at 20 °C [SCHWARZENBACH,RP et al.(1988)]",,,,"Oral
Inhalation
Dermal
(R329)",,"Acute 2,4-dinitrophenol poisoning (from ingestion) involves uncoupling of oxidative phosphorylation, which presumably reduces body's reservoirs of high-energy phosphate. This stimulates oxidative metabolism and, in turn, the heat production of the body. Oxygen consumption, body temperature, respiration and heart rate are all increased. 2,4-Dinitrophenol has been suggested to bind serum proteins such as transthyretin. In fact it was proposed as a therapeutic agent for the prevention/inhibition of amyloid diseases through stabilization of the native fold of transthyretin. (R286, R348, R349)","2,4-DNP can readily enter the body through inhalation and ingestion. It can probably be absorbed through the skin also. Animal studies show that after 2,4-DNP enters the body, the blood can carry it to organs and tissues such as the liver, the kidneys, and the eyes. DNP does not build up in organs and tissues, but it is metabolized via reduction of the nitro groups or broken down to other chemicals. The parent compound and metabolites such as 2-amino-4-nitrophenol, 4-amino-2-nitrophenol and diaminophenol are excreted in the urine. 2,4-DNP is also excreted by mammals, partially unchanged, partially conjugated with glucuronic acid and probably as 2,4-diamenolphenol. (R326, R330)",,"LD50: 14-43 mg/kg (Oral, Human) (R337)",,"2,4-Dinitrophenol has been used to make dyes, other organic chemicals, and wood preservatives. It has also been used to make photographic developer, explosives, and pesticides. 2,4-Dinitrophenol exposure may occur from breathing contaminated air, drinking contaminated water, eating contaminated food, or by contact with contaminated soil. (R326, R328)",Acute Oral: 0.01 mg/kg/day (R326),"2,4-DNP can cause cataracts following ingestion of a small dose for short or long periods. This condition could lead to blindness in both eyes. Breathing in, swallowing, or having skin contact with large amounts of DNP can lead to death.(R326)","Dermal contact may results in redness, roughness, yellow staining of the skin. Nausea, vomiting, palpitations, collapse, sweating occur after inhalation or ingestion. (R329)","There is no specific antidote for 2,4-DNP poisoning. Symptomatic treatment includes replacing oxygen and fluids, controlling  temperature by administering sponge baths and ice packs, and using a fan to promote air flow and evaporation. In fully conscious patients, administer cold, sugar-containing liquids by mouth as tolerated. In cases of skin contact, bathe and shampoo contaminated skin and hair promptly. (R352)",P02766
89,T3D0088,2009-03-06 18:58:03 UTC,2009-08-04 21:27:39 UTC,Bis(2-chloroethyl) ether,Organic Compound;Industrial Precursor/Intermediate;Organochloride,"&beta;, &beta;'-dichloroethyl ether&beta;,&beta;'-dichlorodiethyl ether&beta;,&beta;'-dichloroethyl ether&beta;,&beta;-dichlorodiethyl ether.beta.,.beta.'-dichlorodiethyl ether.beta.,.beta.'-dichloroethyl ether1, {1'-Oxybis[2-chloroethane]}1,1'-Oxybis(2-chloro)ethane1,1'-Oxybis(2-chloroethane)1,1'-Oxybis[2-chloroethane]1,1-oxybis[2-chloroethane]1,5-Dichloro-3-oxapentane1-Chloro-2-(&beta;-chloroethoxy)ethane1-Chloro-2-(.beta.-chloroethoxy)ethane1-Chloro-2-(2-chloroethoxy)ethane1-Chloro-2-(beta-chloroethoxy)ethane1-chloro-2-(2-chloroethoxy)ethane (ACD/Name 4.0)2, 2'-Dichlor-diaethylaether(GERMAN)2, 2'-Dichlorodiethyl ether2, 2'-Dicloroetiletere(ITALIAN)2,2'-Dichloorethylether2,2'-Dichloorethylether [Dutch]2,2'-Dichloorethylether(DUTCH)2,2'-Dichlor-diaethylaether2,2'-Dichlor-diaethylaether [German]2,2'-Dichlorethyl ether2,2'-Dichlorodiethyl ether2,2'-Dichlorodiethyl ether [UN1916] [Poison]2,2'-Dichlorodiethyl oxide2,2'-Dichloroethyl ether2,2'-Dicloroetiletere2,2'-Dicloroetiletere [Italian]2,2'-dichlorodiethylether2-Chloroethyl etherBCEEBeta ,beta'-dichlorodiethyl etherBeta,beta'-dichlorodiethyl etherBeta,beta-dichlorodiethyl etherBeta-chloroethyl etherBis(&beta;-chloroethyl) etherBis(.beta.-chloroethyl) etherBis(2-chloroethyl) etherBis(2-chloroethyl)etherBis(beta-chloroethyl) etherBis(chloro-2-ethyl) oxideBis(chloroethyl) etherBis(chloroethyl)etherBis(chloroethyl)ether (bcee)Bis-2-chloroethyletherCaswell No. 309ChlorexChloroethyl etherClorexDCEEDi(&beta;-chloroethyl) etherDi(.beta.-chloroethyl) etherDi(2-chloroethyl) etherDi(beta-chloroethyl)etherDi(chloroethyl) oxideDichlorodiethyl etherDichloroetherDichloroethyl etherDichloroethyl oxideDicholoroethyl etherDiethylene glycol dichlorideDwuchlorodwuetylowy eterDwuchlorodwuetylowy eter [polish]Dwuchlorodwuetylowy eter(polish)Ethane, 1,1'-oxybis(2-chloro-Ethane, 1,1'-oxybis*2-chloro-Ethane, 1,1'-oxybis[2-chloro-Ethane, {1,1'-oxybis[2-chloro-}Ether dichloreEther dichlore [french]Ether dichlore(french)Ether, bis(2-chloroethyl)Ether, bis(chloroethyl)KhloreksOxybis(2-chloroethane)Oxyde de chlorethyleOxyde de chlorethyle [french]Oxyde de chlorethyle(french)RCRA waste no. U025Rcra waste number U025S-dichloroethyl etherSYM-dichloroethyl etherWLN: G2O2Gbis(2-chloroethyl) ether (ACD/Name 4.0)","Bis(2-chloroethyl) ether (BCEE) is a colorless non-flammable liquid with a strong, unpleasant odor. It does not occur naturally, but is manufactured by humans for use in the production of pesticides and other chemicals. Limited amounts of BCEE dissolve in water and also slowly evaporate into air. In the environment, BCEE is broken down by bacteria in soil and water and by chemical reactions in the air, so it does not tend to persist for long periods. (R357)",,111-44-4,8115,,C14688,"","",GAL-GLCNAC-GAL-GLC,,C006767,Bis(2-chloroethyl) ether,169,,,,InChI=1/C4H8Cl2O/c5-1-3-7-4-2-6/h1-4H2,1-chloro-2-(2-chloroethoxy)ethane,http://www.biospider.ca/saved_files/mol/acfd2f849e5acf567051183470d5dbdd_1237943123.mol,C(CCl)OCCCl,C(CCl)OCCCl,C4H8Cl2O,141.995220,Colorless liquid.,-51.9 °C,,,"17.2 mg/mL at 20 °C [VEITH,GD et al. (1980)]",,,,"Oral
Inhalation
Dermal (R358)",,"BCEE is extremely meabolized, with thiodiglycolic acid (TDGA) being the principal endproduct. The pathway leading to TDGA formation is uncertain, but probably involves oxidative cleavage of the ether bond to yield chloroacetaldehyde and 2-chloroethanol. (R357)","BCEE is absorbed following inhalation exposure, oral administration, as well as contact to the skin. BCEE is distributed through the body, but highest levels are found in the liver, kidney and small intestine, while much lower levels are found in lung, spleen and muscle. BCEE is extensively metabolized to thiodiglycolic acid (TDGA), 2-chloroethoxyacetic acid (CEAA), and N-acetyl-S-[2-(2-chloroethoxy)ethyl]-L-cysteine, with TDGA being the principal endproduct. Smaller amounts of BCEE are metabolized by oxidation or substitution at a chlorine without ether cleavage. Approximately 80% of BCEE administered orally is excreted as TDGA within 48 hours. Smaller amounts are excreted in feces or expired air and only a very small fraction of the dose remains in the body. This indicates that BCEE is effectively excreted, and that it has a low tendency to accumulate in tissues. (R357, R361)",,,,"Bis(2-chloroethyl) ether is used in pesticides. It is also used as a solvent, cleaner, component of paint and varnish, rust inhibitor, or as a chemical intermediate to make other chemicals. Exposure occurs from consumption of drinking water that contains BCEE, breathing BCEE vapors, and dermal contact. (R357)",Intermediate Inhalation: 0.02 ppm (R260),"The principal acute effect of inhalation exposure to BCEE vapor is irritation and injury to the cells of the respiratory epithelium. BCEE vapors can cause loss of weight, nose irritation, severe injury to the lungs, and may lead to death. It might also cause cancer. (R357)","Symptoms of BCEE exposure include coughing, sore throat, nausea, vomiting, burning sensation, redness of the exposed surface, laboured breathing, and abdominal pain, depending on the route of exposure. Symptoms may be delayed. (R358)","",P98194;O75185;P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P78334;Q8N1C3;P18507;Q99928;O00591;P24046;P28476;A8MPY1;Q9UN88;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;P54710;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P03372;Q92731
90,T3D0089,2009-03-06 18:58:03 UTC,2009-08-27 18:21:51 UTC,Thiocyanate,Organic Compound;Cyanide Compound,Ammonium rhodanateAmmonium rhodanideAmmonium sulfocyanateEDOHS-c#nHSCNHydrogen thiocyanateN#c-SHNitridosulfanidocarbonRhodanidRhodanideSCNSilver thiocyanate agscnThallium thiocyanateThiocyanate ionThiocyanic acidThiocyanidWeedazol TL[CN(sh)][c(n)(SH)],"Thiocyanates are a group of compounds formed from a combination of sulfur, carbon, and nitrogen. Thiocyanates are found in various foods and plants and are produced primarily from the reaction of free cyanide with sulfur. This reaction occurs in the environment (for example, in industrial waste streams that contain cyanide) and in the human body after cyanide ingestion. Thiocyanates are present in water primarily because of discharges from coal processing, extraction of gold and silver, and mining industries. Thiocyanate is the major product formed from cyanide that passes into the body as the body attempts to rid itself of cyanide. (R370)",,01762-95-4,781,,C01755,"",18022,HSCN,,,Thiocyanate,,,,http://en.wikipedia.org/wiki/Thiocyanate,InChI=1/CHNS/c2-1-3/h3H,thiocyanic acid,http://www.biospider.ca/saved_files/mol/6652c299ef4de004c17a2181ad4aae03_1237943210.mol,[S-]C#N,[S-]C#N,CNS,57.975140,,"",,,"",,,,"Oral
Inhalation
Dermal
(R370)","Thiosulfate sulfurtransferase (Q16762) 
Sodium/iodide cotransporter (Q92911) 
Cystic fibrosis transmembrane conductance regulator (P13569) 
(R370, R390,R410,R412)","Thiocyanate (sulphocyanate or SCN) is believed to be a goitrogenic compound. It is a competitive inhibitor of the human thyroid sodium/iodide symporter NIS. Thus, the adverse effects of thiocyanate overload are especially noticeable when iodine availability is low. Intake of goitrogenic substances causes an adaptive increase in T3’s binding to brain nuclear receptors and in the activity of type II 5'-deiodinase, which generates T3 from T4. This altered function and availability of T3 is detrimental to the developing brain. Thiocyanate is also known to modulate activity of mammalian peroxidases. For instance, eosinophil peroxidase has been implicated in promoting oxidative tissue damage in a variety of inflammatory conditions, including asthma. Thiocyanate also acts as inhibitor to carbonic anhydrase, which catalyzes the rapid conversion of carbon dioxide to bicarbonate and protons. (R389, R410, R417)","Thiocyanates can appear in the body after metabolization of cyanides by rhodanese. When thiocyanates enter the body, they normally breaks down in aqueous solution to yield sulfate ions. However, thiocyanates are also found in the thyroid fluids. Immediately following exposure to thiocyanate containing solutions, the cystic fibrosis conductance regulator Cl– channel exhibits high unitary SCN– conductance and anomalous mole fraction behaviour. Thiocyanates is normally excreted in urine. (R390, R409, R410, R412)",,"Guanidine Thiocyanate: LD50: 375 mg/kg (Oral, Rat), LD50: 2000 mg/kg (Dermal, Rabbit) (R423)
Potassium Thiocyanate: LD50: 854 mg/kg (Oral, Rat) (R424) 
Amonium Thiocyanate: LD50: 750 mg/kg (Oral, Rat), LD50: 500 mg/kg (Oral, Mouse) (R425)",,"Exposure occurs from breathing air and drinking water, touching soil or water containing thiocyanate, or eating foods that contain thiocyanate. Thiocyanates are present in water primarily because of discharges from coal processing, extraction of gold and silver, and mining industries. Thiocyanate is the major product formed from cyanide that passes into the body as the body attempts to rid itself of cyanide, thus exposure to cyanide also results in exposure to thiocyanate. (R370)",,"Thiocyanates are known to affect the thyroid glands, reducing the ability of the gland to produce hormones that are necessary for the normal function of the body. Exposure to high levels of cyanide for a short time harms the brain and heart and can even cause coma and death. (R370)","Symptoms of thiocyanate exposure include rapid, deep breathing and shortness of breath, followed by convulsions (seizures) and loss of consciousness. (R370)","In cases of thiocyanate exposure, get fresh air and medical attention. If not breathing, give artificial respiration. If breathing is difficult, give oxygen. If swallowed, do not induce vomiting but give large quantities of water. Immediately flush skin with plenty of water for at least 15 minutes in case of exposure to skin or the eyes. (R422)",P22079;P05164;P11678;Q92911;P00918;P22748;P07451;P00915
91,T3D0090,2009-03-06 18:58:03 UTC,2009-08-26 15:10:22 UTC,Asbestos,Inorganic Compound;Mineral,"AetznatronAmianthusAsbest [german]AsbestosAsbestos (friable)Asbestos dustAsbestos fiberAsbestos fibersAsbestos fibreAsbestos, all formsAsbestose [german]AscariteCalidria HPPCalidria R-G 244Carey 4TCaswell No. 061Caswell No. 773Caustic sodaCaustic soda solutionCaustic soda, liquidChlorobestos 25Collo-grillreinCollo-tapettaFerodo C3CFibrous gruneriteFuers rohrHpo (mineral)Hydroxide, sodiumHydroxyde de sodium [french]Lewis-red devil lyeLiquid-plumrMTMMan-made mineral fibresMountain corkMountain leatherMountain woodNatrium causticumNatrium-hydroxid, reinstesNatriumhydroxid [german]Natriumhydroxyde [dutch]P 5-50 (mineral)PlungRohrputzRohrreiniger rofixSM 1 (mineral)SM 2 (mineral)Sepiolex 3Sepiolex 5Soda lyeSoda, causticSoda, hydrateSoda, kaustischeSodio(idrossido di) [italian]Sodium hydrateSodium hydrate solutionSodium hydroxideSodium hydroxide (Na2(OH)2)Sodium hydroxide (na(oh))Sodium hydroxide [usan]Sodium hydroxide dimerSodium hydroxide solutionSodium hydroxide, solid [UN1823] [Corrosive]Sodium hydroxide, solution [UN1824] [Corrosive]Sodium(hydroxyde de) [french]UN 1823 (solid)UN 1824 (solution)White causticWhite caustic solution","Asbestos is the name given to a group of six different fibrous minerals (amosite, chrysotile, crocidolite, and the fibrous varieties of tremolite, actinolite, and anthophyllite) that occur naturally in the environment. One of these, namely chrysotile, belongs to the serpentine family of minerals, while all of the others belong to the amphibole family. All forms of asbestos are hazardous, and all can cause cancer, but amphibole forms of asbestos are considered to be somewhat more hazardous to health than chrysotile. Asbestos minerals consist of thin, separable fibers that have a parallel arrangement. Nonfibrous forms of tremolite, actinolite, and anthophyllite also are found naturally. Abestos is toxic and inhalation of asbestos fibers can cause serious illnesses, including malignant mesothelioma, lung cancer, and asbestosis. (R426, R427)",,1332-21-4,14798,,C16442,"",46661,"",,D001194,Asbestos,6369,,,http://en.wikipedia.org/wiki/Asbestos,InChI=1/Na.H2O/h;1H2/q+1;/p-1,sodium hydroxide,http://www.biospider.ca/saved_files/mol/,[OH-].[Na+],O.[Mg++].[Mg++].[Mg++].O[Si]([O-])([O-])[O-].O[Si]([O-])([O-])[O-],HNaO,39.992510,"Long, thin, fibrous crystals.","",,,"",,,,"Inhalation 
Injection 
(R427)",,"When asbestos fibers are inhaled, many are deposited on the epithelial surface of the respiratory tree. Fibers that are retained in the lung or mesothelium for long periods of time are capable of producing chronic inflammation and fibrotic and tumorigenic effects. These effects may be mediated by direct interactions between the fiber and key cellular macromolecules, or they may be mediated by the production of reactive oxygen species and other cellular factors originating from alveolar macrophages. In addition, the physical-chemical nature of the fiber appears to be an important determinant of toxicity. It is generally agreed that exposure to amphibole fibers can produce mesothelioma, and that the potency of amphibole fibers to produce mesothelioma is greater than that of chrysotile. Asbestos fibers can adsorb to a variety of cellular macromolecules (e.g., proteins,membrane lipids, RNA, DNA). The coulombic forces between the asbestos fiber and some of these macromolecules may induce conformational changes, and these changes could affect protein function and chromosomal fidelity. Chrysotile fibers were found to bind to cytochrome P-450, thereby decreasing mono-oxygenase activity. Chrysotile and crocidolite fibers were also found to bind to artificial lipid membranes in vitro, thereby increasing membrane rigidity. Fibers found to be translocated near the nucleus can interact with the cytoskeleton and interfere with chromosome segregation. (R427)","Asbestos fibers are not metabolized in the normal sense of the word, and amphibole fibers that are retained in the lung do not appear to undergo any major changes. However, chrysotile fibers appear to undergo some type of breakdown or alteration in the lung. Some of the fibers will be deposited in the air passages and on the lung cells. Most fibers are removed from the lungs by being carried away or coughed up in a layer of mucus to the throat, where they are swallowed into the stomach. Fibers that are deposited in the deepest parts of the lung are removed more slowly. In fact, some fibers may move through the lungs and can remain in place for many years and may never be removed from the body. Longer fibers that are retained in the lung may undergo a number of processes including translocation, dissolution, fragmentation, splitting, or protein encapsulation. Long fibers that reside in the lung can become encapsulated in protein, forming what is often referred to as an ""asbestos body"". In response to asbestos fibers, alveolar macrophages produce reactive oxygen species in an attempt to digest the fiber. The reactive oxygen species include hydrogen peroxide and superoxide radical anion (O2-). Fibers that have been swallowed (those present in water, or those moved to the throat from the lungs) almost all pass along the intestines within a few days and are excreted in the feces. (R427)",,,"1, carcinogenic to humans. (R434)","Asbestos are used in building materials (roofing shingles, ceiling and floor tiles, paper products, and asbestos cement products), friction products (automobile clutch, brake, and transmission parts), heat-resistant fabrics, packaging, gaskets, and coatings. Some vermiculite or talc products may contain asbestos. Exposure most likely by breathing air containing asbestos fibers or by drinking asbestos fibers that are present in water. (R427)","","Infected people develop a slow buildup of scar-like tissue in the lungs and in the membrane that surrounds the lungs, so breathing becomes difficult. Blood flow to the lung may also be decreased, and this causes the heart to enlarge. This disease is called asbestosis. Infected people have increased chances of getting two principal types of cancer: cancer of the lung tissue itself and mesothelioma, a cancer of the thin membrane that surrounds the lung and other internal organs. The cellular immune system of the patient can be depressed. Also, deletions of chromosome segments have been noted in human mesothelioma cells or cell lines. (R427)","Symptoms of asbestos exposure include shortness of breath, often accompanied by a cough. (R427)","In vitro studies have shown that the effects of asbestos can be diminished by compounds that reduce the levels of reactive oxygen species, such as free radical scavengers (ascorbic acid, bemitil, mannitol, salicylate, 5,5'-dimetyl-l-proline N-oxide, rutin, vitamin E, vitamin A) and enzymes that catalyze the decomposition of reactive oxygen species (catalase, superoxide dismutase). Patients should quit smoking, perform bronchial drainage and can use chest physical therapy techniques to further aid in removing secretions. Shortness of breath is treated with bronchodilators, inhaled or oral medications that open up the bronchial tubes and allow the passage of air. In more severe asbestosis cases, supplemental oxygen may be required. Productive cough is treated with humidifiers and chest percussion. Asbestosis can be treated, but not cured. (R427, R438)",DNA
92,T3D0091,2009-03-06 18:58:03 UTC,2009-08-27 18:23:46 UTC,Chlorine,Inorganic Compound;Vapour;Solvent;Industrial Precursor/Intermediate;Disinfectant;Halogen,BertholiteBertholite /warfare gas/CLCaswell No. 179ChloorChloor [dutch]ChlorChlor [german]ChloreChlore [french]ChlorideChloride ionChlorinated waterChlorinated water (chlorine)Chlorine [UN1017] [Poison gas]Chlorine gasChlorine molChlorine mol.CholinumCloroCloro [italian]Diatomic chlorineDichlorineHygeol 1% LiquidMolecular chlorine,"Chlorine is a chemical element with atomic number 17 and symbol Cl. It is abundant in nature as the chloride ion, which is part of common salt and other compounds necessary to most forms of life. Chlorine is a greenish-yellow gas with a pungent, irritating odor. It is stored and transported as a liquid under pressure. When chlorine is released into the environment, it reacts with both organic and inorganic substances that it comes into contact with. When chlorine gas is released into water, such as during water chlorination, it quickly dissolves in the water and then disproportionates within seconds to form chloride and hypochlorous acid. Chlorine may be released into the environment from facilities where it is produced or used, or during accidents, such as a chlorine tank rupture or a liquid chlorine spill. (R461, R462)",,7782-50-5,24526,,C00115,"103600
106195
109270
109280
111000
111300
118425
118930
121011
123885
125950
126650
131399
137163
137165
137192
138491
139392
141850
141900
145260
145500
160800
160900
166600
167050
171050
171060
173393
179800
181750
182307
186854
188070
192320
214700
218000
219700
223900
229100
230000
236200
241200
244400
248250
250900
255700
259700
261600
263800
264350
270420
277180
300008
300009
300138
300398
300554
302910
305990
308990
310468
560000
600041
600170
600228
600229
600232
600233
600359
600421
600436
600570
600580
600637
600760
600761
600791
600839
600840
600968
600997
601199
601271
601330
601678
601690
601844
601881
602023
602024
602056
602158
602359
602421
602522
602668
602722
602726
602727
602872
602958
602974
603080
603339
603353
603475
603506
603743
603831
603855
603906
604003
604045
604119
604159
604309
604337
604433
604471
604708
604878
604879
604943
604996
605125
605208
605232
605377
605646
605784
606038
606205
606410
606412
606465
606516
606520
606533
606536
606672
606680
606718
606726
606757
606845
606904
606983
607096
607239
607293
607335
607364
607582
607589
607591
607628
607631
607682
607854
608041
608390
608479
608480
608481
608855
608893
608919
609448
609914
610130
610291
610791
611316
611490
611492",29310,CPD-4521,,D002713,Chlorine,275,,,http://en.wikipedia.org/wiki/Chlorine,InChI=1/ClH/h1H/p-1,chlorine,http://www.biospider.ca/saved_files/mol/98bdcbb3a16d3bbb29db1387aa162b84_1237943607.mol,[Cl-],[Cl-],[Cl]-,34.968849,Green/yellow gas.,-101 °C,,,"6.3 mg/mL at 25 °C [AMOORE,JE & HAUTALA,E (1983)]",,,,"Inhalation
Dermal 
(R463)",,"Chlorine is a strong oxidizer that hydrolyzes in water forming hydrochloric and hypochlorous acids. In this form, it apparently can penetrate the cell and form N-chloro-derivatives that can damage cellular integrity. Chlorine reacts with water in the epithelial lining of the upper respiratory airways. The mechanism of toxicity of aqueous chlorine or a hypochlorous acid/sodium hypochlorite is basically the same as that for chlorine gas. However, hypochlorous acid is a stronger oxidant than chlorine gas as reflected by its higher redox potential. Damage to the upper gastrointestinal tract, as may occur following ingestion of sodium hypochlorite bleach, is likely the result of oxidation reactions of hypochlorous acid with a range of biological molecules. (R464)","Hypochlorous acid reacts with proteins, amino acids, and unsaturated lipids to form chlorinated compounds, whereas the reaction with carbohydrates yields oxidation products. Metabolisation of chlorine results in the production of N-chloramines, tentatively identified as N-chloroalanine, N-chloroglycine, and N-chlorophenylalanine. (R461)",,,"4, probably not carcinogenic to humans. (R461)","Exposure usually results from inhalating contaminated air, ingesting chlorine bleach or directly contacting the skin with aqueous chlorine. (R461)","Acute Inhalation: 0.07 ppm (Chlorine gas) (R461) 
Intermediate Inhalation: 0.02 ppm (Chlorine gas) (R461) 
Chronic Inhalation: 0.00005 ppm (Chlorine gas) (R461)","The principal targets of exposure to chlorine gas are the respiratory airways and the eyes. Exposure to chlorine gas can lead to mild irritation of the nose, eye irritation and headache and throat irritation. Pulmonary edema and hypoxia can follow and further increase capillary permeability. Further complications can lead to pneumonia and even death. The principal targets of exposure to aqueous chlorine are the upper gastrointestinal tract and the skin. Ingestion of chlorine can lead to esophageal and gastric mucosal erosions, perforations at the gastroesophageal junction, and extensive necrosis of adjacent soft tissue. (R461)","If inhaled, chlorine can trigger cough, substernal pain, respiratory distress, shortness of breath, and wheezing. Symptoms may be delayed. Nausea and vomiting are reflex in origin, and headache and loss of consciousness are probably due to the hypoxia caused by pulmonary edema. Dermal contact can lead to redness, pain, and redness of the exposed surface. Eye contact can lead to watering of the eyes. (R461, R463)","In case of inhalation, move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with inhaled beta2 agonist and oral or parenteral corticosteroids. examine mucous membranes, eyes and skin to be certain that corrosive effects have not occurred. In case of acute lung injury, maintain ventilation and oxygenation and evaluate with frequent arterial blood gas or pulse oximetry monitoring. In can of eye exposure, irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes. In case of dermal exposure, remove contaminated clothing and wash exposed area thoroughly with soap and water. (R464)",""
93,T3D0092,2009-03-06 18:58:04 UTC,2009-08-04 21:27:39 UTC,Cyclotrimethylenetrinitramine,Organic Compound;Explosive;Amine;Nitrite,"1,3, 5-Triazine, hexahydro-1,3,5-trinitro-1,3, 5-Trinitrohexahydro-1,3,5-triazine1,3,5-Triaza-1,3,5-trinitrocyclohexane1,3,5-Triazacyclohexane 1,3,5-trinitro-1,3,5-Trinitro-1,3, 5-triazacyclohexane1,3,5-Trinitro-1,3,5-triazacyclohexane1,3,5-Trinitro-1,3,5-triazinane1,3,5-Trinitrohexahydro-1,3,5-triazine1,3,5-Trinitrohexahydro-s-triazine1,3,5-Trinitroperhydro-1,3, 5-triazine1,3,5-Trinitroperhydro-1,3,5-triazine1,3,5-trinitrohexahydro-p-triazineCyclonitCycloniteCyclonite (cyclotrimethylene trinitramine)CyclotrimethylenenitramineCyclotrimethylenetrinitramineCyclotrimethylenetrinitramine (RDX)CyklonitCyklonit [czech]Esaidro-1,3,5-trinitro-1,3,5-triazinaEsaidro-1,3,5-trinitro-1,3,5-triazina [Italian]Esaidro-1,3,5-trinitro-1,3,5-triazina(ITALIAN)GeksogenHeksogenHeksogen [polish]Heksogen(polish)Hexahydro-1,3, 5-trinitro-1,3,5-triazineHexahydro-1,3,5-trinitro-1,3,5-triazinHexahydro-1,3,5-trinitro-1,3,5-triazin [German]Hexahydro-1,3,5-trinitro-1,3,5-triazin(GERMAN)Hexahydro-1,3,5-trinitro-1,3,5-triazineHexahydro-1,3,5-trinitro-s-triazineHexogeenHexogeen [dutch]Hexogeen(dutch)HexogenHexogen (explosive)Hexogen 5WHexoliteHexolite, dry or wetted with < 15% water, by massNuvan 100 ECPBX (af) 108PBX(AF) 108PBXW 108(E)Perhydro-1,3,5-trinitro-1,3,5-triazineRDXSYM-trimethylene trinitramineSYM-trimethylenetrinitramineT4 (VAN)TrimethyleentrinitramineTrimethyleentrinitramine [dutch]Trimethyleentrinitramine(dutch)TrimethylenetrinitramineTrinitrocyclotrimethylene triamineTrinitrohexahydrotriazineTrinitrotrimethylenetriamineWLN: T6N CN ENTJ ANW CNW ENWhexahydro-1,3 ,5-trinitro-1,3 5-triazines-Triazine, hexahydro-1,3,5-trinitro-","Cyclotrimethylenetrinitramine is a chemical compound also called RDX, which stands for Royal Demolition Explosive. It is also known as cyclonite or hexogen. The chemical name for RDX is 1,3,5-trinitro-1,3,5-triazine and it is a very explosive white powder that creates fumes when it is burned with other substances. As such, it is used as an explosive and it is also used in combination with other ingredients in explosives. RDX is a synthetic product that does not occur naturally in the environment. (R478)",,121-82-4,8490,,"","",24556,CPD-9356,,C009160,Cyclotrimethylenetrinitramine,3621,,,,InChI=1/C3H6N6O6/c10-7(11)4-1-5(8(12)13)3-6(2-4)9(14)15/h1-3H2,"1,3,5-trinitro-1,3,5-triazinane",http://www.biospider.ca/saved_files/mol/,C1N(CN(CN1[N+](=O)[O-])[N+](=O)[O-])[N+](=O)[O-],C1N(CN(CN1[N+](=O)[O-])[N+](=O)[O-])[N+](=O)[O-],C3H6N6O6,222.034880,White powder.,205.5 °C,,,"0.0597 mg/mL at 25 °C [YALKOWSKY,SH & HE,Y (2003)]",,,,"Oral
Inhalation
Dermal 
(R478)",,"RDX can get into the lungs after breathing in the fumes of burning RDX or breathing in the dust from powdered RDX. It can also enter the body after ingestion of contaminated water. It may also pass through the skin into the bloodstream or enter through cuts or breaks in the skin. It also blocks electron transport. (R029, R478)","There are no studies available regarding RDX metabolites in humans following inhalation, oral, or dermal exposure. Some studies reported that 4-nitro-2,4-diazabutanal, and nitrite ions are produced through biotransformation of RDX by cytochrome P450. The limited toxicological data show that RDX is absorbed through the gastrointestinal system, lungs, and skin, and is distributed to the cerebrospinal fluid, plasma, urine, and feces. RDX will leaves the body in the breath and urine within a few days. (R478,R489)",,,,"RDX is used as an explosive and is also used in combination with other ingredients in explosives. Exposure may occur by breathing dust containing RDX, contact with the skin, or drinking contaminated water. (R478)","Acute Oral: 0.06 mg/kg/day (Rat) (R478)
Intermediate Oral: 0.03 mg/kg/day (Rat) (R478)","RDX can cause seizures. Inhalation exposure to RDX can lead to gastrointestinal, hematological, hepatic, and renal effects. (R478)","Symptoms of RDX exposure include epileptiform seizures, insomnia, restlessness, headache, dizziness, nausea, vomiting and irritability. Temporary postconvulsive amnesia, malaise, fatigue, and asthenia can follow the seizures. (R491)","Following oral exposure, symptomatic patients should be given adequate respiratory support during seizures. Monitor liver and renal function tests and urinalysis in patients with significant exposure. Following inhalation exposure, move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with inhaled beta2 agonist and oral or parenteral corticosteroids. Following eye exposure, irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist, the patient should be seen in a health care facility. Following dermal exposure, remove contaminated clothing and wash exposed area thoroughly with soap and water. A physician may need to examine the area if irritation or pain persists. (R492)",""
94,T3D0093,2009-03-06 18:58:04 UTC,2009-08-04 21:27:39 UTC,Hexachlorobenzene,Organic Compound;Pesticide;Aromatic Hydrocarbon;Organochloride,"1,2,3,4,5,6-Hexachlorobenzene1,2,3,4,5,6-hexachlorobenzene (ACD/Name 4.0)AmatinAnticarieBunt-cureBunt-no-moreCaswell No. 477Ceku c.bCeku c.b.Co-op hexaEsaclorobenzeneEsaclorobenzene [italian]GranoxGranox NMHCBHexa CBHexa c.bHexa c.b.HexachlorbenzolHexachlorbenzol [german]Hexachlorbenzol(german)HexachlorobenzeneHexachlorobenzene [UN2729] [Poison]Hexachlorobenzene [bsi:iso]HexcachlorbenzenJulen's carbon chlorideJulian's carbon chlorideJulin's carbon chlorideJulin's chlorideNo Bunt 40No Bunt 80No buntNo bunt liquidPS690_SUPELCOPentachlorophenyl chloridePerchlorobenzenePhenyl perchlorylRCRA waste no. U127Rcra waste number U127S anocideSaatbeizfungizidSaatbeizfungizid [german]SanocidSanocideSmut-goSnieciotoxVoronit cWLN: GR bg CG dg eg FG","Hexachlorobenzene is a chlorinated hydrocarbon previously used as a pesticide to protect the seeds of onions and sorghum, wheat, and other grains against fungus. It has since been banned due to its nature as a persistent organic pollutant. It was also used to make fireworks, ammunition, and synthetic rubber. (R435)",,118-74-1,8370,,C11042,"",5692,CPD-1125,,D006581,Hexachlorobenzene,691,,,,InChI=1/C6Cl6/c7-1-2(8)4(10)6(12)5(11)3(1)9,"1,2,3,4,5,6-hexachlorobenzene",http://www.biospider.ca/saved_files/mol/2da1f18043eb9df855e4ce61f8dc163b_1237943941.mol,C1(=C(C(=C(C(=C1Cl)Cl)Cl)Cl)Cl)Cl,C1(=C(C(=C(C(=C1Cl)Cl)Cl)Cl)Cl)Cl,C6Cl6,281.813120,"",231.8 °C,"","","6.2e-06 mg/mL at 25 °C [FARMER,WJ et al. (1976)]","","","","Oral
Inhalation
Dermal 
(R435)",Cytochrome P450 3A4 (P08684) (R435),"Hexachlorobenzene causes porphyria by modifying sulfhydryl groups in the catalytic or substrate-binding sites of uroporphyrinogen decarboxylase. This inhibits uroporphyrinogen decarboxylase, resulting in a deficiency of the decarboxylation of uroporphyrinogen III and accumulation of uroporphyrins in the liver. In addition, metabolism of hexachlorobenzene by the cytochrome P-450 enzymes is believed to produce reactive electrophilic metabolites that covalently bind to cellular proteins and DNA, causing irreversible damage. Exposure to hexochlorobenzene also causes macrophages to be attracted to organs such as the spleen, lungs, and skin, where they become activated by the hexochlorobenzene. This leads to a cascade of reactions involving innate immune cells. The gene expression profiles provide evidence for the importance of macrophages and granulocytes and mediators released by these cells in the adverse inflammatory response against hexochlorobenzene. In this way, co-stimulatory or danger signals are generated that could polyclonally activate T cells. Hexachlorobenzene is a weak agonist for aryl hydrocarbon receptor and may exhibit some of its toxic effects by activating the gene-regulatory properties of this protein, possibly inducing cytochome P-450 enzymes. It may also act at certain endocrine receptors. (R044, R435, R437, R439, R440)","Hexachlorobenzene is mainly absorbed via ingestion, but also through inhalation and oral routes. It preferentially distributes to adipose tissue and other organs with high fat content. In animals, hexachlorobenzene is slowly metabolized to pentachlorophenol by the hepatic cytochrome P-450 system, conjugated with glutathione to yield pentachlorothiophenol, or reductively dechlorinated to form pentachlorobenzene. Other metabolites include less chlorinated benzenes, chlorophenols, S-conjugated phenols, and benzenes. Hexachlorobenzene is slowly metabolized in mammals, and the majority of hexachlorobenzene is excreted unchanged in the feces, while metabolites are excreted in the urine. (R435)","LD50: 3500 mg/kg (Oral, Rat) (R029)","","2B, possibly carcinogenic to humans. (R264)","Hexachlorobenzene was previously used as a pesticide to protect the seeds of onions and sorghum, wheat, and other grains against fungus. It was also used to make fireworks, ammunition, and synthetic rubber. As it can persist in the environment for long periods of time, today exposure occurs mainly from contact with contaminated water, food, soil, or air. (R435)","Acute Oral: 0.008 mg/kg/day (R260)
Intermediate Oral: 0.0001 mg/kg/day (R260)
Chronic Oral: 0.00005 mg/kg/day (R260)","Chronic exposure to hexachlorobenzene can damage the liver, thyroid, nervous system, bones, kidneys, blood, and immune and endocrine systems. It also causes a syndrome, called black sore, that is characterized by dermal blistering and epidermolysis, pigmentation and scarring, alopecia, photosensitivity, hepatomegaly, porphyria, suppurative arthritis, osteomyelitis, and osteoporosis of the bones of the hands. It may also cause a liver disease called porphyria cutanea tarda. This disease can cause red-colored urine, skin sores, change in skin color, arthritis, and problems of the liver, nervous system, and stomach. Hexachlorobenzene also affects development and results in lower survival rates of children of exposed mothers. It is also believed to be a human carcinogen. (R029, R435)","Hexachlorobenzene causes a syndrome, called black sore, that is characterized by dermal blistering and epidermolysis, pigmentation and scarring, alopecia, photosensitivity, hepatomegaly, porphyria, suppurative arthritis, osteomyelitis, and osteoporosis of the bones of the hands. It may also cause a liver disease called porphyria cutanea tarda. This disease can cause red-colored urine, skin sores, change in skin color, arthritis, and problems of the liver, nervous system, and stomach. (R435)","Treatment is mainly symptomatic and may include gastric lavage, administering activated charcoal, and controlling convulsions. (R436)",P06132;P35869;P62508;P10275;DNA;P98194;O75185;P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P78334;Q8N1C3;P18507;Q99928;O00591;P24046;P28476;A8MPY1;Q9UN88;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;P54710;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P03372;Q92731
95,T3D0094,2009-03-06 18:58:04 UTC,2009-08-06 21:37:31 UTC,"2,4-Dinitrotoluene",Organic Compound;Explosive;Industrial Precursor/Intermediate;Plasticizer;Aromatic Hydrocarbon;Nitrite,"1-Methyl-2,4-dinitrobenzene2, 4-Dinitrotoluene2,4-Dinitro-1-methylbenzene2,4-Dinitromethylbenzene2,4-Dinitrotoluene2,4-Dinitrotoluene (containing 0.5% 2,6-dinitrotoluene)2,4-Dinitrotoluene (containing 1.0-1.5% 2,6-dinitrotoluene)2,4-Dinitrotoluene, practical grade2,4-Dinitrotoluol4-Methyl-1,3-dinitrobenzeneBenzene, 1-methyl-2,4-dinitro-, sulfurizedBenzene, methyldinitro-CHEBI:920D.n.tDNTDinitrotolueneDinitrotoluene, 2,4-Dinitrotoluene, technical grade (2,4 (77%)- and 2,6 (19%)-)DinitrotoluolRCRA waste no. U105Rcra waste number U105Toluene, 2, 4-dinitro-Toluene, 2,4-dinitro-WLN: WNR B1 ENWnchembio882-comp9","2,4-Dinitrotoluene is the most common of the six dinitrotoluene isomers. Dinitrotoluene (DNT) or Dinitro is an explosive with the formula C6H3(CH3)(NO2)2. At room temperature it is a pale yellow to orange crystalline solid. It is a high explosive and one of the precursors for trinitrotoluene (TNT), which is synthesized through three separate nitrations of toluene. The first product is mononitrotoluene, DNT is the second, and TNT is the third and final product. (R501)",,121-14-2,8461,,C11006,"",920,CPD-1125,,C016403,"2,4-Dinitrotoluene",539,,,,"InChI=1/C7H6N2O4/c1-5-2-3-6(8(10)11)4-7(5)9(12)13/h2-4H,1H3","1-methyl-2,4-dinitrobenzene",http://www.biospider.ca/saved_files/mol/4692c683511255e306345df8da6d580e_1237944051.mol,CC1=C(C=C(C=C1)[N+](=O)[O-])[N+](=O)[O-],CC1=C(C=C(C=C1)[N+](=O)[O-])[N+](=O)[O-],C7H6N2O4,182.032760,Yellow to orange crystals.,71 °C,,,"0.2 mg/mL at 25 °C [PHELAN,JM & BARNETT,JL (2001)]",,,,"Exposure to skin, eyes, inhalation, or ingestion (R502).","O-acetyltransferase (Q8WZ77)
Xanthine dehydrogenase/oxidase (P47989)
(R511, R353)","2,4-DNT may cause conversion of oxyhemoglobin to methemoglobin via oxidation of iron(II) to iron(III) by its metabolites. High levels of methemoglobin are removed by catabolism, leading to the development of anemia. Some metabolites of 2,4-DNT are also transported back from the bile to the liver, where the amine group is N-hydroxylated by cytochrome P-450 to form an unstable sulfate conjugate. The sulfate conjugate is degraded into carbonium or nitrenium ions. These ions covalently bind to hepatic macromolecules (DNA, RNA), leading to mutations and subsequently liver tumors. They also bind to DNA of the lung and the intestine. (R511, R517, R518, R526)","2,4-Dinitrotoluene can be inhalated as fumes or dust, ingested, or absorbed after contact with the skin. Bioactivation of 2,4-DNT is thought to occur by the following processes: The methyl group is oxidized to an alcohol by a cytochrome P-450 dependent pathway; the benzyl alcohol is conjugated with glucuronic acid and excreted in the bile. Intestinal microflora hydrolyzes the glucuronide and reduces one nitro group, forming an aminonitrobenzyl alcohol which can be readsorbed from the intestine. The amino group is oxidized to an hydroxylamine by hepatic enzymes and conjugated with sulfate, by sulfotransferase. Decomposition of the sulfate ester yields a highly electrophilic nitrenium (or carbonium) ion which can react with DNA and other biological nucleophiles. The major metabolite found in human urine is 2,4-dinitrobenzyl alcohol or its glucuronide conjugate. Other urinary metabolites include 2,4-dinitrobenzoic acid, 4-(N-acetyl)amino-2nitrobenzoic acid, and 2-amino-4-nitrobenzoic acid. The latter two are clearly the product of both oxidative and reductive metabolism. Metabolism is also believed to involve O-acetyltransferase (which transfers the acetyl group of 2,4-DNT) and cytosolic xanthine oxidase (which reduces 2,4-DNT). Small traces of unmetabolized 2,4-DNT can be observed in the urine too. (R511, R512, R515, R516, R534, R535)",,"LD50:268 mg/kg (Oral, Rat) (R522)
LD50: 790 mg/kg (Oral, Mouse) (R522)
LD50: 1300 mg/kg (Oral, Guinea pig) (R522)","2B, possibly carcinogenic to humans. (R264)","It is a high explosive and one of the precursors for trinitrotoluene (TNT), which is synthesized through three separate nitrations of toluene. 2,4-Dinitrotoluene can affect the body if it is inhaled, comes in contact with the eyes or skin, is swallowed, or is absorbed through the skin. Even a small amount absorbed from clothes or shoes may cause toxic symptoms. It is assumed that oral ingestion could be a secondary route for occupationally exposed humans. (R501, R502)","Acute Oral: 0.05 mg/kg/day (R260)
Chronic Oral: 0.002 mg/kg/day (R260)","2,4-Dinitrotoluene poisoning may cause methemoglobinemia, anemia, leukopenia, and liver necrosis. Liver injury may be more common than cyanosis. (R521)","Symptoms of 2,4-dinitrotoluene poisoning include blue lips or finger nails, blue skin, vertigo, fatigue, dizziness, weakness, nausea, vomiting, dyspnea, arthralgia, insomnia, tremor, paralysis, unconsciousness, chest pain, shortness of breath, palpitation, anorexia, and loss of weight. (R504, R505)","Following oral exposure, immediately dilute with 4 to 8 ounces (120 to 240 mL) of water or milk (not to exceed 4 ounces/120 mL in a child). Administer charcoal as a slurry. Gastric lavage and oxygen administration is recommended. Following inhalation exposure, move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with inhaled beta2 agonist and oral or parenteral corticosteroids. Following eyes exposure, irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes. Following dermal exposure, remove contaminated clothing and wash exposed area thoroughly with soap and water, and administer a benzodiazepine IV in case of irritation. In all those cases, a physician may need to examine the area if irritation or pain persists. (R624)",DNA;RNA;P69905;P68871;P02042;P02100;P69891;P69892;Q6B0K9;P09105;P02008
97,T3D0096,2009-03-06 18:58:04 UTC,2009-08-04 21:27:40 UTC,Ethion,Organic Compound;Pesticide;Organophosphate,"Bis(s-(diethoxyphosphinothioyl)mercapto)methaneBladanCaswell No. 427DiethionEmbathionEthanoxEthiolEthiol 100Ethion [ansi:bsi:iso]Ethion mixtureEthodanEthopazEthyl methylene phosphorodithioateEthyl methylene phosphorodithioate ([(EtO)2P(S)S]2CH2)Fosfatox eFosfono 50HylemaxHylemoxItopazKWITMethyleen-s,s'-bis(o,o-diethyl-dithiofosfaat)Methyleen-s,s'-bis(o,o-diethyl-dithiofosfaat) [dutch]Methylene-s,s'-bis(o,o-diaethyl-dithiophosphat)Methylene-s,s'-bis(o,o-diaethyl-dithiophosphat) [german]Niagara 1240NialateO,o,o',o'-tetraaethyl-bis(dithiophosphat)O,o,o',o'-tetraaethyl-bis(dithiophosphat) [german]O,o,o',o'-tetraethyl s,s'-methanediyl bis(dithiophosphate)O,o,o',o'-tetraethyl s,s'-methylene bis(dithiophosphate)O,o,o',o'-tetraethyl s,s'-methylene bisphosphorodithioateO,o,o',o'-tetraethyl s,s'-methylene di(phosphorodithioate)O,o,o',o'-tetraethyl s,s'-methylenebis(phosphorodithioate)O,o,o',o'-tetraethyl s,s'-methylenebisphosphordithioateO,o,o',o'-tetraethyl-s,s'-methylene di(phosphorodithioate)O,o,o',o'-tetraethyl-s,s'-methylenebisphosphorodithioateO,o,o,o-tetraethyl s,s'-methylenebis(dithiophosphate)PS92_SUPELCOPhosphotox eRP-thionRhodiacideRhodocideRodocidRodocideS,s'-methylen-bis(o,o-diaethyl-dithiophosphat)S,s'-methylen-bis(o,o-diaethyl-dithiophosphat) [german]S,s'-methylene bis(o,o-diethyl phosphorodithioate)S,s'-methylene o,o,o',o'-tetraethyl di(phosphorodithioate)S,s'-methylene o,o,o',o'-tetraethyl phosphorodithioateSoprathionTetraethyl s,s'-methylene bis(phosphorothiolothionate)Trecator-SCVegfru fosmiteVegfru-fosmite","Ethion is an organophosphate pesticide. It does not occur naturally in the environment. Ethion is used in agriculture, mainly to control insects on citrus trees, but also on cotton, fruit and nut trees, and some vegetables. It may also be used on lawns and turf grasses, but it is not used in the home for pest control. Ethion affects the nervous systems by inhibiting acetylcholineserases. (S687)",,563-12-2,3286,,"","",38663,ALPHA-METHYLMETHIONINE,,C100038,Ethion,6440,,,http://en.wikipedia.org/wiki/Ethion,"InChI=1/C9H22O4P2S4/c1-5-10-14(16,11-6-2)18-9-19-15(17,12-7-3)13-8-4/h5-9H2,1-4H3",diethoxyphosphinothioylsulfanylmethylsulfanyl-diethoxy-sulfanylidene-$l^{5}-phosphane,http://www.biospider.ca/saved_files/mol/,CCOP(=S)(OCC)SCSP(=S)(OCC)OCC,CCOP(=S)(OCC)SCSP(=S)(OCC)OCC,C9H22O4P2S4,383.987620,Pure ethion is a clear to yellowish liquid with an unpleasant sulfur-like smell.,-13 °C,165 °C at 0.3 mm Hg,1.220 at 20 °C,"0.002 mg/mL at 25 °C [SHIU,WY et al.(1990)]",,,,Oral. Inhalation. Dermal. (S687),,"Ethion is converted, in the liver, into its active form ethion monoxon. Ethion monoxon is a potent inhibitor of cholinesterases and exerts toxicity by reacting with and inhibiting neural acetylcholinesterase. (S687)","Ethion is a small, lipid-soluble molecule that can be absorbed by passive diffusion through the lungs, gastrointestinal tract, or skin. Ethion is desulfurated by cytochrome P-450 enzymes in the liver to its active form, ethion monoxon. Ethion and its oxon form can be detoxified by the action of esterases in the blood and liver, producing diethyl phosphate, diethyl thiophosphate, diethyl dithiophosphate, and other metabolites that have not been characterized. (S687)",,,,"Ethion enters the air, water, and soil during its manufacture and use. It is not known if ethion levels can build up in plants or fish. Chemical plant workers, transport workers, and pesticide applicators are the major occupational groups that might be exposed to ethion. The general population may be exposed to very small amounts of ethion by eating or drinking. People living near hazardous waste sites containing ethion or near its manufacturing, processing, or storage facilities could potentially be exposed. (S687)",,Ethion affects the nervous system. (S687),"Exposure to high levels of ethion can cause nausea, sweating, diarrhea, loss of bladder control, blurring or dimness of vision, muscle tremors, and labored breathing. Severe poisoning may result in coma, inability to breathe, and death. (S687)","",""
98,T3D0097,2009-03-06 18:58:04 UTC,2009-08-04 21:27:40 UTC,"1,1,1-Trichloroethane",Organic Compound;Solvent;Organochloride,"&alpha;-t&alpha;-trichloroethane'chlorothene'.alpha.-t.alpha.-trichloroethane1,1, 1-Trichloraethan (GERMAN)1,1, 1-Tricloroetano (ITALIAN)1,1,1 Trichloroethane1,1,1-TRICHLOROETHANE (METHYL CHLOROFORM)1,1,1-Trichloorethaan1,1,1-Trichloorethaan (DUTCH)1,1,1-Trichloraethan1,1,1-Trichloraethan [German]1,1,1-Trichlorethane1,1,1-Trichloroethane1,1,1-Trichloroethane [UN2831] [Poison]1,1,1-Trichloroethane, technical grade1,1,1-Trichloroethane-surfactants-butane-propane1,1,1-Tricloroetano1,1,1-Tricloroetano [Italian]1,1,1-trichloroethane (ACD/Name 4.0)1,1-TrichloroethaneAerothene TTAlpha-tAlpha-trichloroethaneBaltanaCH3CCl3Caswell No. 875ChloroeteneChloroetheneChloroethene nuChloroform, methyl-ChloroteneChlorothane nuChlorotheneChlorothene SMChlorothene VGChlorothene nuChlorothene, inhibitedChlortenCleaniteCut aidDabco CS90Delf fabric protectorDistillex DS1Dowclene LSEthanaEthana nuGenklene LBHALOGENATED ETHANES CS (1,1, 1-TRICHLOROETHANE)Ici-cf 2InChI=1/C2H3Cl3/c1-2(3,4)5/h1HInhibisolMS-170 1,1,1 trichloroethane solventMethyl chloroformMethylchloroformMethyltrichloromethaneRCRA waste no. U226Rcra waste number U226Solvent 111SolvethaneStrobaneTCEATafcleanThree one aThree one sTri-ethaneTrichloro-1,1, 1-ethane (FRENCH)Trichloro-1,1,1-ethaneTrichloro-1,1,1-ethane [French]TrichloroethaneTrichloroethane (van)Trichloroethane, 1,1,1-TrichloromethylmethaneWLN: GXGG1","The chemical compound 1,1,1-trichloroethane is a chlorinated hydrocarbon that was until recently widely used as an industrial solvent. It does not occur naturally in the environment. 1,1,1-Trichloroethane is a colorless liquid with a sweet, sharp odor, which dissolves slightly in water. The liquid evaporates quickly and becomes a vapor. 1,1,1-Trichloroethane was often used as a solvent to dissolve other substances, such as glues and paints. In industry, it was widely used to remove oil or grease from manufactured parts. In the home, it is used to be an ingredient of products such as spot cleaners, glues, and aerosol sprays. No 1,1,1-trichloroethane is supposed to be manufactured for domestic use in the United States after January 1, 2002, because it affects the ozone layer. (R557,R558)",,71-55-6,6278,,"","",36015,CPD-8985,,,"1,1,1-Trichloroethane",1413,,,"http://en.wikipedia.org/wiki/1,1,1-Trichloroethane","InChI=1/C2H3Cl3/c1-2(3,4)5/h1H3","1,1,1-trichloroethane",http://www.biospider.ca/saved_files/mol/,CC(Cl)(Cl)Cl,CC(Cl)(Cl)Cl,C2H3Cl3,131.930030,Colorless liquid.,"-33 °C (240 K, -27 °F)","74 °C (347 K, 165 °F)",1.32 g/cm3,"1.29 mg/mL at 25 °C [HORVATH,AL et al. (1999)]",,,,"Oral
Inhalation
Dermal 
(R559)","","An involvement of cytochrome P-450-mediated dechlorination in the production of liver injury has been demonstrated. 1,1,1-Trichloroethane is converted by the cytochrome P-450 to chlorinated metabolites after incubation with hepatic nuclei and an NADPH-generating system plus EDTA, with the omission of any component eliminating metabolite production. The production of free radicals via the homolytic cleavage of the carbon-chlorine bond in 1,1,1-trichloroethane occurs in the endoplasmic reticulum of hepatocytes, and the free radicals react with unsaturated lipids and proteins in the endoplasmic reticulum, producing lipid peroxidation and covalent binding. These actions lead to morphological and functional changes in this organelle and, eventually, to cellular dysfunction and necrosis. Moreover, exposure to high concentrations of 1,1,1-trichloroethane can lead to the depression of the nervous system. In general, the highly lipophilic nature of 1,1,1-trichloroethane, allows it to cross the blood-brain barrier readily and partition into lipids in neuronal membranes. This property allows it to interfere with neural membrane function, bringing about central nervous system depression, behavioral changes, and anesthesia. 1,1,1-Trichloroethane has also been shown to inhibit the activity of membrane-bound enzymes such as acetylcholinesterase and magnesium-activated ATPase in human red blood cells and rat synaptosomes. (R557, R569)","Upon first exposure, 1,1,1-trichloroethane is rapidly and efficiently absorbed by the lung, skin, and gastrointestinal tract of humans. 1,1,1-Trichloroethane is distributed by the blood to tissues and organs throughout the body, including to developing fetuses, with preferential distribution to fatty tissues. The predominant pathway of elimination of 1,1,1-trichloroethane in humans, regardless of route of exposure, is exhalation of the unchanged compound. 1,1,1-Trichloroethane is metabolized oxidatively, at low rates, to trichloroethanol and trichloroacetic acid by the cytochrome P-450 mixed-function oxidase system. These metabolites are excreted in the urine, and other minor metabolites (carbon dioxide [CO2] and acetylene) are excreted in expired air. (R557)","LD50: 11 240 mg/kg (Oral, Mouse) (R557) 
LD50: 9470 mg/kg (Oral, Guinea pig) (R557) 
LD50: 5660 mg/kg (Oral, Rabbit) (R557) ","","3, not classifiable as to its carcinogenicity to humans. (R566)","1,1,1-Trichloroethane was often used as a solvent to dissolve other substances, such as glues and paints. In industry, it was widely used to remove oil or grease from manufactured parts. In the home, it is used as an ingredient of products such as spot cleaners, glues, and aerosol sprays. No 1,1,1-trichloroethane is supposed to be manufactured for domestic use in the United States after January 1, 2002, because it affects the ozone layer. Exposure can occur from breathing in air containing it in vapor form, drinking water or eating food containing 1,1,1-trichloroethane. (R557)","Acute Inhalation: 2 ppm (R557) 
Intermediate Inhalation: 0.7 ppm (Gerbil) (R557) 
Intermediate Oral: 20 mg/kg/day (Mouse) (R557)","Dizziness, lightheadedness, cardiac arrhythmias, and loss of coordination are caused by exposure to higher concentrations. Increased levels of serum bilirubin, lactate dehydrogenase (LDH), alkaline phosphatase, and serum glutamic oxaloacetic transaminase (SGOT), all suggestive of liver injury can result from the exposure to high levels of 1,1,1-trichloroethane by inhalation or ingestion. Moreover, inhalation of 1,1,1-trichloroethane can lead to fat accumulation in the liver. Mild erythema and fine scaling can be visible after dermal exposure. Dermal exposure to 1,1,1-trichloroethane can cause reversible effects such as the increase of the blood flow. (R557)","Symptoms include cough, sore throat, headache, dizziness, drowsiness, nausea, ataxia, unconsciousness. Dry skin and redness follow dermal exposure, while nausea, vomiting, abdominal pain, and diarrhoea follw ingestion. (R559)","Gastric lavage is recommended following oral exposure, but must be weighted against potential complications of bleeding or perforation. Avoid administration of adrenergic agonist drugs whenever possible. Following inhalation, move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Following eye exposure, irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes. Remove contaminated clothing and wash exposed area thoroughly with soap and water if the contamination occured through dermal exposure. (R560) ",P22303;DNA;RNA;P98194;O75185;P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P78334;Q8N1C3;P18507;Q99928;O00591;P24046;P28476;A8MPY1;Q9UN88;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;P54710;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P03372;Q92731
100,T3D0099,2009-03-06 18:58:04 UTC,2009-08-04 21:27:40 UTC,Ethylbenzene,Organic Compound;Industrial Precursor/Intermediate;Aromatic Hydrocarbon,"&alpha;-methyltolueneAethylbenzolAethylbenzol [german]Aethylbenzol(german)Alpha-methyltolueneAromatic hydrocarbons, C12-20Aromatic hydrocarbons, C12-2OBenzene, ethenylBenzene, ethenyl-, trimerBenzene, ethyl-Benzene, ethyl-, benzylatedEBEthyl benzeneEthyl benzene(dot)Ethyl-benzeneEthylbenzeenEthylbenzeen [dutch]Ethylbenzeen(dutch)Ethylbenzene [UN1175] [Flammable liquid]Ethylbenzene solutionEthylbenzolEthylenzeneEtilbenzeneEtilbenzene [italian]Etilbenzene(italian)EtylobenzenEtylobenzen [polish]Etylobenzen(polish)HSDB 84PYLPhenylethaneStyrene trimerStyrene trimersWLN: 2Rethylbenzene (ACD/Name 4.0)","Ethylbenzene is an organic compound with the formula C6H5CH2CH3. This aromatic hydrocarbon is important in the petrochemical industry as an intermediate in the production of styrene, which in turn is used for making polystyrene, a commonly used plastic material. Although often present in small amounts in crude oil, ethylbenzene is produced in bulk quantities by combining benzene and ethylene in an acid-catalyzed chemical reaction. (R573)",,100-41-4,7500,,C07111,"",16101,CPD-9502,,C004912,Ethylbenzene,606,,,http://en.wikipedia.org/wiki/Ethylbenzene,"InChI=1/C8H10/c1-2-8-6-4-3-5-7-8/h3-7H,2H2,1H3",ethylbenzene,http://www.biospider.ca/saved_files/mol/76a7d3e05b0d4b13f8d892b8855a80ed_1237944646.mol,CCC1=CC=CC=C1,CCC1=CC=CC=C1,C8H10,106.078250,,-94.9 °C,,,"0.169 mg/mL at 25 °C [SANEMASA,I et al. (1982)]",,,,"Oral
Inhalation
Dermal
(R573)","Cytochrome P450 2B6 (P20813)
Cytochrome P450 2E1 (P05181)
(R573, R595)","Changes in the integrity of the cell membrane after partitioning of ethylbenzene into the lipid bilayer may subsequently affect the function of membrane, particularly as a barrier and in energy transduction, and in the formation of a matrix for proteins and enzymes. Ethybenzene inhibits the activity of the astrocytic membrane ATPases, which helps regulate adequate intercellular levels of ions, nutrients, metabolic intermediates and precursors in the central nervous system. Thus, this may disturb the ability of the cells to maintain homeostasis. (R573, R590)","Ethylbenzene is metabolized mainly through hydroxylation and then through conjugation reactions from which numerous metabolites have been isolated. Hydroxylation of ethylbenzene to 1-phenylethanol is catalyzed by cytochrome P-450 isoforms CYP2E1 and CYP2B6. 1-Phenylethanol is conjugated to glucuronide, which then is either excreted or converted to subsequent metabolites. Oxidation of 1-phenylethanol yields acetophenone, which is both excreted in the urine as a minor metabolite and further transformed. Continued oxidation of the side chain leads to the sequential formation of 2-hydroxyacetophenone, 1-phenyl-1,2-ethanediol, mandelic acid, and phenylglyoxylic acid. Minor pathways (e.g., ring hydroxylation) include glucuronide and sulfate conjugation with hydroxylated derivatives to form glucuronides and sulfates that are excreted in the urine. In humans exposed via inhalation, the major metabolites of ethylbenzene in the urine are mandelic acid (70%) and phenylglyoxylic acid (25%). Following dermal exposure of humans, however, excretion of mandelic acid was shown to be only 4.6% of the absorbed dose, which may indicate differences in the metabolic fate between inhalation and dermal exposure routes. (R573)",,"LD50: 3.5 g/kg (Oral, Rat) (R587) 
LD50: 77.4 g/kg (Dermal, Rabbit)(R587)
LC50: 17.2 g/m3 (4000 ppm) (Inhalation, Rat) (R587)","2B, possibly carcinogenic to humans. (R264)","Ethylbenzene is used in the petrochemical industry as an intermediate in the production of styrene, which in turn is used for making polystyrene, a commonly used plastic material. Exposure may occur from breathing contaminated air, drinking or eating food prepared with ethylbenzene-contaminated water, and through skin contact with products containing ethylbenzene, such as gasoline. (R573)","Acute Inhalation: 10 ppm (R260) 
Intermediate Inhalation: 0.7 ppm (R260)
Chronic Inhalation: 0.3 ppm (R260)
Intermediate Oral: 0.5 mg/kg/day (R260)","Chronic exposure to etylbenzene can lead to an increase in the mean number of lymphocytes and a decrease in hemoglobin levels. Acute duration and intermediate duration studies suggest that the auditory system is a sensitive target of ethylbenzene toxicity. Exposure ethylbenzene can lead to functional and organic disturbances (nervous system disturbances, toxic hepatitis and upper respiratory tract complaints). Metabolites of ethylbenzene have been shown to produce oxidative damage to DNA. (R573, R583)","Cough, sore throat, dizziness, drowsiness, and headache follow inhalation or ingestion exposure to ethylbenzene. Ingestion exposure can also lead to burning sensation in the throat and chest. Skin or eyes contact to ethylbenzene can lead to redness and pain of the exposed surface. (R578)","Following oral exposure, a gastric lavage is recommended. Protect airway by placement in Trendelenburg and left lateral decubitus position or by endotracheal intubation. Control any seizures first. Following inhalation, move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Following eye exposure, irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes. In case of dermal exposure, remove contaminated clothing and wash exposed area thoroughly with soap and water. Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines. Some chemicals can produce systemic poisoning by absorption through intact skin. Carefully observe patients with dermal exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary. (R596)",P54710;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P98194;O75185;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084
101,T3D0100,2009-03-06 18:58:05 UTC,2009-08-25 19:51:10 UTC,Radium-226,Inorganic Compound;Metal;Radium Compound;Radioactive Isotope,"Actinium-xRARADIUM-226RadioRadium bromatumRadium, isotope of mass 226Radium-226 and its decay productsRadon-226Thorium-x","Radium is a radioactive chemical element which has the symbol Ra and atomic number 88. Its appearance is almost pure white, but it readily oxidizes on exposure to air, turning black. Radium is an alkaline earth metal that is formed when uranium and thorium break down in the environment. It is extremely radioactive. Radium-226 is the most stable isotope, has a half-life of 1602 years, and decays into radon gas. Radium has been used as a radiation source for treating cancer, in radiography of metals, and combined with other metals as a neutron source for research and radiation instrument calibration. Until the 1960s, radium was a component of the luminous paints used for watch and clock dials, instrument panels in airplanes, military instruments, and compasses. (S360, W508)",,13982-63-3,6328144,,"","",33325,"",,D011883,Radium-226,6526,,,http://en.wikipedia.org/wiki/Radium,InChI=1/Ra.2H,radium,http://www.biospider.ca/saved_files/mol/,[Ra],[226Ra],Ra,0.000000,"Its appearance is almost pure white, but it readily oxidizes on exposure to air, turning black. (S360)","973  K (700 °C , 1292 °F )",1737 °C,5.5  g·cm−3,"",,,,"Oral
Inhalation
Dermal
(S360)",,"Ionizing radiation produced by radium damages the DNA, resulting in gene mutations and chromosomal aberrations. This can both initiate and promote carcinogenesis, and interfere with reproduction and development. Since radium`s similarity to calcium allows it to deposit in the bones, bone cancer is of particular risk. (W508)","Due to its radioactivity, radium can affect the body following ingestion, inhalation, or dermal exposure. If inhalated, it may accumulate in the lungs. Once in the body radium may deposit in the bones, mainly on the surface and areas where new bone is being formed. Radium is not metabolized and is excreted primarily in the faeces. (W508)",,,"1, carcinogenic to humans. (R264)","Radium has been used as a radiation source for treating cancer, in radiography of metals, and combined with other metals as a neutron source for research and radiation instrument calibration. Until the 1960s, radium was a component of the luminous paints used for watch and clock dials, instrument panels in airplanes, military instruments, and compasses. (W508)",,"Radium is highly radioactive and its decay product, radon gas, is also radioactive. It has been shown to cause effects on the blood (anemia) and eyes (cataracts). Inhalation, injection, ingestion or body exposure to radium can cause cancer and other disorders, due to its radioactivity. Since radium is chemically similar to calcium, it has the potential to cause great harm by replacing it in bones, and bone cancer is of particular risk. (S360, W508)","Exposure to high doses of ionizing radiation results in acute radiation syndrome, which can cause skin burns, hair loss, nausea, vomiting, dizziness, disorientation, low blood pressure, headache, fatigue, weakness, fever, birth defects, illness, infection, and death. (W510, W525)","Treatment reversing the effects of irradiation is currently not possible. Anaesthetics and antiemetics are administered to counter the symptoms of exposure, as well as antibiotics for countering secondary infections due to the resulting immune system deficiency. (W525)",DNA
102,T3D0101,2009-03-06 18:58:05 UTC,2009-08-25 15:50:10 UTC,Thorium,Inorganic Compound;Metal;Thorium Compound;Radioactive Isotope,"THTHORIUM, 99.1%, POWDERThorium atomic absorption standard solutionThorium metal, pyrophoric [UN2975] [Radioactive]Thorium, pyrophoricThorium-232Torio","Thorium is the chemical element of symbol Th and atomic number 90. It is a naturally occurring radioactive metal of the actinide series. In the environment, thorium exists in combination with other minerals, such as silica. Small amounts of thorium are present in all rocks, soil, water, plants, and animals. Twenty-seven radioactive isotopes of thorium, with mass number from 210 to 236, have been characterized. Naturally occurring thorium is composed mainly of one isotope: 232Th. The most abundant and/or stable isotopes are: 232Th (half-life of 14.05 billion years), 230Th (half-life of 75,380 years), 229Th (half-life of 7340 years), and 228Th (half-life of 1.92 years). Thorium is used to make ceramics, gas lantern mantles, and metals used in the aerospace industry and in nuclear reactions. Thorium can also be used as a fuel for generating nuclear energy. Thorium has been linked to increased risk of liver cancer. (S521, W511)",,7440-29-1,23960,,"","",33385,"",,D013910,Thorium,7977,,,http://en.wikipedia.org/wiki/Thorium,InChI=1/Th,thorium,http://www.biospider.ca/saved_files/mol/,[Th],[Th],Th,232.038050,Thorium is an air-stable silvery-white solid metal. (S521),"2115 K (1842 °C, 3348 °F)","5061 K (4788 °C, 8650 °F)",11.7  g·cm−3 (room temperature),"",,,,"Oral
Inhalation
Dermal
(W511)","Serotransferrin (P02787)
(W511)","The ionizing radiation produced by thorium causes cellular damage that includes DNA breakage, accurate or inaccurate repair, apoptosis, gene mutations, chromosomal change, and genetic instability. This leads to loss of normal cell and tissue homeostasis, and development of malignancy. Ionizing radiation that does not directly damage DNA can produce reactive oxygen intermediates that directly affect the stability of p53, an important enzyme in cell-cycle regulation, and produce oxidative damage to individual bases in DNA and point mutations by mispairing during DNA replication. (W510)","Exposure to thorium can occur following inhalation, ingestion, or dermal exposure. Once in the body thorium accumulates mainly in the liver, spleen, lymph nodes, lungs, and bone. Transferrin plays a major role in the transport and cellular uptake of thorium. Thorium may combine with oxygen to form thorotrast (thorium dioxide), a colloid which may affect protein uptake. Thorium and thorotrast are excreted mainly in the faeces. (W511)",,,"1, carcinogenic to humans. (R264)","Thorium can also be used as a fuel for generating nuclear energy. Thorium is used as an alloying element in magnesium, used in aircraft engines, imparting high strength and creep resistance at elevated temperatures. Thorium is also used as an alloying agent in gas tungsten arc welding (GTAW) to increase the melting temperature of tungsten electrodes and improve arc stability. Thorium is used to coat tungsten wire used in electronic equipment, improving the electron emission of heated cathodes. Thorium is used as a fertile material for producing nuclear fuel. Thorium is a very effective radiation shield, although it has not been used for this purpose as much as lead or depleted uranium. Uranium-thorium age dating has been used to date hominid fossils. (S521)",,"Lungs and other internal organs can be penetrated by the alpha radiation produced by thorium. As a result, exposure to an aerosol of thorium can lead to increased risk of cancers of the lung, pancreas and blood. Exposure to thorium internally leads to increased risk of liver diseases. (S521)","Exposure to high doses of ionizing radiation results in acute radiation syndrome, which can cause skin burns, hair loss, nausea, vomiting, dizziness, disorientation, low blood pressure, headache, fatigue, weakness, fever, birth defects, illness, infection, and death. (W510, W525)","Treatment reversing the effects of irradiation is currently not possible. Anaesthetics and antiemetics are administered to counter the symptoms of exposure, as well as antibiotics for countering secondary infections due to the resulting immune system deficiency. (W525)",DNA
103,T3D0102,2009-03-06 18:58:05 UTC,2009-08-04 21:27:41 UTC,"4,6-Dinitro-o-cresol",Organic Compound;Pesticide;Aromatic Hydrocarbon;Nitrite,"2, 4-Dinitro-o-cresol2,4-Dinitro-6-methylphenol2,4-Dinitro-o-cresol2,4-bis(hydroxy(oxido)amino)-6-methylphenol (ACD/Name 4.0)2-Methyl-4,6-dinitrophenol3, 5-Dinitro-2-hydroxytoluene3,5-Dinitro-2-hydroxytoluene4, 6-Dinitro-o-cresolo (ITALIAN)4, 6-Dinitrokresol (DUTCH)4,6-DNOC4,6-Dinitro-2-methylphenol4,6-Dinitro-o-cresol4,6-Dinitro-o-cresol, and salts4,6-Dinitro-o-cresolo4,6-Dinitro-o-cresolo [Italian]4,6-Dinitro-o-kresol4,6-Dinitro-o-kresol (CZECH)4,6-Dinitro-o-kresol [Czech]4,6-Dinitrocresol4,6-Dinitrokresol4,6-Dinitrokresol [Dutch]6-Methyl-2,4-dinitrophenolAntinoninAntinonninArborolCapsineCaswell No. 390Chemsect dnocDNDNCDNOCDNOKDegrassanDekryllDekrysilDetalDetolDillexDinitroDinitro-o-cresolDinitro-o-cresol (van)Dinitro-o-cresol, solidDinitro-o-cresol, solid [UN1598] [Poison]Dinitro-o-cresol, solutionDinitro-o-cresol, solution [UN1598] [Poison]DinitrocresolDinitrodendtroxalDinitrolDinitromethyl cyclohexyltrienolDinitrosolDinocDinokDinuraniaDitrosolDn-dry mix no. 2Dnoc (pesticide)Dnoc [bsi:iso]Dnok (czech)Dnok [czech]Dwunitro-o-krezolDwunitro-o-krezol (polish)Dwunitro-o-krezol [polish]EffusanEffusan 3436ElgetolElgetol 30ElgetoxElipolExtrarFlavin-samdozHedolitHedoliteK IIIK ivKreniteKreozanKresamoneKresonite-eKrezotol 50LE dinitrocresol-4,6 [French]Le dinitrocresol-4,6Le dinitrocresol-4,6 (FRENCH)LipanNeudorff DN 50NitradorNitrofanOranz viktoriaOranz viktoria [czech]PS57_SUPELCOPhenol, 2-methyl-4,6-dinitro-, and saltsProkarbolRCRA waste no. P047RafexRafex 35RaphatoxRcra waste number P047SandolinSandolin aSelinonSinoxToluene, 3,5-dinitro-2-hydroxy-TrifocideTrifrinaWLN: WNR BQ C1 ENWWinterwashZahlreiche bezeichnungenZahlreiche bezeichnungen (german)Zahlreiche bezeichnungen [german]o-Cresol, 4,6,-dinitro-o-Cresol, 4,6-dinitro-","4,6-Dinitro-o-cresol is the most commercially important of the 18 different dinitrocresols, a class of manufactured chemicals. 4,6-Dinitro-o-cresol (DNOC) is used primarily for insect control and crop protection. It may be sold under different trade names, including Antinonnin, Detal, and Dinitrol. DNOC was used in diet pills in the 1930s, but has since been banned for this use. (R380)",,534-52-1,10800,,"","",39349,CPD-10489,,C024132,"4,6-Dinitro-o-cresol",1947,,,,"InChI=1/C7H6N2O5/c1-4-2-5(8(11)12)3-6(7(4)10)9(13)14/h2-3,10H,1H3","2-methyl-4,6-dinitrophenol",http://www.biospider.ca/saved_files/mol/,CC1=CC(=CC(=C1O)[N+](=O)[O-])[N+](=O)[O-],CC1=CC(=CC(=C1O)[N+](=O)[O-])[N+](=O)[O-],C7H6N2O5,198.027670,Yellow solid.,86.6 °C,,,"0.198 mg/mL at 20 °C [SCHWARZENBACH,RP et al.(1988)]",,,,"Oral
Inhalation
Dermal
(R380)",Serum albumin (P02768) (R380),"4,6-Dinitro-o-cresol is an uncoupler of oxidative phosphorylation. It is believed to cause an acceleration of metabolic processes that are part of the tricarboxylic acid (TCA) cycle. DNOC produces its accelerative effect by increasing the permeability of the inner mitochondrial membrane to Ca+, altering the proton electrochemical gradient and thus interrupting the phosphate transfer to adenosine diphosphate (ADP) to form ATP. Uncoupling allows electron transport to proceed unchecked even when ATP synthesis is inhibited. As a consequence, more ADP and inorganic phosphate are available to drive the TCA cycle, and most of the energy produced from catabolism of glucose is not stored in high energy phosphate bonds as ATP but is given off as heat. This results in the elevated body temperature and related effects characteristic of DNOC toxicity. (R380)","4,6-Dinitro-o-cresol is absorbed via oral, inhalation, and dermal routes, then binds to albumin and is distributed to most tissues, including the lungs, heart, liver, kidney, brain, spleen, and muscle. Although small quantities of DNOC may be conjugated, most of it appears to be reduced to less toxic mono amino derivatives, such as 6-amino-4-nitro-o-cresol and 6-acetamido-4-nitro-o-cresol, and then subsequently conjugated. DNOC and its metabolites are eliminated primarily via the urine. (R380)","LD50: 200 mg/kg (Dermal, Rat) (R287)
LD50: 21 mg/kg (Oral, Mouse) (R287)
LD50: 19 mg/kg (Intraperitoneal, Mouse) (R287)
LD50: 25,600 ug/kg (Subcutaneous, Rat) (R263)",29 mg/kg (oral) or 1 mg/m3 (inhaled) for an adult human. (R293),,"4,6-Dinitro-o-cresol is used primarily for insect control and crop protection. (R380)",,"Exposure to DNOC may cause mild damage to the stomach, kidneys, and liver. Ingesting DNOC for long periods may cause cataracts and skin rashes. (R380)
","Exposure to high levels of DNOC for short periods may cause convulsions, unconsciousness, and death. Exposure to low levels of DNOC may result in an increased basal metabolic rate, increased sweating, weight loss, and increased heart rate, breathing rate, and body temperature. Other effects from DNOC exposure may include difficulty in breathing, headache, drowsiness, dizziness, and a yellowing of skin and the whites of the eyes. (R380)
","",Q99643;O14521;P31040;P21912
104,T3D0103,2009-03-06 18:58:05 UTC,2009-08-04 21:27:41 UTC,"1,3,5-Trinitrobenzene",Organic Compound;Explosive;Aromatic Hydrocarbon;Nitrite,"1,3, 5-Trinitrobenzene1,3,5-Trinitrobenzol2,4,6-trinitrobenzeneBenzene, 1,3,5-trinitro-Benzene, trinitro- (wet)Benzene,1,3,5-trinitro-BenziteRCRA waste no. U234Rcra waste number U234S-trinitrobenzeneSYM-trinitrobenzeneSYN-trinitrobenzeneSymmetric trinitrobenzeneTNBTrinitrobenzeenTrinitrobenzeen [dutch]Trinitrobenzeen(dutch)TrinitrobenzeneTrinitrobenzene, DRYTrinitrobenzene, DRY(dot)Trinitrobenzene, dry or wetted with < 30% water, by massTrinitrobenzene, wetTrinitrobenzene, wet (dot)TrinitrobenzenesTrinitrobenzolTrinitrobenzol [german]Trinitrobenzol(german)WLN: WNR cnw enw","1,3,5-Trinitrobenzene (1,3,5-TNB) is a synthetic substance that is used in explosives. (R382)",,99-35-4,7434,,"","",48113,"",,C029222,"1,3,5-Trinitrobenzene",1437,,,"http://en.wikipedia.org/wiki/1,3,5-Trinitrobenzene",InChI=1/C6H3N3O6/c10-7(11)4-1-5(8(12)13)3-6(2-4)9(14)15/h1-3H,"1,3,5-trinitrobenzene",http://www.biospider.ca/saved_files/mol/,C1=C(C=C(C=C1[N+](=O)[O-])[N+](=O)[O-])[N+](=O)[O-],C1=C(C=C(C=C1[N+](=O)[O-])[N+](=O)[O-])[N+](=O)[O-],C6H3N3O6,213.002180,Yellow solid.,121.5 °C,,,"0.278 mg/mL at 15 °C [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral
Inhalation
Dermal
(R382)",,"In the red blood cell, 1,3,5-TNB induces formation of methemoglobin, leading to cyanosis. Reduction of the nitrogroup(s) of 1,3,5-TNB produces reactive nitroaromatic radical anions which redox cycle to produce other reactive species such as superoxide anion. Redox cycling of these intermediates probably causes the methemoglobinemia. 1,3,5-TNB may also exert neurotoxic effects by damaging the blood-brain barrier.(R382, R386)","1,3,5-Trinitrobenzene is absorbed via oral, inhalation, and dermal routes and is believed to penetrate the red blood cell membrane. The metabolism of 1,3,5-TNB includes both oxidative and reductive biotransformations, followed by conjugation. The main route of excretion of 1,3,5-TNB metabolites is the urine. (R382)","LD50: 250 mg/kg (Oral, Rat) (R261)
LD50: 32 mg/kg (Intravenous, Mouse) (R261)",,,"1,3,5-Trinitrobenzene is used in explosives. Waste discharges from army ammunitions plants or other chemical manufacturers are the primary sources for release into the air, water, and soil. (R382)",,"Chronic exposure to 1,3,5-trinitrobenzene can cause a reduction (or loss) in the number of red blood cells (anemia). 1,3,5-TNB may also have neurotoxic effects. (R382, R386)","Exposure to high concentrations of 1,3,5-trinitrobenzene can reduce the ability of blood to carry oxygen and can cause skin bluishing. Other symptoms nclude headache, nausea, and dizziness. (R382)","Treatment is mainly symptomatic and may include gastric lavage and/or the administration of activated charcoal. Benzodiazepine may be administered if seizures occur. If methemoglobinemia is evident, 1 to 2 mg/kg of 1% methylene blue should be administered via IV. (R383)",""
105,T3D0104,2009-03-06 18:58:05 UTC,2009-08-04 21:27:41 UTC,Chlorobenzene,Organic Compound;Solvent;Industrial Precursor/Intermediate;Aromatic Hydrocarbon;Organochloride,"Abluton T30Benzene chlorideCaswell No. 183AChloorbenzeenChloorbenzeen [dutch]Chloorbenzeen(dutch)ChlorbenzeneChlorbenzolChlorobenzenChlorobenzen [polish]Chlorobenzen(polish)ChlorobenzeneChlorobenzene [UN1134] [Flammable liquid]Chlorobenzene monoChlorobenzene(italian)Chlorobenzene, mono-Chlorobenzene-UL-14CChlorobenzenuChlorobenzenu [czech]ChlorobenzolChlorobenzol(dot)ClorobenzeneClorobenzene [italian]Clorobenzene(italian)HSDB 55I P Carrier T 40MCBMonochloorbenzeenMonochloorbenzeen [dutch]Monochloorbenzeen(dutch)MonochlorbenzeneMonochlorbenzolMonochlorbenzol [german]Monochlorbenzol(german)MonochlorobenzeneMonochlorobenzolMonoclorobenzeneMonoclorobenzene [italian]Monoclorobenzene(italian)PHCLPhenyl chlorideRCRA waste no. U037Tetrosin SPWLN: GRchlorobenzene (ACD/Name 4.0)","Chlorobenzene is a synthetic aromatic organochloride. It was used in the past to make other chemicals, such as phenol and DDT. Now chlorobenzene is used as a solvent for some pesticide formulations, to degrease automobile parts, and as a chemical intermediate to make several other chemicals. (R391)",,108-90-7,7964,,C06990,"",28097,CPD-1125,,C031294,Chlorobenzene,300,,,,InChI=1/C6H5Cl/c7-6-4-2-1-3-5-6/h1-5H,chlorobenzene,http://www.biospider.ca/saved_files/mol/9736f45e8f14be7c25e92089cd00c00d_1237945152.mol,C1=CC=C(C=C1)Cl,C1=CC=C(C=C1)Cl,C6H5Cl,112.007980,Colorless liquid.,-45.2 °C,,,"0.498 mg/mL at 25 °C [HORVATH,AL (1982)]",,,,"Oral
Inhalation
(R391)",,"The reactive metabolites of chlorobenzene are believed to bind both liver and kidney proteins, causing direct damage. Chlorobenzene also activates nuclear factor-kappa B (NF-kappa B) and p38 mitogen-activated protein kinase, inducing the release of monocyte chemoattractant protein 1 (MCP-1) by lung epithelial cells, causing an inflammatory reponse. (R383, R392)","Chlorobenzene is known to be absorbed via ingestion and inhahation. As it is a lipophilic compound, chlorobenzene distributes preferentially to adipose tissue. It is metabolized by cytochrome P-450 enzymes into its major metabolite 4-chlorocatechol. Unchanged chlorobenzene is exhalted and its metabolites are excreted mainly in the urine. (R391)","LD50: 515 mg/kg (Intraperitoneal, Mouse) (R293)
LD50: 2290 mg/kg (Oral, Rat) (R293)
LD50: 1110 mg/kg (Subcutaneous, Rat) (R293)",,,"Chlorobenzene is used as a solvent for some pesticide formulations, to degrease automobile parts, and as a chemical intermediate to make several other chemicals. (R391)",Intermediate Oral: 0.4 mg/kg/day (R260),Effects on the central nervous system from breathing chlorobenzene may include unconsciousness and death. Chronic exposure can cause liver and kidney damage. (R391),"Symptoms of chlorobenzene exposure include headaches, nausea, sleepiness, numbness, and vomiting. Effects on the central nervous system from breathing chlorobenzene include unconsciousness, tremors, restlessness, and death. (R391)",Treatment is mainly symptomatic and supportive. (R383),P98194;O75185;P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P78334;Q8N1C3;P18507;Q99928;O00591;P24046;P28476;A8MPY1;Q9UN88;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;P54710;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P03372;Q92731
106,T3D0105,2009-03-06 18:58:05 UTC,2009-08-25 15:50:14 UTC,Radon,Inorganic Compound;Nobel Gas;Radioactive Isotope,"ActinonAlphatronNitonNiton /(222)Radon/RNRadium emanationRadon 222Radon, radioactiveThoronThoron (element)","Radon is the chemical element of symbol Rn and atomic number 86. It is a rare radioactive gas, belonging to the noble gas series, and is formed as part of three radioactive decay chains that begin with uranium or thorium. Thirty-six radioactive isotopes of radon, with mass number from 193 to 228, have been characterized. The most stable isotope is Rn-222 (half-life of 3.8 days); it is generated naturally by the decay of 238U and emits alpha particles. Rn-220 (half-life of 55.6 seconds) is a natural decay product of thorium and also emits alpha radiation. Because of its radioactivity and unreactivity as a chemical element, radon has few uses and is seldom used in academic research. Radon is responsible for the majority of the mean public exposure to ionizing radiations. (S494)",,10043-92-2,24857,,"","",33314,"",,D011886,Radon,,,,http://en.wikipedia.org/wiki/Radon,InChI=1/Rn,radon,http://www.biospider.ca/saved_files/mol/,[Rn],[Rn],Rn,0.000000,"Radon is a colorless, odorless, tasteless gas. (S494)","202 K (−71.15 °C, −96 °F)","211.3 K (−61.85 °C, −79.1 °F)",9.73 kg/m3 (standard temperature and pression),"",,,,"Oral
Inhalation
Dermal
(W509)",,"The ionizing radiation produced by radon causes cellular damage that includes DNA breakage, accurate or inaccurate repair, apoptosis, gene mutations, chromosomal change, and genetic instability. This leads to loss of normal cell and tissue homeostasis, and development of malignancy. Ionizing radiation that does not directly damage DNA can produce reactive oxygen intermediates that directly affect the stability of p53, an important enzyme in cell-cycle regulation, and produce oxidative damage to individual bases in DNA and point mutations by mispairing during DNA replication. (W509)","Exposure to radon can occur from inhalation or dermal contact. It can also enter the body via ingestion if dissolved in water. Radon distributes mainly to the fat. It is not metabolized and may be eliminated in the urine, faeces, or expired air. (W509)",,,"1, carcinogenic to humans. (R264)","Radon has few uses and is seldom used in academic research. Radon gas from natural sources can accumulate in buildings, especially in confined areas such as basements. Radon can be found in some spring waters and hot springs. (S494)",,"Radon is responsible for the majority of the mean public exposure to ionizing radiations. Due to it's radioactivity, breathing high concentrations of radon can cause lung cancer. According to the United States Environmental Protection Agency, radon could be the second most frequent cause of lung cancer, after cigarette smoking; and radon-induced lung cancer the 6th leading cause of cancer death overall, causing 21,000 lung cancer deaths per year in the United States. (S494)","Exposure to high doses of ionizing radiation results in acute radiation syndrome, which can cause skin burns, hair loss, nausea, vomiting, dizziness, disorientation, low blood pressure, headache, fatigue, weakness, fever, birth defects, illness, infection, and death. (W510, W525)","Treatment reversing the effects of irradiation is currently not possible. Anaesthetics and antiemetics are administered to counter the symptoms of exposure, as well as antibiotics for countering secondary infections due to the resulting immune system deficiency. (W525)",DNA
107,T3D0106,2009-03-06 18:58:05 UTC,2009-08-25 15:54:51 UTC,Radium-228,Inorganic Compound;Metal;Radium Compound;Radioactive Isotope,"Radium, isotope of mass 228Radium-228Radium-228 and its decay products","Radium is a radioactive chemical element which has the symbol Ra and atomic number 88. Its appearance is almost pure white, but it readily oxidizes on exposure to air, turning black. Radium is an alkaline earth metal that is formed when uranium and thorium break down in the environment. It is extremely radioactive. Radium has been used as a radiation source for treating cancer, in radiography of metals, and combined with other metals as a neutron source for research and radiation instrument calibration. Until the 1960s, radium was a component of the luminous paints used for watch and clock dials, instrument panels in airplanes, military instruments, and compasses. (S360, W508)",,15262-20-1,6328553,,C16457,"","","",,,Radium-228,,,,,InChI=1/Ra.2H/i1+2;;,radium-228,http://www.biospider.ca/saved_files/mol/cf72d6509be50e1ba8e9536af9e0140a_1237945505.mol,[228Ra],[228Ra],Ra,0.000000,,"",,,"",,,,"Oral
Inhalation
Dermal
(S360)",,"Ionizing radiation produced by radium damages the DNA, resulting in gene mutations and chromosomal aberrations. This can both initiate and promote carcinogenesis, and interfere with reproduction and development. Since radium`s similarity to calcium allows it to deposit in the bones, bone cancer is of particular risk. (W508)","Due to its radioactivity, radium can affect the body following ingestion, inhalation, or dermal exposure. If inhalated, it may accumulate in the lungs. Once in the body radium may deposit in the bones, mainly on the surface and areas where new bone is being formed. Radium is not metabolized and is excreted primarily in the faeces. (W508)",,,"1, carcinogenic to humans. (R264)","Radium has been used as a radiation source for treating cancer, in radiography of metals, and combined with other metals as a neutron source for research and radiation instrument calibration. Until the 1960s, radium was a component of the luminous paints used for watch and clock dials, instrument panels in airplanes, military instruments, and compasses. (W508)",,"Radium is highly radioactive and its decay product, radon gas, is also radioactive. It has been shown to cause effects on the blood (anemia) and eyes (cataracts). Inhalation, injection, ingestion or body exposure to radium can cause cancer and other disorders, due to its radioactivity. Since radium is chemically similar to calcium, it has the potential to cause great harm by replacing it in bones, and bone cancer is of particular risk. (S360, W508)","Exposure to high doses of ionizing radiation results in acute radiation syndrome, which can cause skin burns, hair loss, nausea, vomiting, dizziness, disorientation, low blood pressure, headache, fatigue, weakness, fever, birth defects, illness, infection, and death. (W510, W525)","Treatment reversing the effects of irradiation is currently not possible. Anaesthetics and antiemetics are administered to counter the symptoms of exposure, as well as antibiotics for countering secondary infections due to the resulting immune system deficiency. (W525)",DNA
108,T3D0107,2009-03-06 18:58:05 UTC,2009-08-25 17:59:25 UTC,Thorium-230,Inorganic Compound;Metal;Thorium Compound;Radioactive Isotope,"Thorium, isotope of mass 230Thorium-230","Thorium is the chemical element of symbol Th and atomic number 90. It is a naturally occurring radioactive metal of the actinide series. In the environment, thorium exists in combination with other minerals, such as silica. Small amounts of thorium are present in all rocks, soil, water, plants, and animals. Twenty-seven radioactive isotopes of thorium, with mass number from 210 to 236, have been characterized. Naturally occurring thorium is composed mainly of one isotope: 232Th. The most abundant and/or stable isotopes are: 232Th (half-life of 14.05 billion years), 230Th (half-life of 75,380 years), 229Th (half-life of 7340 years), and 228Th (half-life of 1.92 years). Thorium is used to make ceramics, gas lantern mantles, and metals used in the aerospace industry and in nuclear reactions. Thorium can also be used as a fuel for generating nuclear energy. Thorium has been linked to increased risk of liver cancer. (S521, W511)",,14269-63-7,61723,,"","","","",,,Thorium-230,,,,http://en.wikipedia.org/wiki/Thorium-230,InChI=1/Th/i1-2,thorium-230,http://www.biospider.ca/saved_files/mol/,[230Th],[238Th],Th,232.038050,,"",,,"",,,,"Oral
Inhalation
Dermal
(W511)","Serotransferrin (P02787)
(W511)","The ionizing radiation produced by thorium causes cellular damage that includes DNA breakage, accurate or inaccurate repair, apoptosis, gene mutations, chromosomal change, and genetic instability. This leads to loss of normal cell and tissue homeostasis, and development of malignancy. Ionizing radiation that does not directly damage DNA can produce reactive oxygen intermediates that directly affect the stability of p53, an important enzyme in cell-cycle regulation, and produce oxidative damage to individual bases in DNA and point mutations by mispairing during DNA replication. (W510)","Exposure to thorium can occur following inhalation, ingestion, or dermal exposure. Once in the body thorium accumulates mainly in the liver, spleen, lymph nodes, lungs, and bone. Transferrin plays a major role in the transport and cellular uptake of thorium. Thorium may combine with oxygen to form thorotrast (thorium dioxide), a colloid which may affect protein uptake. Thorium and thorotrast are excreted mainly in the faeces. (W511)",,,"1, carcinogenic to humans. (R264)","Thorium can also be used as a fuel for generating nuclear energy. Thorium is used as an alloying element in magnesium, used in aircraft engines, imparting high strength and creep resistance at elevated temperatures. Thorium is also used as an alloying agent in gas tungsten arc welding (GTAW) to increase the melting temperature of tungsten electrodes and improve arc stability. Thorium is used to coat tungsten wire used in electronic equipment, improving the electron emission of heated cathodes. Thorium is used as a fertile material for producing nuclear fuel. Thorium is a very effective radiation shield, although it has not been used for this purpose as much as lead or depleted uranium. Uranium-thorium age dating has been used to date hominid fossils. (S521)",,"Lungs and other internal organs can be penetrated by the alpha radiation produced by thorium. As a result, exposure to an aerosol of thorium can lead to increased risk of cancers of the lung, pancreas and blood. Exposure to thorium internally leads to increased risk of liver diseases. (S521)","Exposure to high doses of ionizing radiation can result in skin burns, hair loss, nausea, birth defects, illness, and death. (W510)","",DNA
109,T3D0108,2009-03-06 18:58:05 UTC,2009-08-25 15:54:56 UTC,Uranium-235,Inorganic Compound;Metal;Uranium Compound;Radioactive Isotope,"Uranium, isotope of mass 235Uranium-235","Uranium-235 is an isotope of uranium. Uranium is a chemical element that has the symbol U and atomic number 92. It is a normal part of rocks, soil, air, and water, and occurs in nature in the form of minerals. Natural uranium is a mixture of three radioactive isotopes called uranium-234, uranium-235, and uranium-238. Uranium-235 is used as a fuel for nuclear reactors and nuclear weapons. Uranium is also used as a colorant in uranium glass, producing orange-red to lemon yellow hues. (R465, R466)",,15117-96-1,61784,,"","","","",,,Uranium-235,,,,,InChI=1/U/i1-3,uranium-235,http://www.biospider.ca/saved_files/mol/,[235U],[235U],U,238.050780,Silver metallic solid.,"",,,"",,,,"Oral 
Inhalation 
Dermal 
Radiation 
(R466)","Serotransferrin (P02787) 
Serum albumin (P02768) 
Ceruloplasmin (P00450) 
Hemopexin (P02790) 
Complement C3 (P01024) 
Complement C4-A (P0C0L4) 
Complement C4-B (P0C0L5) 
(R465, R468)","Uranium is combined with either bicarbonate or a plasma protein in the blood but once in the kidney, it is released and forms complexes with phosphate ligands and proteins in the tubular wall, causing damage. Uranium may also inhibit both sodium transport-dependent and independent ATP utilization and mitochondrial oxidative phosphorylation in the renal proximal tubule. Uranium causes respiratory diseases by damaging alveolar epithelium type II cells in the lungs. Uranium induces c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (p38 MAPK) activation, which in turn induces tumor necrosis factor alpha (TNF-alpha) secretion and generates and inflammatory response in the lungs. Studies have shown that the more soluble the uranium salt, the more toxic it is. Ionizing radiation produced by uranium damages the DNA, resulting in gene mutations and chromosomal aberrations. This can both both initiate and promote carcinogenesis, and interfere with reproduction and development. (R466, R467)","Uranium is absorbed in low amounts via oral, inhalation, and dermal routes. Uranium in body fluids generally exists as the uranyl ion (UO2)2+ complexed with anions, such as citrate and bicarbonate, or plasma proteins. Uranium preferentially distributes to bone, liver, and kidney. The large majority of uranium that enters the body is not absorbed and is eliminated from the body via the urine and faeces. (R465)",,,,"Uranium-235 is used as a fuel for nuclear reactors and nuclear weapons. Uranium is also used as a colorant in uranium glass, producing orange-red to lemon yellow hues. (R465, R466)","Intermediate Inhalation: 0.0004 mg/m3 (Soluble salts) (R260)
Chronic Inhalation: 0.0003 mg/m3 (Soluble salts) (R260)
Intermediate Oral: 0.002 mg/kg/day (Soluble salts) (R260)
Intermediate Inhalation: 0.008 mg/m3 (Insoluble compounds) (R260)","Uranium primarily damages the kidney, but may also damage the lungs, central nervous system, and immune system. Uranium's radioactivity is believed to damage the DNA, resulting in carcinogenic effects and reproductive and developmental damage. (R465, R466)","Ingestion of uranium may cause vomiting and diarrhea. Exposure to high doses of ionizing radiation results in acute radiation syndrome, which can cause skin burns, hair loss, nausea, vomiting, dizziness, disorientation, low blood pressure, headache, fatigue, weakness, fever, birth defects, illness, infection, and death. (W510, W525, R465)","Treatment reversing the effects of irradiation is currently not possible. Anaesthetics and antiemetics are administered to counter the symptoms of exposure, as well as antibiotics for countering secondary infections due to the resulting immune system deficiency. (W525)",DNA
110,T3D0109,2009-03-06 18:58:05 UTC,2009-08-04 21:27:42 UTC,Barium,Inorganic Compound;Metal;Barium Compound,"Acb Pws 93%Anatrast Pst 55%BABANBARIUM, 99%Baricon for suspensionBarioBario [spanish]Barium Chloride Liquid (S#128)Barium [UN1400] [Dangerous when wet]Barium and compoundsBarium and soluble compoundsBarium atomic absorption standard solutionBarium nitrate solutionBarium standard for aasBarium standard for icBarium standard for icpBarium, soluble compoundsBarium, water-soluble compounds, n.o.sBarium, water-soluble compounds, n.o.s.Baro Bag Enema 98%Barocat Susp 1.5%Barosperse Disposable Enema Units 95%Barosperse for Susp 95%Baryta Carbonica 4ch-30chBaryta Carbonica Dps D3-C1000Baryta Carbonica Drops 5ch-9chBaryta Carbonica Liquid (S No. 40)Baryta carbonicaBaryta carbonica homaccordBaryta muriaticaBaryumBaryum Carbonicum-Injeel Forte Liq (6d,12d,30d,200d/1.1ml)Baryum [french]Baryum carbonicumCheetahE-Z-Cat Liq 4.6%E-Z-Paque Powder for Suspension 95%E-z-HDEnhancerEnterovu liquidEntrobar Suspension 50%EntroeaseEsobarEsopho-Cat Crm 3%Flo-Coat Susp 100%Hd 85 Barium Sulfate Susp 51%Intropaste - Pst Orl 44%W/WLiqui-Coat Hd - Sus Orl 210%W/V 81%W/WLiquid Barosperse- Sus Orl Rt 60%W/V 40%W/WMedebar Plus - Sus Orl Rt 56%W/W 100%W/VPekana - baryta carbonicaPolibar Liq 55%Polibar Rapid 57% (P/P)Polibar plusPrepcat 1.5%Readi-Cat 2.0% W/WReadi-Cat Liq 1.2%Recto-bariumTomo Cat Barium Sulfate Susp 5%UNLUltra-rUnibar 100 Sus 100%barium(0)","Barium is a metallic alkaline earth metal with the symbol Ba, and atomic number 56. It never occurs in nature in its pure form due to its reactivity with air, but combines with other chemicals such as sulfur or carbon and oxygen to form barium compounds found as minerals such as barium sulfate and barium carbonate. Barium compounds are used by the oil and gas industries to make drilling muds, and can also be used in the production of paint, bricks, ceramics, glass, and rubber. They are also often used in pyrotechnics, as they emit a green light when burned. (R407, 408)",,7440-39-3,5355457,,C13881,"",32595,CPD0-1592,,D001464,Barium,6373,,,http://en.wikipedia.org/wiki/Barium,InChI=1/Ba/q+2,barium,http://www.biospider.ca/saved_files/mol/b07389da7f8dc69da4c35117bc654699_1237945734.mol,[Ba++],[Ba++],[Ba]2+,137.905243,Silvery white metal.,710 °C,,,"",,,,"Oral 
Inhalation 
(R407)",,"Barium is a competitive potassium channel antagonist that blocks the passive efflux of intracellular potassium, resulting in a shift of potassium from extracellular to intracellular compartments. The intracellular translocation of potassium results in a decreased resting membrane potential, making the muscle fibers electrically unexcitable and causing paralysis. (R407)","Barium compounds are absorbed via ingestion and inhalation. Barium is principally found in the bone, while small amounts exists in the muscle, adipose tissue, skin, and connective tissue. Barium is not metabolized, but may be transported and incorporated into complexes or tissues. Barium is excreted in the urine and faeces. (R407)",,1 to 15 grams for an adult human (barium salts). (R321),,"Barium compounds are used by the oil and gas industries to make drilling muds, and can also be used in the production of paint, bricks, ceramics, glass, and rubber. They are also often used in pyrotechnics, as they emit a green light when burned. (R407, R408)","Intermediate Oral: 0.2 mg/kg/day (Barium salts) (R260)
Chronic Oral: 0.2 mg/kg/day (Barium salts) (R260)","The health effects of the different barium compounds depend on how well the compound dissolves in water or the stomach contents. At low doses, barium acts as a muscle stimulant, while higher doses affect the nervous system, causing cardiac irregularities, tremors, weakness, anxiety, dyspnea, paralysisand possibly death. Barium may also cause gastrointestinal disturbances, damage the kidneys and cause decreases in body weight. (R407)","Ingesting excess barium may cause vomiting, abdominal cramps, diarrhea, difficulties in breathing, increased or decreased blood pressure, numbness around the face, and muscle weakness. High levels may result in changes in heart rhythm or paralysis and possibly death. (R407)",Intravenous infusion of potassium often relieves many of the symptoms of barium toxicity. (R407),P62158;O60928;Q9NPI9;P63252;P48050;P48549;P48051;Q92806;P48544;P48048;P78508;Q14654;Q14500;Q9UNX9;Q99712;Q15842;P51787;O43526;O43525;P56696;Q9NR82
111,T3D0110,2009-03-06 18:58:06 UTC,2009-08-04 21:27:42 UTC,Fluoranthene,Organic Compound;Industrial By-product/Pollutant;Aromatic Hydrocarbon;Polycyclic Aromatic Hydrocarbon,"1,2-(1, 8-Naphthylene)benzene1,2-(1,8-Naphthalene)benzene1,2-(1,8-Naphthalenediyl)benzene1,2-(1,8-Naphthylene)benzene1,2-BenzacenaphtheneBCR160R_FLUKABenzacenaphthyleneBenzene, 1,2-(1, 8-naphthylene)-Benzene, 1,2-(1,8-naphthalenediyl)-Benzene, 1,2-(1,8-naphthylene)-Benzo(JK)fluoreneBenzo[JK]fluoreneBenzo[JK]fluorene, idrylBenzo[j,k]fluoreneF807_ALDRICHFAFLAFluoranthene solutionFluoranthreneFluroantheneIdrylRCRA waste no. U120Rcra waste number U120WLN: L C6566 1A PJfluoranthene (ACD/Name 4.0){benzo[JK]fluorene}","Fluoranthene is one of over 100 different polycyclic aromatic hydrocarbons (PAHs). PAHs are are formed during the incomplete burning of organic substances, such as fossil fuels. They are usually found as a mixture containing two or more of these compounds. (R028)",,206-44-0,9154,,"","",33083,"",,C007738,Fluoranthene,6445,,,http://en.wikipedia.org/wiki/Fluoranthene,InChI=1/C16H10/c1-2-8-13-12(7-1)14-9-3-5-11-6-4-10-15(13)16(11)14/h1-10H,fluoranthene,http://www.biospider.ca/saved_files/mol/,C1=CC=C2C(=C1)C3=CC=CC4=C3C2=CC=C4,C1=CC=C2C(=C1)C3=CC=CC4=C3C2=CC=C4,C16H10,202.078250,Pale yellow solid.,107.8 °C,"","","0.00026 mg/mL at 25 °C [MACKAY,D & SHIU,WY (1977)]","","","",Oral Inhalation (R028),Serum albumin (P02768) Cytochrome P450 1A1 (P04798) Cytochrome P450 1A2 (P05177) Cytochrome P450 1B1 (Q16678) (R060),"The ability of PAH's to bind to blood proteins such as albumin allows them to be transported throughout the body. Many PAH's induce the expression of cytochrome P450 enzymes, especially CYP1A1, CYP1A2, and CYP1B1, by binding to the aryl hydrocarbon receptor or glycine N-methyltransferase protein. These enzymes metabolize PAH's into their toxic intermediates. The reactive metabolites of PAHs (epoxide intermediates, dihydrodiols, phenols, quinones, and their various combinations) covalently bind to DNA and other cellular macromolecules, initiating mutagenesis and carcinogenesis. (R028, R060, R068, R073)","PAH metabolism occurs in all tissues, usually by cytochrome P-450 and its associated enzymes. PAHs are metabolized into reactive intermediates, which include epoxide intermediates, dihydrodiols, phenols, quinones, and their various combinations. The phenols, quinones, and dihydrodiols can all be conjugated to glucuronides and sulfate esters; the quinones also form glutathione conjugates. (R028)","LD50: 2000 mg/kg (Oral, Rat) (R372)
LD50: 100 mg/kg (Intravenous, Mouse) (R372) 
LD50: 3180 mg/kg (Dermal, Rabbit) (R372)","","3, not classifiable as to its carcinogenicity to humans. (R264)","PAHs are released into the environment via the combustion of fossil fuels, coke oven emissions and vehicle exhausts, as well as naturally from forest fires and volcanic eruptions. PAHs from these sources may contaminate nearly water systems. They are also found in coal tar and charbroiled food. (R028)","","PAHs are carcinogens and have been associated with the increased risk of skin, respiratory tract, bladder, stomach, and kidney cancers. They may also cause reproductive effects and depress the immune system. (R028)","Acute exposure to PAHs causes irritation and inflammation of the skin and lung tissue. (R034)
",There is no known antidote for PAHs. Exposure is usually handled with symptomatic treatment. (R028),P35869;Q14749;DNA
112,T3D0111,2009-03-06 18:58:06 UTC,2009-08-25 19:49:53 UTC,Uranium-234,Inorganic Compound;Metal;Uranium Compound;Radioactive Isotope,"Uranium, isotope of mass 234Uranium-234","Uranium-234 is an isotope of uranium. Uranium is a chemical element that has the symbol U and atomic number 92. It is a normal part of rocks, soil, air, and water, and occurs in nature in the form of minerals. Natural uranium is a mixture of three radioactive isotopes called uranium-234, uranium-235, and uranium-238. Uranium is also used as a colorant in uranium glass, producing orange-red to lemon yellow hues. (R465, R466)",,13966-29-5,61704,,"","","","",,,Uranium-234,,,,,InChI=1/U/i1-4,uranium-234,http://www.biospider.ca/saved_files/mol/,[234U],[234U],U,238.050780,Silver metallic solid.,"",,,"",,,,"Oral 
Inhalation 
Dermal 
Radiation 
(R466)","Serotransferrin (P02787) 
Serum albumin (P02768) 
Ceruloplasmin (P00450) 
Hemopexin (P02790) 
Complement C3 (P01024) 
Complement C4-A (P0C0L4) 
Complement C4-B (P0C0L5) 
(R465, R468)","Uranium is combined with either bicarbonate or a plasma protein in the blood but once in the kidney, it is released and forms complexes with phosphate ligands and proteins in the tubular wall, causing damage. Uranium may also inhibit both sodium transport-dependent and independent ATP utilization and mitochondrial oxidative phosphorylation in the renal proximal tubule. Uranium causes respiratory diseases by damaging alveolar epithelium type II cells in the lungs. Uranium induces c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (p38 MAPK) activation, which in turn induces tumor necrosis factor alpha (TNF-alpha) secretion and generates and inflammatory response in the lungs. Studies have shown that the more soluble the uranium salt, the more toxic it is. Ionizing radiation produced by uranium damages the DNA, resulting in gene mutations and chromosomal aberrations. This can both both initiate and promote carcinogenesis, and interfere with reproduction and development. (R466, R467)","Uranium is absorbed in low amounts via oral, inhalation, and dermal routes. Uranium in body fluids generally exists as the uranyl ion (UO2)2+ complexed with anions, such as citrate and bicarbonate, or plasma proteins. Uranium preferentially distributes to bone, liver, and kidney. The large majority of uranium that enters the body is not absorbed and is eliminated from the body via the urine and faeces. (R465)",,,,"Uranium is also used as a colorant in uranium glass, producing orange-red to lemon yellow hues. (R465, R466)","Intermediate Inhalation: 0.0004 mg/m3 (Soluble salts) (R260)
Chronic Inhalation: 0.0003 mg/m3 (Soluble salts) (R260)
Intermediate Oral: 0.002 mg/kg/day (Soluble salts) (R260)
Intermediate Inhalation: 0.008 mg/m3 (Insoluble compounds) (R260)","Uranium primarily damages the kidney, but may also damage the lungs, central nervous system, and immune system. Uranium's radioactivity is believed to damage the DNA, resulting in carcinogenic effects and reproductive and developmental damage. (R465, R466)","Ingestion of uranium may cause vomiting and diarrhea. Exposure to high doses of ionizing radiation results in acute radiation syndrome, which can cause skin burns, hair loss, nausea, vomiting, dizziness, disorientation, low blood pressure, headache, fatigue, weakness, fever, birth defects, illness, infection, and death. (W510, W525, R465)","Treatment reversing the effects of irradiation is currently not possible. Anaesthetics and antiemetics are administered to counter the symptoms of exposure, as well as antibiotics for countering secondary infections due to the resulting immune system deficiency. (W525)",DNA
113,T3D0112,2009-03-06 18:58:06 UTC,2009-08-04 21:27:43 UTC,n-Nitrosodi-n-propylamine,Organic Compound;Industrial By-product/Pollutant;Amine;Nitrite,"2-Oxo-1,1-dipropylhydrazine2-oxo-1,1-dipropylhydrazine (ACD/Name 4.0)DPNDPNADi-n-propylnitrosamineDi-n-propylnitrosoamineDipropylamine, n-nitroso-DipropylnitrosamineN,n-di-n-propylnitrosamineN,n-dipropylnitrosamineN-Nitroso-N -propyl-1-propanamineN-Nitroso-N-propyl-1-propanamineN-nitroso di-n-propylamineN-nitroso(di-n-propyl)amineN-nitroso-N-propylpropan-1-amineN-nitroso-n-dipropylamineN-nitrosodi-n-propylamineN-nitrosodipropylamineNDPANitrosodipropylamineNitrous dipropylamidePropanamine, n-nitroso-n-propyl-Propylamine, n-nitroso-n-di-RCRA waste no. U111Rcra waste number U111WLN: ONN3&3","n-Nitrosodi-n-propylamine is a chemical produced by industry in small amounts for research. Small amounts of n-nitrosodi-n-propylamine are also produced as a side reaction during some manufacturing processes, as a contaminant in some weed killers, and during the manufacture of some rubber products. (R420) ",,621-64-7,12130,,"","","",CPD-630,,C013161,n-Nitrosodi-n-propylamine,1053,,,,"InChI=1/C6H14N2O/c1-3-5-8(7-9)6-4-2/h3-6H2,1-2H3","N,N-dipropylnitrous amide",http://www.biospider.ca/saved_files/mol/,CCCN(CCC)N=O,CCCN(CCC)N=O,C6H14N2O,130.110610,Yellow liquid.,Boiling Pt : 206 oC,206 °C,,"13 mg/mL at 24 °C [MIRVISH,SS et al.(1976)]",,,,"Oral
Inhalation
Dermal
(R420)",Cytochrome P450 2E1 (P05181) (R421),"Reactive metabolites of n-nitrosodi-n-propylamine are believed to form adducts with DNA, resulting in carcinogenic effects. (R420)","n-Nitrosodi-n-propylamine can be absorbed through oral, inhalation, or dermal routes. It is metabolized by cytochrome p-450 enzymes (mainly CYP 2E1) into its reactive metabolites via oxidation at the alpha, beta and gamma carbon positions. Alpha carbon oxidation is regarded as the primary pathway, resulting in formation of propionaldehyde, 1-propanol, and 2-propanol. The metabolites of n-nitrosodi-n-propylamine are excreted mainly in the urine. (R420, R421)","LD50: 480 mg/kg (Oral, Rat) (R373)
LD50: 487 mg/kg (Subcutaneous, Rat) (R373)",,"2B, possibly carcinogenic to humans. (R264)","Small amounts of n-nitrosodi-n-propylamine are also produced as a side reaction during some manufacturing processes, as a contaminant in some weed killers, and during the manufacture of some rubber products. (R420)",Acute Oral: 0.095 mg/kg/day (R260),"High levels of n-nitrosodi-n-propylamine may damage the liver, lung, stomach, kidneys, and heart. n-Nitrosodi-n-propylamine is also a likely carcinogen. (R420)",,"",DNA
114,T3D0113,2009-03-06 18:58:06 UTC,2009-08-25 19:49:29 UTC,Thorium-228,Inorganic Compound;Metal;Thorium Compound;Radioactive Isotope,"Thorium, isotope of mass 228Thorium-228","Thorium is the chemical element of symbol Th and atomic number 90. It is a naturally occurring radioactive metal of the actinide series. In the environment, thorium exists in combination with other minerals, such as silica. Small amounts of thorium are present in all rocks, soil, water, plants, and animals. Twenty-seven radioactive isotopes of thorium, with mass number from 210 to 236, have been characterized. Naturally occurring thorium is composed mainly of one isotope: 232Th. The most abundant and/or stable isotopes are: 232Th (half-life of 14.05 billion years), 230Th (half-life of 75,380 years), 229Th (half-life of 7340 years), and 228Th (half-life of 1.92 years). Thorium is used to make ceramics, gas lantern mantles, and metals used in the aerospace industry and in nuclear reactions. Thorium can also be used as a fuel for generating nuclear energy. Thorium has been linked to increased risk of liver cancer. (S521, W511)",,14274-82-9,61724,,"","","","",,,Thorium-228,,,,http://en.wikipedia.org/wiki/Thorium-228,InChI=1/Th/i1-4,thorium-228,http://www.biospider.ca/saved_files/mol/,[228Th],[228Th],Th,232.038050,,"",,,"",,,,"Oral
Inhalation
Dermal
(W511)","Serotransferrin (P02787)
(W511)","The ionizing radiation produced by thorium causes cellular damage that includes DNA breakage, accurate or inaccurate repair, apoptosis, gene mutations, chromosomal change, and genetic instability. This leads to loss of normal cell and tissue homeostasis, and development of malignancy. Ionizing radiation that does not directly damage DNA can produce reactive oxygen intermediates that directly affect the stability of p53, an important enzyme in cell-cycle regulation, and produce oxidative damage to individual bases in DNA and point mutations by mispairing during DNA replication. (W510)","Exposure to thorium can occur following inhalation, ingestion, or dermal exposure. Once in the body thorium accumulates mainly in the liver, spleen, lymph nodes, lungs, and bone. Transferrin plays a major role in the transport and cellular uptake of thorium. Thorium may combine with oxygen to form thorotrast (thorium dioxide), a colloid which may affect protein uptake. Thorium and thorotrast are excreted mainly in the faeces. (W511)",,,"1, carcinogenic to humans. (R264)","Thorium can also be used as a fuel for generating nuclear energy. Thorium is used as an alloying element in magnesium, used in aircraft engines, imparting high strength and creep resistance at elevated temperatures. Thorium is also used as an alloying agent in gas tungsten arc welding (GTAW) to increase the melting temperature of tungsten electrodes and improve arc stability. Thorium is used to coat tungsten wire used in electronic equipment, improving the electron emission of heated cathodes. Thorium is used as a fertile material for producing nuclear fuel. Thorium is a very effective radiation shield, although it has not been used for this purpose as much as lead or depleted uranium. Uranium-thorium age dating has been used to date hominid fossils. (S521)",,"Lungs and other internal organs can be penetrated by the alpha radiation produced by thorium. As a result, exposure to an aerosol of thorium can lead to increased risk of cancers of the lung, pancreas and blood. Exposure to thorium internally leads to increased risk of liver diseases. (S521)","Exposure to high doses of ionizing radiation results in acute radiation syndrome, which can cause skin burns, hair loss, nausea, vomiting, dizziness, disorientation, low blood pressure, headache, fatigue, weakness, fever, birth defects, illness, infection, and death. (W510, W525)","Treatment reversing the effects of irradiation is currently not possible. Anaesthetics and antiemetics are administered to counter the symptoms of exposure, as well as antibiotics for countering secondary infections due to the resulting immune system deficiency. (W525)",DNA
115,T3D0114,2009-03-06 18:58:06 UTC,2009-08-25 19:48:49 UTC,Radon-222,Inorganic Compound;Metal;Radium Compound;Radioactive Isotope,"radon, isotope of mass 222radon-222","Radon is the chemical element of symbol Rn and atomic number 86. It is a rare radioactive gas, belonging to the noble gas series, and is formed as part of three radioactive decay chains that begin with uranium or thorium. Thirty-six radioactive isotopes of radon, with mass number from 193 to 228, have been characterized. The most stable isotope is Radon-222 (half-life of 3.8 days); it is generated naturally by the decay of 238U and emits alpha particles. Because of its radioactivity and unreactivity as a chemical element, radon has few uses and is seldom used in academic research. Radon is responsible for the majority of the mean public exposure to ionizing radiations. (S494)",,14859-67-7,61773,,C16454,"",33492,"",,,Radon-222,6527,,,,InChI=1/Rn/i1+0,radon-222,http://www.biospider.ca/saved_files/mol/2159a50dd2f21aa3ad551dfcbfa3d6b7_1237946219.mol,[222Rn],[222Rn],Rn,0.000000,,"",,,"",,,,"Oral
Inhalation
Dermal
(W509)",,"The ionizing radiation produced by radon causes cellular damage that includes DNA breakage, accurate or inaccurate repair, apoptosis, gene mutations, chromosomal change, and genetic instability. This leads to loss of normal cell and tissue homeostasis, and development of malignancy. Ionizing radiation that does not directly damage DNA can produce reactive oxygen intermediates that directly affect the stability of p53, an important enzyme in cell-cycle regulation, and produce oxidative damage to individual bases in DNA and point mutations by mispairing during DNA replication. (W509)","Exposure to radon can occur from inhalation or dermal contact. It can also enter the body via ingestion if dissolved in water. Radon distributes mainly to the fat. It is not metabolized and may be eliminated in the urine, faeces, or expired air. (W509)",,,"1, carcinogenic to humans. (R264)","Radon has few uses and is seldom used in academic research. Radon gas from natural sources can accumulate in buildings, especially in confined areas such as basements. Radon can be found in some spring waters and hot springs. (S494)",,"Radon is responsible for the majority of the mean public exposure to ionizing radiations. Due to it's radioactivity, breathing high concentrations of radon can cause lung cancer. According to the United States Environmental Protection Agency, radon could be the second most frequent cause of lung cancer, after cigarette smoking; and radon-induced lung cancer the 6th leading cause of cancer death overall, causing 21,000 lung cancer deaths per year in the United States. (S494)","Exposure to high doses of ionizing radiation results in acute radiation syndrome, which can cause skin burns, hair loss, nausea, vomiting, dizziness, disorientation, low blood pressure, headache, fatigue, weakness, fever, birth defects, illness, infection, and death. (W510, W525)","Treatment reversing the effects of irradiation is currently not possible. Anaesthetics and antiemetics are administered to counter the symptoms of exposure, as well as antibiotics for countering secondary infections due to the resulting immune system deficiency. (W525)",DNA
116,T3D0115,2009-03-06 18:58:06 UTC,2009-08-04 21:27:43 UTC,"Hexachlorocyclohexane, alpha-",Organic Compound;Pesticide;Organochloride,"&alpha;-1,2,3,4,5,6-Hexachlorcyclohexane&alpha;-1,2,3,4,5,6-Hexachlorocyclohexane&alpha;-BHC&alpha;-HCH&alpha;-benzene hexachloride&alpha;-hexachloran&alpha;-hexachlorane&alpha;-hexachlorcyclohexane&alpha;-hexachlorocyclohexane(1R,2R,3R,4R,5S,6S)-1,2,3,4,5,6-hexachlorocyclohexane(1R,2R,3S,4S,5S,6S)-1,2,3,4,5,6-hexachlorocyclohexane(1r,2R,3S,4r,5R,6S)-1,2,3,4,5,6-hexachlorocyclohexane(1r,2R,3S,4s,5R,6S)-1,2,3,4,5,6-hexachlorocyclohexane(1r,2c,3c,4t,5c,6t)-1,2,3,4,5,6-hexachlorocyclohexane(1r,2c,3t,4t,5c,6t)-1,2,3,4,5,6-hexachlorocyclohexane(1r,2r,3r,4r,5r,6r)-1,2,3,4,5,6-hexachlorocyclohexane(1s,2R,3R,4s,5S,6S)-1,2,3,4,5,6-hexachlorocyclohexane1,2,3,4,5,6-Hexachlorocyclohexane1,2,3,4,5,6-Hexachlorocyclohexane (all stereo isomers)1,2,3,4,5,6-Hexachlorocyclohexane (mixture of isomers)1,2,3,4,5,6-Hexachlorocyclohexane gamma isomer1,2,3,4,5,6-Hexachlorocyclohexane, gamma-isomer1,2,3,4,5,6-hexachlorocyclohexane (ACD/Name 4.0)1,2,3,4,5,6-hexachlorocyclohexane, alpha isomer1a,2a,3b,4a,5b,6b-hexachlorocyclohexane1a,2b,3a,4b,5a,6b-hexachlorocyclohexaneAalindanAficideAgrocideAgrocide IIIAgrocide WPAgronexitAlpha- BHCAlpha-BHCAlpha-HCHAlpha-HCH [hexachlorocyclohexanes]Alpha-HCH solutionAlpha-benzene hexachlorideAlpha-benzenehexachlorideAlpha-hexachloranAlpha-hexachloraneAlpha-hexachlorocyclohexaneAlpha-hexachlorocyclohexanesAlpha-lindaneAm eisenatodAmeisenatodAmeisenmittel merckAmeisentodAparasinAphtiriaAphtitriaAplidalArbitexArcotal sBBHBCHBHCBHC &alpha;BHC (alpha-, beta-, gamma-)BHC (insecticide)BHC insecticideBHC or HCHBHC-&alpha; isomerBen-hexBenhexachlorBenhexolBenzanexBenzene hexachlorideBenzene hexachloride (ambiguous)Benzene hexachloride, all isomersBenzene hexachloride-&alpha;-isomerBenzene hexachloride-alpha-isomerBenzene hexachloride-gamma isomerBenzene hexachloride-gamma-isomerBenzene-1,2,3,4,5,6-hexachloride ((Ambiguous)Benzene-cis-hexachlorideBenzene-trans-hexachlorideBenzenehexachloride, mixed isomersBenzenehexachloride-alpha-isomerBenzexBeta-BHCBeta-HCHBeta-HCH [hexachlorocyclohexanes]Beta-HCH solutionBeta-benzene hexachlorideBeta-hexac hlorocyclohexaneBeta-hexachloranBeta-hexachlorobenzeneBeta-hexachlorocyclohexaneBeta-hexachlorocyclohexanesBeta-isomerBeta-lindaneBexolBorer sprayCPD with unspecified stereochemistryCaswell No. 079Caswell No. 527CelanexChinoin brand of lindaneChloreseneCodechineCyclohexane, &alpha;-1,2,3,4,5,6-hexachloro-Cyclohexane, 1,2,3,4,5,6-hexachloro-Cyclohexane, 1,2,3,4,5,6-hexachloro-, &alpha;-Cyclohexane, 1,2,3,4,5,6-hexachloro-, &alpha;-isomerCyclohexane, 1,2,3,4,5,6-hexachloro-, (mixed isomers)Cyclohexane, 1,2,3,4,5,6-hexachloro-, alpha-Cyclohexane, 1,2,3,4,5,6-hexachloro-, alpha-isomerCyclohexane, 1,2,3,4,5,6-hexachloro-, beta-isomerCyclohexane, 1,2,3,4,5,6-hexachloro-, delta-Cyclohexane, 1,2,3,4,5,6-hexachloro-, delta-isomerCyclohexane, 1,2,3,4,5,6-hexachloro-, gamma-Cyclohexane, 1,2,3,4,5,6-hexachloro-, gamma-isomerCyclohexane, beta-1,2,3,4,5,6-hexachloro-Cyclohexane, delta-1,2,3,4,5,6-hexachloro-DBHDelitexDelta-BHCDelta-HCHDelta-benzene hexachlorideDelta-benzenehexachlorideDelta-hexachlorocyclohexaneDelta-lindaneDetmol extractDetmol-extraktDevoranDol granuleDolmixDrill tox-spezial aglukonDrilltox-spezial aglukonEntomoxanEpsilon HCHEpsilon-HCHEpsilon-benzenehexachlorideEpsilon-hexachlorocyclohexaneEso dermEsodermExagamaFenoform forteForlinForst-nexenGallogamaGamacarbatoxGamacidGamacideGamacide 20GamaphexGameneGamisoGamma 666Gamma BHCGamma benzene hexachlorideGamma hexachlorGamma hexachlorocyclohexaneGamma-666Gamma-:hexachlorocyclohexaneGamma-BHCGamma-BHC (lindane)Gamma-BHC benhexachlorGamma-HCHGamma-HCH [hexachlorocyclohexanes]Gamma-HCH or gamma-BHCGamma-benzene hexachlorideGamma-benzenehexachlorideGamma-benzohexachlorideGamma-colGamma-hexachloraneGamma-hexachlorcyclohexanumGamma-hexachlorobenzeneGamma-hexachlorocyclohexaneGamma-linda neGamma-lindaneGamma-mean 400Gamma666GammahexaGammahexaneGammalinGammaterrGammexGammexaneGammopazGamtoxGeobilanGexaneGybenH.c.hHCCHCCHHCHHCH (alpha)HCH (beta)HCH [bsi]HCH [iso]HCH, technical grade [hexachlorocyclohexanes]HCH-&alpha;HEXAHGIHeclotoxHecoltoxHexablancHexachlorHexachloranHexachloraneHexachlorcyclohexanHexachlorcyclohexan [german]Hexachloride, benzeneHexachloride, gamma-benzeneHexachlorocyclohexaneHexachlorocyclohexane (all isomers)Hexachlorocyclohexane (mixed isomers)Hexachlorocyclohexane (mixture)Hexachlorocyclohexane (technical grade)Hexachlorocyclohexane, alpha-Hexachlorocyclohexane, beta-Hexachlorocyclohexane, delta-Hexachlorocyclohexane, gamma isomerHexachlorocyclohexane, gamma-Hexachlorocyclohexane, gamma-isomerHexachlorocyclohexane, technicalHexachlorocyclohexane, technical gradeHexachlorocyclohexane-alphaHexachlorocyclohexane-betaHexachlorocyclohexanesHexachlorzyklohexanHexamulHexapoudreHexatoxHexavermHexcidumHexicideHexit Shampoo 1.0%Hexit lotionHexyclanHilbeec hHilbeechHortexInexitInfectopharm brand of lindaneInsecticide, BHCIsatoxIsot oxIsotoxJacutinKokotineKwellKwell-rLacco hi linLasochronLatka 666 [Czech]LendineLentoxLidenalLindaforLindagamLindagrainLindagranoxLindaloLindam ulLindamulLindane (benzene hexachloroide-gamma isomer)Lindane (gamma-HCH)Lindane [hexachlorocyclohexanes]Lindane [usan:inn:ban]Lindano [inn-spanish]Lindanum [inn-latin]LindapoudreLindaterraLindatoxLindexLindosepLintoxLinvurLorexaneMglawik lMixture nameMszycolNeo-scabicidolNexen FBNexen-FBNexi t-starkNexitNexit-starkNexol-eNicochloranNovigamNoviganOmnitoxOvadziakOwadziakPLKPMS lindanePMS-lindanePS71_SUPELCOPedraczakPflanzolPharmascience brand of lindanePms-Lindane Lot 1%Pms-Lindane Shp 1%PmslindaneQuelladaRCRA waste no. U129RCRA waste number U129Sang gammaScabecidScabeneScabisanSilvanolSpritz-rapidinSpritzlindaneSpruehpflanzolStiefel brand of lindaneStreunexSubmarT-HCHTBHTechnical HCHTechnical hexachlorocyclohexaneTetocidTrans-alpha-benzenehexachlorideTri-6Trives-tVerindal ultraVitonagrisol g-20agrocide 2agrocide 6gagrocide 7alpha-1,2,3,4,5,6-Hexachlorocyclohexanebentox 10beta-1,2,3,4,5,6-Hexachlorocyclohexanedelta-(Aeeeee)-1,2,3,4,5,6-hexachlorocyclohexanedelta-1,2,3,4,5,6-Hexachlorocyclohexanedetox 25gamma-1,2,3,4,5,6-Hexachlorocyclohexanegammalin 20geolin g 3hungaria l7milbol 49","Hexachlorocyclohexane, Alpha- is one of eight isoforms of the commercially manufactured chemical hexachlorocyclohexane. It is used as an insecticide on fruit, vegetables, and forest crops and is also available as a prescription (lotion, cream, or shampoo) to treat head and body lice, and scabies. (R186)",,319-84-6,727,,C15214,"",32888,GAMMA-HCH,,C040534,"Hexachlorocyclohexane, alpha-",693,,,http://en.wikipedia.org/wiki/Lindane,"InChI=1/C6H6Cl6/c7-1-2(8)4(10)6(12)5(11)3(1)9/h1-6H/t1-,2-,3-,4-,5+,6+/m0/s1","1,2,3,4,5,6-hexachlorocyclohexane",http://www.biospider.ca/saved_files/mol/57830bd6718f9d331d3e1525f91378f5_1237946309.mol,C1(C(C(C(C(C1Cl)Cl)Cl)Cl)Cl)Cl,C1(C(C(C(C(C1Cl)Cl)Cl)Cl)Cl)Cl,C6H6Cl6,287.860070,White solid or colorless vapor.,159.5 °C,"","","0.002 mg/mL at 25 °C [WEIL,L et al. (1974)]","","","",Oral Inhalation Dermal (R186),Cytochrome P450 2E1 (P05181) Cytochrome P450 1A1 (P04798) Cytochrome P450 1A2 (P05177) (R186),"Hexachlorocyclohexane is a neurotoxin that interferes with GABA neurotransmitter function by interacting with the GABA-A receptor-chloride channel complex at the picrotoxin binding site, causing over stimulation of the central nervous system. It is also believed to inhibit sodium/potassium-transporting ATPases and to be an endocrine disruptor. In the liver, hexachlorocyclohexane is thought to cause oxidative stress by interfering with hepatic oxidative capacity and glutathione metabolism, increasing lipid metabolism, and inhibiting magnesium ATPase activity. Hexachlorocyclohexane may also inhibit gap junction and intercellular communication, leading to uncontrolled cell growth and tumor promotion. (R186, R187, R188)","Hexachlorocyclohexane is absorbed through the skin, lungs, and intestines, then distributed mainly to the adipose tissue but also to the brain, kidney, muscle, and blood. Metabolism occurs via dechlorination, dehydrogenation, dehydrochlorination, and hydroxylation by hepatic cytochrome P-450 enzymes. The main metabolites are polychlorophenols and 1,2,4-trichlorocyclohexane-4,5-epoxide, which are excreted in the urine. (R186)","LD50: 177 mg/kg (Oral, Rat) (R261)","","2B, possibly carcinogenic to humans. (R264)","Hexachlorocyclohexane is used as an insecticide on fruit, vegetables, and forest crops and is also available as a prescription (lotion, cream, or shampoo) to treat head and body lice, and scabies. (R186)",Chronic Oral: 0.008 mg/kg/day (R260),"Exposure to large amounts of hexachlorocyclohexane can harm the nervous system, producing a range of symptoms from headache and dizziness to seizures, convulsions and more rarely death. Hexachlorocyclohexane is known to damage the liver, kidneys, and immune system, as well as cause blood disorders and reproductive and developmental defects. Hexachlorocyclohexane is also potentially carcinogenic. (R186, R187)","Exposure to large amounts of hexachlorocyclohexane can harm the nervous system, producing a range of symptoms from headache and dizziness to seizures, convulsions and more rarely death. (R187)","Hexachlorocyclohexane poisoning is treated symptomatically. Gastric lavage, followed by the administration of activated charcoal, may be performed upon ingestion. (R284)",P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P18507;Q99928;O00591;P24046;P28476;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P54710;P62508;P10275;P06401;Q8N1C3;A8MPY1;Q9UN88;P78334;P98194;O75185;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;P03372;Q92731
117,T3D0116,2009-03-06 18:58:06 UTC,2009-08-04 21:27:44 UTC,"1,2,3-Trichlorobenzene",Organic Compound;Solvent;Aromatic Hydrocarbon;Organochloride,"*chlorobenzens1,2, 3-Trichlorobenzene1,2,3-Trichlorbenzol1,2,3-Trichlorobenzene1,2,3-trichlorobenzene (ACD/Name 4.0)1,2,6-TrichlorobenzeneBenzene, trichloro-Invalon TCPyranol 1478TCBTrichlorbenzeneTrichlorobencenos [spanish]TrichlorobenzeneTrichlorobenzenesVic-trichlorobenzene","1,2,3-Trichlorobenzene is an organochloride aromatic compound and one of the three isomeric forms of trichlorobenzene. Trichlorobenzene is used as a solvent. (R428)",,87-61-6,6895,,C14408,"",35289,CPD-1125,,,"1,2,3-Trichlorobenzene",3345,,,,InChI=1/C6H3Cl3/c7-4-2-1-3-5(8)6(4)9/h1-3H,"1,2,3-trichlorobenzene",http://www.biospider.ca/saved_files/mol/d7bbe866a002c36c4896850c4be05ac0_1237946497.mol,C1=CC(=C(C(=C1)Cl)Cl)Cl,C1=CC(=C(C(=C1)Cl)Cl)Cl,C6H3Cl3,179.930030,White crystals.,53.5 °C,,,"0.018 mg/mL at 25 °C [CHIOU,CT et al. (1986)]",,,,Oral Inhalation Dermal (R430),,"Trichlorobenzene may uncouple mitochondrial oxidative phosphorylation, inducing potassium ion release and inhibiting respiratory control. It's metabolites may covalently bind to cellular proteins and alkylate DNA. (R432, R433)","Trichlorobenzene is absorbed via oral, inhalation, and dermal routes. It is believed to be metabolized via cytochrome p-450 enzymes into metabolites that include phenols, mercapturic acid, and catechols.(R430)","LD50: 756 mg/kg (Oral, Rat) (R285)",,,"Trichlorobenzene is used as a solvent in chemical manufacturing, as well as in dyes, dielectric fluid, synthetic transformer oils, lubricants, heat-transfer medium, and insecticides. (R431)",,"High levels of trichlorobenzene may damage the liver, kidney, and thyroid. (R429)",Trichlorobenzene irritates the eyes and respiratory tract. (R285),"",P98194;O75185;P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P78334;Q8N1C3;P18507;Q99928;O00591;P24046;P28476;A8MPY1;Q9UN88;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;P54710;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P03372;Q92731
118,T3D0117,2009-03-06 18:58:06 UTC,2009-08-04 21:27:44 UTC,Manganese,Inorganic Compound;Metal;Manganese Compound,"ASTM A601Chelazome Manganese Cap 15mgColloidal manganeseCutavalDienolMANGANESE, 99.5%MNMN(II)MN(III)MNNMagnacatManganMangan [polish]Mangan nitridovanyMangan nitridovany [czech]Manganese Acetate Liquid (S#147)Manganese Amino Acid Chelate Tab 15mgManganese Amino Acid Chelate Tab 5mgManganese Chelated 25mgManganese Oligosol Liq 0.59mg/2mlManganese Tab 25mgManganese and inorganic compoundsManganese chloride in plastic containerManganese compoundsManganese compounds and fumes (as MN)Manganese fumeManganese metal alloyManganese, elementalManganesoManganumManganum Aceticum-Injeel Forte Liq (6d,12d,30d,200d/1.1ml)Manganum Met 4ch-30chManganum aceticumManganum carbonicumManganum metallicumManganum muriaticumManganum sulfuricumManganum sulphuricumMicro MNOligostim manganeseTripart liquid manganeseTronamangTronamang electrolytic manganese metalmanganese(0)","Manganese is a naturally occurring metal with the symbol Mn and the atomic number 25. It does not occur naturally in its pure form, but is found in many types of rocks in combination with other substances such as oxygen, sulfur, or chlorine. Manganese occurs naturally in most foods and small amounts are needed to stay healthy, as manganese ions act as cofactors for a number of enzymes. Manganese is used principally in steel production to improve hardness, stiffness, and strength. It may also be used as an additive in gasoline to improve the octane rating of the gas. Manganese ions have various colors and are used industrially as pigments. (R441, R442)",,7439-96-5,23930,,C00034,"153550
173470",18291,MN%2b3,,D008345,Manganese,6475,,,http://en.wikipedia.org/wiki/Manganese,InChI=1/Mn,manganese,http://www.biospider.ca/saved_files/mol/a0c444039b1330fd17c2a5a6fb0e808b_1237946609.mol,[Mn++],[Mn++],[Mn]2+,54.938049,,1244 °C,,,"",,,,"Oral 
Inhalation 
(R441) ","Alpha-2-macroglobulin (P01023) 
Serum albumin (P02768) 
Serotransferrin (P02787) 
Superoxide dismutase [Mn], mitochondrial (P04179)
(R441) ","Manganese is a cellular toxicant that can impair transport systems, enzyme activities, and receptor functions. It primarily targets the central nervous system, particularily the globus pallidus of the basal ganglia. It is believed that the manganese ion, Mn(II), enhances the autoxidation or turnover of various intracellular catecholamines, leading to increased production of free radicals, reactive oxygen species, and other cytotoxic metabolites, along with a depletion of cellular antioxidant defense mechanisms, leading to oxidative damage and selective destruction of dopaminergic neurons. In addition to dopamine, manganese is thought to interact with other neurotransmitters, such as GABA and glutamate. Manganese overwhelms the manganese superoxide dismutase and produce oxidative damage. The neurotoxicity of Mn(II) has also been linked to its ability to substitute for Ca(II) under physiological conditions. It can enter mitochondria via the calcium uniporter and inhibit mitochondrial oxidative phosphorylation. It may also inhibit the efflux of Ca(II), which can result in a loss of mitochondrial membrane integrity. Mn(II) has been shown to inhibit mitochondrial aconitase activity to a significant level, altering amino acid metabolism and cellular iron homeostasis. (R441)","Manganese is mainly absorbed via ingestion, but can also be inhaled. It binds to alpha-2-macroglobulin, albumin, or transferrin in the plasma and is distributed to the brain and all other mammalian tissues, though it tends to accumulate more in the liver, pancreas, and kidney. Manganese exists in a number of oxidation states and is believed to undergo changes in oxidation state within the body. Manganese oxidation state can influence tissue toxicokinetic behavior, and possibly toxicity. Manganese is excreted primarily in the faeces. (R441)","LD50: 9 g/kg (Oral, Rat) (R293)",,,"Manganese is used principally in steel production to improve hardness, stiffness, and strength. It may also be used as an additive in gasoline to improve the octane rating of the gas. Manganese ions have various colors and are used industrially as pigments. (R441, R442)",Chronic Inhalation: 0.0003 mg/m3 (R260),"Manganese mainly affects the nervous system and may cause behavioral changes and other nervous system effects, which include movements that may become slow and clumsy. This combination of symptoms when sufficiently severe is referred to as “manganism”. High levels of manganese may also cause damage to the reproductive system. (R441)","Manganese mainly affects the nervous system and may cause behavioral changes and other nervous system effects, which include movements that may become slow and clumsy. This combination of symptoms when sufficiently severe is referred to as “manganism”. (R441)","",P04156;Q86SH4;Q99798;P21399;P48200 
120,T3D0119,2009-03-06 18:58:07 UTC,2009-08-26 15:10:30 UTC,Chrysotile asbestos,Inorganic Compound;Mineral,"7-45 AsbestosAntigoriteAsbestos (chrysotile)Asbestos, Serpentine, Chrysotile (Mg3(OH)4(Si2O5))Asbestos, chrysotileAsbestos, chrysotile(SR)Asbestos, chrysotile(ir)Asbestos, chrysotile(ir) + dimethyl hydrazineAsbestos, serpentineAvibest cCalidria RG 100Calidria RG 144Calidria RG 600Cassiar akChrysotileChrysotile (Mg3(OH)4(SiO5))Chrysotile [asbestos]Chrysotile aChrysotile a asbestosChrysotile asbestosChrysotile uiccHooker No. 1 chrysotile asbestosJenkinsiteMetaxitePlastibest 20SerpentineSerpentine (mineral)Serpentine asbestosSerpentine chrysotileSylodexWhite asbestos","Chrysotile is one of the six naturally occuring minerals that may compose asbestos. Asbestos minerals consist of thin, separable fibers that have a parallel arrangement. Chrysotile belongs to the serpentine family of minerals and has curly fibres that can be spun and woven into fabric. The most common use for chrysotile asbestos is within corrugated asbestos cement roof sheets typically used for outbuildings, warehouses and garages. It is also found as flat sheets used for ceilings and sometimes for walls and floors. Abestos is toxic and inhalation of asbestos fibers can cause serious illnesses, including malignant mesothelioma, lung cancer, and asbestosis. While all forms of asbestos are hazardous and can cause cancer, chrysotile is considered to be somewhat less hazardous that its amphibole counterparts. (R426, R427)",,12001-29-5,25477,,"","",46664,"",,,Chrysotile asbestos,,,,,"InChI=1/3Mg.2HO4Si.H2O/c;;;2*1-5(2,3)4;/h;;;2*1H;1H2/q3*+2;2*-3;",trimagnesium hydroxy(trioxido)silane hydrate,http://www.biospider.ca/saved_files/mol/,O.O[Si]([O-])([O-])[O-].O[Si]([O-])([O-])[O-].[Mg+2].[Mg+2].[Mg+2],O.O[Si]([O-])([O-])[O-].O[Si]([O-])([O-])[O-].[Mg+2].[Mg+2].[Mg+2],H4Mg3O9Si2,275.894510,Grey to green fibrous crystals.,"",,,"",,,,"Inhalation 
Injection 
(R427)",,"When asbestos fibers are inhaled, many are deposited on the epithelial surface of the respiratory tree. Fibers that are retained in the lung or mesothelium for long periods of time are capable of producing chronic inflammation and fibrotic and tumorigenic effects. These effects may be mediated by direct interactions between the fiber and key cellular macromolecules, or they may be mediated by the production of reactive oxygen species and other cellular factors originating from alveolar macrophages. In addition, the physical-chemical nature of the fiber appears to be an important determinant of toxicity. It is generally agreed that exposure to amphibole fibers can produce mesothelioma, and that the potency of amphibole fibers to produce mesothelioma is greater than that of chrysotile. Asbestos fibers can adsorb to a variety of cellular macromolecules (e.g., proteins,membrane lipids, RNA, DNA). The coulombic forces between the asbestos fiber and some of these macromolecules may induce conformational changes, and these changes could affect protein function and chromosomal fidelity. Chrysotile fibers were found to bind to cytochrome P-450, thereby decreasing mono-oxygenase activity. Chrysotile and crocidolite fibers were also found to bind to artificial lipid membranes in vitro, thereby increasing membrane rigidity. Fibers found to be translocated near the nucleus can interact with the cytoskeleton and interfere with chromosome segregation. (R427)","Asbestos fibers are not metabolized in the normal sense of the word, and amphibole fibers that are retained in the lung do not appear to undergo any major changes. However, chrysotile fibers appear to undergo some type of breakdown or alteration in the lung. Some of the fibers will be deposited in the air passages and on the lung cells. Most fibers are removed from the lungs by being carried away or coughed up in a layer of mucus to the throat, where they are swallowed into the stomach. Fibers that are deposited in the deepest parts of the lung are removed more slowly. In fact, some fibers may move through the lungs and can remain in place for many years and may never be removed from the body. Longer fibers that are retained in the lung may undergo a number of processes including translocation, dissolution, fragmentation, splitting, or protein encapsulation. Long fibers that reside in the lung can become encapsulated in protein, forming what is often referred to as an ""asbestos body"". In response to asbestos fibers, alveolar macrophages produce reactive oxygen species in an attempt to digest the fiber. The reactive oxygen species include hydrogen peroxide and superoxide radical anion (O2-). Fibers that have been swallowed (those present in water, or those moved to the throat from the lungs) almost all pass along the intestines within a few days and are excreted in the feces. (R427)",,,"1, carcinogenic to humans. (R434)","Asbestos are used in building materials (roofing shingles, ceiling and floor tiles, paper products, and asbestos cement products), friction products (automobile clutch, brake, and transmission parts), heat-resistant fabrics, packaging, gaskets, and coatings. Some vermiculite or talc products may contain asbestos. Exposure most likely by breathing air containing asbestos fibers or by drinking asbestos fibers that are present in water. (R427)","","Infected people develop a slow buildup of scar-like tissue in the lungs and in the membrane that surrounds the lungs, so breathing becomes difficult. Blood flow to the lung may also be decreased, and this causes the heart to enlarge. This disease is called asbestosis. Infected people have increased chances of getting two principal types of cancer: cancer of the lung tissue itself and mesothelioma, a cancer of the thin membrane that surrounds the lung and other internal organs. The cellular immune system of the patient can be depressed. Also, deletions of chromosome segments have been noted in human mesothelioma cells or cell lines. (R427)","Symptoms of asbestos exposure include shortness of breath, often accompanied by a cough. (R427)","In vitro studies have shown that the effects of asbestos can be diminished by compounds that reduce the levels of reactive oxygen species, such as free radical scavengers (ascorbic acid, bemitil, mannitol, salicylate, 5,5'-dimetyl-l-proline N-oxide, rutin, vitamin E, vitamin A) and enzymes that catalyze the decomposition of reactive oxygen species (catalase, superoxide dismutase). Patients should quit smoking, perform bronchial drainage and can use chest physical therapy techniques to further aid in removing secretions. Shortness of breath is treated with bronchodilators, inhaled or oral medications that open up the bronchial tubes and allow the passage of air. In more severe asbestosis cases, supplemental oxygen may be required. Productive cough is treated with humidifiers and chest percussion. Asbestosis can be treated, but not cured. (R427, R438)",DNA
121,T3D0120,2009-03-06 18:58:07 UTC,2009-08-25 15:55:13 UTC,Strontium-90,Inorganic Compound;Metal;Strontium Compound;Radioactive Isotope,"STRONTIUM 90Strontium, isotope of mass 90Strontium-90","Strontium is a naturally occurring element found in rocks, soil, dust, coal, and oil. Strontium-90 is a radioactive isotope of strontium (Sr) with a half-life of 28.8 years. Strontium-90 is a product of nuclear fission and is obtained during nuclear reprocessing of spent nuclear fuel and is a beta-emitter. Strontium 90 is extensively used in medicine and industry. Strontium-90 is a radioactivity hazard and is linked to cancers. (S573, W512)",,10098-97-2,5486204,,"","","","",,,Strontium-90,,,,http://en.wikipedia.org/wiki/Strontium-90,InChI=1/Sr.2H/i1+2;;,strontium-90,http://www.biospider.ca/saved_files/mol/,[90Sr],[90Sr],Sr,87.905610,,"",,,"",,,,"Oral
Inhalation
Dermal
(W512)",,"The fact that strontium is chemically similar to calcium allows it to exchange for calcium in bone. It affects bone development and strength by binding directly to hydroxyapatite crystals, which interferes with the normal crystalline structure of bone. Strontium can also interact with secondary cell messenger systems and transporter systems that normally use calcium. It is thought to bind to the calcium receptor of the parathyroid gland, thereby suppressing parathyroid hormone levels, preventing vitamin D3 activiation, and reducing calcium absorption. The ionizing radiation produced by strontium-90 causes cellular damage that includes DNA breakage, accurate or inaccurate repair, apoptosis, gene mutations, chromosomal change, and genetic instability. This leads to loss of normal cell and tissue homeostasis, and development of malignancy. Strontium's ability to mimick calcium makes bone cancer a particular risk. Ionizing radiation that does not directly damage DNA can produce reactive oxygen intermediates that directly affect the stability of p53, an important enzyme in cell-cycle regulation, and produce oxidative damage to individual bases in DNA and point mutations by mispairing during DNA replication. (W510, W512)","The radioactivity of strontium-90 allow it to penetrate the body following inhalation, ingestion, or dermal exposure. Strontium-90 exhibits biochemical behavior similar to calcium. After entering the organism, about 70-80% of the dose is excreted. Virtually all remaining strontium-90 is deposited in bones and bone marrow, with the remaining 1% remaining in blood and soft tissues. The metabolism of strontium consists of binding interactions with proteins and, based on its similarity to calcium, probably complex formation with various inorganic anions such as carbonate and phosphate, and carboxylic acids such as citrate and lactate. Strontium-90 is eliminated mainly in the urine and faeces. (S573)",,,,"Strontium-90 is widely used in medicine and industry, as a radioactive source for thickness gauges, and for superficial radiotherapy of some cancers. Being cheaper than the alternative 238Pu, it is used as a heat source in many Russian and Soviet radioisotope thermoelectric generators. It is also used as a radioactive tracer in medicine and agriculture. (S573)",Intermediate Oral: 2 mg/kg/day (R260),"High levels of radioactive strontium can damage bone marrow, cause anemia and prevent the blood from clotting properly. Strontium-90 present in bones could cause bone cancer, cancer of nearby tissues, and leukemia. (S573, W512)","High levels of radioactive strontium can damage bone marrow, cause anemia and prevent the blood from clotting properly. Exposure to high doses of ionizing radiation results in acute radiation syndrome, which can cause skin burns, hair loss, nausea, vomiting, dizziness, disorientation, low blood pressure, headache, fatigue, weakness, fever, birth defects, illness, infection, and death. (W510, W525, W512)","Treatment reversing the effects of irradiation is currently not possible. Anaesthetics and antiemetics are administered to counter the symptoms of exposure, as well as antibiotics for countering secondary infections due to the resulting immune system deficiency. (W525)",DNA
122,T3D0121,2009-03-06 18:58:07 UTC,2009-08-25 15:55:17 UTC,Plutonium-239,Inorganic Compound;Metal;Plutonium Compound;Radioactive Isotope,"239-PlutoniumPlutonium, isotope of mass 239Plutonium, isotope of mass 239 (239Pu4+)Plutonium-239","Plutonium is an element with the symbol Pu and atomic number 94. It is a rare transuranic radioactive element that normally exhibits six allotropes and four oxidation states. It is also a radioactive poison that accumulates in bone marrow. Plutonium-239 is the most important isotope of plutonium, with a half-life of 24,100 years. It is fissile and can therefore sustain a nuclear chain reaction, leading to applications in nuclear weapons and nuclear reactors. Pu-239 is synthesized by irradiating uranium-238 with neutrons in a nuclear reactor, then recovered via nuclear reprocessing of the fuel. (W513)",,15117-48-3,61782,,"","","","",,,Plutonium-239,,,,,InChI=1/Pu/i1-5,plutonium-239,http://www.biospider.ca/saved_files/mol/,[239Pu],[239Pu],Pu,0.000000,,"",,,"",,,,"Oral
Inhalation
(R513)","Serum albumin (P02768)
Serotransferrin (P02787)
Ferritin light chain (P02792)
Ferritin heavy chain (P02794)
Ferritin, mitochondrial (Q8N4E7)
(W514)","The alpha radiation plutonium emits does not penetrate the skin but can irradiate internal organs when plutonium is inhaled or ingested. Particularly at risk are the skeleton, where it is likely to be absorbed by the bone surface, and the liver, where it collects and becomes concentrated. The ionizing radiation produced by plutonium causes cellular damage that includes DNA breakage, accurate or inaccurate repair, apoptosis, gene mutations, chromosomal change, and genetic instability. This leads to loss of normal cell and tissue homeostasis, and development of malignancy. Ionizing radiation that does not directly damage DNA can produce reactive oxygen intermediates that directly affect the stability of p53, an important enzyme in cell-cycle regulation, and produce oxidative damage to individual bases in DNA and point mutations by mispairing during DNA replication. (W510, W514)","Plutonium-238 can affect the body following ingestion or inhalation. When inhaled, Pu-239 tends to accumulate in the lungs, though it also distributes to the liver and skeleton. Ingested plutonium is found in the liver and bone. Plutonium metabolism consists primarily of hydrolytic reactions and formation of complexes with protein and nonprotein ligands, such as albumin, globulins, ferritin, citrate, and lactate. Plutonium is excreted in feces and urine. (W514)",,,"1, carcinogenic to humans. (R264)","Plutonium-239 is a key fissile component in nuclear weapons, due to its ease of fission and availability. (W513)",,"Plutonium's radioactivity can cause cancers of the bone, liver, and lungs if ingested or inhaled. Large amounts may also cause acute radiation poisoning. (W513, W514)","Exposure to high doses of ionizing radiation results in acute radiation syndrome, which can cause skin burns, hair loss, nausea, vomiting, dizziness, disorientation, low blood pressure, headache, fatigue, weakness, fever, birth defects, illness, infection, and death. (W510, W525)","Treatment reversing the effects of irradiation is currently not possible. Anaesthetics and antiemetics are administered to counter the symptoms of exposure, as well as antibiotics for countering secondary infections due to the resulting immune system deficiency. (W525)",DNA
123,T3D0122,2009-03-06 18:58:07 UTC,2009-08-26 20:25:17 UTC,Polonium-210,Inorganic Compound;Metal;Plutonium Compound;Radioactive Isotope,"210-PoloniumPolonium, isotope of mass 210Polonium-210Radium f","Polonium is a chemical element with the symbol Po and atomic number 84, discovered in 1898 by Marie and Pierre Curie. A rare and highly radioactive metalloid, polonium is chemically similar to bismuth and tellurium, and it occurs in uranium ores. When it is mixed or alloyed with beryllium, polonium can be a neutron source and has been used in this capacity as a neutron trigger or initiator for nuclear weapons. Polonium has also been studied for possible use in heating spacecraft. It is unstable and all isotopes of polonium are radioactive. (W515)",,13981-52-7,6328544,,"","",37340,"",,,Polonium-210,,,,,InChI=1/Po/i1+1,polonium-210,http://www.biospider.ca/saved_files/mol/,[210Po],[210Po],Po,0.000000,,"",,,"",,,,"Oral
Inhalation
(W515)",,"The alpha radiation polonium emits does not penetrate the skin but can irradiate internal organs when polonium is inhaled or ingested. The ionizing radiation produced by plutonium causes cellular damage that includes DNA breakage, accurate or inaccurate repair, apoptosis, gene mutations, chromosomal change, and genetic instability. This leads to loss of normal cell and tissue homeostasis, and development of malignancy. Ionizing radiation that does not directly damage DNA can produce reactive oxygen intermediates that directly affect the stability of p53, an important enzyme in cell-cycle regulation, and produce oxidative damage to individual bases in DNA and point mutations by mispairing during DNA replication. (W510, W515)",,,,,"When it is mixed or alloyed with beryllium, polonium can be a neutron source and has been used in this capacity as a neutron trigger or initiator for nuclear weapons. Polonium has also been studied for possible use in heating spacecraft. (W515)",,"Polonium's radioactivity can cause cancer, especially of the lung, if ingested of inhaled. (W515)","Exposure to high doses of ionizing radiation results in acute radiation syndrome, which can cause skin burns, hair loss, nausea, vomiting, dizziness, disorientation, low blood pressure, headache, fatigue, weakness, fever, birth defects, illness, infection, and death. (W510, W525)","Chelation agents such as British Anti-Lewisite (dimercaprol) can be used to decontaminate humans. Treatment reversing the effects of irradiation is currently not possible. Anaesthetics and antiemetics are administered to counter the symptoms of exposure, as well as antibiotics for countering secondary infections due to the resulting immune system deficiency. (W525, W515)",DNA
124,T3D0123,2009-03-06 18:58:07 UTC,2009-08-04 21:27:45 UTC,Methylmercury,Organic Compound;Mercury Compound;Organometallic,"CH3Hg(+)HGCMEHGMMCMercury(1+), methyl-Mercury(1+), methyl-, ionMethyl mercuryMethylmercuryMethylmercury IIMethylmercury ionMethylmercury ion(1+)Methylmercury(1+)Methylmercury(II)Methylmercury(II) cationMonomethylmercury cation[HgCH3](+)[hgme](+)","Methylmercury is an organometallic cation. It is formed by the burning of wastes and fossil fuels containing inorganic mercury, as well as by the action of anaerobic organisms on inorganic mercury. It is particularily hazardous due to its ability to bioaccumulate in the environment, particularily in aquatic systems. (R479)",,22967-92-6,6860,,"","",49747,"",,C030957,Methylmercury,6484,,,,InChI=1/CH3.Hg/h1H3;/q;+1,methylmercury,http://www.biospider.ca/saved_files/mol/,C[Hg+],C[Hg+],CH3Hg+,"","","","","","","","","","Oral 
Inhalation
Dermal 
(R022)","Metallothionein-2 (P02795) Metallothionein-1G (P13640) Metallothionein-1H (P80294) Metallothionein-3 (P25713) Metallothionein-1F (P04733) Metallothionein-1E (P04732) Metallothionein-1X (P80297) Metallothionein-1A (P04731) Metallothionein-1B (P07438) Metallothionein-1M (Q8N339) Metallothionein-4 (P47944) Metallothionein-1L (Q93083) Catalase (P04040) Hemoglobin subunit alpha (P69905) Hemoglobin subunit beta (P68871) Hemoglobin subunit gamma-1 (P69891) Hemoglobin subunit gamma-2 (P69892) Hemoglobin subunit delta (P02042) Hemoglobin subunit epsilon (P02100) Hemoglobin subunit theta-1 (P09105) Hemoglobin subunit zeta (P02008) Hemoglobin subunit mu (Q6B0K9) (R022, R164)","High-affinity binding of the divalent mercuric ion to thiol or sulfhydryl groups of proteins is believed to be the major mechanism for the activity of mercury. Through alterations in intracellular thiol status, mercury can promote oxidative stress, lipid peroxidation, mitochondrial dysfunction, and changes in heme metabolism. Mercury is known to bind to microsomal and mitochondrial enzymes, resulting in cell injury and death. For example, mercury is known to inhibit aquaporins, halting water flow across the cell membrane. It also inhibits the protein LCK, which causes decreased T-cell signalling and immune system depression. Mercury is also believed to inhibit neuronal excitability by acting on the postsynaptic neuronal membrane. It also affects the nervous system by inhibiting protein kinase C and alkaline phosphatase, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Organic mercury exerts developmental effects by binding to tubulin, preventing microtubule assembly and causing mitotic inhibition. Mercury also produces an autoimmune response, likely by modification of major histocompatibility complex (MHC) class II molecules, self peptides, T-cell receptors, or cell-surface adhesion molecules. (R022, R025, R066, R067)","Organic mercury is absorbed mainly by the gastrointestinal tract, then distributed throughout the body via the bloodstream. Organic mercury complexes with free cysteine and the cysteine and sulfhydryl groups on proteins such as haemoglobin. These complexes are able to mimic methionine and thus be transported throughout the body, including through the blood-brain barrier and placenta. Organic mercury is metabolized into inorganic mercury, which is eventually excreted in the urine and faeces. (R033)","LD50: 58 mg/kg (Oral, Rat) (R480)
LD50: 14 mg/kg (Intraperitoneal, Mouse) (R480)",100 mg/kg for an adult human (average for organic mercurials). (R273),"2B, possibly carcinogenic to humans. (R264)",Methylmercury is a pollutant producted by the burning of fossil fuels and wastes containing inorganic mercury. It bioaccumulates in aquatic systems and exposure can result from ingesting contaminated fish. (R479),Chronic Oral: 0.00005 mg/kg (R260),"Mercury mainly affects the nervous system. Exposure to high levels of metallic, inorganic, or organic mercury can permanently damage the brain, kidneys, and developing fetus. Effects on brain functioning may result in irritability, shyness, tremors, changes in vision or hearing, and memory problems. Acrodynia, a type of mercury poisoning in children, is characterized by pain and pink discoloration of the hands and feet. Mercury poisoning can also cause Hunter-Russell syndrome and Minamata disease. (R022)","Common symptoms include peripheral neuropathy, skin discoloration, edema, and desquamation. (R020)","Mercury poisoning is treated by immediate decontamination and chelation therapy using DMSA, DMPS, DPCN, or dimercaprol. (R023)",P06239;P68363;Q13748;P68366;P07437;Q13885;P68371;Q13509;P04350;P23258;P29972;P41181;Q92482;P55087;P55064;Q13520;O14520;O94778;O43315;Q71U36;Q9BQE3;Q6PEY2;Q9H4B7;Q9BVA1;Q9NY65;Q3ZCM7;Q9BUF5;Q9UJT1;Q9UJT0;Q9NRH3;Q96PS8;Q8NBQ7;Q8IXF9;P05186;A6NM10;P30301;P17252;P05771;Q05655;Q02156;P24723;P05129;P41743;Q04759;Q05513;A6NKZ8 ;Q99867;Q9H853;A6NHL2;A6NNZ2
125,T3D0124,2009-03-06 18:58:07 UTC,2009-08-25 19:50:12 UTC,Plutonium-238,Inorganic Compound;Metal;Plutonium Compound;Radioactive Isotope,"PLUTONIUM-238Plutonium, isotope of mass 238","Plutonium is an element with the symbol Pu and atomic number 94. It is a rare transuranic radioactive element that normally exhibits six allotropes and four oxidation states. It is also a radioactive poison that accumulates in bone marrow. Plutonium-238 has a half-life of 88 years and emits alpha particles. It is a heat source in radioisotope thermoelectric generators, which are used to power some spacecraft.  (W513)",,13981-16-3,61709,,"","","","",,,Plutonium-238,,,,,InChI=1/Pu/i1-6,plutonium-238,http://www.biospider.ca/saved_files/mol/,[238Pu],[238Pu],Pu,0.000000,,"",,,"",,,,"Oral
Inhalation
(R513)","Serum albumin (P02768)
Serotransferrin (P02787)
Ferritin light chain (P02792)
Ferritin heavy chain (P02794)
Ferritin, mitochondrial (Q8N4E7)
(W514)","The alpha radiation plutonium emits does not penetrate the skin but can irradiate internal organs when plutonium is inhaled or ingested. Particularly at risk are the skeleton, where it is likely to be absorbed by the bone surface, and the liver, where it collects and becomes concentrated. The ionizing radiation produced by plutonium causes cellular damage that includes DNA breakage, accurate or inaccurate repair, apoptosis, gene mutations, chromosomal change, and genetic instability. This leads to loss of normal cell and tissue homeostasis, and development of malignancy. Ionizing radiation that does not directly damage DNA can produce reactive oxygen intermediates that directly affect the stability of p53, an important enzyme in cell-cycle regulation, and produce oxidative damage to individual bases in DNA and point mutations by mispairing during DNA replication. (W510, W514)","Plutonium-238 can affect the body following ingestion or inhalation. When inhaled, Pu-239 tends to accumulate in the lungs, though it also distributes to the liver and skeleton. Ingested plutonium is found in the liver and bone. Plutonium metabolism consists primarily of hydrolytic reactions and formation of complexes with protein and nonprotein ligands, such as albumin, globulins, ferritin, citrate, and lactate. Plutonium is excreted in feces and urine. (W514)",,,"1, carcinogenic to humans. (R264)","Plutonium-238 is a heat source in radioisotope thermoelectric generators, which are used to power some spacecraft.  (W513)",,"Plutonium's radioactivity can cause cancers of the bone, liver, and lungs if ingested or inhaled. Large amounts may also cause acute radiation poisoning. (W513, W514) ","Exposure to high doses of ionizing radiation results in acute radiation syndrome, which can cause skin burns, hair loss, nausea, vomiting, dizziness, disorientation, low blood pressure, headache, fatigue, weakness, fever, birth defects, illness, infection, and death. (W510, W525)","Treatment reversing the effects of irradiation is currently not possible. Anaesthetics and antiemetics are administered to counter the symptoms of exposure, as well as antibiotics for countering secondary infections due to the resulting immune system deficiency. (W525)",DNA
127,T3D0126,2009-03-06 18:58:07 UTC,2009-08-25 19:48:32 UTC,Plutonium,Inorganic Compound;Metal;Plutonium Compound,"PUPlutonioPlutonium, ion(4+)Plutonium, ion(Pu5 )",Plutonium is an element with the symbol Pu and atomic number 94. It is a rare transuranic radioactive element that normally exhibits six allotropes and four oxidation states. It is also a radioactive poison that accumulates in bone marrow. (W513),,7440-07-5,23940,,"","",33388,"",,D011005,Plutonium,,,,http://en.wikipedia.org/wiki/Plutonium,InChI=1/Pu,plutonium,http://www.biospider.ca/saved_files/mol/,[Pu],[Pu],Pu,0.000000,"Plutonium is a solid metal. It has a bright silvery appearance at first, much like nickel, but it oxidizes very quickly to a dull gray, although yellow and olive green are also reported. (S443)","912.5 K (639.4 °C, 1182.9 °F)","3505 K (3228 °C, 5842 °F)",19.816  g·cm−3 (room temperature) and 16.63  g·cm −3 (melting point),"",,,,"Oral 
Inhalation 
(R513)","Serum albumin (P02768)
Serotransferrin (P02787)
Ferritin light chain (P02792)
Ferritin heavy chain (P02794)
Ferritin, mitochondrial (Q8N4E7)
(W514)","The alpha radiation plutonium emits does not penetrate the skin but can irradiate internal organs when plutonium is inhaled or ingested. Particularly at risk are the skeleton, where it is likely to be absorbed by the bone surface, and the liver, where it collects and becomes concentrated. The ionizing radiation produced by plutonium causes cellular damage that includes DNA breakage, accurate or inaccurate repair, apoptosis, gene mutations, chromosomal change, and genetic instability. This leads to loss of normal cell and tissue homeostasis, and development of malignancy. Ionizing radiation that does not directly damage DNA can produce reactive oxygen intermediates that directly affect the stability of p53, an important enzyme in cell-cycle regulation, and produce oxidative damage to individual bases in DNA and point mutations by mispairing during DNA replication. (W510, W514)","Plutonium-238 can affect the body following ingestion or inhalation. When inhaled, Pu-239 tends to accumulate in the lungs, though it also distributes to the liver and skeleton. Ingested plutonium is found in the liver and bone. Plutonium metabolism consists primarily of hydrolytic reactions and formation of complexes with protein and nonprotein ligands, such as albumin, globulins, ferritin, citrate, and lactate. Plutonium is excreted in feces and urine. (W514)",,,"1, carcinogenic to humans. (R264)","In nature, plutonium is only found in trace quantities. Artificially, Pu-238 and Pu-239 are synthesized by bombarding uranium-238 with deuterons and neutrons, respectively. Plutonium is used in explosives and the isotope Pu-239 is a key fissile component in nuclear weapons. Plutonium is also a source of power and heat; for example in radioisotope thermoelectric generators and radioisotope heater units, artificial heart pacemakers, or supplemental heat providing to scuba diving. (S443)",,"Plutonium's radioactivity can cause cancers of the bone, liver, and lungs if ingested or inhaled. Large amounts may also cause acute radiation poisoning. (W513)  ","Exposure to high doses of ionizing radiation results in acute radiation syndrome, which can cause skin burns, hair loss, nausea, vomiting, dizziness, disorientation, low blood pressure, headache, fatigue, weakness, fever, birth defects, illness, infection, and death. (W510, W525)","Treatment reversing the effects of irradiation is currently not possible. Anaesthetics and antiemetics are administered to counter the symptoms of exposure, as well as antibiotics for countering secondary infections due to the resulting immune system deficiency. (W525)",DNA
128,T3D0127,2009-03-06 18:58:07 UTC,2009-08-04 21:27:45 UTC,Chlorpyrifos,Organic Compound;Pesticide;Aromatic Hydrocarbon;Organochloride;Organophosphate,"BonidelBrodanC9H11Cl3NO3PSCPFCaswell No. 219AAChloropyrifosChloropyrifos solutionChloropyriphosChlorpyrifos (ban)Chlorpyrifos (dursban)Chlorpyrifos [ansi:bsi:iso]Chlorpyrifos [ban]Chlorpyrifos ethylChlorpyrifos solutionChlorpyrifos-ethylChlorpyriphosChlorpyriphos [iso-french]Chlorpyriphos-ethylChlorpyritosChlorpyrofosChlorpyrophosClorpyrifosCorobanCrossfireDanusbanDetmol u. aDetmol u.aDetmol u.a.Detmol uaDhanusbanDiethyl O-(3,5,6-trichloro-2-pyridyl) phosphorothioateDowcoDowco 179DurmetDursbanDursban 10CRDursban 14GDursban 2EDursban 44Dursban 4EDursban fDursban rEmpireEquityEradexEthion, DRYEthyl chlorpyriphosGeodinfosGrofoKillmasterLentrekLock-onLorsbanLorsban 50SLLoxiranM-chlorpyrifosO,O-Diaethyl-O-3,5,6-trichlor-2-pyridylmonothiophosphatO,O-Diethyl O-(3,5,6-Trichloro-2-pyridyl) phosphorothioateO,O-Diethyl O-(3,5,6-trichloro-2-pyridinyl)phosphorothioateO,O-Diethyl O-(3,5,6-trichloro-2-pyridyl) phsophorothioateO,O-Diethyl O-3,5,6-trichloro-2-pyridyl phosphorothioateO,O-Diethyl-o-(3,5,6-trichloro-2-pyridyl)phosphorothiolateO,O-diethyl O-(3,5,6-trichloropyridin-2-yl) thiophosphatePageantPiridanePyrinexRadarRadar (fungicide)SilrifosSpannitStipendSusconSuscon blueSuscon greenTafabanTalonTerialTerial 40LTrichlorpyrphosZidilZodiacZodiac (TN)nchembio.86-comp19o,o-Diethyl o-(3,5,6-trichloro-2-pyridinyl) thiophosphateo,o-Diethyl-o-(3,5,6-trichloro-2-pyridyl)phosphorothioate","Chlorpyrifos is an  organophosphate insecticide. In the home, it is used to control cockroaches, fleas, and termites; it is also used in some pet flea and tick collars. On the farm, it is used to control ticks on cattle and as a spray to control crop pests. (R488)",,2921-88-2,2730,,C14322,"",34631,"",,D004390,Chlorpyrifos,465,,,http://en.wikipedia.org/wiki/Chlorpyrifos,"InChI=1/C9H11Cl3NO3PS/c1-3-14-17(18,15-4-2)16-9-7(11)5-6(10)8(12)13-9/h5H,3-4H2,1-2H3","diethoxy-sulfanylidene-(3,5,6-trichloropyridin-2-yl)oxy-$l^{5}-phosphane",http://www.biospider.ca/saved_files/mol/e9c3aa2783ad289c65f8bd185ff5b697_1237947708.mol,CCOP(=S)(OCC)OC1=NC(=C(C=C1Cl)Cl)Cl,CCOP(=S)(OCC)OC1=NC(=C(C=C1Cl)Cl)Cl,C9H11Cl3NO3PS,348.926280,White crystals.,42 °C,,,"0.00112 mg/mL at 24 °C [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral
Inhalation
Dermal
(R488)","Serum paraoxonase/arylesterase 1 (P27169)
Serum paraoxonase/arylesterase 2 (Q15165)
(R488)","Chlorpyrifos and its bioactivation product, chlorpyrifos oxon, inhibit neural acetylcholinesterase by forming a stable covalent bond at the active site. The result of this acetylcholinesterase inhibition is cholinergic overstimulation of the central nervous system. Chlorpyrifos oxon also binds to muscarinic receptors, altering the signal transduction, which affects cellular signalling and disrupts neurological function. It also inhibits an endogenous signaling modulator, fatty acid amide hydrolase, producing secondary neurotoxicity. Chlorpyrifos alters cytochrome P-450 levels, controlling the metabolism of itself and other xenobiotics, and inhibits neuropathy target esterase, producing ataxia. (R488, R495, R497, R499, R973))","Chlorpyrifos is absorbed mainly via ingestion and inhalation, but may also be absorbed to a lesser extent through the skin. Chlorpyrifos rapidly distributes to all the major organs and is bioactivated to chlorpyrifos oxon in the liver via cytochrome P-450-dependent desulfuration. The oxon is hydrolyzed by A-esterase to diethylphosphate and 3,5,6-trichloro-2-pyridinol (TCP), the major metabolite. Chlorpyrifos is primarily excreted in the urine in the form of TCP conjugates. (R488)","LD50: 102 mg/kg (Oral, Rat) (R490)
LD50: 1233 mg/kg (Dermal, Rabbit) (R490)
LC50: 560 mg/m3 over 4 hours (Inhalation, Rat) (R490)
LC50: 192 mg/kg (Intraperitoneal, Mouse) (R263)",300 mg/kg for an adult human. (R293),,"Chlorpyrifos is used as a pesticide. In the home, it is used to control cockroaches, fleas, and termites; it is also used in some pet flea and tick collars. On the farm, it is used to control ticks on cattle and as a spray to control crop pests. (R488)","Acute Oral: 0.003 mg/kg/day (R260)
Intermediate Oral: 0.003 mg/kg/day (R260)
Chronic Oral: 0.001 mg/kg/day (R260)","Chlorpyrifos damages the nervous system. High levels may result in severe sweating, loss of bowel control, severe muscle tremors, seizures, loss of consciousness, coma, or death. (R488)","Chlorpyrifos exposure may produce a variety of effects on the nervous system including headaches, blurred vision, lacrimation, excessive salivation, runny nose, dizziness, confusion, muscle weakness or tremors, nausea, diarrhea, and sudden changes in heart rate. High levels may result in severe sweating, loss of bowel control, severe muscle tremors, seizures, loss of consciousness, coma, or death. (R488)","The effects of chlorpyrifos can be reversed by administration of the cholinergic blocking agent, atropine. (R488)",P22303;P11229;P08172;P20309;P08173;P08912;P02768;P08684;Q8IY17;P21554;O00519;Q6GMR7;P98194;O75185;P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P78334;Q8N1C3;P18507;Q99928;O00591;P24046;P28476;A8MPY1;Q9UN88;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;P54710;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P03372;Q92731
129,T3D0128,2009-03-06 18:58:08 UTC,2009-08-04 21:27:46 UTC,Copper,Inorganic Compound;Metal;Copper Compound,"Allbri natural copperAnode copperArwood copperBlister copperBronze powderC 100 (metal)C.I. Pigment Metal 2CDX (metal)CE 7 (metal)CI Pigment metal 2COPPER T MODEL TCU 380ACUCU M3CUNCasting copperCaswell No. 227Cathode copperChelazome Copper Cap 5mgCobreCopper 2mgCopper Amino Acid Chelate Tab 2mgCopper Caps 2mgCopper Chelate - 5mg TabCopper M 1Copper bronzeCopper citrateCopper dustCopper fulleride (CuC20)Copper metal powderCopper powderCopper precipitatesCopper slag-airborneCopper slag-milledCopper(III) cationCopper, dusts and mistsCopper, elementalCopper, fumeCopper, metallic powderCopper-airborneCopper-milledCu(II)Cu(III)Cu+CuivreCuivre Oligosol Liq 5.18mg/2mlCuprumCuprum Drops D3-C1000Cuprum Gtte 4ch-30chCuprum Metallicum 4ch-30chCuprum Metallicum Liquid (S#103)-LiqCuprum Sulfuricum Granule 1ch-30chCuprum [latin]Cuprum met.Cuprum metallicumCuprum sulphuricumCuprum tabsCuprum-Injeel Forte Liq (6d,12d,30d,200d/1.1ml)E 115 (metal)Electrolytic refinery billet copperElectrolytic refinery wirebar copperGold bronzeHVP chelated copperKafar copperKupferM1 (Copper)M2 (Copper)M3 (Copper)M4 (Copper)Micro cuMicroheterogeneityOfhc cuOligostim Ciuvre - Tab 6dhOpti-copper capletPekana - cuprum metallicumPigment metal 2RAMERaney copperRaney copper or baney coppercopper(0)copper(3+)copper(3+) ion","Copper is a chemical element with the symbol Cu and atomic number 29. Copper is an essential element in plants and animals as it is required for the normal functioning of more than 30 enzymes. It occurs naturally throughout the environment in rocks, soil, water, and air. It is used as a thermal conductor, an electrical conductor, a building material, and a constituent of various metal alloys such as brass and bronze. Copper compounds are known in several oxidation states, usually 2+, where they often impart blue or green colors to natural minerals such as turquoise and have been used historically widely as pigments. Copper as both metal and pigmented salt, has a significant presence in decorative art. Copper compounds are also commonly used in agriculture to treat plant diseases like mildew, for water treatment and, as preservatives for wood, leather, and fabrics. (R513, R514)",,7440-50-8,23978,,C00070,"121270
147450
215600
309400
602268
603085
603088
603735
603864
607238
610101",30052,CUCL2,,D003300,Copper,6411,,,http://en.wikipedia.org/wiki/Copper,InChI=1/Cu,copper,http://www.biospider.ca/saved_files/mol/b814d90490fab9daf5d0817429a81cff_1237947835.mol,[Cu++],[Cu++],[Cu]2+,62.929600,Reddish metallic solid.,1083 °C,,,"",,,,"Oral
Inhalation
Dermal
(R513)","High affinity copper uptake protein 1 (O15431) Probable low affinity copper uptake protein 2 (O15432) Serum albumin (P02768) Ceruloplasmin (P00450) Copper-transporting ATPase 1 (Q04656) Copper-transporting ATPase 2 (P35670) Copper transport protein ATOX1 (O00244) Copper chaperone for superoxide dismutase (O14618) Cytochrome c oxidase copper chaperone (Q14061) Metallothionein-2 (P02795) Metallothionein-1G (P13640) Metallothionein-1H (P80294) Metallothionein-3 (P25713) Metallothionein-1F (P04733) Metallothionein-1E (P04732) Metallothionein-1X (P80297) Metallothionein-1A (P04731) Metallothionein-1B (P07438) Metallothionein-1M (Q8N339) Metallothionein-4 (P47944) Metallothionein-1L (Q93083) (R513, R528)","Excess copper is sequestered within hepatocyte lysosomes, where it is complexed with metallothionein. Copper hepatotoxicity is believed to occur when the lysosomes become saturated and copper accumulates in the nucleus, causing nuclear damage. This damage is possibly a result of oxidative damage, including lipid peroxidation. Copper inhibits the sulfhydryl group enzymes such as glucose-6-phosphate 1-dehydrogenase, glutathione reductase, and paraoxonases, which protect the cell from free oxygen radicals. It also influences gene expression and is a co-factor for oxidative enzymes such as cytochrome C oxidase and lysyl oxidase. In addition, the oxidative stress induced by copper is thought to activate acid sphingomyelinase, which lead to the production of ceramide, an apoptotic signal, as well as cause hemolytic anemia. Copper-induced emesis results from stimulation of the vagus nerve. (R513, R523, R525, R526)","Copper is mainly absorbed through the gastrointestinal tract, but it can also be inhalated and absorbed dermally. It passes through the basolateral membrane, possibly via regulatory copper transporters, and is transported to the liver and kidney bound to serum albumin. The liver is the critical organ for copper homeostasis. In the liver and other tissues, copper is stored bound to metallothionein, amino acids, and in association with copper-dependent enzymes, then partitioned for excretion through the bile or incorporation into intra- and extracellular proteins. The transport of copper to the peripheral tissues is accomplished through the plasma attached to serum albumin, ceruloplasmin or low-molecular-weight complexes. Copper may induce the production of metallothionein and ceruloplasmin. The membrane-bound copper transporting adenosine triphosphatase (Cu-ATPase) transports copper ions into and out of cells. Physiologically normal levels of copper in the body are held constant by alterations in the rate and amount of copper absorption, compartmental distribution, and excretion. (R513, R520)","LD50: 3500 ug/kg (Intraperitoneal, Mouse) (R293)",10 to 20 grams for an adult human. (R273),,"Copper is used as a thermal conductor, an electrical conductor, a building material, and a constituent of various metal alloys such as brass and bronze. Copper compounds have been widely used historically as pigments in decorative art. Copper compounds are also commonly used in agriculture to treat plant diseases like mildew, for water treatment, and as preservatives for wood, leather, and fabrics. (R513, R514)","Acute Oral: 0.01 mg/kg/day (R260)
Intermediate Oral: 0.01 mg/kg/day (R260)","People must absorb small amounts of copper every day because copper is essential for good health, however, high levels of copper can be harmful. Very-high doses of copper can damage liver and kidneys, and can even cause death. Copper may induce allergic responses in sensitive individuals. (R514, R520)","Breathing high levels of copper can cause irritation of the nose and throat. Ingesting high levels of copper can cause nausea, vomiting, diarrhea, headache, dizziness, and respiratory difficulty. (R514, R520)","",P37840;P05067;P00390;P27169;P11413;Q15166
130,T3D0129,2009-03-06 18:58:08 UTC,2009-08-25 15:58:54 UTC,Americium-241,Inorganic Compound;Metal;Americium Compound;Radioactive Isotope,"Americium 241Americium, isotope of mass 241Americium, isotope of mass 241 (241Am3+)Americium-241","Americium is a synthetic element that has the symbol Am and atomic number 95. It is a radioactive metallic element of the actinide series. Eighteen radioisotopes of americium, with mass number from 231 to 249, have been characterized. The most used isotope is Am-241 because it is easiest to produce. Americium is widely used in commercial ionization-chamber smoke detectors as well as in neutron sources and industrial gauges. Americium emits alpha and gamma radiation, which represents a serious health hazard. (S530)",,86954-36-1,104726,,"","","","",,,Americium-241,,,,,InChI=1/Am/i1-2,americium-241,http://www.biospider.ca/saved_files/mol/,[241Am],[241Am],Am,0.000000,,"",,,"",,,,"Oral
Inhalation
(W516)",,"Americium toxicity results primarily from the damage done by the alpha particle emitted during radioactive decay. This alpha particle has very limited penetration in tissue, and hence, the cellular damage occurs only in the immediate vicinity of the sequestered americium. The ionizing radiation produced by americium causes cellular damage that includes DNA breakage, accurate or inaccurate repair, apoptosis, gene mutations, chromosomal change, and genetic instability. This leads to loss of normal cell and tissue homeostasis, and development of malignancy. Ionizing radiation that does not directly damage DNA can produce reactive oxygen intermediates that directly affect the stability of p53, an important enzyme in cell-cycle regulation, and produce oxidative damage to individual bases in DNA and point mutations by mispairing during DNA replication. (W510)","Americium can be absorbed following ingestion, inhalation, and dermal exposure. In the body it distributes primarily to the liver, as well as to the bone and skeletal muscle. The metabolism of americium involves binding interactions with proteins and probably complex formation with various inorganic anions, such as carbonate and phosphate, and carboxylic acids, such as citrate and lactate. Americium is excreted in faeces and urine. (W516)",,,,Americium is widely used in commercial ionization-chamber smoke detectors as well as in neutron sources and industrial gauges. (S530),"Acute Radiation: 4 mSv (R260)
Chronic Radiation: 1 mSv/yr (R260)","Americium's radioactivity can cause cancer, especially of the bone, where it is known to accumulate. Exposure to large amount of americium may also damage the lungs, liver, and thyroid. (W516)","Exposure to high doses of ionizing radiation results in acute radiation syndrome, which can cause skin burns, hair loss, nausea, vomiting, dizziness, disorientation, low blood pressure, headache, fatigue, weakness, fever, birth defects, illness, infection, and death. (W510, W525)","Treatment reversing the effects of irradiation is currently not possible. Anaesthetics and antiemetics are administered to counter the symptoms of exposure, as well as antibiotics for countering secondary infections due to the resulting immune system deficiency. (W525)",DNA
131,T3D0130,2009-03-06 18:58:08 UTC,2009-08-25 15:59:02 UTC,Radon-220,Inorganic Compound;Metal;Radium Compound;Radioactive Isotope,"TNThoronThoron (Radon-220)radon, isotope of mass 220radon-220","Radon is the chemical element of symbol Rn and atomic number 86. It is a rare radioactive gas, belonging to the noble gas series, and is formed as part of three radioactive decay chains that begin with uranium or thorium. Thirty-six radioactive isotopes of radon, with mass number from 193 to 228, have been characterized. Radon-220 (half-life of 55.6 seconds) is a natural decay product of thorium and emits alpha radiation. Because of its radioactivity and unreactivity as a chemical element, radon has few uses and is seldom used in academic research. Radon is responsible for the majority of the mean public exposure to ionizing radiations. (S494)",,22481-48-7,62761,,"","",33491,"",,,Radon-220,,,,,InChI=1/Rn/i1-2,radon-220,http://www.biospider.ca/saved_files/mol/,[220Rn],[220Rn],Rn,0.000000,,"",,,"",,,,"Oral
Inhalation
Dermal
(W509)",,"The ionizing radiation produced by radon causes cellular damage that includes DNA breakage, accurate or inaccurate repair, apoptosis, gene mutations, chromosomal change, and genetic instability. This leads to loss of normal cell and tissue homeostasis, and development of malignancy. Ionizing radiation that does not directly damage DNA can produce reactive oxygen intermediates that directly affect the stability of p53, an important enzyme in cell-cycle regulation, and produce oxidative damage to individual bases in DNA and point mutations by mispairing during DNA replication. (W509)","Exposure to radon can occur from inhalation or dermal contact. It can also enter the body via ingestion if dissolved in water. Radon distributes mainly to the fat. It is not metabolized and may be eliminated in the urine, faeces, or expired air. (W509)",,,"1, carcinogenic to humans. (R264)","Radon has few uses and is seldom used in academic research. Radon gas from natural sources can accumulate in buildings, especially in confined areas such as basements. Radon can be found in some spring waters and hot springs. (S494)",,"Radon is responsible for the majority of the mean public exposure to ionizing radiations. Due to it's radioactivity, breathing high concentrations of radon can cause lung cancer. According to the United States Environmental Protection Agency, radon could be the second most frequent cause of lung cancer, after cigarette smoking; and radon-induced lung cancer the 6th leading cause of cancer death overall, causing 21,000 lung cancer deaths per year in the United States. (S494)","Exposure to high doses of ionizing radiation results in acute radiation syndrome, which can cause skin burns, hair loss, nausea, vomiting, dizziness, disorientation, low blood pressure, headache, fatigue, weakness, fever, birth defects, illness, infection, and death. (W510, W525)","Treatment reversing the effects of irradiation is currently not possible. Anaesthetics and antiemetics are administered to counter the symptoms of exposure, as well as antibiotics for countering secondary infections due to the resulting immune system deficiency. (W525)",DNA
132,T3D0131,2009-03-06 18:58:08 UTC,2009-08-26 15:11:34 UTC,Amosite asbestos,Inorganic Compound;Mineral,Cis-dihydronarciclasineTrans-dihydronarciclasine,"Amosite is one of the six naturally occuring minerals that may compose asbestos. Asbestos minerals consist of thin, separable fibers that have a parallel arrangement. Amosite belongs to the amphibole family of minerals and has needlelike fibres. The most common use for amosite asbestos is as a fire retardant in thermal insulation products and ceiling tiles. Abestos is toxic and inhalation of asbestos fibers can cause serious illnesses, including malignant mesothelioma, lung cancer, and asbestosis. While all forms of asbestos are hazardous and can cause cancer, amphibole forms of asbestos are considered to be somewhat more hazardous than their serpentine counterpart (chrysotile). (R426, R427)",,12172-73-5,436050,,"","",46678,"",,D017639,Amosite asbestos,,,,,"InChI=1/C14H15NO7/c16-6-1-5-4-2-7-13(22-3-21-7)11(18)8(4)14(20)15-9(5)12(19)10(6)17/h2,5-6,9-10,12,16-19H,1,3H2,(H,15,20)","2,3,4,7-tetrahydroxy-2,3,4,4a,5,11b-hexahydro-1H-[1,3]dioxolo[4,5-j]phenanthridin-6-one",http://www.biospider.ca/saved_files/mol/,"",C1C2C(C(C(C1O)O)O)NC(=O)C3=C(C4=C(C=C23)OCO4)O,C14H15NO7,309.084850,Grey to green fibrous crystals.,"",,,"",,,,"Inhalation 
Injection 
(R427)",,"When asbestos fibers are inhaled, many are deposited on the epithelial surface of the respiratory tree. Fibers that are retained in the lung or mesothelium for long periods of time are capable of producing chronic inflammation and fibrotic and tumorigenic effects. These effects may be mediated by direct interactions between the fiber and key cellular macromolecules, or they may be mediated by the production of reactive oxygen species and other cellular factors originating from alveolar macrophages. In addition, the physical-chemical nature of the fiber appears to be an important determinant of toxicity. It is generally agreed that exposure to amphibole fibers can produce mesothelioma, and that the potency of amphibole fibers to produce mesothelioma is greater than that of chrysotile. Asbestos fibers can adsorb to a variety of cellular macromolecules (e.g., proteins,membrane lipids, RNA, DNA). The coulombic forces between the asbestos fiber and some of these macromolecules may induce conformational changes, and these changes could affect protein function and chromosomal fidelity. Fibers found to be translocated near the nucleus can interact with the cytoskeleton and interfere with chromosome segregation. (R427)","Asbestos fibers are not metabolized in the normal sense of the word, and amphibole fibers that are retained in the lung do not appear to undergo any major changes. Some of the fibers will be deposited in the air passages and on the cells that make up your lungs. Most fibers are removed from the lungs by being carried away or coughed up in a layer of mucus to the throat, where they are swallowed into the stomach. Fibers that are deposited in the deepest parts of the lung are removed more slowly. In fact, some fibers may move through the lungs and can remain in place for many years and may never be removed from the body. Longer fibers that are retained in the lung may undergo a number of processes including translocation, dissolution, fragmentation, splitting, or protein encapsulation. Long fibers that reside in the lung can become encapsulated in protein, forming what is often referred to as an ""asbestos body"". In response to asbestos fibers, alveolar macrophages produce reactive oxygen species in an attempt to digest the fiber. The reactive oxygen species include hydrogen peroxide and superoxide radical anion (O2-). Fibers that have been swallowed (those present in water, or those moved to the throat from the lungs) almost all pass along the intestines within a few days and are excreted in the feces. (R427)",,,"1, carcinogenic to humans. (R434)","Asbestos are used in building materials (roofing shingles, ceiling and floor tiles, paper products, and asbestos cement products), friction products (automobile clutch, brake, and transmission parts), heat-resistant fabrics, packaging, gaskets, and coatings. Some vermiculite or talc products may contain asbestos. Exposure most likely by breathing air containing asbestos fibers or by drinking asbestos fibers that are present in water. (R427)","","Infected people develop a slow buildup of scar-like tissue in the lungs and in the membrane that surrounds the lungs, so breathing becomes difficult. Blood flow to the lung may also be decreased, and this causes the heart to enlarge. This disease is called asbestosis. Infected people have increased chances of getting two principal types of cancer: cancer of the lung tissue itself and mesothelioma, a cancer of the thin membrane that surrounds the lung and other internal organs. The cellular immune system of the patient can be depressed. Also, deletions of chromosome segments have been noted in human mesothelioma cells or cell lines. (R427)","Symptoms of asbestos exposure include shortness of breath, often accompanied by a cough. (R427)","In vitro studies have shown that the effects of asbestos can be diminished by compounds that reduce the levels of reactive oxygen species, such as free radical scavengers (ascorbic acid, bemitil, mannitol, salicylate, 5,5'-dimetyl-l-proline N-oxide, rutin, vitamin E, vitamin A) and enzymes that catalyze the decomposition of reactive oxygen species (catalase, superoxide dismutase). Patients should quit smoking, perform bronchial drainage and can use chest physical therapy techniques to further aid in removing secretions. Shortness of breath is treated with bronchodilators, inhaled or oral medications that open up the bronchial tubes and allow the passage of air. In more severe asbestosis cases, supplemental oxygen may be required. Productive cough is treated with humidifiers and chest percussion. Asbestosis can be treated, but not cured. (R427, R438)",DNA
133,T3D0132,2009-03-06 18:58:08 UTC,2009-08-25 15:59:16 UTC,Iodine-131,Inorganic Compound;Halogen;Radioactive Isotope,"IODINE-131Iodine, isotope of mass 131","Iodine is a chemical element that has the symbol I and atomic number 53. Chemically, iodine is the second least reactive of the halogens, and the second most electropositive halogen; trailing behind astatine in both of these categories. However, the element does not occur in the free state in nature. As with all other halogens, when freed from its compounds iodine forms diatomic molecules. Iodine naturally occurs in the environment chiefly as a dissolved iodide in seawater, although it is also found in some minerals and soils. Iodine is an essential trace element for life, mainly as constituents of the thyroid hormones, thyroxine (T4) and triiodothyronine (T3). Iodine-131 is used in nuclear medicine both diagnostically and therapeutically. Examples of its use in radiation therapy include the treatment of thyrotoxicosis and thyroid cancer. Diagnostic tests exploit the mechanism of absorption of iodine by the normal cells of the thyroid gland. Iodine-131 is also used as a radioactive label for radiopharmaceuticals that can be used for imaging and therapy. (W518, W519)",,10043-66-0,24855,,"","","","",,,Iodine-131,,,,,"InChI=1/I2/c1-2/i1+4,2+4","",http://www.biospider.ca/saved_files/mol/,[131I][131I],[131I],I2,253.808940,Grey solid.,"",,,"",,,,"Oral
Inhalation
Dermal
(W517)","Thyroid peroxidase (P07202)
(W517)","Iodide inhibits adenylate cyclase in thyroid gland follicle cells and decreases the TSH-induced rise in intracellular cAMP. This results in decreased iodination of thyroglobulin and inhibited production and release of T4 and T3, causing hypothyroidism. The ionizing radiation produced by radioiodine causes cellular damage that includes DNA breakage, accurate or inaccurate repair, apoptosis, gene mutations, chromosomal change, and genetic instability. This leads to loss of normal cell and tissue homeostasis, and development of malignancy. Ionizing radiation that does not directly damage DNA can produce reactive oxygen intermediates that directly affect the stability of p53, an important enzyme in cell-cycle regulation, and produce oxidative damage to individual bases in DNA and point mutations by mispairing during DNA replication. (W510, W514, W517)","Iodine can enter the body following ingestion, inhalaiton, or dermal exposure. In the body, iodine and iodide accumulates in the thyroid gland, where it is used for producing the thyroid hormones T4 and T3. Iodide in the thyroid gland is incorporated into a protein, thyroglobulin, as covalent complexes with tyrosine residues. The iodination of thyroglobulin is catalyzed by the enzyme thyroid peroxidase. The iodination reactions occur at the follicular cell-lumen interface and consist of the oxidation of iodide to form a reactive intermediate, the formation of monoiodotyrosine and diiodotyrosine residues in thyroglobulin, and the coupling of theiodinated tyrosine residues to form T4 (coupling of two diiodotyrosine residues) or T3 (coupling of a monoiodotyrosine and diiodotyrosine residue) in thyroglobulin. The major pathways of metabolism of iodine that occur outside of the thyroid gland involve the catabolism of T4 and T3, and include deiodination reactions, ether bond cleavage of thyronine, oxidative deamination and decarboxylation of the side chain of thyronine, and conjugation of the phenolic hydroxyl group on thyronine with glucuronic acid and sulfate. Absorbed iodine is excreted primarily in the urine and feces, but is also excreted in breast milk, exhaled air, sweat, and tears. (W517)",,,"1, carcinogenic to humans. (R264)",Iodine-131 is used in nuclear medicine both diagnostically and therapeutically. Examples of its use in radiation therapy include the treatment of thyrotoxicosis and thyroid cancer. Diagnostic tests exploit the mechanism of absorption of iodine by the normal cells of the thyroid gland. Iodine-131 is also used as a radioactive label for radiopharmaceuticals that can be used for imaging and therapy. (W519),,"Exposure to high levels of nonradioactive and radioactive iodine can damage the thyroid. Damage to the thyroid gland can result in effects in other parts of your body, such as your skin, lung, and reproductive organs. Concentrated iodine is very corrosive and can damage the mucous membrane if swallowed. Radioactive iodine can also cause cancer, especially of the thyroid, where it tends to concentrate. (W517, W519, W521)","Ingestion of iodine may cause corrosive effects such as oedema of the glottis, with asphyxia, aspiration pneumonia, pulmonary oedema and shock, as well as vomiting and bloody diarrhea. The CNS, cardiovascular and renal toxicity following acute iodine ingestion appear to be due to the corrosive gastroenteritis and resultant shock. Vomiting, hypotension and circulatory collapse may be noted following severe intoxication. Exposure to high doses of ionizing radiation results in acute radiation syndrome, which can cause skin burns, hair loss, nausea, vomiting, dizziness, disorientation, low blood pressure, headache, fatigue, weakness, fever, birth defects, illness, infection, and death. (W510, W525, W521)","Sodium thiosulphate, 100 mL orally of a 1% solution, has been recommended as an antidote because it immediately reduces iodine to iodide. Treatment reversing the effects of irradiation is currently not possible. Anaesthetics and antiemetics are administered to counter the symptoms of exposure, as well as antibiotics for countering secondary infections due to the resulting immune system deficiency. (W525, W521)",Q08828;Q08462;O60266;Q8NFM4;O95622;O43306;P51828;P40145;O60503;Q96PN6;DNA
134,T3D0133,2009-03-06 18:58:08 UTC,2009-08-04 21:27:47 UTC,Hydrogen cyanide,Organic Compound;Cyanide Compound,"ACAcide cyanhydriqueAcide cyanhydrique [french]Acide cyanhydrique [iso-french]Acido cianidricoAcido cianidrico [italian]Aero liquid HCNAero@ liquid HCNAgent acArbon hydride nitrideBlausaeureBlausaeure (german)Blausaeure [german]BlauwzuurBlauwzuur [dutch]CNCN-, cyanoCYNCarbon hydride nitrideCarbon hydride nitride (CHN)Caswell No. 483CyaanwaterstofCyaanwaterstof [dutch]CyanideCyanide groupCyanwasserstoffCyanwasserstoff [german]CyclonCyclone bCyjanowodorCyjanowodor [polish]EvercynFormic anammonideFormonitrileHCNHydridonitridocarbonHydrocyanic acidHydrocyanic acid (prussic), unstabilized [forbidden]Hydrocyanic acid, anhydrous, stabilizedHydrogen cyanide [iso]Hydrogen cyanide, anhydrous, stabilizedHydrogen isocyanideHydrogen(nitridocarbonate)MethanenitrileNitrilomethanePrussic acidPrussic acid, anhydrous, stabilizedPrussic acid, unstabilizedRCRA waste no. P063Rcra waste number P063ZaclondiscoidsZootic acidZyklonZyklon b[CHN]","Hydrogen cyanide is a chemical compound of cyanide. Certain bacteria, fungi, and algae can produce cyanide, and cyanide is found in a number of foods and plants. Hydrogen cyanide is a precursor to many chemical compounds, ranging from polymers to pharmaceuticals. (R177)",,74-90-8,768,,C01326,"",18407,HCN,,D006856,Hydrogen cyanide,6076,,,http://en.wikipedia.org/wiki/Hydrogen cyanide,InChI=1/CHN/c1-2/h1H,formonitrile,http://www.biospider.ca/saved_files/mol/42a6a8b6172e25f1ed7f80737bb4aa7e_1237948397.mol,C#N,C#N,CHN,27.010900,Colorless gas or liquid.,-13.4 °C,"","","1000 mg/mL at 25 °C [METCALF,RL (1978)]","","","",Oral Inhalation Dermal (R172),"Thiosulfate sulfurtransferase (Q16762)
3-mercaptopyruvate sulfurtransferase (P25325)
(R172)","Cyanide complexes with ferric iron of cytochrome c oxidase in the fourth complex of the electron transport chain, leading to the inhibition of the electron transport from cytochrom c to oxygen, and thus inhibition of ATP production. Tissues that mainly depend on aerobic respiration, such as the central nervous system and the heart, are particularly affected. Cyanide is also known to produce some of its toxic effects by binding to catalase, glutathione peroxidase, methemoglobin, hydroxocobalamin, phosphatase, tyrosinase, ascorbic acid oxidase, xanthine oxidase, succinic dehydrogenase, and Cu/Zn superoxide dismutase. Cyanide binds to the ferric ion of methemoglobin to form inactive cyanmethemoglobin. (R173)","Cyanide is rapidly alsorbed through oral, inhalation, and dermal routes and distributed throughout the body. Cyanide is mainly metabolized into thiocyanate by either rhodanese or 3-mercaptopyruvate sulfur transferase. Cyanide metabolites are excreted in the urine. (R172)","LC50: 158 mg/m3 (Inhalation, Rat) LD50: 3700 ug/kg (Acute subcutaneous, Rat) LD50: 810 ug/kg (Acute intravenous, Rat) LD50: 3700 ug/kg (Acute oral, Mouse) LD50: 2990 ug/kg (Acute intraperitoneal, Mouse)","50 to 60 mg (oral) or 270 ppm (inhaled for an adult human. (R411, R555)",,"Hydrogen cyanide is a precursor to many chemical compounds, ranging from polymers to pharmaceuticals. (R177)","","Exposure to high levels of cyanide for a short time harms the brain and heart and can even cause coma, seizures, apnea, cardiac arrest and death. Chronic inhalation of cyanide causes breathing difficulties, chest pain, vomiting, blood changes, headaches, and enlargement of the thyroid gland. Skin contact with cyanide salts can irritate and produce sores. (R172, R173)","Cyanide poisoning is identified by rapid, deep breathing and shortness of breath, general weakness, giddiness, headaches, vertigo, confusion, convulsions/seizures and eventually loss of consciousness. (R172, R173)","Antidotes to cyanide poisoning include hydroxocobalamin and sodium nitrite, which release the cyanide from the cytochrome system, and rhodanase, which is an enzyme occurring naturally in mammals that combines serum cyanide with thiosulfate, producing comparatively harmless thiocyanate. Oxygen therapy can also be administered. (R173)",P00395;P00403;P00414;P13073;P20674;P10606;P12074;Q02221;P14854;P09669;P24310;P14406;P24311;P15954;P10176;P04040;P07203;P18283;P22352;P36969;O75715;P59796;P14679;Q6YFQ2;Q96KJ9;Q8TF08;Q7Z4L0;Q96SL4;P10696;P05186;P08294;P00390;Q8TED1 ;P00441;Q99643;O14521;P31040;P21912
135,T3D0134,2009-03-06 18:58:08 UTC,2009-08-04 21:27:47 UTC,Tributyltin,Organic Compound;Tin Compound;Organometallic,"Stannane, tri-n-butyl-, hydrideStannane, tributyl-TBTC chlorideTBYTin tributyl hydrideTin, tri-n-butyl-, hydrideTri-n-butyl tin maleateTri-n-butylstannane hydrideTri-n-butyltinTributyl tinTributylstannaneTributylstannic hydrideTributyltinTributyltin acetateTributyltin chlorideTributyltin fluorideTributyltin hydrideTributyltin tetrafluoroboratetributyltin ion (1+)","Tributyltin refers to the group of organotin compounds that contain the (C4H9)3Sn functional group. They are the main active ingredients in certain biocides used to control a broad spectrum of organisms, and are also used in wood preservation, marine paints (as antifouling pesticides), and textiles and industrial water systems (as antifungal agents).  They are also considered moderately to highly persistent organic pollutants and are especially hazardous to marine ecosystems. The main toxic component of tributyltins is tin, a natural element of the earth's crust. (R562, R562)",,0688-73-3,3032732,,"","",27086,"",,,Tributyltin,,,,http://en.wikipedia.org/wiki/Tri-n-butyltin hydride,"InChI=1/3C4H9.Sn/c3*1-3-4-2;/h3*1,3-4H2,2H3;",tributyltin,http://www.biospider.ca/saved_files/mol/,CCCC[Sn](CCCC)CCCC,CCCC[Sn](CCCC)CCCC,C12H27Sn,291.113470,,Boiling Pt : 80 oC  at  4.00E-01 mm Hg,80 °C at  4.00E-01 mm Hg,,"",,,,"Oral
Inhalation
Dermal
(R562)","Hemoglobin subunit alpha (P69905) 
Hemoglobin subunit beta (P68871) 
Hemoglobin subunit gamma-1 (P69891) 
Hemoglobin subunit gamma-2 (P69892) 
Hemoglobin subunit delta (P02042) 
Hemoglobin subunit epsilon (P02100) 
Hemoglobin subunit theta-1 (P09105) 
Hemoglobin subunit zeta (P02008) 
Hemoglobin subunit mu (Q6B0K9) 
Cytochrome P450 2C6 (P05178)
(R562)","Organotin compounds produce neurotoxic and immunotoxic effects. Organotins may directly activate glial cells contributing to neuronal cell degeneration by local release of pro-inflammatory cytokines, tumor necrosis factor-α, and/or interleukins. They may also induce apoptosis by direct action on neuronal cells. Organotin compounds stimulate the neuronal release of and/or decrease of neuronal cell uptake of neurotransmitters in brain tissue, including aspartate, GABA, glutamate, norepinephrine, and serotonin. This may be either a contributing factor to or a result of the neuronal cell loss. The immunotoxic effects of organotins are characterized by thymic atrophy caused by the suppression of proliferation of immature thymocytes and apoptosis of mature thymocytes. Organotin compounds are believed to exert these effects by suppressing DNA and protein synthesis, inducing the expression of genes involved in apoptosis (such as nur77), and disrupting the regulation of intracellular calcium levels, giving rise to the uncontrolled production of reactive oxygen species, release of cytochrome c to the cytosol, and the proteolytic and nucleolytic cascade of apoptosis. The suppression of proliferation of immature thymocytes further results in the suppression of T-cell-mediated immune responses. Organotins are also endocrine disruptors and are believed to contribute to obesity by inappropriate receptor activation, leading to adipocyte differentiation. (R562, R568, R571) ","Organotin compounds are readily absorbed via oral, inhalation, or dermal routes. Tin may enter the bloodstream and bind to hemoglobin, where it is distributed and accumulates mainly in the kidney, liver, lung, and bone. Organotin compounds may undergo dealkylation, hydroxylation, dearylation, and oxidation catalyzed by cytochrome P-450 enzymes in the liver. Dealkylation of butyltin compounds produces di- and monobutyltin compounds, while oxidation of butyltin compounds produces the 3-hydroxybutyl, 4-hydroxybutyl, 3-oxobutyl, and 3-carboxy metabolites. The alkyl products of dealkylation are conjugated with glutathione and further metabolized to mercapturic acid derivatives. Tin and its metabolites are excreted mainly in the urine and feces. (R562)",,,,"Tributyltins are the main active ingredients in certain biocides used to control a broad spectrum of organisms, and are also used in wood preservation, marine paints (as antifouling pesticides), and textiles and industrial water systems (as antifungal agents). (R561)",,"Breathing or swallowing, or skin contact with organotins, can interfere with the way the brain and nervous system work, causing death in severe cases. Organic tin compounds may also damage the immune and reproductive system. (R561, R562)",Organic tin contact with the skin or the eyes can produce irritation. (R562),"",P28074;P07327;P00325;P00326;P08319;P28332;P40394;P11766;P37231;P10276;P10826;P13631;Q16881;Q9NNW7;Q86VQ6
136,T3D0135,2009-03-06 18:58:08 UTC,2009-08-04 21:27:47 UTC,Guthion,Organic Compound;Pesticide;Organophosphate,"AzimilAzinfos-methylAzinfos-methyl [dutch]Azinophos-methylAzinphosAzinphos methylAzinphos methyl mixtureAzinphos-meAzinphos-methyl [bsi:iso]Azinphos-metileAzinphos-metile [italian]AzinphosmethylBAYBeetle busterBenzotriazine derivative of a methyl dithiophosphateBenzotriazinedithiophosphoric acid dimethoxy esterCarfeneCaswell No. 374CotneonCotnionCotnion methylCotnion-methylCrysthion 2LCrysthyonCrysthyon 2LDBDDimethyl dithiophosphoric acid n-methylbenzazimidyl esterDimethyldithiophosphoric acid n-methylbenzazimide esterGo thnionGothnionGusathionGusathion 25Gusathion kGusathion mGusathion methylGusathion-20Gusthion mGuthionGuthion (azinphos-methyl)Guthion mixtureGuthion(r)Guthion, gusationGutionKetokil No. 52MetazintoxMethyl azinphosMethyl gusathionMethyl guthionMethylazinphosMethylgusathionMethyltriazotinMetiltriazotionN-methylbenzazimide, dimethyl dithiophosphoric acid esterN-methylbenzazimide, dimethyldithiophosphoric acid esterNetherlandshylNitrinalO,O-Dimethyl-S-(4-oxobenzotriazin-3-methyl)-dithiophosphatO,o-dimethyl s-(be nzaziminomethyl) dithiophosphateO,o-dimethyl s-(benzaziminomethyl) dithiophosphateO,o-dimethyl-s-(benzaziminomethyl) dithiophosphateZinphos methyl","Guthion, also called azinphos-methyl, is a synthetic organophosphorous pesticide. It has been used on many different crops, especially apples, pears, cherries, peaches, almonds, and cotton. Due to its toxicity, its use has been banned or tightly regulated in most areas today. (R904)",,86-50-0,2268,,C11018,"",2953,"",,D001387,Guthion,123,,,http://en.wikipedia.org/wiki/Azinphos-methyl,"InChI=1/C10H12N3O3PS2/c1-15-17(18,16-2)19-7-13-10(14)8-5-3-4-6-9(8)11-12-13/h3-6H,7H2,1-2H3","3-(dimethoxyphosphinothioylsulfanylmethyl)-1,2,3-benzotriazin-4-one",http://www.biospider.ca/saved_files/mol/3f60310bfc12e9f137c3f510eb49fd7d_1237948562.mol,COP(=S)(OC)SCN1C(=O)C2=CC=CC=C2N=N1,COP(=S)(OC)SCN1C(=O)C2=CC=CC=C2N=N1,C10H12N3O3PS2,317.005770,Colorless to white crystals.,73 °C,,,"0.0209 mg/mL at 20 °C [BOWMAN,BT & SANS,WW (1983)]",,,,"Oral
Inhalation
Dermal
(R904)","Cytochrome P450 2A1 (P05177)
Cytochrome P450 3A4 (P08684)
Cytochrome P450 2B6 (P20813)
(R904)","Guthion and its reactive metabolite, gutoxon, directly affect the nervous system by inhibiting acetylcholinesterase (AChE) in the central and peripheral nervous system. Gutoxon reacts with a serine hydroxyl group at the active site of AChE, rendering it largely unreactive. Thus acetylcholine accumulates in the neuromuscular juntions of cholinergic nerves, causing continual stimulation of electrical activity by both muscarinic and nicotinic receptors. Gutoxon has been shown to be the more potent inhibitor. (R904)","Guthion may be absorbed through oral, inhalation, and dermal routes. In the liver it is metabolized into its reactive intermediate, gutoxon, by cytochrome P-450 enzymes, in specific CYP1A2, CYP3A4, and CYP2B6. Further detoxification involves CYP450-mediated cleavage of the P-S-C bond, as well as glutathione-mediated dealkylation and dearylation. This produces numerous metabolites, including mercaptomethyl benzazimide, mono- and di-demethylated guthion, benzazimide, dimethyl phosphorodithioate, and dimethyl thiophosphate, which are excreted in the urine. (R904)","LD50: 11 mg/kg (Oral, Rat) (R907)
LD50: 4900 ug/kg (Intraperitoneal, Rat) (R263)
LD50: 7500 ug/kg (Intravenous, Rat) (R263)
LD50: 65 mg/kg (Dermal, Mouse) (R263)
LC50: 0.15 mg/L over 4 hours (Inhalation, Rat) (R907)",5 to 50 mg/kg for an adult human. (R921),,"Guthion is used as a pesticide, thus exposure usually occurs from eating contaminated food. (R904)","Acute Inhalation: 0.02 mg/m3 (R260)
Intermediate Inhalation: 0.01 mg/m3 (R260)
Chronic Inhalation: 0.01 mg/m3 (R260)
Acute Oral: 0.01 mg/kg/day (R260)
Intermediate Oral: 0.003 mg/kg/day (R260)
Chronic Oral: mg/kg/day (R260)","Guthion interferes with the nerves and brain normal way. However, after exposition to high amounts of guthion, a rapidly given appropriate treatment can prevent long-term harmful effects. (R904)","Guthion interferes with the nerves and brain normal way. Exposure to very high levels of guthion for a short period in air, water, or food may cause difficulty breathing, chest tightness, vomiting, cramps, diarrhea, blurred vision, sweating, headaches, dizziness, loss of consciousness, and death. (R904)","If contacted, guthion should be washed from the body. If ingested, gastric lavage should be perfomed. Patients exhibiting severe symptoms and/or respiratory difficulties should be administered atropine. When administered early, pralidoxime may also be used to relieve nicotinic effects. Diazepam can be given to control convulsions. (R921)",P22303
137,T3D0136,2009-03-06 18:58:09 UTC,2009-08-25 19:47:58 UTC,Neptunium-237,Inorganic Compound;Metal;Radioactive Isotope,"Neptunium, isotope of mass 237Neptunium, isotope of mass 237 (237Np5+)Neptunium-237","Neptunium is a chemical element with the symbol Np and atomic number 93. A radioactive metallic element, neptunium is the first transuranic element and belongs to the actinide series. Its most stable isotope, 237Np, is a by-product of nuclear reactors and plutonium production and it can be used as a component in neutron detection equipment. Neptunium is also found in trace amounts in uranium ores due to transmutation reactions. (W522)",,13994-20-2,104783,,"","","","",,,Neptunium-237,,,,,InChI=1/Np/i1+0,neptunium-237,http://www.biospider.ca/saved_files/mol/,[237Np],[237Np],Np,0.000000,Silver metal.,"",,,"",,,,"Oral
Inhalation
(W510)",,"The ionizing radiation produced by neptunium causes cellular damage that includes DNA breakage, accurate or inaccurate repair, apoptosis, gene mutations, chromosomal change, and genetic instability. This leads to loss of normal cell and tissue homeostasis, and development of malignancy. Ionizing radiation that does not directly damage DNA can produce reactive oxygen intermediates that directly affect the stability of p53, an important enzyme in cell-cycle regulation, and produce oxidative damage to individual bases in DNA and point mutations by mispairing during DNA replication. (W510)",,,,,237Np is a by-product of nuclear reactors and plutonium production and it can be used as a component in neutron detection equipment. (W522),,237-Neptunium's radioactivity can cause cancer. (W510),"Exposure to high doses of ionizing radiation results in acute radiation syndrome, which can cause skin burns, hair loss, nausea, vomiting, dizziness, disorientation, low blood pressure, headache, fatigue, weakness, fever, birth defects, illness, infection, and death. (W510, W525)","Treatment reversing the effects of irradiation is currently not possible. Anaesthetics and antiemetics are administered to counter the symptoms of exposure, as well as antibiotics for countering secondary infections due to the resulting immune system deficiency. (W525)",DNA
138,T3D0137,2009-03-06 18:58:09 UTC,2009-08-04 21:27:47 UTC,Chrysene,Organic Compound;Industrial By-product/Pollutant;Aromatic Hydrocarbon;Polycyclic Aromatic Hydrocarbon,"1,2, 5,6-Dibenzonaphthalene1,2,5,6-Dibenzonaphthalene1,2-Benzophenanthrene1,2-BenzphenanthreneAmbap84BCR269_FLUKABenz(a)phenanthreneBenz[a]phenanthreneBenzo(a)phenanthreneBenzo(a)phenanthrene [polycyclic aromatic compounds]Benzo[a]phenanthreneBenzophenanthreneChrysenCoal tar pitch volatiles: chryseneCryseneRCRA waste no. U050Rcra waste number U050WLN: L E6 B666Jchrysene (ACD/Name 4.0){benz[a]phenanthrene}{benzo[a]phenanthrene}","Chrysene is one of over 100 different polycyclic aromatic hydrocarbons (PAHs). PAHs are chemicals that are formed during the incomplete burning of organic substances, such as fossil fuels. They are usually found as a mixture containing two or more of these compounds. (R028)",,218-01-9,9171,,C14222,"",51687,"",,C031180,Chrysene,6410,,,http://en.wikipedia.org/wiki/Chrysene,InChI=1/C18H12/c1-3-7-15-13(5-1)9-11-18-16-8-4-2-6-14(16)10-12-17(15)18/h1-12H,chrysene,http://www.biospider.ca/saved_files/mol/bdcb591df86f9257f359ff2a06db88ed_1237948748.mol,C1=CC=C2C(=C1)C=CC3=C2C=CC4=CC=CC=C43,C1=CC=C2C(=C1)C=CC3=C2C=CC4=CC=CC=C43,C18H12,228.093900,Colorless solid.,258.2 °C,"","","2e-06 mg/mL at 25 °C [MILLER,MM et al. (1985)]","","","",Oral Inhalation (R028),Serum albumin (P02768) Cytochrome P450 1A1 (P04798) Cytochrome P450 1A2 (P05177) Cytochrome P450 1B1 (Q16678) (R060),"The ability of PAH's to bind to blood proteins such as albumin allows them to be transported throughout the body. Many PAH's induce the expression of cytochrome P450 enzymes, especially CYP1A1, CYP1A2, and CYP1B1, by binding to the aryl hydrocarbon receptor or glycine N-methyltransferase protein. These enzymes metabolize PAH's into their toxic intermediates. The reactive metabolites of PAHs (epoxide intermediates, dihydrodiols, phenols, quinones, and their various combinations) covalently bind to DNA and other cellular macromolecules, initiating mutagenesis and carcinogenesis. (R028, R060, R068, R073) ","PAH metabolism occurs in all tissues, usually by cytochrome P-450 and its associated enzymes. PAHs are metabolized into reactive intermediates, which include epoxide intermediates, dihydrodiols, phenols, quinones, and their various combinations. The phenols, quinones, and dihydrodiols can all be conjugated to glucuronides and sulfate esters; the quinones also form glutathione conjugates. (R028)","LD50: > 320 mg/kg (Intraperitoneal, Mouse) (R373)","","2B, possibly carcinogenic to humans. (R264)","PAHs are released into the environment via the combustion of fossil fuels, coke oven emissions and vehicle exhausts, as well as naturally from forest fires and volcanic eruptions. PAHs from these sources may contaminate nearly water systems. They are also found in coal tar and charbroiled food. Chrysene is also used in the manufacture of some wood preservatives and dyes. (R028)","","PAHs are carcinogens and have been associated with the increased risk of skin, respiratory tract, bladder, stomach, and kidney cancers. They may also cause reproductive effects and depress the immune system. (R028)","Acute exposure to PAHs causes irritation and inflammation of the skin and lung tissue. (R034)
",There is no known antidote for PAHs. Exposure is usually handled with symptomatic treatment. (R028),P35869;Q14749;DNA
139,T3D0138,2009-03-06 18:58:09 UTC,2009-08-04 21:27:47 UTC,Chlordecone,Organic Compound;Pesticide;Organochloride,"Caswell No. 275ChlordecaneChlordeconeChlordecone (kepone)Chlordecone [iso]ChlorodeconeClordeconeCompound 1189Decachloro-1,3,4-metheno-2H-cyclobuta(cd)pentalen-2-oneDecachloroketoneDecachloropentacyclo(5.3.0.02,6.04,10.05,9)decan-3-oneDecachloropentacyclo[5.2.1.0(2,6).0(3,9).0(5,8)]decan-4-oneDecachlorotetracyclodecanoneGeneral chemicals 1189HlordecaneKepone-2-one, decachlorooctahydro-MerexPS701_SUPELCOPerchloropentacyclo(5.3.0.0(2,6).0(3,9).0(4,8))decan-5-onePerchloropentacyclo[5.3.0.02,6.03,9.04,8]decan-5-oneRCRA waste no. U142Rcra waste number U142decachlorooctahydrokepone-2-onedecachlorotetrahydro-4,7-methanoindeneoneperchloropentacyclo[5.3.0.0(2,6).0(3,9).0(4,8)]decan-5-one","Chlordecone is a manufactured insecticide also known as Kepone. It was used mainly on tobacco, ornamental shrubs, bananas, and citrus trees, and in ant and roach traps. However, its use was banned in 1975 due to its toxicity and nature as a persistent organic pollutant. (R933, R934)",,143-50-0,299,,C01792,"",16548,"",,D007631,Chlordecone,784,,,http://en.wikipedia.org/wiki/Kepone,"InChI=1/C10Cl10O/c11-2-1(21)3(12)6(15)4(2,13)8(17)5(2,14)7(3,16)9(6,18)10(8,19)20","",http://www.biospider.ca/saved_files/mol/53b5692c048d5336c360b93dc08116bc_1237948866.mol,C1(=O)C2(C3(C4(C1(C5(C2(C3(C(C45Cl)(Cl)Cl)Cl)Cl)Cl)Cl)Cl)Cl)Cl,C1(=O)C2(C3(C4(C1(C5(C2(C3(C(C45Cl)(Cl)Cl)Cl)Cl)Cl)Cl)Cl)Cl)Cl,C10Cl10O,485.683440,White powder.,350 °C,,,"0.0027 mg/mL at 25 °C [KILZER,L et al. (1979)]",,,,"Oral
Inhalation
Dermal
(R933)","Albumin (P02768)
(R933)","It is believed that the α-noradrenergic and serotonergic transmitter systems in the central nervous system are the primary neurotransmitter systems affected by chlordecone's neurotoxicity. Chlordecone causes spontaneous neurotransmitter release and increases in free intracellular calcium in synaptosomes by increasing permeability of the plasma membrane, activating voltage-dependent calcium channels, inhibiting of brain mitochondrial calcium uptake, and decreasing the activity of calmodulin-stimulated enzymes and Na+/K+, Mg+, and Ca+ ATPases. This inhibition of membrane ATPases also impairs energy-dependent cellular processes. Chlordecone causes its reproductive effects by binding to the estrogen and androgen receptors. (R933, R965, R966)","Chlordecone is well absorbed orally and through inhalation, but may also be absorbed dermally to a lesser extent. It is widely distributed throughout the body and concentrates in the liver, where it is metabolized to chlordecone alcohol by chlordecone reductase. Chlordecone, chlordecone alcohol, and their glucuronide conjugates are slowly excreted in the bile and eliminated in the feces. (R933)","LD50: 132 mg/kg (Oral, Rat) (R327)
LD50: 410 mg/kg (Percutaneous, Rabbit) (R327)",,"2B, possibly carcinogenic to humans. (R264)",Chlordecone is an insecticide. (R933),"Acute Oral: 0.01 mg/kg/day (R260)
Intermediate Oral: 0.0005 mg/kg/day (R260)
Chronic Oral: 0.0005 mg/kg/day (R260)","Chlordecone damages the nervous system, skin, liver, and male reproductive system. Animal studies indicate that it may also have harmful kidney effects, developmental effects, and effects on the ability of females to reproduce. (R933)","Exposure to chlordecone may cause tremors, jerky eye movements, memory loss, headaches, slurred speech, unsteadiness, lack of coordination, loss of weight, rash, enlarged liver, decreased libido, sterility, chest pain, arthralgia, and an increased risk of developing cancer. (R934)",Treatment of chlordecone exposure is symptomatic. (R935),P03372;P10275;Q08828;O60266;P40145;P98194;O75185;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;P54710;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P78334;Q8N1C3;P18507;Q99928;O00591;P24046;P28476;A8MPY1;Q9UN88;Q92731
140,T3D0139,2009-03-06 18:58:09 UTC,2009-08-25 19:47:31 UTC,Iodine-129,Inorganic Compound;Halogen;Radioactive Isotope,"Iodine 129Iodine, isotope of mass 129Iodine-129","Iodine is a chemical element that has the symbol I and atomic number 53. Chemically, iodine is the second least reactive of the halogens, and the second most electropositive halogen; trailing behind astatine in both of these categories. However, the element does not occur in the free state in nature. As with all other halogens, when freed from its compounds iodine forms diatomic molecules. Iodine naturally occurs in the environment chiefly as a dissolved iodide in seawater, although it is also found in some minerals and soils. Iodine is an essential trace element for life, mainly as constituents of the thyroid hormones, thyroxine (T4) and triiodothyronine (T3). Iodine-129 is used for a variety of dating applications, including groundwater age dating and meteorite age dating. (W518, W520)",,15046-84-1,6433622,,"","","","",,,Iodine-129,,,,,InChI=1/HI/h1H/i1+2,iodane,http://www.biospider.ca/saved_files/mol/,[129IH],[129I],HI,127.912290,Grey solid.,"",,,"",,,,"Oral
Inhalation
Dermal
(W517)","Thyroid peroxidase (P07202)
(W517)","Iodide inhibits adenylate cyclase in thyroid gland follicle cells and decreases the TSH-induced rise in intracellular cAMP. This results in decreased iodination of thyroglobulin and inhibited production and release of T4 and T3, causing hypothyroidism. The ionizing radiation produced by radioiodine causes cellular damage that includes DNA breakage, accurate or inaccurate repair, apoptosis, gene mutations, chromosomal change, and genetic instability. This leads to loss of normal cell and tissue homeostasis, and development of malignancy. Ionizing radiation that does not directly damage DNA can produce reactive oxygen intermediates that directly affect the stability of p53, an important enzyme in cell-cycle regulation, and produce oxidative damage to individual bases in DNA and point mutations by mispairing during DNA replication. (W510, W514, W517)","Iodine can enter the body following ingestion, inhalaiton, or dermal exposure. In the body, iodine and iodide accumulates in the thyroid gland, where it is used for producing the thyroid hormones T4 and T3. Iodide in the thyroid gland is incorporated into a protein, thyroglobulin, as covalent complexes with tyrosine residues. The iodination of thyroglobulin is catalyzed by the enzyme thyroid peroxidase. The iodination reactions occur at the follicular cell-lumen interface and consist of the oxidation of iodide to form a reactive intermediate, the formation of monoiodotyrosine and diiodotyrosine residues in thyroglobulin, and the coupling of theiodinated tyrosine residues to form T4 (coupling of two diiodotyrosine residues) or T3 (coupling of a monoiodotyrosine and diiodotyrosine residue) in thyroglobulin. The major pathways of metabolism of iodine that occur outside of the thyroid gland involve the catabolism of T4 and T3, and include deiodination reactions, ether bond cleavage of thyronine, oxidative deamination and decarboxylation of the side chain of thyronine, and conjugation of the phenolic hydroxyl group on thyronine with glucuronic acid and sulfate. Absorbed iodine is excreted primarily in the urine and feces, but is also excreted in breast milk, exhaled air, sweat, and tears. (W517)",,,"1, carcinogenic to humans. (R264)","Iodine-129 is used for a variety of dating applications, including groundwater age dating and meteorite age dating. (W520)",,"Exposure to high levels of nonradioactive and radioactive iodine can damage the thyroid. Damage to the thyroid gland can result in effects in other parts of your body, such as your skin, lung, and reproductive organs. Concentrated iodine is very corrosive and can damage the mucous membrane if swallowed. Radioactive iodine can also cause cancer, especially of the thyroid, where it tends to concentrate. (W517, W519, W521)","Ingestion of iodine may cause corrosive effects such as oedema of the glottis, with asphyxia, aspiration pneumonia, pulmonary oedema and shock, as well as vomiting and bloody diarrhea. The CNS, cardiovascular and renal toxicity following acute iodine ingestion appear to be due to the corrosive gastroenteritis and resultant shock. Vomiting, hypotension and circulatory collapse may be noted following severe intoxication. Exposure to high doses of ionizing radiation results in acute radiation syndrome, which can cause skin burns, hair loss, nausea, vomiting, dizziness, disorientation, low blood pressure, headache, fatigue, weakness, fever, birth defects, illness, infection, and death. (W510, W525, W521)","Sodium thiosulphate, 100 mL orally of a 1% solution, has been recommended as an antidote because it immediately reduces iodine to iodide. Treatment reversing the effects of irradiation is currently not possible. Anaesthetics and antiemetics are administered to counter the symptoms of exposure, as well as antibiotics for countering secondary infections due to the resulting immune system deficiency. (W525, W521)",Q08828;Q08462;O60266;Q8NFM4;O95622;O43306;P51828;P40145;O60503;Q96PN6;DNA
141,T3D0140,2009-03-06 18:58:09 UTC,2009-08-25 15:59:46 UTC,Plutonium-240,Inorganic Compound;Metal;Plutonium Compound;Radioactive Isotope,"Plutonium, isotope of mass 240Plutonium-240","Plutonium is an element with the symbol Pu and atomic number 94. It is a rare transuranic radioactive element that normally exhibits six allotropes and four oxidation states. It is also a radioactive poison that accumulates in bone marrow. Plutonium-240 has a high rate of spontaneous fission, raising the background neutron radiation of plutonium containing it. Plutonium is graded by proportion of Pu-240. Lower grades are less suited for nuclear weapons and thermal reactors but can fuel fast reactors. Pu-240 is not fissile, but is fertile material like U-238. (W513)",,14119-33-6,104728,,"","","","",,,Plutonium-240,,,,,InChI=1/Pu/i1-4,plutonium-240,http://www.biospider.ca/saved_files/mol/,[240Pu],[240Pu],Pu,0.000000,,"",,,"",,,,"Oral
Inhalation
(R513)","Serum albumin (P02768)
Serotransferrin (P02787)
Ferritin light chain (P02792)
Ferritin heavy chain (P02794)
Ferritin, mitochondrial (Q8N4E7)
(W514)","The alpha radiation plutonium emits does not penetrate the skin but can irradiate internal organs when plutonium is inhaled or ingested. Particularly at risk are the skeleton, where it is likely to be absorbed by the bone surface, and the liver, where it collects and becomes concentrated. The ionizing radiation produced by plutonium causes cellular damage that includes DNA breakage, accurate or inaccurate repair, apoptosis, gene mutations, chromosomal change, and genetic instability. This leads to loss of normal cell and tissue homeostasis, and development of malignancy. Ionizing radiation that does not directly damage DNA can produce reactive oxygen intermediates that directly affect the stability of p53, an important enzyme in cell-cycle regulation, and produce oxidative damage to individual bases in DNA and point mutations by mispairing during DNA replication. (W510, W514)","Plutonium-240 can affect the body following ingestion or inhalation. When inhaled, Pu-240 distributes to the lungs, liver and skeleton. Ingested plutonium is found in the liver and bone. Plutonium metabolism consists primarily of hydrolytic reactions and formation of complexes with protein and nonprotein ligands, such as albumin, globulins, ferritin, citrate, and lactate. Plutonium is excreted in feces and urine. (W514)",,,"1, carcinogenic to humans. (R264)","Plutonium-240 has a high rate of spontaneous fission, raising the background neutron radiation of plutonium containing it. Plutonium is graded by proportion of Pu-240. Lower grades are less suited for nuclear weapons and thermal reactors but can fuel fast reactors. (W513)",,"Plutonium's radioactivity can cause cancers of the bone, liver, and lungs if ingested or inhaled. Large amounts may also cause acute radiation poisoning. (W513, W514) ","Exposure to high doses of ionizing radiation results in acute radiation syndrome, which can cause skin burns, hair loss, nausea, vomiting, dizziness, disorientation, low blood pressure, headache, fatigue, weakness, fever, birth defects, illness, infection, and death. (W510, W525)","Treatment reversing the effects of irradiation is currently not possible. Anaesthetics and antiemetics are administered to counter the symptoms of exposure, as well as antibiotics for countering secondary infections due to the resulting immune system deficiency. (W525)",DNA
142,T3D0141,2009-03-06 18:58:09 UTC,2009-08-04 21:27:48 UTC,"S,S,S-Tributyl phosphorotrithioate",Organic Compound;Pesticide;Organophosphate,"ButifosButiphosButyl Phosphorotrithioate ((BuS)3PO)Butyl phosphorotrithioateButyphosCaswell No. 864Chemagro 1,776Chemagro B-1776DEFDe-greenDef defoliantDeleaf defoliantE-z-off dEasy off-dFolex 6ECFos-fall &quot;a&quot;Fos-fall aFosfallFossfallMerphos oxideMerphos-oxonOrtho phosphate defoliantPhosphorotrithioic acid, s,s,s-tributyl esterS,s,s-tributyl trithiophosphateS,s,s-tributylphosphorotrithioateS,s,s-tributyltrithiofosfatS,s,s-tributyltrithiofosfat [czech]S,s,s-tributyltrithiophosphateTBTPTribufosTribuphosTributyl s,s,s-phosphorotrithioateTributylphosphorotrithioate","S,S,S-Tributyl phosphorotrithioate (Tribufos) is a plant growth regulator belonging to the organophosphate group of pesticides. Tribufos was registered for use on cotton as a defoliant. (R601)",,78-48-8,5125,,"","",38737,SER,,C006863,"S,S,S-Tributyl phosphorotrithioate",6478,,,,"InChI=1/C12H27OPS3/c1-4-7-10-15-14(13,16-11-8-5-2)17-12-9-6-3/h4-12H2,1-3H3",1-bis(butylsulfanyl)phosphorylsulfanylbutane,http://www.biospider.ca/saved_files/mol/,CCCCSP(=O)(SCCCC)SCCCC,CCCCSP(=O)(SCCCC)SCCCC,C12H27OPS3,314.096160,Colorless liquid.,<-25 °C,,,"0.0023 mg/mL at 20 °C [TOMLIN,C (1994)]",,,,"Inhalation
Dermal
(R605)",,"Like other organophosphate compounds, S,S,S-tributyl phosphorotrithioate causes neurotoxic effects by inhibiting acetylcholinesterase. This results in overstimulation of the central nervous system. It also inhibits an endogenous signaling modulator, fatty acid amide hydrolase, producing secondary neurotoxicity. (R973)",,"LD50: 97 mg/kg (Dermal, Rabbit) (R261)
LD50: 290 mg/kg (Intraperitoneal, Rat) (R261)
LD50: 150 mg/kg (Oral, Rat) (R261)
LC50: 4.65 mg/L over 4 hours (Inhalation, Rat) (R971)",,,"S,S,S-Tributyl phosphorotrithioate is a plant growth regulator and pesticides. It was registered for use on cotton as a defoliant. (R601)",,"S,S,S-Tributyl phosphorotrithioate affects the central nervous system. (R605)","Symptoms include nausea, vomiting, abdominal cramps, diarrhea, excessive salivation, headache, giddiness, vertigo and weakness. Rhinorrhea and sensation of tightness in chest are common in inhalation exposure. Blurring or dimness of vision, miosis, tearing, ciliary muscle spasm, loss of accommodation, ocular pain, and mydriasis may also occur. (R605)","",P22303;O00519;Q6GMR7
143,T3D0142,2009-03-06 18:58:09 UTC,2009-08-04 21:27:48 UTC,Bromine,Inorganic Compound;Halogen,"BRBR(-)BR-BROMBromeBromide ionBromide ionsBromine anionBromine ionBromine, ionBromoBroomCaswell No. 499DDibromineInorganic bromidesbromide(1-)","Bromine is a halogen element with the symbol Br and atomic number 35. Diatomic bromine does not occur naturally, but bromine salts can be found in crustal rock. There are also several organic bromine compounds that occur in marine organisms. It is used mainly in fire retardants and fine chemicals. Bromine salts have also been used as gasoline additives and pesticides. Bromine vapours are corrosive and toxic. (R987)",,7726-95-6,259,,C01324,"",29224,BR-,,D001966,Bromine,8170,,,http://en.wikipedia.org/wiki/Bromide,InChI=1/BrH/h1H/p-1,bromide,http://www.biospider.ca/saved_files/mol/e2770d3e6257c47e7fa75a2aec7bd345_1237949253.mol,[Br-],[Br-],[Br]-,78.918343,Red liquid.,-7.25 °C,,,"35 mg/mL at 20 °C [MILLS, JF (1985)]",,,,"Oral
Inhalation
Dermal
(R989)",,"Bromine is a powerful oxidizing agent and is able to release oxygen free radicals from the water in mucous membranes. These free radicals are also potent oxidizers and produce tissue damage. In additon, the formation of hydrobromic and bromic acids will result in secondary irritation. The bromide ion is also known to affect the central nervous system, causing bromism. This is believed to be a result of bromide ions substituting for chloride ions in the in actions of neurotransmitters and transport systems, thus affecting numerous synaptic processes. (R989, R990, R991)","Bromine is mainly absorbed via inhalation, but may also enter the body through dermal contact. Bromine salts can be ingested. Due to its reactivity, bromine quickly forms bromide and may be deposited in the tissues, displacing other halogens. (R989)","LD50: 85.2 ppm (Intraperitoneal, Rat) (R988)
LD50: 2600 mg/kg (Oral, Rat) (R988)
LC50: 750 ppm over 9 minutes (Inhalation, Mouse) (R988)",,,Bromine is used mainly in fire retardants and fine chemicals. Bromine salts have also been used as gasoline additives and pesticides. (R987),,"Bromine vapour causes irritation and direct damage to the mucous membranes. Elemental bromine also burns the skin. The bromide ion is a central nervous system depressant and chronic exposure produces neuronal effects. This is called bromism and can result in central reactions reaching from somnolence to coma, cachexia, exicosis, loss of reflexes or pathologic reflexes, clonic seizures, tremor, ataxia, loss of neural sensitivity, paresis, papillar edema of the eyes, abnormal speech, cerebral edema, delirium, aggressiveness, and psychoses. (R987, R989, R990)","Bromine vapour causes irritation and direct damage to the mucous membranes. Symptoms include lacrimation, rhinorrhoea, eye irritation with mucous secretions from the oropharyngeal and upper airways, coughing, dyspnoea, choking, wheezing, epistaxis, and headache. The bromide ion is a central nervous system depressant producing ataxia, slurred speech, tremor, nausea, vomiting, lethargy, dizziness, visual disturbances, unsteadiness, headaches, impaired memory and concentration, disorientation and hallucinations. (R989, R990)","Bromine should be washed with water from any areas of dermal or ocular contact. If inhaled, treatment is mainly symptomatic and may include maintaining an adequate airway, administering oxygen, antibronchospasm therapy, and/or antibiotics. (R989)",""
144,T3D0143,2009-03-06 18:58:09 UTC,2009-08-04 21:27:48 UTC,Polybrominated biphenyls,Organic Compound;Polybrominated Biphenyl;Aromatic Hydrocarbon;Organobromide,"1,1'-Biphenyl, 2,2',4,4',5,5'-hexabromo-2,2',4,4',5,5'-Hexabromo-1,1'-biphenyl2,2',4,4',5,5'-Hexabromobiphenyl2,2'4,4',5,5'-Hexabromo-1,1'-biphenyl2,2'4,4'5,5'-Hexabromo-1,1'-biphenyl2,4,5,2',4',5'-HexabromobiphenylBrominated biphenylFiremaster FF-1Firemaster FF-1, technical grade [Polybrominated biphenyls]HexabromobiphenylPBBPolybrominated biphenylPolybrominated biphenyl mixturePolybrominated biphenyl mixture (Firemaster FF-1)Polybrominated biphenylspolybrominated biphenyl (ff-1)","Polybrominated biphenyls (PBBs) are a group of 209 synthetic organic compounds with 1-10 bromine atoms attached to biphenyl. They can be used as flame retardants and may be added to the plastics used to make products like computer monitors, televisions, textiles, and plastic foams to prevent them to burn. However, the use of PBBs is banned or restricted in most areas due to their toxicity and persistence in the environment. (R994, R995)",,67774-32-7,42948,,"","","","",,C027365,Polybrominated biphenyls,,,,,InChI=1/C12H4Br6/c13-7-3-11(17)9(15)1-5(7)6-2-10(16)12(18)4-8(6)14/h1-4H,"1,2,4-tribromo-5-(2,4,5-tribromophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=C(C(=CC(=C1Br)Br)Br)C2=CC(=C(C=C2Br)Br)Br,C1=C(C(=CC(=C1Br)Br)Br)C2=CC(=C(C=C2Br)Br)Br,C12H4Br6,621.541330,Colorless to white solid.,"",,,"",,,,"Oral
Inhalation
Dermal
(R994)",,"The exact mechanism of toxicty of PBBs varies depending on the specific congener. The predominant interaction is believed to involve the aryl hydrocarbon receptor (AhR). PBBs bind to and activate the AhR, which in turn initiates the transcriptional upregulation of a number of genes, affecting biochemical and endocrine pathways, cell cycle regulation, morphogenesis, oxidative stress response, and various other processes. This results in the numerous toxic responses characteristic of PBBs. Some of the known induced genes include the cytochrome P-450-dependent monooxygenases CYP1A1 and CYP1A2. (R994)","PBBs can be absorbed via oral, inhalation, and dermal routes. Due to their lipophilic nature, PBBs, especially the highly brominated congeners, tend to accumulate in lipid-rich tissues such as the liver, adipose tissue, skin, and breast milk. Certain PBB compounds are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 of the type induced by phenobarbital. The rate of metabolism may depends on the bromine substitution pattern. PBB congeners of low bromine content are transformed into hydroxylated derivatives that are predominately eliminated in the urine. Highly brominated congeners are either retained or excreted unchanged in the feces. (R994)",,,"2B, possibly carcinogenic to humans. (R264)","PBBs can be used as flame retardants and may be added to the plastics used to make products like computer monitors, televisions, textiles, and plastic foams to prevent them to burn. However, the use of PBBs is banned or restricted in most areas due to their toxicity and persistence in the environment. (R994, R995)",Acute Oral: 0.01 mg/kg/day (R260),"PBB exposure may cause weight loss, skin disorders (such as acne), nervous and immune systems effects, and effects on the liver, kidneys, and thyroid gland. (R994)","Symptoms of PBB exposure may include nausea, abdominal pain, loss of appetite, joint pain, fatigue, and weakness. (R995)","",P35869
145,T3D0144,2009-03-06 18:58:09 UTC,2009-08-04 21:27:48 UTC,Dicofol,Organic Compound;Pesticide;Aromatic Hydrocarbon;Organochloride,"1,1,1-Trichlor-2,2-bis(4-chlorphenyl)-aethanol1,1,1-Trichlor-2,2-bis(4-chlorphenyl)-aethanol [German]1,1-Bis(4-chlorophenyl)-2,2,2-trichloroethanol1,1-Bis(chlorophenyl)-2,2,2-trichloroethanol1,1-Bis(p-Chlorophenyl)-2,2,2-trichloroethanol1,1-Bis-(p-chlorophenyl)-2,2,2-trichloroethanol1,1-bis-(chlorophenyl)-2,2,2-trichloroethanol2,2,2-Trichloor-1,1-bis(4-chloor fenyl)-ethanol2,2,2-Trichloor-1,1-bis(4-chloor-fenyl)-ethanol [Dutch]2,2,2-Trichlor-1,1-bis(4-chlor-phenyl)-aethanol2,2,2-Trichlor-1,1-bis(4-chlor-phenyl)-aethanol [German]2,2,2-Trichloro-1,1-bis(4-chlorophenyl)-ethanol [French]2,2,2-Trichloro-1,1-bis(4-chlorophenyl)ethanol2,2,2-Trichloro-1,1-bis(4-cloro-fenil)-etanolo2,2,2-Trichloro-1,1-bis(4-cloro-fenil)-etanolo [Italian]2,2,2-Trichloro-1,1-bis(p-chlorophenyl)ethanol2,2,2-Trichloro-1,1-di(4-chlorophenyl)ethanol2,2,2-Trichloro-1,1-di-(4-chlorophenyl)ethanol4,4'-Dichloro-&alpha;-(trichloromethyl)benzhydrol4,4'-Dichloro-.alpha.-(trichloromethyl)benzhydrol4,4'-Dichloro-alpha-(trichloromethyl)benzhydrolAcarinBenzhydrol, 4,4'-dichloro-&alpha;-(trichloromethyl)-Benzhydrol, 4,4'-dichloro-alpha-(trichloromethyl)-Bis(chlorophenyl)-2,2,2-trichl oroethanolBis(chlorophenyl)-2,2,2-trichloroethanolCPCACarbaxCarboxCaswell No. 093CekudifolDTMCDecofolDi-(p-chlorophenyl)trichloromethylcarbinolDichlorokelthaneDicofolDicofol (kelthane)Dicofol [bsi:iso]DicomiteEthanol, 2,2,2-Trichloro-1,1-bis(4-chlorophenyl)-Ethanol, 2,2,2-trichloro-1,1-bis(p-chlorophenyl)-Ethanol,1,1-bis(p-chlorophenyl)-2,2,2-trichloro-Fumite dicofolHifolHilfolHilfol 18.5 ecKeltaneKelthaneKelthane aKelthane dust baseKelthanethanolKelthoneMifolMilbolMitiganP,p'-di cofolP,p'-dicofolP,p'-kelthaneP,p-dicofolPara,para'-kelthaneTricofol","Dicofol is an organochlorine pesticide that is chemically related to DDT. Specifically, it is used as a miticide against the red spider mite. Though difocol is not extremely toxic, its use is controverial because one of the intermediates used in its production is DDT. It also may accumulate in the environment and its use is restricted in many areas. (R1001)",,115-32-2,8268,,C14301,"",34692,CPD-121,,D004010,Dicofol,456,,,,"InChI=1/C14H9Cl5O/c15-11-5-1-9(2-6-11)13(20,14(17,18)19)10-3-7-12(16)8-4-10/h1-8,20H","2,2,2-trichloro-1,1-bis(4-chlorophenyl)ethanol",http://www.biospider.ca/saved_files/mol/8660acfe1b80ea5db4ad28fd48a0cc6a_1237949522.mol,C1=CC(=CC=C1C(C2=CC=C(C=C2)Cl)(C(Cl)(Cl)Cl)O)Cl,C1=CC(=CC=C1C(C2=CC=C(C=C2)Cl)(C(Cl)(Cl)Cl)O)Cl,C14H9Cl5O,367.909600,"",77.5 °C,"","","0.0008 mg/mL at 25 °C [TOMLIN,C (1997)]","","","","Oral
Inhalation
Dermal
(R1001)","","Like other organochloride pesticides, dicofol is believed to act by at least four mechanisms, possibly all functioning simultaneously. It may reduce potassium transport across the membrane. Dicofol also alters the porous channels through which sodium ions pass. These channels activate (open) normally but are inactivated (closed) slowly, thus interfering with the active transport of sodium out of the nerve axon during repolarization. Dicofol inhibits neuronal adenosine triphosphatases (ATPases), particularly Na+K+-ATPase, and Ca2+-ATPase which play vital roles in neuronal repolarization. Dicofol also inhibits the ability of calmodulin, a calcium mediator in nerves, to transport calcium ions that are essential for the release of neurotransmitters. All these inhibited functions reduce the rate of depolarization and increase the sensitivity of neurons to small stimuli that would not elicit a response in a fully depolarized neuron. Difocol is also an endocrine disruptor and binds both the androgen and estrogen receptor. In addition, it may alter sex hormone metabolism by directly inhibiting cytochrome P-450 19A1. Difocol is able to competitively bind transthyretin, which lowers plasma thyroid hormone levels. (R029, R966, R1002, R1003)","Dicofol can be absorbed via oral, inhahation, and dermal routes. It is distributed primarily to the adipose tissue, as well as the adrenal glands, thyroid, and liver. Metabolism of dicofol produces the metabolites 4,4'-dichloro-benzophenone and 4,4'-dichlorodicofol. Dicofol and its metabolites are excreted mainly in the faeces. (R1001, R1004)","LD50: 595 mg/kg (Oral, Rat) (R926)
LD50: 2100 mg/kg (Percutaneous, Rabbit) (R715)","","3, not classifiable as to its carcinogenicity to humans. (R264)","Dicofol is used as a pesticide on agricultural crops and ornamental plants, as well as for agricultural and domestic buildings for mite control. (R1001)","","Dicofol poisoning affects the liver, kidneys and the central nervous system. Very severe cases may result in convulsions, coma, or death from respiratory failure. High doses may also cause reproductive damage. (R1001)","Symptoms exposure include nausea, dizziness, weakness and vomiting. Dermal exposure may cause skin irritation or a rash, and eye contact may cause conjunctivitis. (R029, R1001)","Treatment of dicofol poisoning is mainly symptomatic. Areas of contact should be washed with soap and water, and gastric lavage may be performed if ingested. (R1004)",P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P54710;P98194;O75185;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;P62158;P03372;P10275;Q9Y3Q4;Q9UL51;O60741;Q9P1Z3 ;P35498;Q9Y5Y9;Q9UI33;Q99250;Q9NY46;P35499;Q14524;Q01118;Q9UQD0;Q15858;Q07699;O60939;Q9NY72;Q8IWT1;P11511;P02766;P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P78334;Q8N1C3;P18507;Q99928;O00591;P24046;P28476;A8MPY1;Q9UN88;Q92731
146,T3D0145,2009-03-06 18:58:10 UTC,2009-08-04 21:27:48 UTC,Parathion,Organic Compound;Pesticide;Aromatic Hydrocarbon;Organophosphate,"0, 0-Diethyl 0-(p-nitrophenyl) phosphorothioate0,0-Diethyl 0-(p-nitrophenyl) phosphorothioate0,0-Diethyl 0-(p-nitrophenyl) thiophosphateAATAATPAlkronAlleronAphamiteAqua 9-ParathionAral oAraloBayer E-605BladanBladan fBladenCaswell No. 637Compound 3422CorothionCorthionCorthioneDNTPDPPDanthionDiethoxy, nitro-phenoxy phosphorothioateDiethyl o-p-nitrophenyl phosphorothioateDiethyl p-nitroph enyl monothiophosphateDiethyl p-nitrophenyl monothiophosphateDiethyl p-nitrophenyl phosphorothionateDiethyl p-nitrophenyl thionophosphateDiethyl p-nitrophenyl thiophosphateDiethyl para-nitrophenol thiophosphateDiethyl parathionDiethyl-p-nitrophenyl monothiophosphateDiethylparathionDietil tiofosfato de p-nitrofenila [portuguese]DurathionE 605 FORTEEcatoxEcatox 20Ekatin WF & WF ulvEkatoxEkatox 20EthlonEthyl parathionEthyl parathion (o,o-diethyl-o-p-nitrophenylthiophosphate)Ethyl parathion 50 ECEthyle-parathionEthylparathionEthylparathioneEtilonEtylparationEtylparation (czech)Etylparation [czech]FoliclalFolidolFolidol E &amp; E 605Folidol E-605Folidol eFolidol oilFosfermoFosfernoFosferno 50FosfexFosfiveFosovaFosternFostoxGearphosGenithionIsotoxJacutinKokotineKolphosKwellKypthionLi rothionLirothionMurfosMurphosNIUIF 100NiranNiran E-4NitrostigminNitrostigmin [german]NitrostigmineNitrostygmineNourithionO, O-Diethyl O-(4-nitrophenyl) phosphorothioateO, O-Dietil-O-(4-nitro-fenil)-monotiofosfato (ITALIAN)O, O-diaethyl-O-(4-nitro-phenyl)-monothiophosphat (GERMAN)O, O-diethyl-O-(4-nitro-fenil)monothiofosfaat (DUTCH)O, o-dietyl-o-p-nitrofenyltiofosfat (czech)O,O-Diaethyl-O-(4-nitro-phenyl)-monothiophosphat [German]O,O-Diethyl O-(4-nitrophenyl) phosphorothioateO,O-Diethyl O-(4-nitrophenyl) thiophosphateO,O-Diethyl O-4-nitrophenyl thiophosphateO,O-Diethyl-O-(4-nitro-fenil)-monothiofosfaat [Dutch]O,O-Diethyl-O-(4-nitrophenyl) phosphorothioateO,O-Dietil-O-(4-nitro-fenil)-monotiofosfatoO,O-Dietil-O-(4-nitro-fenil)-monotiofosfato [Italian]O,O-diaethyl-O-(4-nitro-phenyl)-monothiophosphatO,O-diethyl-O-(4-nitro-fenil)monothiofosfaatO,o-diethyl o-(p-nitrophenyl) phosphorothioateO,o-diethyl o-(p-nitrophenyl) thionophosphateO,o-diethyl o-(p-nitrophenyl) thiophosphateO,o-diethyl o-p-nitrophenyl phosphorothioateO,o-diethyl o-p-nitrophenyl thiophosphateO,o-diethyl o-p-nitrophenylphosphorothioateO,o-diethyl-o-(p-nitrophenyl)thionophosphateO,o-diethyl-o-p-nitrofenylester kyseliny thiofosforecneO,o-diethyl-o-p-nitrophenylthiophosphateO,o-dietyl-o-p-nitrofenyltiofosfatO,o-dietyl-o-p-nitrofenyltiofosfat [czech]OleoparapheneOleoparatheneOleoparathionOrthophosP- nitrophenol o-ester with o,o-diethylphosphorothioateP-nitrophenol o-ester with o,o-diethylphosphorothioateP-nitrophenyl diethyl thiophosphatePACPH osphenolPacolPanthionParadustParamarParaphosParatheneParathion 20 wpParathion [NA2783] [Poison]Parathion [bsi:iso]Parathion and compressed gas mixture [NA1967] [Poison gas]Parathion ethylParathion mixtureParathion solutionParathion, ethylParathion, liquidParathion, liquid (dot)Parathion-aethylParathion-aethyl [german]Parathion-eParathion-ethylParathion-ethyl solutionParawetParthionPenncap ePestox plusPethionPhenol, p-nitro-, 0-ester with 0,0-diethyl phosphorothioatePhenol, p-nitro-, o-ester with o,o-diethyl phosphorothioatePhenol, p-nitro-, o-ester with o,o-diethylphosphorothioatePhoskilPhosphemolPhosphenolPhosphorothioic acid O,O-diethyl-O-(4-nitrophenyl) esterPhosphorothioic acid, O,O-diethyl O-(4-nitrophenyl) esterPhosphorothioic acid, o,o-diethyl o-(p-nitrophenyl) esterPhosphostigmineRBRCRA waste no. P089Rcra waste number P089RhodiasolRhodiatoxRhodiatroxRodiatoxS.n.p.SNPSelephosSixty-three special e.cSixty-three special e.c.Sixty-three special e.c. insecticideSixty-three special ec insecticideSoprathionSoprothionStabilized ethyl parathionStathionStrathionSul fosSulfosSulphosSuper rodiatoxThiofosThiomexThionspray No.84ThiophosThiophos parathion 4 E.C.Thiophosphate de O,O-diethyle et de O-(4-nitrophenyle)TiofosVapophosViranVitrexVitrex hgiWLN: WNR DOPS&O2&O2american cyanamid 3422deoxynucleoside 5'-triphosphatediethyl 4-nitrophenyl phosphorothionatedrexel parathion 8Efolidol e & e 605folidol e e 605folidol e605lethalaire g-54niuif-100oleofos 20paramar 50thiophos 3422","Parathion, also called parathion-ethyl or diethyl parathion, is an organophosphate compound. It is a potent insecticide and acaricide that is generally applied by spraying, most often to cotton, rice, and fruit trees. As parathion is highly toxic to non-target organisms, its use is banned or restricted in many areas. (R1005)",,56-38-2,991,,C06604,"",27928,PARATHION,,D010278,Parathion,1126,,,http://en.wikipedia.org/wiki/Parathion,"InChI=1/C10H14NO5PS/c1-3-14-17(18,15-4-2)16-10-7-5-9(6-8-10)11(12)13/h5-8H,3-4H2,1-2H3",diethoxy-(4-nitrophenoxy)-sulfanylidene-phosphorane,http://www.biospider.ca/saved_files/mol/5dad4cf38e6f44db24999d06ea1a6374_1237949600.mol,CCOP(=S)(OCC)OC1=CC=C(C=C1)[N+]([O-])=O,CCOP(=S)(OCC)OC1=CC=C(C=C1)[N+]([O-])=O,C10H14NO5PS,291.033030,White crystals.,6.1 °C,,,"0.011 mg/mL at 20 °C [TOMLIN,CDS (1997)]",,,,"Oral
Inhalation
Dermal
(R1005)","Cytochrome P450 3A4 (P08684) 
Cytochrome P450 2C8 (P10632) 
Serum paraoxonase/arylesterase 1 (P27169)
Glutathione S-transferase A1 (P08263)
Glutathione S-transferase theta-1 (P30711)
Serum albumin (P02768)
(R1006, R1011, R1012, R1013)","The active metabolite of parathion, paraoxon, inactivates acetylcholinesterase by phosphorylating the active site of the enzyme, thus inhibiting its activity in the nervous system and at the motor end-plate. As a result, the neurotransmitter acetylcholine accumulates in the nerve synapse or neuromuscular junction, producing overstimulation of cholinergic end organs. The immunotoxicity of parathion and other organophosphates is thought to result from their inhibition of esterases and stabilization of the lysosomal membrane of lymphocytes, thus blocking release of lymphokines. (R1005, R1006)","Parathion can be readily absorbed by humans following inhalation, oral, or dermal exposure. It is widely distributed in organs and tissues, then rapidly metabolized in the liver, to polar substances that are quickly excreted in the urine. Oxidative desulfuration by microsomal oxidases transforms methyl parathion into the neurotoxic, active metabolite, paraoxon. Other reactions include oxidation, hydrolysis, dearylation, and dealkylation detoxify parathion. (R1005, R1006)","LD50: 2 mg/kg (Oral, Rat) (R263) 
LD50: 6800 ug/kg (Dermal, Rat) (R263) 
LD05: 3600 ug/kg (Intraperitoneal, Rat) (R263) 
LD50: 6 mg/kg (Intramuscular, Rat) (R263) 
LC50: 84.0 mg (Inhalation, Rat) (R1009)",7143 mg/kg for an adult human. (R293),"3, not classifiable as to its carcinogenicity to humans. (R264)","Parathion is an insecticide and acaricide that is generally applied by spraying, most often to cotton, rice, and fruit trees. (R1005)",,"Parathion affects the central nervous system. Changes in mental state may last several months after exposure to high levels of parathion has ended. Parathion may also affect the immune system. (R1005, R1006)","Parathion exposure can result in headaches, convulsions, poor vision, vomiting, abdominal pain, severe diarrhea, unconsciousness, tremor, dyspnea, and finally lung-edema as well as respiratory arrest. (R1005)",Parathion poisoning should be treated by administering the antidote atropine. (R1005),P22303
147,T3D0146,2009-03-06 18:58:10 UTC,2009-08-04 21:27:49 UTC,"1,1,2,2-Tetrachloroethane",Organic Compound;Refrigerant;Solvent;Industrial Precursor/Intermediate;Organochloride,"(CHCl2)21, 1,2,2-Tetrachlorethane (FRENCH)1,1,2, 2-Tetrachloorethaan (DUTCH)1,1,2, 2-Tetracloroetano (ITALIAN)1,1,2,2-Czterochloroetan1,1,2,2-Czterochloroetan (POLISH)1,1,2,2-Czterochloroetan [Polish]1,1,2,2-Tetrachloorethaan1,1,2,2-Tetrachloorethaan [Dutch]1,1,2,2-Tetrachloraethan1,1,2,2-Tetrachloraethan (GERMAN)1,1,2,2-Tetrachloraethan [German]1,1,2,2-Tetrachlorethane1,1,2,2-Tetrachlorethane [French]1,1,2,2-Tetrachloroethane1,1,2,2-Tetracloroetano1,1,2,2-Tetracloroetano [Italian]1,1,2,2-tetrachloroethane (ACD/Name 4.0)1,1-Dichloro-2, 2-dichloroethane1,1-Dichloro-2,2-dichloroethaneAcetosalAcetosolAcetylene tetrachlorideBonoformCaswell No. 826CellonCellon, bonoformDichloro 2,2 dichloroethaneDichloro-2,2-dichloroethaneETHANE,1,1,2,2-TETRACHLOROHALOGENATED ETHANES CS (1,1, 2,2-TETRACHLOROETHANE)RCRA waste no. U209Rcra waste number U209S-tetrachloroethaneSYM-tetrachloroethaneSymmetrical tetrachloroethaneTCETce (ambiguous)TetrachlorethaneTetrachloroe thane, 1,1,2,2-TetrachloroethaneTetrachloroethane (van)Tetrachloroethane, 1,1,2,2-Tetrachlorure d'acetyleneTetrachlorure d'acetylene (french)Tetrachlorure d'acetylene [french]WLN: GYGYGGWestrolWestron","1,1,2,2-Tetrachloroethane is a chlorinated derivative of ethane. It has the highest solvent power of any chlorinated hydrocarbon. As a refrigerant, it is used under the name R-130. It was once widely used as a solvent and as an intermediate in the industrial production of trichloroethylene, tetrachloroethylene, and 1,2-dichloroethylene. 1,1,2,2-Tetrachloroethane was also used to separate fats and oils from other substances, to clean and degrease metals, and in paints and pesticides. However, 1,1,2,2-tetrachloroethane is no longer used much in the United States due to concerns about its toxicity. Less toxic chemicals are now available to replace this solvent, and largescale commercial production has stopped, although some production still occurs (R608, R610).",,79-34-5,6591,,"","",36026,CPD-8985,,C015530,"1,1,2,2-Tetrachloroethane",1349,,,"http://en.wikipedia.org/wiki/1,1,2,2-Tetrachloroethane",InChI=1/C2H2Cl4/c3-1(4)2(5)6/h1-2H,"1,1,2,2-tetrachloroethane",http://www.biospider.ca/saved_files/mol/,C(C(Cl)Cl)(Cl)Cl,C(C(Cl)Cl)(Cl)Cl,C2H2Cl4,165.891060,,-43.8 °C,,,"2.83 mg/mL at 25 °C [HORVATH,AL et al. (1999)]",,,,"Oral
Inhalation
Eye and dermal contact 
(R612)","Cytochrome P450 2A6 (P11509)
Cytochrome P450 2A7 (P20853)
Cytochrome P450 2A13 (Q16696)
Cytochrome P450 2B6 (P20813)
Cytochrome P450 2E1 (P05181)
Cytochrome P450 3A4 (P08684)
Cytochrome P450 3A5 (P20815)
Cytochrome P450 3A7 (P24462)
Cytochrome P450 3A43 (Q9HB55)
(R608)","The presence of the functional group consisting of a terminal dichloromethyl moiety in a molecule is known to confer toxicity. Moreover, the metabolism of 1,1,2,2-tetrachloroethane to reactive products is also likely to play a key role in its toxicity. Both nuclear and microsomal cytochrome P450 enzymes (of the CYPIIA, CYPIIB, CYPIIE, and CYPIIIA subfamilies) have been implicated in the metabolism of the compound, possibly releasing a number of biologically active compounds, including aldehydes, alkenes, acids, and free radicals that may react with biological tissues. In general, the highly lipophilic nature of chlorinated hydrocarbons, such as 1,1,2,2-tetrachloroethane, allows them to cross the blood-brain barrier readily and partition into lipids in neuronal membranes. This property allows them to interfere with neural membrane function, bringing about central nervous system depression, behavioral changes, and anesthesia. 1,1,2,2-Tetrachloroethane has been shown to bind to DNA in the liver and several other organs, indicating that this mechanism may contribute to the carcinogenic process. Several studies of 1,1,2,2-tetrachloroethane toxicity have reported increases in the number of hepatocytes in mitosis, but the possible role these effects may have on the carcinogenicity of 1,1,2,2-tetrachloroethane has not been evaluated. (R608)","1,1,2,2-tetrachloroethane appears to be distributed throughout the body, but may selectively accumulate to a degree in certain cells and tissues. Because it is a volatile, lipophilic molecule of small molecular size that appears to be readily absorbed from the respiratory and gastrointestinal tracts, passive diffusion is the most likely mechanism of absorption. The metabolism of 1,1,2,2-tetrachloroethane proceeds via multiple pathways. The predominant pathway appears to involve production of dichloroacetic acid, formed as an initial metabolite via stagewise hydrolytic cleavage of 1,1,2,2-tetrachloroethane, or by cytochrome P450-based oxidation of 1,1,2,2-tetrachloroethane. Dichloroacetic acid has been identified as the major urinary metabolite. Dichloroacetic acid can be further metabolized to glyoxylic acid, formic acid, and carbon dioxide, with carbon dioxide a potential major component of the end products. Other pathways involve the formation of trichloroethylene or tetrachloroethylene as initial metabolites, with subsequent reactions yielding trichloroethanol, trichloroacetic acid, and oxalic acid as important end products. Metabolism of 1,1,2,2-tetrachloroethane is generally extensive, with 68% or more of a total administered dose found as metabolites. Following absorption into the body, 1,1,2,2-tetrachloroethane is eliminated mainly as metabolites in the urine and as carbon dioxide and unchanged compound in expired air. (R608)","LD50: 250 mg/kg/day (Oral, Rat) (R608) 
LD50: 6,360 mg/kg (Dermal, Rabbit) (R608)","","3, not classifiable as to its carcinogenicity to humans. (R264)","1,1,2,2-Tetrachloroethane was used as a refrigerant, a solvent, and as an intermediate in the industrial production of trichloroethylene, tetrachloroethylene, and 1,2-dichloroethylene. 1,1,2,2-Tetrachloroethane was also used to separate fats and oils from other substances, to clean and degrease metals, and in paints and pesticides. Exposure may occur from breathing concentrated fumes of 1,1,2,2-tetrachloroethane, drinking contaminated water or eating contaminated food, or through skin or eye contact. (R608)","Intermediate Oral: 0.5 mg/kg/day (Rat) (R260, R608)","Liver, gastro-intestinal tract and nervous system (central peripheral) are the targets in chronic exposure. Toxic effects are also reported in the hematopoietic system. Breathing high levels of 1,1,2,2-tetrachloroethane for a long time can cause liver damage. Drinking very large amounts of 1,1,2,2-tetrachloroethane can cause shallow breathing, faint pulse, decreased blood pressure, and possibly unconsciousness. Central nervous system effects include general anesthesia, somnolence, hallucinations, and distorted perceptions. Other effects include narcosis, acute yellow atrophy of the liver, liver cirrhosis, fatty degeneration of the kidneys and heart, brain changes, changes in the peripheral nerves, hematemesis, purpuric rashes, and blood changes, including an increase in mononuclear leukocytes, progressive anemia, and slight thrombocytosis, hemolysis, salivation, restlessness, dizziness, nausea, vomiting, coma, and death. Monocytosis, dermatitis, liver tenderness and damage, delirium and convulsions may occur. Oliguria, cyanosis, uremia, peripheral paresthesia, and hypesthesia may also occur. (R608, R617)","Abdominal pain, cough, sore throat, headache, nausea, vomiting, dizziness, drowsiness, confusion, tremor and convulsions can occur following inhalation, ingestion, as well as dermal contact with 1,1,2,2-tetrachloroethane. Redness and dry skin can follow dermal exposure. Eye exposure can lead to redness and pain of the eye(s). Exposure may also cause prickling sensation and numbness of limbs, loss of kneejerk, an unpleasant taste in the mouth, sweating, a deep dusky coloration of the skin, weight loss, pain over the liver, dark urine, and bilirubinuria. (R612, R617)","There is no specific treatment for trichloroethane poisoning. Gastric lavage is recommended after oral exposure. Protect airway by placement in Trendelenburg and left lateral decubitus position or by endotracheal intubation. Control any seizures first. In case od seizures foolwing ingestion, administer a benzodiazepine IV; Following inhalation, move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with inhaled beta2 agonist and oral or parenteral corticosteroids. After eye exposure, irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes. If the exposure occurs through dermal contact, remove contaminated clothing and wash exposed area thoroughly with soap and water. In any case, a physician may need to examine the area if irritation or pain persists. (R624)",DNA;P98194;O75185;P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P78334;Q8N1C3;P18507;Q99928;O00591;P24046;P28476;A8MPY1;Q9UN88;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;P54710;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P03372;Q92731
148,T3D0147,2009-03-06 18:58:10 UTC,2009-08-04 21:27:49 UTC,Selenium,Inorganic Compound;Non-Metal;Selenium Compound,"Colloidal seleniumElemental seleniumFormula 2Gnc Selenium 100mcg TabletMicro seMoisturizing selsun blueOligostim Selenium - Tab 6dhPekana - selenium metallicumSESelanedIIdeSelegelSelenSelenateSelenideSelenium 100 McgSelenium 100mcgSelenium 100mcg Hvp ChelateSelenium 200 McgSelenium 200 Mcg TabletsSelenium 200mcgSelenium 200mcg TabletsSelenium 50mcgSelenium Dps 3ch-1000chSelenium Gtte 4ch-30chSelenium Metallicum 4ch - 30chSelenium Tab 100mcgSelenium Tab 200mcgSelenium Tab 50mcgSelenium Tablets 100mcgSelenium Tablets 50mcgSelenium alloySelenium baseSelenium citrateSelenium dustSelenium elementalSelenium homopolymerSelenium ion (Se2+)Selenium metallicumSelenium oligosolSelenium yeastSelenium, ion (Se2+)Selenium-Injeel Forte Liq (6d,12d,30d,200d/1.1ml)Selsun 2.5%Selsun Blue, 2-in-1Selsun blue, normal oily hairSelsun blue, revitalizingVandexVersel Lotion 2.5%selenide(2-)","Selenium is a nonmetal element with the atomic number 34 and the chemical symbol Se. Isolated selenium occurs in several different forms, the most stable of which is a dense purplish-gray semiconductor form. Selenium rarely occurs in its elemental state in nature and is usually found in sulfide ores such as pyrite, partially replacing the sulfur in the ore matrix. It may also be found in silver, copper, lead, and nickel minerals. Selenium is mainly used in the electronics industry, in glassmaking, and in chemicals and pigments. Though selenium salts are toxic in large amounts, trace amounts of the element are necessary for cellular function in most animals, forming the active center of the enzymes glutathione peroxidase, thioredoxin reductase, and three known deiodinase enzymes. (R976)",,7782-49-2,107674,,C01529,"138319
138320
138321
138322
147892
176803
226600
229300
600902
601112
601148
601413
601484
603235
604188
604687
606210
606216
606218
606235
606254
606448
611056",27568,CPD0-1561,,D012643,Selenium,1291,,,http://en.wikipedia.org/wiki/Selenium,InChI=1/Se/q-2,selenium,http://www.biospider.ca/saved_files/mol/7ce33992e339762cfe27d95ba66aba03_1237949797.mol,[Se--],[Se--],[Se]2-,79.916519,Gray to black crystals.,221 °C,,,"",,,,"Oral
Inhalation
Dermal
(R975)",,"Selenium readily substitutes for sulfur in biomolecules and in many biochemical reactions, especially when the concentration of selenium is high and the concentration of sulfur is low. Inactivation of the sulfhydryl enzymes necessary for oxidative reactions in cellular respiration, through effects on mitochondrial and microsomal electron transport, might contribute to acute selenium toxicity. Selenomethionine (a common organic selenium compound) also appears to randomly substitute for methionine in protein synthesis. This substitution may affect the structure and functionability of the protein, for example, by altering disulfide bridges. Inorganic forms of selenium appear to react with tissue thiols by redox catalysis, resulting in formation of reactive oxygen species and causing damage by oxidative stress. (R975)","Selenium may be absorbed through inhalation and ingestion, while some selenium compounds may also be absorbed dermally. Once in the body, selenium is distributed mainly to the liver and kidney. Selenium is an essential micronutrient and is a component of glutathione peroxidase, iodothyronine 5'-deiodinases, and thioredoxin reductase. Organic selenium is first metabolized into inorganic selenium. Inorganic selenium is reduced stepwise to the intermediate hydrogen selenide, which is either incorporated into selenoproteins after being transformed to selenophosphate and selenocysteinyl tRNA or excreted into the urine after being transformed into methylated metabolites of selenide. Elemental selenium is also methylated before excretion. Selenium is primarily eliminated in the urine and feces, but certain selenium compounds may also be exhaled. (R975)","LD50: 6700 mg/kg (Oral, Rat) (R263)",,"3, not classifiable as to its carcinogenicity to humans. (R264)","Most processed selenium is used in the electronics industry, but it is also used as a nutritional supplement, in the glass industry, in the preparation of pharmaceuticals, as a nutritional feed additive for poultry and livestock, in pesticide formulations, in rubber production, as an ingredient in antidandruff shampoos, and as a constituent of fungicides. It may also be found in pigments in plastics, paints, enamels, inks, and rubber. (R975)",Chronic Oral: 0.005 mg/kg/day (R260),"Chronic oral exposure to high concentrations of selenium compounds can produce a disease called selenosis. The major signs of selenosis are hair loss, nail brittleness, and neurological abnormalities (such as numbness and other odd sensations in the extremities). Animal studies have shown that selenium may also affect sperm production and the female reproductive cycle. (R975)","Short-term oral exposure to high concentrations of selenium may cause nausea, vomiting, and diarrhea. Brief exposures to high levels of elemental selenium or selenium dioxide in air can result in respiratory tract irritation, bronchitis, difficulty breathing, and stomach pains. Longer-term exposure to either of these air-borne forms can cause respiratory irritation, bronchial spasms, and coughing. (R975)","",""
149,T3D0148,2009-03-06 18:58:10 UTC,2009-08-04 21:27:49 UTC,"Hexachlorocyclohexane, technical Grade",Organic Compound;Pesticide;Organochloride,"(1R,2R,3R,4R,5S,6S)-1,2,3,4,5,6-hexachlorocyclohexane(1R,2R,3S,4S,5S,6S)-1,2,3,4,5,6-hexachlorocyclohexane(1r,2R,3S,4r,5R,6S)-1,2,3,4,5,6-hexachlorocyclohexane(1r,2R,3S,4s,5R,6S)-1,2,3,4,5,6-hexachlorocyclohexane(1r,2c,3c,4t,5c,6t)-1,2,3,4,5,6-hexachlorocyclohexane(1r,2c,3t,4t,5c,6t)-1,2,3,4,5,6-hexachlorocyclohexane(1r,2r,3r,4r,5r,6r)-1,2,3,4,5,6-hexachlorocyclohexane(1s,2R,3R,4s,5S,6S)-1,2,3,4,5,6-hexachlorocyclohexane1,2,3,4,5,6-Hexachlorocyclohexane1,2,3,4,5,6-Hexachlorocyclohexane (all stereo isomers)1,2,3,4,5,6-Hexachlorocyclohexane (mixture of isomers)1,2,3,4,5,6-Hexachlorocyclohexane gamma isomer1,2,3,4,5,6-Hexachlorocyclohexane, gamma-isomer1,2,3,4,5,6-hexachlorocyclohexane, alpha isomer1a,2a,3b,4a,5b,6b-hexachlorocyclohexane1a,2b,3a,4b,5a,6b-hexachlorocyclohexaneAalindanAficideAgrocideAgrocide IIIAgrocide WPAgronexitAlpha- BHCAlpha-BHCAlpha-HCHAlpha-HCH [hexachlorocyclohexanes]Alpha-HCH solutionAlpha-benzene hexachlorideAlpha-benzenehexachlorideAlpha-hexachloranAlpha-hexachloraneAlpha-hexachlorocyclohexaneAlpha-hexachlorocyclohexanesAlpha-lindaneAm eisenatodAmeisenatodAmeisenmittel merckAmeisentodAparasinAphtiriaAphtitriaAplidalArbitexArcotal sBBHBCHBHCBHC (alpha-, beta-, gamma-)BHC (insecticide)BHC insecticideBHC or HCHBen-hexBenhexachlorBenhexolBenzanexBenzene hexachlorideBenzene hexachloride (BHC)Benzene hexachloride (ambiguous)Benzene hexachloride, all isomersBenzene hexachloride-alpha-isomerBenzene hexachloride-gamma isomerBenzene hexachloride-gamma-isomerBenzene-1,2,3,4,5,6-hexachloride ((Ambiguous)Benzene-cis-hexachlorideBenzene-trans-hexachlorideBenzenehexachloride, mixed isomersBenzenehexachloride-alpha-isomerBenzexBeta-BHCBeta-HCHBeta-HCH [hexachlorocyclohexanes]Beta-HCH solutionBeta-benzene hexachlorideBeta-hexac hlorocyclohexaneBeta-hexachloranBeta-hexachlorobenzeneBeta-hexachlorocyclohexaneBeta-hexachlorocyclohexanesBeta-isomerBeta-lindaneBexolBorer sprayCPD with unspecified stereochemistryCaswell No. 079Caswell No. 527CelanexChinoin brand of lindaneChloreseneCodechineCompound-666Cyclohexane, 1,2,3,4,5,6-hexachloro-Cyclohexane, 1,2,3,4,5,6-hexachloro-, (mixed isomers)Cyclohexane, 1,2,3,4,5,6-hexachloro-, alpha-Cyclohexane, 1,2,3,4,5,6-hexachloro-, alpha-isomerCyclohexane, 1,2,3,4,5,6-hexachloro-, beta-isomerCyclohexane, 1,2,3,4,5,6-hexachloro-, delta-Cyclohexane, 1,2,3,4,5,6-hexachloro-, delta-isomerCyclohexane, 1,2,3,4,5,6-hexachloro-, gamma-Cyclohexane, 1,2,3,4,5,6-hexachloro-, gamma-isomerCyclohexane, beta-1,2,3,4,5,6-hexachloro-Cyclohexane, delta-1,2,3,4,5,6-hexachloro-DBHDelitexDelta-BHCDelta-HCHDelta-benzene hexachlorideDelta-benzenehexachlorideDelta-hexachlorocyclohexaneDelta-lindaneDetmol extractDetmol-extraktDevoranDol granuleDolmixDrill tox-spezial aglukonDrilltox-spezial aglukonEntomoxanEpsilon HCHEpsilon-HCHEpsilon-benzenehexachlorideEpsilon-hexachlorocyclohexaneEso dermEsodermExagamaFenoform forteForlinForst-nexenGallogamaGamacarbatoxGamacidGamacideGamacide 20GamaphexGameneGamisoGamma 666Gamma BHCGamma benzene hexachlorideGamma hexachlorGamma hexachlorocyclohexaneGamma-666Gamma-:hexachlorocyclohexaneGamma-BHCGamma-BHC (lindane)Gamma-BHC benhexachlorGamma-HCHGamma-HCH [hexachlorocyclohexanes]Gamma-HCH or gamma-BHCGamma-benzene hexachlorideGamma-benzenehexachlorideGamma-benzohexachlorideGamma-colGamma-hexachloraneGamma-hexachlorcyclohexanumGamma-hexachlorobenzeneGamma-hexachlorocyclohexaneGamma-linda neGamma-lindaneGamma-mean 400Gamma666GammahexaGammahexaneGammalinGammaterrGammexGammexaneGammopazGamtoxGeobilanGexaneGybenH.c.hHCCHCCHHCHHCH (alpha)HCH (beta)HCH [bsi]HCH [iso]HCH, technical grade [hexachlorocyclohexanes]HEXAHGIHeclotoxHecoltoxHexablancHexachlorHexachloranHexachloraneHexachlorcyclohexanHexachlorcyclohexan [german]Hexachloride, benzeneHexachloride, gamma-benzeneHexachlorocyclohexaneHexachlorocyclohexane (all isomers)Hexachlorocyclohexane (mixed isomers)Hexachlorocyclohexane (mixture)Hexachlorocyclohexane (technical grade)Hexachlorocyclohexane, alpha-Hexachlorocyclohexane, beta-Hexachlorocyclohexane, delta-Hexachlorocyclohexane, gamma isomerHexachlorocyclohexane, gamma-Hexachlorocyclohexane, gamma-isomerHexachlorocyclohexane, technicalHexachlorocyclohexane, technical gradeHexachlorocyclohexane-alphaHexachlorocyclohexane-betaHexachlorocyclohexanesHexachlorzyklohexanHexaklorHexamulHexapoudreHexatoxHexavermHexcidumHexicideHexit Shampoo 1.0%Hexit lotionHexyclanHexylanHilbeec hHilbeechHortexInexitInfectopharm brand of lindaneInsecticide, BHCIsatoxIsot oxIsotoxJacutinKokotineKwellKwell-rLacco hi linLasochronLatka 666Latka 666 [Czech]LendineLentoxLidenalLindaforLindagamLindagrainLindagranoxLindaloLindam ulLindamulLindane (benzene hexachloroide-gamma isomer)Lindane (gamma-HCH)Lindane [hexachlorocyclohexanes]Lindane [usan:inn:ban]Lindano [inn-spanish]Lindanum [inn-latin]LindapoudreLindaterraLindatoxLindexLindosepLintoxLinvurLorexaneMglawik lMixture nameMszycolNeo-scabicidolNexen FBNexen-FBNexi t-starkNexitNexit-starkNexol-eNicochloranNovigamNoviganOmnitoxOvadziakOwadziakPLKPMS lindanePMS-lindanePS71_SUPELCOPedraczakPflanzolPharmascience brand of lindanePms-Lindane Lot 1%Pms-Lindane Shp 1%PmslindaneQuelladaRCRA waste no. U129RCRA waste number U129Sang gammaScabecidScabeneScabisanSilvanolSpritz-rapidinSpritzlindaneSpruehpflanzolStiefel brand of lindaneStreunexSubmarT-HCHTBHTechnical HCHTechnical hexachlorocyclohexaneTetocidTrans-alpha-benzenehexachlorideTri-6Trives-tVerindal ultraVitonagrisol g-20agrocide 2agrocide 6gagrocide 7alpha-1,2,3,4,5,6-Hexachlorocyclohexanebentox 10beta-1,2,3,4,5,6-Hexachlorocyclohexanedelta-(Aeeeee)-1,2,3,4,5,6-hexachlorocyclohexanedelta-1,2,3,4,5,6-Hexachlorocyclohexanedetox 25gamma-1,2,3,4,5,6-Hexachlorocyclohexanegammalin 20geolin g 3hungaria l7milbol 49","Technical grade hexachlorocyclohexane is a manufactured chemical that typically consists of the alpha, beta, delta, epsilon, and gamma isomers of hexachlorocyclohexane. It is used as an insecticide on fruit, vegetables, and forest crops and is also available as a prescription (lotion, cream, or shampoo) to treat head and body lice, and scabies. (R186)",,608-73-1,727,,C06988,"",24536,GAMMA-HCH,,,"Hexachlorocyclohexane, technical Grade",696,,,http://en.wikipedia.org/wiki/Lindane,"InChI=1/C6H6Cl6/c7-1-2(8)4(10)6(12)5(11)3(1)9/h1-6H/t1-,2-,3+,4+,5-,6-","1,2,3,4,5,6-hexachlorocyclohexane",http://www.biospider.ca/saved_files/mol/bcb85a438d3b4793b7e7a0733e922b4a_1237949987.mol,C1(C(C(C(C(C1Cl)Cl)Cl)Cl)Cl)Cl,C1(C(C(C(C(C1Cl)Cl)Cl)Cl)Cl)Cl,C6H6Cl6,287.860070,White solid or colorless vapor.,112.5 °C,"","",0.008 mg/mL at 25 °C [CHEM INSPECT TEST INST (1992)],"","","","Oral 
Inhalation 
Dermal 
(R186)","Cytochrome P450 2E1 (P05181) 
Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
(R186)","Hexachlorocyclohexane is a neurotoxin that interferes with GABA neurotransmitter function by interacting with the GABA-A receptor-chloride channel complex at the picrotoxin binding site, causing over stimulation of the central nervous system. It is also believed to inhibit sodium/potassium-transporting ATPases and to be an endocrine disruptor. In the liver, hexachlorocyclohexane is thought to cause oxidative stress by interfering with hepatic oxidative capacity and glutathione metabolism, increasing lipid metabolism, and inhibiting magnesium ATPase activity. Hexachlorocyclohexane may also inhibit gap junction and intercellular communication, leading to uncontrolled cell growth and tumor promotion. (R186, R187, R188)","Hexachlorocyclohexane is absorbed through the skin, lungs, and intestines, then distributed mainly to the adipose tissue but also to the brain, kidney, muscle, and blood. Metabolism occurs via dechlorination, dehydrogenation, dehydrochlorination, and hydroxylation by hepatic cytochrome P-450 enzymes. The main metabolites are polychlorophenols and 1,2,4-trichlorocyclohexane-4,5-epoxide, which are excreted in the urine. (R186)","LD50: 100 mg/kg (Oral, Rat) (R261)
LD50: 75 mg/kg (Subcutaneous, Rabbit) (R261)","","2B, possibly carcinogenic to humans. (R264)","Hexachlorocyclohexane is used as an insecticide on fruit, vegetables, and forest crops and is also available as a prescription (lotion, cream, or shampoo) to treat head and body lice, and scabies. (R186)","","Exposure to large amounts of hexachlorocyclohexane can harm the nervous system, producing a range of symptoms from headache and dizziness to seizures, convulsions and more rarely death. Hexachlorocyclohexane is known to damage the liver, kidneys, and immune system, as well as cause blood disorders and reproductive and developmental defects. Hexachlorocyclohexane is also potentially carcinogenic. (R186, R187)","Exposure to large amounts of hexachlorocyclohexane can harm the nervous system, producing a range of symptoms from headache and dizziness to seizures, convulsions and more rarely death. (R187)","Hexachlorocyclohexane poisoning is treated symptomatically. Gastric lavage, followed by the administration of activated charcoal, may be performed upon ingestion. (R284)",P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P18507;Q99928;O00591;P24046;P28476;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P54710;P62508;P10275;P06401;Q8N1C3;A8MPY1;Q9UN88;P78334;P03372;Q92731
152,T3D0151,2009-03-06 18:58:10 UTC,2009-08-04 21:27:50 UTC,"DDD, O,P'-",Organic Compound;Pesticide;Organochloride,"(2,4'-Dichlorodiphenyl)dichloroethane(o,p)-DDD1, 1-Dichloro-2,2-bis(2,4'-dichlorophenyl)ethane1, 1-Dichloro-2-(o-chlorophenyl)-2-(p-chlorophenyl)ethane1,1-Dichloro-2,2-bis(2,4'-dichlorophenyl)ethane1,1-Dichloro-2-(o-chlorophenyl)-2-(p-chlorophenyl)ethane1,1-Dichloro-2-(p-chlorophenyl)-2-(o-chlorophenyl)ethane1-(2-Chlorophenyl)-1-(4-chlorophenyl)-2,2-dichloroethane1-(o-Chlorophenyl)-1-(p-chlorophenyl)-2,2-dichloroethane1-Chloro-2-(2,2-dichloro-1-(4-chlorophenyl)ethyl)benzene1-Chloro-2-[2,2-dichloro-1-(4-chlorophenyl)ethyl]benzene1-chloro-4-[2,2-dichloro-1-(2-chlorophenyl)ethyl]benzene2, 2-Bis(2-chlorophenyl-4-chlorophenyl)-1,1-dichloroethane2, 4'-Dichlorodiphenyldichloroethane2,2-Bis(2-Chlorophenyl-4-chlorophenyl)-1,1-dichloroethane2,4'-DDD solution2,4'-Dichlorodiphenyldichloroethane2,4'-Dichlorophenyldichlorethane2-(2-Chlorophenyl)-2-(4-chlorophenyl)-1,1-dichloroethane2-(o-Chlorophenyl)-2-(p-chlorophenyl)-1,1-dichloroethaneBenzene, 1-chloro-2-(2,2-dichloro-1-(4-chlorophenyl)ethyl)-Benzene, 1-chloro-2-[2,2-dichloro-1-(4-chlorophenyl)ethyl]-ChloditanChlodithanChlodithaneDDD, o,p'-DDD-o,p'Ethane, 1,1-dichloro-2-(o-chlorophenyl)-2-(p-chlorophenyl)-Ethane, 2-(o-chlorophenyl)-2-(p-chlorophenyl)-1,1-dichloro-KhloditanKhlodithanLysodrenLysodren (TN)MitotanMitotane (jan/usp/inn)Mitotane [usan:inn:jan]Mitotane(usan)Mitotano [inn-spanish]Mitotanum [inn-latin]MytotanO, p'-tdeO,p'-DDDO,p'-ddeO,p'-dichlorodiphenyldichloroethaneO,p'-tdeO,p-DDDO,p-tdeOpeprimOrtho,para-DDDPS694_SUPELCOPrestwick_75WLN: GYGYR bg&r DG","DDD, O,P'- is an isomer of dichlorodiphenyldichloroethane, an organochlorine insecticide. It is a component of commercial mixtures of DDT. DDT was once a widely used pesticide, but today its agricultural use has been banned worldwide due to its toxicity and tendency to bioaccumulate. However, it still has limited use in disease vector control. (R152)",,53-19-0,4211,,"","","","",,D008939,"DDD, O,P'-",378,,,http://en.wikipedia.org/wiki/Mitotane,"InChI=1/C14H10Cl4/c15-10-7-5-9(6-8-10)13(14(17)18)11-3-1-2-4-12(11)16/h1-8,13-14H","1-chloro-4-[2,2-dichloro-1-(2-chlorophenyl)ethyl]benzene",http://www.biospider.ca/saved_files/mol/903e0375f9b6362fdd95f50b1d964167_1237950413.mol,C1=CC=C(C(=C1)C(C2=CC=C(C=C2)Cl)C(Cl)Cl)Cl,C1=CC=C(C(=C1)C(C2=CC=C(C=C2)Cl)C(Cl)Cl)Cl,C14H10Cl4,317.953660,White solid.,77 °C,"","","0.0001 mg/mL at 25 °C [BIGGAR,JW & RIGGS,RI (1974)]","","","","Ingestion 
(R153)","Cytochrome P450 2B6 (Q16678) 
Cytochrome P450 3A4 (P08684) 
Cytochrome P450 3A5 (P20815) 
Cytochrome P450 3A7 (P24462) 
Cytochrome P450 3A43 (Q9HB55) 
(R153)","DDD toxicity occurs via at least four mechanisms, possibly all functioning simultaneously. DDD reduces potassium transport across the membrane. DDD inhibits the inactivation of voltaged-gated sodium channels. The channels activate (open) normally but are inactivated (closed) slowly, thus interfering with the active transport of sodium out of the nerve axon during repolarization and resulting in a state of hyperexcitability. DDD inhibits neuronal adenosine triphosphatases (ATPases), particularly Na+K+-ATPase, and Ca2+-ATPase which play vital roles in neuronal repolarization. DDD also inhibits the ability of calmodulin, a calcium mediator in nerves, to transport calcium ions that are essential for the release of neurotransmitters. All these inhibited functions reduce the rate of depolarization and increase the sensitivity of neurons to small stimuli that would not elicit a response in a fully depolarized neuron. DDD is also believed to adversely affect the reproductive system by mimicking endogenous hormones and binding to the estrogen and adrogen receptors. (R029, R153)","DDD is absorbed in the stomach and intestine, after which it enters the lymphatic system and is carried throughout the body and incorporated into fatty tissues. Metabolism of DDD occurs mainly via cytochrome P-450 enzymes in the liver and kidney. Its metabolites, mainly DDA (bis(p-chlorophenyl) acetic acid), are excreted in the urine. (R153)","LD50: 113 mg/kg (Oral, Rat) (R270)",5 g/kg for an adult human. (R270),"2B, possibly carcinogenic to humans. (R264)","DDD is found in DDT, which is used as a pesticide and in disease vector control. (R152)","","DDT has been shown to cause mild anemia. Exposure to DDT causes loss of weight and anorexia. DDT poisoning affects CNS function in humans, but pathologic changes are observed in the liver and reproductive organs. Hypertrophy of hepatocytes and subcellular organelles such as mitochondria, proliferation of smooth endoplasmic reticulum, centrolobular necrosis after exposure to high concentrations, and an increase in the incidence of hepatic tumors have been noted. (R029)",DDT exposure causes ataxia and abnormal stepping. Acute signs of DDT poisoning include paresthesia after oral ingestion. Studies have shown that a mammal poisoned with DDT-type agents displays periodic persistent tremoring and/or convulsive seizures that are suggestive of repetitive discharges in neurons. These repetitive tremors and seizures can be initiated by tactile and auditory stimuli. (R029),"Treatment of DDT exposure should be primarily directed towards decontamination and supportive care, as there is no specific antidote. The use of gastric lavage and activated charcoal for large ingestions may be effective. (R274)",P10275;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P54710;P98194;O75185;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;P62158;P03372;Q92731;Q9UL51;Q9Y3Q4;O60741;Q9P1Z3 ;P35498;Q9Y5Y9;Q9UI33;Q99250;Q9NY46;P35499;Q14524;Q01118;Q9UQD0;Q15858;Q07699;O60939;Q9NY72;Q8IWT1
153,T3D0152,2009-03-06 18:58:10 UTC,2009-08-04 21:27:50 UTC,"4,4'-Methylenebis(2-chloroaniline)",Organic Compound;Pesticide;Organochloride,",4'-Methylenebiso-chloroaniline2,2'-dichloro-4,4'-methylendianiline2,2'Dichloro-4,4'-methylene dianiline3,3'-Dichlor-4, 4'-diaminodiphenylmethan(GERMAN)3,3'-Dichlor-4,4'-diaminodiphenylmethan3,3'-Dichlor-4,4'-diaminodiphenylmethan [German]3,3'-Dichloro-4, 4'-diaminodiphenylmethane3,3'-Dichloro-4,4'-Diaminodiphenylmethane3,3'-Dichloro-4,4'-diaminodifenilmetano3,3'-Dichloro-4,4'-diaminodifenilmetano [Italian]3,3'-Dichloro-4,4'-diaminodiphenyl methane3,3'-Dicloro-4, 4'-diaminodifenilmetano(ITALIAN)3,3'-Dicloro-4,4'-diaminodifenilmetano3,3'-Dicloro-4,4'-diaminodifenilmetano [Italian]4, 4-Metilene-bis-o-cloroanilina(ITALIAN)4, {4'-Methylenebis[2-chloroaniline]}4, {4'-Methylenebis[2-chloroaniline}4, {4'-Methylenebis[2-chlorobenzenamine]}4, {4'-Methylenebis[o-chloroaniline]}4,4'-Diamino-3, 3'-(dichlorodiphenyl)methane4,4'-Diamino-3,3'-(dichlorodiphenyl)methane4,4'-Diamino-3,3'-dichlorodiphenyl methane4,4'-Diamino-3,3'-dichlorodiphenylmethane4,4'-Methylene bis(2-chloroaniline)4,4'-Methylene(bis)-chloroaniline4,4'-Methylene-bis(2-chloroaniline)4,4'-Methylene-bis-(2-chloroaniline)4,4'-Methylene-bis-2-chloroaniline4,4'-Methylenebis(2-chloroaniline)4,4'-Methylenebis(2-chlorobenzenamine)4,4'-Methylenebis(o-chloroaniline)4,4'-Methylenebis-(2-Chlorobenzenamine )4,4'-Methylenebis-(2-Chlorobenzenamine)4,4'-Methylenebis-2-chlorobenzenamine4,4'-Methylenebis[2-chloroaniline4,4'-Methylenebis[2-chloroaniline]4,4'-Methylenebis[2-chlorobenzenamine]4,4'-Methylenebis[o-chloroaniline]4,4'-Methylenebiso-chloroaniline4,4-Methylene bis(2-chloroaniline)4,4-Metilene-bis-o-cloroanilina4,4-Metilene-bis-o-cloroanilina [Italian]4-(4-Amino-3-chlorobenzyl)-2-chlorophenylamineAniline, 4, {4'-methylenebis[2-chloro-}Aniline, 4,4'-methylenebis(2-chloro-Aniline, 4,4'-methylenebis(2-chloro- (8CI)Aniline, 4,4'-methylenebis*2-chloro-Aniline, 4,4'-methylenebis[2-chloro-BOCABenzenamine, 4, {4'-methylenebis[2-chloro-}Benzenamine, 4,4'-methylenebis(2-chloro)-Benzenamine, 4,4'-methylenebis(2-chloro-Benzenamine, 4,4'-methylenebis*2-chloro-Benzenamine, 4,4'-methylenebis[2-chloro-Bis amineBis(3-chloro-4-aminophenyl)methaneBis(4-amino-3-chlorophenyl)methaneBis-amine aBisamineBisamine sCL-mdaCuamine MTCuamine mCuralin mCurene 442CyanasetDacpmDi(-4-amino-3-chlorophenyl)methaneDi(4-amino-3-chlorophenyl)methaneDi-(4-amino-3-clorofenil)metanoDi-(4-amino-3-clorofenil)metano [Italian]Di-(4-amino-3-clorofenil)metano(ITALIAN)Diamet KHMOCAMbocaMet hylene-bis(2-chloroaniline), 4,4'-Methylene 4,4'-bis(o-chloroaniline)Methylene bis(chloroaniline)Methylene-4,4'-bis(o-chloroaniline)Methylene-bis(2-chloroaniline), 4,4'-Methylene-bis-orthochloroanilineMethylenebis(2-chloroaniline)Methylenebis(3-chloro-4-aminobenzene)Methylenebis(chloroaniline)Methylenebis[3-Chloro-4-aminobenzene]Millionate mMoca (curing agent)P, {p'-methylenebis[o-chloroaniline]}P,p'-methylenebis(&alpha;-chloroaniline)P,p'-methylenebis(alpha-chloroaniline)P,p'-methylenebis(o-chloroaniline)P,p'-methylenebis(ortho-chloroaniline)P,p'-methylenebis[.alpha.-chloroaniline]P,p'-methylenebis[o-chloroaniline]QuodoroleRCRA waste no. U158Rcra waste number U158WLN: ZR CG D1R DZ CG{p,p'-methylenebis[&alpha;-chloroaniline]}","4,4'-Methylenebis(2-chloroaniline) (MBOCA) is a synthetic chemical used primarily to make polyurethane products. It may be found in gears, gaskets, sport boots, roller skate wheels, shoe soles, rolls and belt drives in cameras, computers and copy machines, wheels and pulleys for escalators and elevators, components in home appliances, and various military applications. It is also used as a coating in chemical reactions to set glues, plastics, and adhesives. (S193)",,101-14-4,7543,,C10999,"",25520,34-DICHLOROANILINE,,D008753,"4,4'-Methylenebis(2-chloroaniline)",882,,,,"InChI=1/C13H12Cl2N2/c14-10-6-8(1-3-12(10)16)5-9-2-4-13(17)11(15)7-9/h1-4,6-7H,5,16-17H2",4-[(4-amino-3-chlorophenyl)methyl]-2-chloroaniline,http://www.biospider.ca/saved_files/mol/96be837fde21c0a56ec2185505d42d43_1237950567.mol,C1=CC(=C(C=C1CC2=CC(=C(C=C2)N)Cl)Cl)N,C1=CC(=C(C=C1CC2=CC(=C(C=C2)N)Cl)Cl)N,C13H12Cl2N2,266.037750,"",110 °C,"","","0.0139 mg/mL at 24 °C [VOORMAN,R & PENNER,D (1986A)]","","","","Oral
Inhalation
Dermal
(S193)",Cytochrome P450 2A6 (P11509) (S194),"MBOCA's carcinogenicity is thought to be a result of its ability to bind to DNA, hemoglobin, and serum albumin. One metabolite in particular, N-hydroxy-N,N’-diacetyl MBOCA, is known to bind nucleic acids, forming DNA adducts. Other N-oxidized MBOCA metabolites, such as n-hydroxy MBOCA and mononitroso-MBOCA, have been shown to form hemoglobin adducts. (R029, S193)","4,4'-Methylenebis(2-chloroaniline) may be absorbed via oral, inhalation, or dermal exposure. It distributes throughout the body, concentrating in the liver, kidney, and adipose tissue. Metabolism involves N-acetylation, N-hydroxylation (which may be followed by n-oxidation), and ring hydroxylation. The mainy enzymes involves are phenobarbital-inducible cytochrome P-450 enzymes. MBOCA and its metabolites are excreted mainly in the urine. (S193)","LD50: >5 g/kg (Dermal, Rabbit) (R263)
LD50: 400 mg/kg (Oral, Guinea Pig) (R263)
LD50: 64 mg/kg (Intraperitoneal, Mouse) (R263)
","","1, carcinogenic to humans. (R264)","4,4'-Methylenebis(2-chloroaniline) is used primarily to make polyurethane products. It may be found in gears, gaskets, sport boots, roller skate wheels, shoe soles, rolls and belt drives in cameras, computers and copy machines, wheels and pulleys for escalators and elevators, components in home appliances, and various military applications. It is also used as a coating in chemical reactions to set glues, plastics, and adhesives. (S193) ",Chronic Oral: 0.003 mg/kg/day (R260),"4,4'-Methylenebis(2-chloroaniline) is a known human carcinogen. It may also damage the liver and kidneys. (S193)","","",DNA;P02768;P69905;P68871;P02042;P02100;P69891;P69892;Q6B0K9;P09105;P02008;P98194;O75185;P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P78334;Q8N1C3;P18507;Q99928;O00591;P24046;P28476;A8MPY1;Q9UN88;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;P54710;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P03372;Q92731
154,T3D0153,2009-03-06 18:58:10 UTC,2009-08-25 18:00:08 UTC,Hexachlorodibenzo-p-dioxin,Organic Compound;Industrial By-product/Pollutant;Chlorinated Dibenzo-p-dioxin;Aromatic Hydrocarbon;Organochloride,"-7-yl esterAzuleno[4,5-b]furan, Octanoic Acid Deriv.T9033_SIGMAThapsigarginThapsingarginalpha,6beta,6abeta,7beta,8alpha(Z),9balpha]]-n-7-yl ester (9CI)","Hexachlorodibenzo-p-dioxins are chlorinated dibenzo-p-dioxin (CDD) congeners. CDDs are a class of manufactured chemicals that consist of dioxin skeletel structures with chlorine substituents. They are also persistent organic pollutants (POPs), thus their production is regulated in most areas. Dioxins occur as by-products from the manufacture of organochlorides, the bleaching of paper, chlorination by waste and drinking water treatment plants, municipal solid waste and industrial incinerators, and natural sources such as volcanoes and forest fires. (R346, R347)",,34465-46-8,446378,,"","",25520,"",,C018073,Hexachlorodibenzo-p-dioxin,,,,,"InChI=1/C34H50O12/c1-9-12-13-14-15-17-24(37)43-28-26-25(20(5)27(28)44-30(38)19(4)11-3)29-34(41,33(8,40)31(39)45-29)22(42-23(36)16-10-2)18-32(26,7)46-21(6)35/h11,22,26-29,40-41H,9-10,12-18H2,1-8H3/b19-11-/t22-,26+,27-,28-,29-,32-,33+,34+/m0/s1","[(3S,3aR,4S,6S,6aR,7S,8S,9bS)-6-acetyloxy-4-butanoyloxy-3,3a-dihydroxy-3,6,9-trimethyl-8-[(Z)-2-methylbut-2-enoyl]oxy-2-oxo-4,5,6a,7,8,9b-hexahydroazuleno[4,5-b]furan-7-yl] octanoate",http://www.biospider.ca/saved_files/mol/,"",CCCCCCCC(=O)O[C@@H]1[C@@H](OC(=O)C(\C)=C/C)C(C)=C2[C@@H]3OC(=O)[C@@](C)(O)[C@@]3(O)[C@H](C[C@](C)(OC(C)=O)[C@@H]12)OC(=O)CCC |t:20|,C34H50O12,650.330230,Colorless solid.,250 °C,,,"4e-09 mg/mL at 20 °C [FISCHER,J et al. (1992)]",,,,"Oral 
Inhalation 
Dermal 
(R346)",,"CDDs cause their toxic effects by binding to the aryl hydrocarbon receptor and subsequently altering the transcription of certain genes. The affinity for the Ah receptor depends on the structure of the specific CDD. The change in gene expression may result from the direct interaction of the Ah receptor and its heterodimer-forming partner, the aryl hydrocarbon receptor nuclear translocator, with gene regulatory elements or the initiation of a phosphorylation/dephosphorylation cascade that subsequently activates other transcription factors. The affected genes include several oncogenes, growth factors, receptors, hormones, and drug-metabolizing enzymes. The change in transcription/translation of these genes is believed to be the cause of most of the toxic effects of CDDs. (R346)","CDDs are absorbed through oral, inhalation, and dermal routes of exposure. CDDs are carried in the plasma by serum lipids and lipoproteins, distributing mainly to the liver and adipose tissue. CDDs are very slowly metabolized by the microsomal monooxygenase system to polar metabolites that can undergo conjugation with glucuronic acid and glutathione. They may increase the rate of their own metabolism by inducing both phase I and phase II enzymes. The major routes of excretion of CDDs are the bile and the faeces, though smaller amounts are excreted in the urine and via lactation. (R346)",,,"3, not classifiable as to its carcinogenicity to humans. (R264) ","Dioxins occur as by-products from the manufacture of organochlorides, the bleaching of paper, chlorination by waste and drinking water treatment plants, municipal solid waste and industrial incinerators, and natural sources such as volcanoes and forest fires. (R346, R347) ","Acute Oral: 0.0002 ug/kg/day (R260) 
Intermediate Oral: 0.00002 ug/kg/day (R260) 
Chronic Oral: 0.000001 ug/kg/day (R260) ","Exposure to large amounts of CDDs causes chloracne, a severe skin disease with acne-like lesions that occur mainly on the face and upper body. CDDs may also cause liver damage and induce long-term alterations in glucose metabolism and subtle changes in hormonal levels. In addition, studies have shown that CDDs may disrupt the endocrine system and weaken the immune system, as well as cause reproductive damage and birth defects, central and peripheral nervous system pathology, thyroid disorders, endometriosis, and diabetes. (R346, R347) ","In addition to chloracne, CDD exposure causes skin rashes, discoloration, and excessive body hair. (R346) ","Treatment of CDD exposure may include washing the area of contact, GI decontamination, administering an IV, or forced alkaline diuresis. (R622) ",P35869;P03372;Q92731
155,T3D0154,2009-03-06 18:58:11 UTC,2009-08-04 21:27:50 UTC,Heptachlorodibenzo-p-dioxin,Organic Compound;Industrial By-product/Pollutant;Chlorinated Dibenzo-p-dioxin;Aromatic Hydrocarbon;Organochloride,"","Heptachlorodibenzo-p-dioxins are chlorinated dibenzo-p-dioxin (CDD) congeners. CDDs are a class of manufactured chemicals that consist of dioxin skeletel structures with chlorine substituents. They are also persistent organic pollutants (POPs), thus their production is regulated in most areas. Dioxins occur as by-products from the manufacture of organochlorides, the bleaching of paper, chlorination by waste and drinking water treatment plants, municipal solid waste and industrial incinerators, and natural sources such as volcanoes and forest fires. (R346, R347)",,37871-00-4,235956,,"","","","",,,Heptachlorodibenzo-p-dioxin,,,,,"InChI=1/C30H40N2O7S/c1-19-11-10-13-22-29(39-18-37-3)23(16-24-30(22)40-17-27(35)32-24)31-26(34)15-21(38-4)12-8-6-5-7-9-14-25(33)20(2)28(19)36/h5-9,11-12,16,20-21,25,28,33,36H,10,13-15,17-18H2,1-4H3,(H,31,34)(H,32,35)/b6-5+,9-7+,12-8+,19-11+/t20-,21-,25-,28",4-(2-methyl-5-propan-2-ylcyclopenten-1-yl)butan-2-ol,http://www.biospider.ca/saved_files/mol/,CC1=C(C(CC1)C(C)C)CCC(C)O,CC1=C(C(CC1)C(C)C)CCC(C)O,C13H24O,196.182720,Colorless solid.,264 °C,,,"1.41e-09 mg/mL at 23 °C [FRIESEN,KJ et al. (1990B)]",,,,"Oral 
Inhalation 
Dermal 
(R346)",,"CDDs cause their toxic effects by binding to the aryl hydrocarbon receptor and subsequently altering the trascription of certain genes. The affinity for the Ah receptor depends on the structure of the specific CDD. The change in gene expression may result from the direct interaction of the Ah receptor and its heterodimer-forming partner, the aryl hydrocarbon receptor nuclear translocator, with gene regulatory elements or the initiation of a phosphorylation/dephosphorylation cascade that subsequently activates other transcription factors. The affected genes include several oncogenes, growth factors, receptors, hormones, and drug-metabolizing enzymes. The change in transcription/translation of these genes is believed to be the cause of most of the toxic effects of CDDs. (R346)","CDDs are absorbed through oral, inhalation, and dermal routes of exposure. CDDs are carried in the plasma by serum lipids and lipoproteins, distributing mainly to the liver and adipose tissue. CDDs are very slowly metabolized by the microsomal monooxygenase system to polar metabolites that can undergo conjugation with glucuronic acid and glutathione. They may increase the rate of their own metabolism by inducing both phase I and phase II enzymes. The major routes of excretion of CDDs are the bile and the faeces, though smaller amounts are excreted in the urine and via lactation. (R346)",,,"3, not classifiable as to its carcinogenicity to humans. (R264) ","Dioxins occur as by-products from the manufacture of organochlorides, the bleaching of paper, chlorination by waste and drinking water treatment plants, municipal solid waste and industrial incinerators, and natural sources such as volcanoes and forest fires. (R346, R347) ","Acute Oral: 0.0002 ug/kg/day (R260) 
Intermediate Oral: 0.00002 ug/kg/day (R260) 
Chronic Oral: 0.000001 ug/kg/day (R260) ","Exposure to large amounts of CDDs causes chloracne, a severe skin disease with acne-like lesions that occur mainly on the face and upper body. CDDs may also cause liver damage and induce long-term alterations in glucose metabolism and subtle changes in hormonal levels. In addition, studies have shown that CDDs may disrupt the endocrine system and weaken the immune system, as well as cause reproductive damage and birth defects, central and peripheral nervous system pathology, thyroid disorders, endometriosis, and diabetes. (R346, R347) ","In addition to chloracne, CDD exposure causes skin rashes, discoloration, and excessive body hair. (R346) ","Treatment of CDD exposure may include washing the area of contact, GI decontamination, administering an IV, or forced alkaline diuresis. (R622) ",P35869;P03372;Q92731
157,T3D0156,2009-03-06 18:58:11 UTC,2009-08-04 21:27:50 UTC,"1,3-Butadiene",Organic Compound;Industrial Precursor/Intermediate,"&alpha;,&laquo;gamma&raquo;-butadiene(E)-CH2=CHCH=CH2.alpha.,.gamma.-butadiene1,3-Butadien1,3-butadiene, various grades1,4-PolybutadieneAlpha,gamma-butadieneAlpha-gamma-butadieneBiethyleneBivinylButa-1,3-dieenButa-1,3-dieen [Dutch]Buta-1,3-dienButa-1,3-dien [German]Buta-1,3-dieneButadieenButadieen [dutch]ButadienButadien [polish]ButadieneButadiene monomerButadiene, 1,3-Butadiene-1,3-uninhibitedCH2=CH-CH=CH2DivinylErythrenePolybutadienePolybutadiene, cisPolybutadiene, dicarboxy terminatedPolybutadiene, phenyl terminatedPolybutadiene, predominantly 1,2-additionPolybutadiene, surface-modifiedPyrrolyleneTrans-butadieneVinyl ethyleneVinylethylene","1,3-Butadiene is a chemical made from the processing of petroleum. It is a colorless gas with a mild gasoline-like odor. 1,3-Butadiene is used mainly to make synthetic rubber for tires. It is also used to make plastics such as acrylics, and small amounts can be found in gasoline. (S355)",,106-99-0,7845,,C16450,"",39478,BUTADIENE,,C031763,"1,3-Butadiene",204,,,"http://en.wikipedia.org/wiki/1,3-Butadiene","InChI=1/C4H6/c1-3-4-2/h3-4H,1-2H2","buta-1,3-diene",http://www.biospider.ca/saved_files/mol/88b9cf0950a45dcc70c7671fc1118922_1237950949.mol,C=CC=C,C=CC=C,C4H6,54.046950,Colorless gas.,-108.9 °C,,,"0.735 mg/mL at 25 °C [MCAULIFFE,C (1966)]",,,,"Inhalation
(S355)","Epoxide hydrolase 1 (P07099)
Cytochrome P450 2E1 (P05181)
Glutathione S-transferase Mu 1 (P09488)
Glutathione S-transferase theta-1 (P30711)
(S355, S357, S358)","Certain metabolites of 1,3-butadiene have been shown to bind to DNA and nucleoproteins, forming protein-DNA and DNA-DNA crosslinks. Specifically, 1,2-epoxybutene-3 and diepoxybutane react with guanine to cause crosslinking. (S355, S356)","1,3-Butadiene is absorbed following inhalation and is distributed to the adipose tissue, brain, liver, septum, and kidney. 1,3-Butadiene is believed to be metabolized in the liver by cytochrome P-450 enzymes, forming 1,2-epoxybutene-3 as the main metabolite. 1,2-Epoxybutene-3 is further transformed into 3-butene-1,2-diol by microsomal epoxide hydrolase. The metabolites of 1,3-butadiene are exhaled as carbon dioxide or excreted in the urine. (S355)","LD50: 3.21 g/kg  (Oral, Mouse) (S359)
LC50: 270 000 mg/m3 over 2 hours (Inhalation, Mouse) (S359)",,"1, carcinogenic to humans. (R264)","1,3-Butadiene is made from the processing of petroleum. It is used mainly to make synthetic rubber for tires. It is also used to make plastics such as acrylics, and small amounts can be found in gasoline. (S355)",,"Breathing high levels of 1,3-butadiene causes central nervous system damage. Chronic exposure may also cause lung damage and kidney, liver, and cardiovascular disease. In addition, 1,3-butadiene is a known human carcinogen. (S355)","Breathing 1,3-butadiene may cause irritation of the eyes, nose, and throat. High levels of 1,3-butadiene can also cause, blurred vision, nausea, fatigue, headache, decreased blood pressure and pulse rate, and unconsciousness. Skin contact with liquid 1,3-butadiene can cause irritation and frostbite. (S355)","",DNA
158,T3D0157,2009-03-06 18:58:11 UTC,2009-08-04 21:27:51 UTC,Ammonia,Organic Compound;Industrial Precursor/Intermediate;Fertilizer,"After biteAm-folAmmonia (conc 20% or greater)Ammonia anhydrousAmmonia gasAmmonia inhalantAmmonia solutionAmmonia solution strong (NF)Ammonia solution strong [usan]Ammonia solution, strong [usan]Ammonia waterAmmonia water (JP15)Ammonia, anhydrousAmmoniac [french]Ammoniaca [italian]Ammoniacum gummiAmmoniakAmmoniak [german]Ammoniak kconzentrierterAmmoniakgasAmmonium ionAmoniak [polish]Anhydrous ammoniaAromatic ammonia vaporoleAromatic ammonia, vaporoleAzaneCaswell No. 041Liquid ammoniaNitro-silPrimaeres aminSekundaeres aminSpirit of hartshornTertiaeres aminUN 1005 (anhydrous gas or >50% solution)UN 2073 (>44% solution)UN 2672 (between 12% and 44% solution)UNX","Ammonia is a gas that occurs naturally in nature (produced by bacteria) and may also be synthetically manufactured. It is an important source of nitrogen, which is needed by plants and animals, thus it often serves as a precursor to foodstuffs and fertilizers. It may also be applied directly to some crops. Ammonia is a building block for the synthesis of many pharmaceuticals, and is also used in commercial cleaning products. (S307, S308)",,7664-41-7,222,,C00014,"102770
124450
138130
138290
139260
179800
180297
182128
201450
207800
207900
212138
215700
222700
232600
235800
237300
237310
238700
238970
245349
258870
261600
266150
309000
311250
312170
600346
601003
602268
603859
604618
605381
605899
606673
606762
607079
608158
608285
608307
608310
608490
609060
609457
610021
610505
611261
611470
611719",16134,AMMONIA,,D000641,Ammonia,6151,,,http://en.wikipedia.org/wiki/Ammonia,InChI=1/H3N/h1H3,ammonia,http://www.biospider.ca/saved_files/mol/7b4b7509ff1d622dd7194b18eaf713c4_1237951082.mol,N,N,NH3,17.026550,Colorless gas.,-77.7 °C,,,"482 mg/mL at 24 °C [DEAN,JA (1985)]",,,,"Oral
Inhalation
Skin and eyes
(S307)","Carbamoyl-phosphate synthase [ammonia], mitochondrial (P31327) 
Glutamine synthetase (P15104)
(S308, S310)","The topical damage caused by ammonia is probably due mainly to its alkaline properties. Its high water solubility allows it to dissolve in moisture on the mucous membranes, skin, and eyes, forming ammonium hydroxide. Ammonium hydroxide causes saponification of cell membrane lipids, resulting in cell disruption and death. Additionally, it extracts water from the cells and initiates an inflammatory response, which further damages the surrounding tissues. Excess circulating levels of ammonia (hyperammonemia) can cause serious neurological effects. This is thought to involve the alteration of glutamate metabolism in the brain and resultant increased activation of NMDA receptors, which causes decreased protein kinase C-mediated phosphorylation of Na+/K+ ATPase, increased activity of Na+/K+ ATPase, and depletion of ATP. Ammonia can chemically interact with an internal thiolester bond of
complement 3 (C3). This causes a conformation change in C3, which activates the alternative complement pathway, causing the release of chemoattractants and the assembly of the membrane attack complex of complement. The altered C3 can also bind directly to phagocyte complement receptors, which causes the release of toxic oxygen species. (S307)","Ammonia can be absorbed by inhalation and oral routes exposure, and also to a much lesser extent through the skin and eyes. Most of the inhaled ammonia is retained in the upper respiratory tract and is subsequently eliminated in expired air, while ingested ammonia is readily absorbed in the intestinal tract. Ammonia that reaches the circulation is widely distributed to all body compartments although substantial first pass metabolism occurs in the liver where it is transformed into urea and glutamine. Ammonia or ammonium ion reaching the tissues is taken up by glutamic acid, which participates in transamination and other reactions. Ammonia is mainly excreted in the urine. (S307)","LD50: 350 mg/kg (Oral, Rat) (S309)
LC50: 3 360 mg/m3 over 1 hour (Inhalation, Mouse) (S309)",2500 to 4500 ppm over 30 minutes for an adult human. (S307),,"Ammonia is used directly on farm crops, and is also a precursor to foodstuffs and fertilizers. It is also found in many household and industrial cleaners. (S307)","Acute Inhalation: 1.7 ppm (R260)
Chronic Inhalation: 0.1 ppm (R260)","Exposure to high levels of ammonia in air may be irritating to skin, eyes, throat, and lungs and cause coughing and burns. Lung damage and death may occur after exposure to very high concentrations of ammonia. Swallowing concentrated solutions of ammonia can cause burns in mouth, throat, and stomach. Splashing ammonia into eyes can cause burns and even blindness. (S307)",Exposure to high levels of ammonia can cause irritation and burning at the site of exposure. (S307),"",P01024
159,T3D0158,2009-03-06 18:58:11 UTC,2009-08-04 21:27:51 UTC,2-Methylnaphthalene,Organic Compound;Industrial By-product/Pollutant;Aromatic Hydrocarbon;Polycyclic Aromatic Hydrocarbon,"&beta;-methylnaphthalene.beta.-methylnaphthalene2-Methylnaphthalene2-Methylnaphthalene (beta)2-Naphthylmethyl radical2-methyInaphthalene2-methylnaphthalene (ACD/Name 4.0)2-methylnaphthalene, ion(1+)2-methylnaphthalene, ion(1-)2-methylnaphthalene, lithium salt, ion(1-)2-methylnaphthalene, methyl-13C-labeled2-methylnaphthalene, naphthalene-1-(13)C-labeledBeta-methyl naphthalenesBeta-methylnaphthaleneMethyl-2-naphthaleneNAPHTALENE,2-METHYL MFC11 H10Naphthalene, beta-methyl-WLN: L66J C1","2-Methylnaphthalene is one of over 100 different polycyclic aromatic hydrocarbons (PAHs). PAHs are chemicals that are formed during the incomplete burning organic substances, such as fossil fuels. They are usually found as a mixture containing two or more of these compounds. (R028)",,91-57-6,7055,,C14098,"",50720,ALPHA-NAPHTHALENEACETAMIDE,,C027384,2-Methylnaphthalene,898,,,,"InChI=1/C11H10/c1-9-6-7-10-4-2-3-5-11(10)8-9/h2-8H,1H3",2-methylnaphthalene,http://www.biospider.ca/saved_files/mol/962666e68e0e1a09b5a2f879e14595fe_1237951324.mol,CC1=CC2=CC=CC=C2C=C1,CC1=CC2=CC=CC=C2C=C1,C11H10,142.078250,White solid.,34.4 °C,"","","0.0246 mg/mL at 25 °C [YALKOWSKY,SH & DANNENFELSER,RM (1992)]","","","","Oral 
Inhalation 
(R028)","Serum albumin (P02768) 
Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 1B1 (Q16678) 
(R060)","The ability of PAH's to bind to blood proteins such as albumin allows them to be transported throughout the body. Many PAH's induce the expression of cytochrome P450 enzymes, especially CYP1A1, CYP1A2, and CYP1B1, by binding to the aryl hydrocarbon receptor or glycine N-methyltransferase protein. These enzymes metabolize PAH's into their toxic intermediates. The reactive metabolites of PAHs (epoxide intermediates, dihydrodiols, phenols, quinones, and their various combinations) covalently bind to DNA and other cellular macromolecules, initiating mutagenesis and carcinogenesis. (R028, R060, R068, R073)","PAH metabolism occurs in all tissues, usually by cytochrome P-450 and its associated enzymes. PAHs are metabolized into reactive intermediates, which include epoxide intermediates, dihydrodiols, phenols, quinones, and their various combinations. The phenols, quinones, and dihydrodiols can all be conjugated to glucuronides and sulfate esters; the quinones also form glutathione conjugates. (R028)","LD50: 1630 mg/kg (Oral, Rat) (R263)","",,"PAHs are released into the environment via the combustion of fossil fuels, coke oven emissions and vehicle exhausts, as well as naturally from forest fires and voLcanic eruptions. PAHs from these sources may contaminate nearly water systems. They are also found in coal tar and charbroiled food. 2-Methylnaphthalene is used to make other chemicals such as dyes and resins. (R028, R035)","","PAHs are carcinogens and have been associated with the increased risk of skin, respiratory tract, bladder, stomach, and kidney cancers. They may also cause reproductive effects and depress the immune system. Exposure to large amounts of 2-methylnapthalene may damage or destroy the red blood cells, resulting in hemolytic anemia. (R028, R035)","Acute exposure to PAHs causes irritation and inflammation of the skin and lung tissue. Some symptoms of hemolytic anemia are fatigue, lack of appetite, restlessness, and pale skin. Exposure to large amounts of  2-methylnapthalene may also cause nausea, vomiting, diarrhea, blood in the urine, and a yellow color to the skin. (R034, R035)
",There is no known antidote for PAHs. Exposure is usually handled with symptomatic treatment. (R028),P35869;Q14749;DNA
160,T3D0159,2009-03-06 18:58:11 UTC,2009-08-04 21:27:51 UTC,"1,4-Dichlorobenzene",Organic Compound;Pesticide;Industrial Precursor/Intermediate;Aromatic Hydrocarbon;Organochloride,"1, 4-Dichloorbenzeen(DUTCH)1, 4-Dichlorobenzene1,3-Cyclohexadien-5-yne, 1,4-dichloro-1,3-Cyclohexadien-5-yne,1,4-dichloro-1,4 dichlorobenzene1,4-Dichloorbenzeen1,4-Dichloorbenzeen [Dutch]1,4-Dichlor-benzol1,4-Dichlor-benzol [German]1,4-Dichlor-benzol(GERMAN)1,4-Dichlorobenzene1,4-Dichlorobenzene (p-dichlorobenzene)1,4-Dichlorobenzene paste1,4-Dichlorobenzene-UL-14C1,4-Diclorobenzene1,4-Diclorobenzene [Italian]1,4-Diclorobenzene(ITALIAN)1,4-chlorobenzene1,4-dichlorobenzene (ACD/Name 4.0)4-DichlorobenzeneBenzene, 1, 4-dichloro-Benzene, p-dichloro-Caswell No. 632DCBDi-chloricideDi-choricideDichloricideDichlorobenzeneDichlorobenzene, 1,4-Dichlorobenzene, p-Dichlorobenzene, p-, solidDichlorobenzene, paraDichlorocideEvolaGlobolKaydoxP-chlorophenyl chlorideP-dichloorbenzeenP-dichloorbenzeen [dutch]P-dichloorbenzeen(dutch)P-dichlorbenzeneP-dichlorbenzolP-dichlorbenzol [german]P-dichlorbenzol(german)P-dichlorobenzeneP-dichlorobenzolP-diclorobenzeneP-diclorobenzene [italian]P-diclorobenzene(italian)PARAPDBPDCBPara crystalsPara-dichlorobenzenePara-zeneParacideParadiParadichlorbenzolParadichlorbenzol [german]ParadichlorobenzeneParadichlorobenzolParadowParamothParanuggetsParazenePersia-perazolRCRA waste no. D027RCRA waste no. U072Rcra waste number U070Rcra waste number U071Rcra waste number U072SantochlorWLN: GR DGnchembio791-comp2","1,4-Dichlorobenzene (para-dichlorobenzene, p-DCB, PDB) is an organic compound with the formula C6H4Cl2. This colourless solid has an odour akin to that of camphor. It consists of two chlorine atoms substituted at opposing sites on a benzene ring. 1,4-DCB is used a pesticide and a deodorant, most famously in mothballs in which it is a replacement for the more traditional naphthalene. 1,4-DCB is also used as a precursor in the production of the polymer poly(p-phenylene sulfide). 1,4-DCB also is used to make deodorant blocks used in garbage cans and restrooms, and to help control odors in animal-holding facilities. 1,4-DCB has been used as an insecticide on fruit and as an agent to control mold and mildew growth on tobacco seeds, leather, and some fabrics. Recently, using 1,4-DCB to make resins has become very important. (R675, R677)",,106-46-7,4685,,C07092,"",28618,CPD-1125,,C018511,"1,4-Dichlorobenzene",434,,,,InChI=1/C6H4Cl2/c7-5-1-2-6(8)4-3-5/h1-4H,"1,4-dichlorobenzene",http://www.biospider.ca/saved_files/mol/469fb8b7e55706f68a8b739621d876e9_1237951413.mol,C1=CC(=CC=C1Cl)Cl,C1=CC(=CC=C1Cl)Cl,C6H4Cl2,145.969010,,52.7 °C,,,"0.0813 mg/mL at 25 °C [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Inhalation 
Ingestion 
Skin and eye exposure 
(R680)","Cytochrome P450 1A1 (P04798)
Cytochrome P450 1A2 (P05177)
Cytochrome P450 2E1 (P05181)
(R687)","The hepatotoxicity and nephrotoxicity observed in laboratory animals are likely due to the formation of toxic intermediates formed while converting 1,4-DCB to 2,5-dichlorophenol by cytochrome P-450, or by depletion of GSH at higher doses of 1,4-DCB, or both. (R677)","Absorption of 1,4-DCB is rapid and essentially complete following inhalation or oral exposure. It is distributed throughout the body, preferentially to the fat tissue and organ-specific sites within the body, following the order: adipose > kidney > liver > blood. 1,4-DCB is initially metabolized by cytochrome P-450 enzymes, specifically P4502E1, to an active epoxide followed by hydrolysis to 2,5-dichlorophenol, which may be further oxidized to dichlorocatechols, or possibly a dichlorohydroquinone. More often, it might be conjugated to sulfate, or to form the glucuronide, or mercapturic acid; conjugation occurs extensively, with virtually no unconjugated metabolites reported in the available studies. Metabolism is believed to occur mainly in the liver, but may occur at lower levels in other tissues, such as the kidney or lung. 1,4-DCB is eliminated almost exclusively in the urine, primarily as conjugates of 2,5-dichlorophenol. (R677)","LD50: >6,000 mg/kg/day (Dermal, Sherman rat) (R677)
LD50: 500 mg/kg/day (Oral, rat) (R677);","","2B, possibly carcinogenic to humans. (R264)","1,4-DCB is used a pesticide and a deodorant, most famously in mothballs in which it is a replacement for the more traditional naphthalene. 1,4-DCB is also used as a precursor in the production of the polymer poly(p-phenylene sulfide). 1,4-DCB also is used to make deodorant blocks used in garbage cans and restrooms, and to help control odors in animal-holding facilities. 1,4-DCB has been used as an insecticide on fruit and as an agent to control mold and mildew growth on tobacco seeds, leather, and some fabrics. Recently, using 1,4-DCB to make resins has become very important. Exposure may result from breathing vapors from 1,4-DCB products, drinking contaminated water or eating contaminated food (However, the levels of p-DCB in foods are generally low), and eye exposure. (R675, R677, R680)","Acute Inhalation: 2 ppm (R677) 
Intermediate Inhalation: 0.2 ppm (R677) 
Chronic Inhalation: 0.01 ppm (R677)
Intermediate Oral: 0.07 mg/kg/day (Rodents) (R677)
Chronic Oral: 0.07 mg/kg/day (Rats) (R677)","Prolonged exposure to high concentration of 1,4-DCB may cause weakness, dizziness, loss of weight, liver injury. Chronic (months to years) ingestion of 1,4-DCB products can provoque skin blotches and problems with red blood cells, such as anemia. There is an indication that 1,4-DCB can affect the development of the nervous system after birth. 1,4-DCB is possibly a human carcinogen. (R677, R682)","Burning sensation, cough, drowsiness, headache, nausea, shortness of breath, and vomiting can follow inhalation or ingestion of 1,4-DCB. Moreover, its ingestion can cause diarrhoea. Eye exposure can lead to redness and pain of the contact surface. Vapors may cause irritation to skin, nose, throat, and eyes. Solid p-dichlorobenzene has very little effect on the skin. (R677, R682)","Administer charcoal as a slurry (240 mL water/30 g charcoal). Following inhalation, move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with inhaled beta2 agonist and oral or parenteral corticosteroids. After eye exposure, irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes. If the exposure occurs through dermal contact, remove contaminated clothing and wash exposed area thoroughly with soap and water. In any case, a physician may need to examine the area if irritation or pain persists. (R624)",P98194;O75185;P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P78334;Q8N1C3;P18507;Q99928;O00591;P24046;P28476;A8MPY1;Q9UN88;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;P54710;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P03372;Q92731
161,T3D0160,2009-03-06 18:58:11 UTC,2009-08-04 21:27:51 UTC,"1,1-Dichloroethane",Organic Compound;Solvent;Industrial Precursor/Intermediate;Organochloride,"1,1-Dichloorethaan1,1-Dichloorethaan [Dutch]1,1-Dichloraethan1,1-Dichloraethan [German]1,1-Dichlorethane1,1-Dichloroethane1,1-Dichloroethane Ethlidene chloride1,1-Dichloroethane [UN2362] [Flammable liquid]1,1-Dicloroetano1,1-Dicloroetano [Italian]1,1-Ethylidene dichloride1,2-dichloroethaneAethylidenchloridAethylidenchlorid [german]Alpha,alpha-dichloroethaneAssymmetrical dichloroethaneCH3CHCl2Chlorinated hydrochloric etherChlorure d'ethylideneChlorure d'ethylidene [french]Cloruro di etilideneCloruro di etilidene [italian]Dichloroethane, 1,1-DichloromethylmethaneEthylidene chlorideEthylidene dichlorideHSDB 64InChI=1/C2H4Cl2/c1-2(3)4/h2H,1HRCRA waste no. U076Rcra waste number U076","1,1-Dichloroethane is a colorless, oily, man-made liquid. It evaporates quickly at room temperature and has an odor like ether. 1,1-Dichloroethane burns easily. When 1,1-dichloroethane is released to the environment, it usually exists as a vapor rather than a liquid. It is used primarily to make 1,1,1-trichloroethane and a number of other chemicals. It is also used to dissolve other substances such as paint, varnish and finish removers, and to remove grease. 1,1-Dichloroethane was used as a surgical anesthetic, but is no longer. (R688)",,75-34-3,6365,,"","","",CPD-8985,,C501196,"1,1-Dichloroethane",442,,,,"InChI=1/C2H4Cl2/c1-2(3)4/h2H,1H3","1,1-dichloroethane",http://www.biospider.ca/saved_files/mol/,CC(Cl)Cl,CC(Cl)Cl,C2H4Cl2,97.969010,,-96.9 °C,,,"5.04 mg/mL at 25 °C [HORVATH,AL et al. (1999)]",,,,"Inhalation 
Oral
Dermal and eye exposure
(R689)",,"The limited information available about 1,1-dichloroethane suggests that it may be nephrotoxic, fetotoxic, and possibly carcinogenic. 1,1-Dichloroethane has been observed to enhance cell transformation and results suggest that 1,1-dichloroethane or a metabolite can bind to cellular macromolecules such as DNA. It had been reported that 1,1-dichloroethane binds to nucleic acids and proteins in vivo and in vitro. This binding is also mediated by the liver cytochrome-P-450 system. Phenobarbital enhances the extent of covalent macromolecular binding. Hence, metabolites of 1,1-dichloroethane bind to the DNA, RNA, and tissue proteins. (R688)","After absorption, 1,1-dichloroethane is distributed to the liver, kidney, lung, and stomach. In general, the identification of specific metabolites and the monitoring of enzyme activities indicate that the biotransformation of 1,1-dichloroethane is mediated by hepatic microsomal cytochrome P-450 system. Metabolism of 1,1-dichloroethane by hepatic microsomes results in the production of acetic acid as the major metabolite and 2,2-dichloroethanol, mono-, and dichloroacetic acid as minor metabolites. The initial steps in the metabolism of 1,1-dichloroethane were proposed to involve cytochrome P-450-dependent hydroxylations at either carbon. Hydroxylation at C-l would result in the production of an unstable alpha-haloalcohol, which can lose HCl to yield acetyl chloride. An alternative, but less favorable reaction, would be a chlorine shift to yield chloroacetyl chloride. These acyl chlorides can react with water to generate free acids or react with cellular constituents. Hydroxylation at C-2 would produce 2,2-dichloroethanol, which would undergo subsequent oxidation to dichloroacetaldehyde and dichloroacetic acid. 1,1-dichloroethane metabolites are excreted in urine and breathed out air. (R688)","LD50: 750 mg/kg (Oral, Rat) (R711) 
LD50: 14.1 g/kg (Oral, Rat) (R712)","","2B, possibly carcinogenic to humans. (R264)","1,1-Dichloroethane is used primarily to make 1,1,1-trichloroethane and a number of other chemicals. It is also used to dissolve other substances such as paint, varnish and finish removers, and to remove grease. Exposure may results from breathing air containing vapors of 1,1-dichloroethane, drinking contaminated water, and through eye and skin contact. (R688)",,"1,1-dichloroethane can cause kidney disease after long-term, high-level exposure in the air. It is also known to cause liver damage, as well as central nervous system depression. 1,1-Dichloroethane can cause dermatitis on prolonged dermal exposure. (R688, R698)","Burning sensation, cough, drowsiness, headache, nausea, dullness, salivation, sneezing, and vomiting can follow inhnalation or ingestion of 1,1-dichloroethane. Eye exposure can lead to redness and pain of the contact surface. Dermal exposure can lead to roughness and dry skin. has very little effect on the skin. Especially, persons with existing skin disorders may be more susceptible to the effects of this agent. (R689, R692)","Following oral exposure, immediately dilute with 4 to 8 ounces (120 to 240 mL) of water or milk and administer charcoal as a slurry (240 mL water/30 g charcoal). Consider insertion of a small, flexible nasogastric or orogastric tube to suction gastric contents after recent large ingestions (the risk of further mucosal injury must be weighed against potential benefits). Following inhalation exposure, Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. After eye exposure, irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes. If the exposure occurs through dermal contact, remove contaminated clothing and wash exposed area thoroughly with soap and water. In any case, a physician may need to examine the area if irritation or pain persists. (R624)",DNA;RNA;P98194;O75185;P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P78334;Q8N1C3;P18507;Q99928;O00591;P24046;P28476;A8MPY1;Q9UN88;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;P54710;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P03372;Q92731
162,T3D0161,2009-03-06 18:58:11 UTC,2009-08-04 21:27:51 UTC,Acenaphthene,Organic Compound;Industrial By-product/Pollutant;Aromatic Hydrocarbon;Polycyclic Aromatic Hydrocarbon,"1, 2-Dihydroacenaphthylene1,2-Dihydroacenaphthylene1,2-dihydroacenaphthylene (ACD/Name 4.0)1,8-Dihydroacenaphthalene1,8-EthylenenaphthaleneA104_ALDRICHAcenaphteneAcenaphthene solutionAcenaphthyleneAcenaphthylene, 1,2-dihydro-EthylenenaphthaleneNaphthyleneethylenePeri-ethylenenaphthalene","Acenaphthene is one of over 100 different polycyclic aromatic hydrocarbons (PAHs). PAHs are chemicals that are formed during the incomplete burning of organic substances, such as fossil fuels. They are usually found as a mixture containing two or more of these compounds. (R028)",,83-32-9,6734,,"","",22154,--TRANS-ACENAPHTHENE-12-DIOL,,C042552,Acenaphthene,1735,,,http://en.wikipedia.org/wiki/Acenaphthene,"InChI=1/C12H10/c1-3-9-4-2-6-11-8-7-10(5-1)12(9)11/h1-6H,7-8H2","1,2-dihydroacenaphthylene",http://www.biospider.ca/saved_files/mol/,C1CC2=CC=CC3=C2C1=CC=C3,C1CC2=CC=CC3=C2C1=CC=C3,C12H10,154.078250,White solid.,93.4 °C,"","","0.0039 mg/mL at 25 °C [MILLER,MM et al. (1985)]","","","","Oral 
Inhalation 
(R028)","Serum albumin (P02768) 
Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 1B1 (Q16678) 
(R060)","The ability of PAH's to bind to blood proteins such as albumin allows them to be transported throughout the body. Many PAH's induce the expression of cytochrome P450 enzymes, especially CYP1A1, CYP1A2, and CYP1B1, by binding to the aryl hydrocarbon receptor or glycine N-methyltransferase protein. These enzymes metabolize PAH's into their toxic intermediates. The reactive metabolites of PAHs (epoxide intermediates, dihydrodiols, phenols, quinones, and their various combinations) covalently bind to DNA and other cellular macromolecules, initiating mutagenesis and carcinogenesis. (R028, R060, R068, R073)","PAH metabolism occurs in all tissues, usually by cytochrome P-450 and its associated enzymes. PAHs are metabolized into reactive intermediates, which include epoxide intermediates, dihydrodiols, phenols, quinones, and their various combinations. The phenols, quinones, and dihydrodiols can all be conjugated to glucuronides and sulfate esters; the quinones also form glutathione conjugates. (R028)","LD50: 600 mg/kg (Acute intraperitoneal, Rat)","","3, not classifiable as to its carcinogenicity to humans. (R264)","PAHs are released into the environment via the combustion of fossil fuels, coke oven emissions and vehicle exhausts, as well as naturally from forest fires and volcanic eruptions. PAHs from these sources may contaminate nearly water systems. They are also found in coal tar and charbroiled food. (R028)","","PAHs are carcinogens and have been associated with the increased risk of skin, respiratory tract, bladder, stomach, and kidney cancers. They may also cause reproductive effects and depress the immune system. (R028)","Acute exposure to PAHs causes irritation and inflammation of the skin and lung tissue. (R034)
",There is no known antidote for PAHs. Exposure is usually handled with symptomatic treatment. (R028),P35869;Q14749;DNA
163,T3D0162,2009-03-06 18:58:12 UTC,2009-08-16 02:18:16 UTC,"1,2,3,4,6,7,8,9-Octachlorodibenzofuran",Organic Compound;Industrial By-product/Pollutant;Aromatic Hydrocarbon;Organochloride;Dibenzofuran,"1,2,3,4,6,7,8,9-Octachlorodibenzo[b,d]furan1,2,3,4,6,7,8,9-octachlorodibenzofuranOctachlorodibenzofuranOctapolychlorinated dibenzofuranPerchlorodibenzofuran","Chlorinated dibenzofurans (CDFs) are a family of chemical that contain one to eight chlorine atoms attached to the carbon atoms of the parent chemical, dibenzofuran. The CDF family contains 135 individual compounds (known as congeners) with varying harmful health and environmental effects. Of these 135 compounds, those that contain chlorine atoms at the 2,3,7,8-positions of the parent dibenzofuran molecule are especially harmful. Other than for laboratory use of small amounts of CDFs for research and development purposes, these chemicals are not deliberately produced by industry. Most CDFs are produced in very small amounts as unwanted impurities of certain products and processes utilizing chlorinated compounds. Only a few of the 135 CDF compounds have been produced in large enough quantities so that their properties, such as color, smell, taste, and toxicity could be studied. (S290)",,"39001-02-0
",38200,,"","","",CPD-926,,,"1,2,3,4,6,7,8,9-Octachlorodibenzofuran",,,,,InChI=1/C12Cl8O/c13-3-1-2-4(14)6(16)8(18)10(20)12(2)21-11(1)9(19)7(17)5(3)15,"1,2,3,4,6,7,8,9-octachlorodibenzofuran",http://www.biospider.ca/saved_files/mol/,C12=C(C(=C(C(=C1Cl)Cl)Cl)Cl)OC3=C2C(=C(C(=C3Cl)Cl)Cl)Cl,C12=C(C(=C(C(=C1Cl)Cl)Cl)Cl)OC3=C2C(=C(C(=C3Cl)Cl)Cl)Cl,C12Cl8O,439.745740,Colorless crystals.,258 °C,,,"1.16e-09 mg/mL at 25 °C [DOUCETTE,WJ & ANDREN,AW (1988)]",,,,"Occupational exposure to dibenzofuran may occur through inhalation and dermal contact, particularly at sites where coal tar, coal tar derivatives, and creosote are produced and used. Consumption of contaminated water and food are the primary sources of exposure for the general population. (S290)",,"Dibenzofurans bind the aryl hydrocarbon receptor, which increases its ability to activate transcription in the XRE promoter region. This alters the expression of a number of genes. (S285)","No information on the metabolism of dibenzofuran in mammalian organisms was found in the available literature. The bacteria Sphingomonas, Brevibacterium, Terrabacter, and Staphylococcus auricularis degrade dibenzofuran to 2,2',3-trihydroxybiphenyl via dibenzofuran 4,4a-dioxygenase. (S290)",,,"3, not classifiable as to its carcinogenicity to humans. (R264)","CDFs are created from production of coal tar and during incineration. They are used as insecticides, in the production of PVC, and in industrial bleaching. (S290)",,"CDFs cause vomiting and diarrhea, anemia, more frequent lung infections, numbness and other effects on the nervous system, and mild changes in the liver. However, there were no permanent liver changes or definite liver damage found in  people who ingested CDFs. (S290)","Skin and eye irritations, especially severe acne, darkened skin color, and swollen eyelids with discharge are the most obvious health effects of the CDF poisoning. (S290)",,P03372;Q92731;P35869
164,T3D0163,2009-03-06 18:58:12 UTC,2009-08-04 21:27:52 UTC,"1,1,2-Trichloroethane",Organic Compound;Solvent;Organochloride,"&beta;-t&beta;-trichloroethane.beta.-t.beta.-trichloroethane1,1, 2-Trichloroethane1,1,2-TRICHLOROETHANE (VINYL TRICHLORIDE)1,1,2-Trichloraethan1,1,2-Trichlorethane1,1,2-Trichloroethane1,1,2-trichloroethane (ACD/Name 4.0)1,2,2-TrichloroethaneBeta-tBeta-trichloroethaneCHCl2CH2ClCaswell No. 875AEthane trichlorideEthane, 1,1, 2-trichloro-InChI=1/C2H3Cl3/c3-1-2(4)5/h2H,1HRCRA waste no. U227Rcra waste number U227Rcra waste number U359TrichloroethaneTrichloroethane, 1,1,2-Trojchloroetan(1,1,2)Trojchloroetan(1,1,2) (POLISH)Trojchloroetan(1,1,2) [Polish]Vinyl trichlorideVinyltrichlorideWLN: GYG1G","1,1,2-Trichloroethane is a colorless, sweet-smelling liquid that does not burn easily and boils at a higher temperature than water. It is used mostly where 1,1-dichloroethene (vinylidene chloride) is made. 1,1,2-Trichloroethane is used as a solvent. When it is released into the environment, most 1,1,2-trichloroethane finally ends up in the air, but some may enter groundwater. Breakdown in both the air and groundwater is slow. (R717)",,79-00-5,6574,,"","",36018,CPD-8985,,C024567,"1,1,2-Trichloroethane",1412,,,"http://en.wikipedia.org/wiki/1,1,2-Trichloroethane","InChI=1/C2H3Cl3/c3-1-2(4)5/h2H,1H2","1,1,2-trichloroethane",http://www.biospider.ca/saved_files/mol/,C(C(Cl)Cl)Cl,C(C(Cl)Cl)Cl,C2H3Cl3,131.930030,Colorless liquid.,-36.6 °C,110 - 115 °C,1.435 g/cm³,"4.59 mg/mL at 25 °C [HORVATH,AL et al. (1999)]",,,,"Inhalation 
Oral
Dermal
(R718)",,"Acyl chlorides and free radicals formed during the metabolism of 1,1,2-trichloroethane are reactive metabolites that can bind to proteins and nucleic acids (DNA, RNA), and are suspected of being cytotoxic, mutagenic, and carginogenic. (R717, R733)","After 1,1,2-trichloroethane enters the body, it is carried by the blood to organs and tissues such as the liver, kidney, brain, heart, spleen, and fat. The primary metabolites identified are chloroacetic acid, S-carboxymethylcysteine, and thiodiacetic acid. S-carboxymethycysteine and thiodiacetic acid are formed from 1,1,2-trichloroethane following conjugation with glutathione. Chloroacetic acid is formed by hepatic cytochrome P-450. This reaction is thought to proceed via the acyl chloride. Cytochrome P-450 can also produce free radicals from 1,1,2-trichloroethane. Experiments show that most 1,1,2-trichloroethane leaves the body unchanged in the breath and as other substances that it is changed into in the urine in about 1 day. (R717)","LD50: 837 mg/kg (Oral, Rat) (R720) 
LD50: 5.38 g/kg (Dermal, Rabbit) (R720)","","3, not classifiable as to its carcinogenicity to humans. (R264)","1,1,2-Trichloroethane is used as a solvent. Exposure to 1,1,2-trichloroethane would most likely be from breathing vapors of the chemical or from skin contact. Drinking contaminated water is also a route of exposure. (R717)","Acute Oral: 0.3 mg/kg/day (Mice) (R717)
Intermediate Oral: 0.04 mg/kg/day (Mice) 9R717)","Inhalation of high levels of 1,1,2-trichloroethanein can affect the nervous system and cause sleepiness. 1,1,2-Trichloroethane may also affect the liver, kidney, and digestive tract, produce skin irritation, and affect the body's ability to fight infections. (R717)","Inhalation or ingestion of 1,1,2-trichloroethane can cause dizziness, drowsiness, headache, nausea, shortness of breath, and unconsciousness. The compound can be absorbed following dermal contact. Skin exposure can also lead to temporary stinging and burning pain. Other symptoms of exposure to this compound may include irritation of the skin, eyes, nose, mucous membranes, and upper respiratory tract. (R718, R719)","Following ingestion, administer charcoal as a slurry (240 mL water/30 g charcoal). Usual dose: 25 to 100 g in adults/adolescents, 25 to 50 g in children (1 to 12 years), and 1 g/kg in infants less than 1 year old. Consider gastric lavage after ingestion of a potentially life-threatening amount of poison if it can be performed soon after ingestion. In case of seizures, administer a benzodiazepine IV. Following inhalation exposure, move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with inhaled beta2 agonist and oral or parenteral corticosteroids. In case of eye exposure, irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes. In case of dermal exposure, remove contaminated clothing and wash exposed area thoroughly with soap and water. (R624)",DNA;RNA;P03372;Q92731
166,T3D0165,2009-03-06 18:58:12 UTC,2009-08-04 21:27:52 UTC,Hexachlorocyclopentadiene,Organic Compound;Industrial Precursor/Intermediate;Organochloride,"1, 3-Cyclopentadiene, hexachloro-1,2,3,4,5,5-Hexachloro-1,3-cyclopentadiene1,2,3,4,5,5-Hexachloro-cyclopenta-1,3-diene1,2,3,4,5,5-Hexachlorocyclopentadiene1,2,3,4,5,5-hexachloro-1,3-cyclopentadiene (ACD/Name 4.0)1,2,3,4,5,5-hexachlorocyclopenta-1,3-diene1,3-Cyclopentadiene, 1,2,3,4,5, 5-hexachloro-1,3-Cyclopentadiene, hexachloro-Caswell No. 478Cyclopentadiene, hexachloro-GraphloxH6002_ALDRICHHccpdHexachlorcyklopentadienHexachlorcyklopentadien (czech)Hexachlorcyklopentadien [czech]Hexachloro-1,3-cyclopentadieneHexachlorocyclopentadieneHexachlorocyclopentadiene [UN2646] [Poison]PCLPerchloro-1, 3-cyclopentadienePerchloro-1,3-cyclopentadienePerchlorocyclopentadie nePerchlorocyclopentadieneRCRA waste no. U130Rcra waste number U130WLN: L5 AHJ AG AG BG CG DG EG","Hexachlorocyclopentadiene (HCCPD) is a light, lemon-yellow liquid that has a sharp, musty odor. It easily turns from a liquid to a vapor when exposed to air. The vapor looks like a blue haze. HCCPD is a manufactured chemical and does not occur naturally in the environment. It is made by adding chlorine to cyclopentadiene, or by removing chlorine from octachlorocyclopentane. HCCPD is used to make a group of related pesticides (aldrin, chlordane, dieldrin, endosulfan, endrin, heptachlor, isodrin, mirex, and pentac) referred to cyclodienes. Only two of these pesticides, endosulfan and pentac, are currently registered for use in the United States. (R734)",,77-47-4,6478,,"","","",1-AMINO-PROPAN-2-OL,,C016488,Hexachlorocyclopentadiene,697,,,,"InChI=1/C5Cl6/c6-1-2(7)4(9)5(10,11)3(1)8","1,2,3,4,5,5-hexachlorocyclopenta-1,3-diene",http://www.biospider.ca/saved_files/mol/,C1(=C(C(C(=C1Cl)Cl)(Cl)Cl)Cl)Cl,C1(=C(C(C(=C1Cl)Cl)(Cl)Cl)Cl)Cl,C5Cl6,269.813120,,-9 °C,,,"0.0018 mg/mL at 25 °C [CALLAHAN,MA et al. (1979)]",,,,"Inhalation
Oral 
Dermal and eye exposure 
(R739)",,"HCCPD may interact with the microsomes that binds to secretory molecules and changes their ability to be transported from the cell. It can be postulated, that some of its toxic properties are a consequence of its reactivity in Diels-Alder reactions where a conjugated diene combines with a substituted or unsubstituted alkene (a dienophile) in a cycloaddition reaction. Biological tissues contain a large number of potential reactants for cycloaddition reactions. HCCPD can also undergo addition and substitution reactions or be oxidized by way of the mixed function oxidase system. Effects of HCCPD on the brain may also be a reflection of the reaction of either HCCPD or a metabolite with brain lipids. The effects of HCCPD on the adrenal glands may be a reflection of its ability to combine with the unsaturated carbons in sterols produced by this gland. The hydroxyl functional group of a sterol is on a carbon adjacent to the double bond and can activate that bond to cycloaddition reactions. Such reactions would require exposure to large doses of HCCPD so that reactive material would reach the adrenal gland. HCCPD is excreted in urine and feces. (R734)","HCCPD is rapidly metabolized and distributed to blood, liver, kidneys, and lungs before being distributed to the peripheral tissues. (R734)","LD50: 471 mg/kg (Oral, Rat) (R734)","",,"HCCPD is used to make a group of related pesticides (aldrin, chlordane, dieldrin, endosulfan, endrin, heptachlor, isodrin, mirex, and pentac) referred to cyclodienes. Exposure may result from eating contaminated food, drinking contaminated water, and exposing the skin or eye to hexachlorocyclopentadiene. (R734)","Intermediate Inhalation: 0.01 ppm (Rat) (R734)
Chronic Inhalation 0.2 ppb (Rat) (R734)
Intermediate Oral: 0.1 mg/kg/day (Rat) (R734)","Patients exposed to HCCPD may get a sore throat or have shortness of breath and chest discomfort. Bleeding, swelling, and fluid buildup can occur in the lungs. The linings of the respiratory passages and the lungs are very susceptible to damage from low concentrations of HCCPD following inhalation exposure. Inflammation of the tissues can be followed by necrosis, exfoliation, and hemorrhage. Tissue repair is often fibrous in appearance. Long-term exposure to very low levels of HCCPD can produce granular yellow-brown pigmentation of the epithelium of the nose, trachea, larynx, and lungs. High acute oral doses of HCCPD are associated with liver necrosis and tissue degeneration. The kidneys also appear to be a target tissue for HCCPD toxicity. Degenerative lesions in the tubules can result from small oral doses. (R734)","Inhalation of HCCPD can cause cough, sore throat, headache, diarrhoea, dizziness, nausea, vomiting, and laboured breathing. Ingestion of HCCPD can cause abdominal pain,burning sensation, shock or collapse. Dermal exposure can cause redness, pain and skin burns. Eye exposure can cause redness, pain, blurred vision, and severe deep burns. (R739)","After oral exposure of HCCPD, gastric lavage is recommended. Following inhalation, move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with inhaled beta2 agonist and oral or parenteral corticosteroids. Irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes in case of eye exposure. If the exposure occurs through dermal contact with the toxin, remove contaminated clothing and wash exposed area thoroughly with soap and water. Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines. (R624)",P98194;O75185;P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P78334;Q8N1C3;P18507;Q99928;O00591;P24046;P28476;A8MPY1;Q9UN88;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;P54710;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P03372;Q92731
167,T3D0166,2009-03-06 18:58:12 UTC,2009-08-25 16:17:04 UTC,Heptachlorodibenzofuran,Organic Compound;Industrial By-product/Pollutant;Aromatic Hydrocarbon;Organochloride;Dibenzofuran,"1,2,3,4,6,7,8-HEPTACHLORODIBENZOFURAN1,2,3,4,6,7,8-Hepta polychlorinated dibenzofuran1,2,3,4,6,7,8-Heptachlorodibenzo[b,d]furanDibenzofuran, 1,2,3,4,6,7,8-heptachloro-Dibenzofuran, heptachloro-HCDBF CPDHeptachlorodibenzofuran","Chlorinated dibenzofurans (CDFs) are a family of chemical that contain one to eight chlorine atoms attached to the carbon atoms of the parent chemical, dibenzofuran. The CDF family contains 135 individual compounds (known as congeners) with varying harmful health and environmental effects. Of these 135 compounds, those that contain chlorine atoms at the 2,3,7,8-positions of the parent dibenzofuran molecule are especially harmful. Other than for laboratory use of small amounts of CDFs for research and development purposes, these chemicals are not deliberately produced by industry. Most CDFs are produced in very small amounts as unwanted impurities of certain products and processes utilizing chlorinated compounds. Only a few of the 135 CDF compounds have been produced in large enough quantities so that their properties, such as color, smell, taste, and toxicity could be studied. (S290)",,38998-75-3,38199,,"","","","",,,Heptachlorodibenzofuran,,,,,InChI=1/C12HCl7O/c13-3-1-2-4-6(15)7(16)8(17)10(19)12(4)20-11(2)9(18)5(3)14/h1H,"1,2,3,4,6,7,8-heptachlorodibenzofuran",http://www.biospider.ca/saved_files/mol/,C1=C2C3=C(C(=C(C(=C3Cl)Cl)Cl)Cl)OC2=C(C(=C1Cl)Cl)Cl,C1=C2C3=C(C(=C(C(=C3Cl)Cl)Cl)Cl)OC2=C(C(=C1Cl)Cl)Cl,C12HCl7O,405.784710,Colorless crystals.,"",,,"",,,,"Occupational exposure to dibenzofuran may occur through inhalation and dermal contact, particularly at sites where coal tar, coal tar derivatives, and creosote are produced and used. Consumption of contaminated water and food are the primary sources of exposure for the general population. (S290)",,"Dibenzofurans bind the aryl hydrocarbon receptor, which increases its ability to activate transcription in the XRE promoter region. This alters the expression of a number of genes. (S285)","No information on the metabolism of dibenzofuran in mammalian organisms was found in the available literature. The bacteria Sphingomonas, Brevibacterium, Terrabacter, and Staphylococcus auricularis degrade dibenzofuran to 2,2',3-trihydroxybiphenyl via dibenzofuran 4,4a-dioxygenase. (S290)",,,"3, not classifiable as to its carcinogenicity to humans. (R264)","CDFs are created from production of coal tar and during incineration. They are used as insecticides, in the production of PVC, and in industrial bleaching. (S290)",,"CDFs cause vomiting and diarrhea, anemia, more frequent lung infections, numbness and other effects on the nervous system, and mild changes in the liver. However, there were no permanent liver changes or definite liver damage found in  people who ingested CDFs. (S290)","Skin and eye irritations, especially severe acne, darkened skin color, and swollen eyelids with discharge are the most obvious health effects of the CDF poisoning. (S290)",,P03372;Q92731;P35869
168,T3D0167,2009-03-06 18:58:12 UTC,2009-08-04 21:27:52 UTC,"1,2-Diphenylhydrazine",Organic Compound;Aromatic Hydrocarbon;Organochloride;Amine,"(SYM)-diphenylhydrazine1, 2-Diphenylhydrazine1,1'-Hydrazodibenzene1,2-Diphenyldrazine1,2-Diphenylhydrazine1,2-Diphenylhydrazine (9CI)1,2-diphenylhydrazine (ACD/Name 4.0)Benzene, 1,1'-hydrazobis-Benzene, hydrazodi-DPHDiphenylhydrazineDiphenylhydrazine, 1,2-Hydrazine, 1, 2-diphenyl-Hydrazine, diphenyl-HydrazobenzenHydrazobenzen [czech]Hydrazobenzen(czech)HydrazobenzeneHydrazodibenzeneN, n'-bianilineN,n'-bianilineN,n'-diphenylhydrazineRCRA waste no. U109Rcra waste number U109SYM-diphenylhydrazineSymmetrical diphenyl hydrazineWLN: RMMR","1,2-Diphenylhydrazine is a white solid. It dissolves only slightly in water and does not change into a gas unless it is heated to very high temperatures. It sticks to soil and can be carried into the air along with windblown dust. Once in water or exposed to air it is changed into other chemicals within minutes. These chemicals include the toxic chemicals azobenzene and benzidine. 1,2-Diphenylhydrazine is used to make fabric dyes in other countries, and to make certain medicines. (R761)",,122-66-7,31222,,"","","",4-HYDROXYMETHYLPHENYLHYDRAZINE,,C032041,"1,2-Diphenylhydrazine",721,,,,"InChI=1/C12H12N2/c1-3-7-11(8-4-1)13-14-12-9-5-2-6-10-12/h1-10,13-14H","1,2-di(phenyl)hydrazine",http://www.biospider.ca/saved_files/mol/,C1=CC=C(C=C1)NNC2=CC=CC=C2,C1=CC=C(C=C1)NNC2=CC=CC=C2,C12H12N2,184.100050,,131 °C,,,"0.221 mg/mL at 25 °C [KUHNE,R et al. (1995)]",,,,,,"Two of the known metabolites, aniline and benzidine, may contribute to the toxicity and/or carcinogenicity of 1,2-diphenylhydrazine. Nonneoplastic liver lesions, hepatocellular carcinomas and/or neoplastic liver nodules indicate that the liver is a target of 1,2-diphenylhydrazine toxicity. As aniline and other aromatic amino metabolites of 1,2-diphenylhydrazine (e.g., aminophenols) are methemoglobinforming compounds by either oral or inhalation routes of exposure, it is possible that 1,2-diphenylhydrazine may cause methemoglobinemia in humans. (R761)","Unchanged 1,2-diphenylhydrazine was detected following treatment by all routes, and aniline and benzidine were identified following oral and intraperitoneal treatments. Other metabolites included two unspecified hydroxy derivatives of benzidine (oral route), 2- and 4- aminophenol (intraperitoneal route), and unidentified compounds (oral, intravenous, and intratracheal routes). Aniline is oxidized by hydroxylation of a ring carbon to form 2-or 4-aminophenol or of the nitrogen to form phenylhydroxylamine, and then is conjugated to glucuronic or sulfuric acid. Benzidine is formed readily from 1,2-diphenylhydrazine by acid rearrangement. It has been suggested that benzidine may be produced from 1,2-diphenylhydrazine by acidity in the stomach. (R761)","LD50: 959 mg/kg (Oral, Rat) (R761)","",,"1,2-Diphenylhydrazine is used to make fabric dyes in other countries, and to make certain medicines. Exposure may result from breathing in dust coated with 1,2-diphenylhydrazine and eating dirt or smearing contaminated dirt on the skin. (R761)",,"Nonneoplastic liver lesions, hepatocellular carcinomas and/or neoplastic liver nodules; seizures and coma. (R761)","Irritatinon to the eyes, nose and respiratory system, depending on the route of exposure. Cough, redness of the exposed surface. (R761)","Consider gastric lavage after ingestion of a potentially life-threatening amount of poison if it can be performed soon after ingestion. Following inhalation, move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with inhaled beta2 agonist and oral or parenteral corticosteroids. Irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes in cse of eye exposure. If the exposure occurs through dermal contact Remove contaminated clothing and wash exposed area thoroughly with soap and water. A physician may need to examine the area if irritation or pain persists. (R624)",P03372;Q92731
169,T3D0168,2009-03-06 18:58:12 UTC,2009-08-04 21:27:52 UTC,"2,3,4,7,8-Pentachlorodibenzofuran",Organic Compound;Industrial By-product/Pollutant;Aromatic Hydrocarbon;Organochloride;Dibenzofuran,"2,3,4,7,8-Pentapolychlorinated dibenzofuran2,3,4,7,8-pentachlorodibenzo[b,d]furan2,3,4,7,8-pentachlorodibenzofuran (PeCDF)4-PeCDFDibenzofuran, 2,3,4,7,8-pentachloro-PCB 126 / PECDF mixturePecdfTef transgenics (pecdf)","Chlorinated dibenzofurans (CDFs) are a family of chemical that contain one to eight chlorine atoms attached to the carbon atoms of the parent chemical, dibenzofuran. The CDF family contains 135 individual compounds (known as congeners) with varying harmful health and environmental effects. Of these 135 compounds, those that contain chlorine atoms at the 2,3,7,8-positions of the parent dibenzofuran molecule are especially harmful. Other than for laboratory use of small amounts of CDFs for research and development purposes, these chemicals are not deliberately produced by industry. Most CDFs are produced in very small amounts as unwanted impurities of certain products and processes utilizing chlorinated compounds. Only a few of the 135 CDF compounds have been produced in large enough quantities so that their properties, such as color, smell, taste, and toxicity could be studied. (S290)",,57117-31-4,42128,,"","","",1-AMINO-PROPAN-2-OL,,C038890,"2,3,4,7,8-Pentachlorodibenzofuran",6787,,,,InChI=1/C12H3Cl5O/c13-6-1-4-5-2-8(15)10(16)11(17)12(5)18-9(4)3-7(6)14/h1-3H,"2,3,4,7,8-pentachlorodibenzofuran",http://www.biospider.ca/saved_files/mol/,C1=C2C3=CC(=C(C(=C3OC2=CC(=C1Cl)Cl)Cl)Cl)Cl,C1=C2C3=CC(=C(C(=C3OC2=CC(=C1Cl)Cl)Cl)Cl)Cl,C12H3Cl5O,337.862650,Colorless crystals.,196 °C,,,"2.35e-07 mg/mL at 23 °C [FRIESEN,KJ et al. (1990B)]",,,,"Occupational exposure to dibenzofuran may occur through inhalation and dermal contact, particularly at sites where coal tar, coal tar derivatives, and creosote are produced and used. Consumption of contaminated water and food are the primary sources of exposure for the general population. (S290)",,"Dibenzofurans bind the aryl hydrocarbon receptor, which increases its ability to activate transcription in the XRE promoter region. This alters the expression of a number of genes. (S285)","No information on the metabolism of dibenzofuran in mammalian organisms was found in the available literature. The bacteria Sphingomonas, Brevibacterium, Terrabacter, and Staphylococcus auricularis degrade dibenzofuran to 2,2',3-trihydroxybiphenyl via dibenzofuran 4,4a-dioxygenase. (S290)",,,"3, not classifiable as to its carcinogenicity to humans. (R264)","CDFs are created from production of coal tar and during incineration. They are used as insecticides, in the production of PVC, and in industrial bleaching. (S290)",,"CDFs cause vomiting and diarrhea, anemia, more frequent lung infections, numbness and other effects on the nervous system, and mild changes in the liver. However, there were no permanent liver changes or definite liver damage found in  people who ingested CDFs. (S290)","Skin and eye irritations, especially severe acne, darkened skin color, and swollen eyelids with discharge are the most obvious health effects of the CDF poisoning. (S290)",,P03372;Q92731;P35869
171,T3D0170,2009-03-06 18:58:12 UTC,2009-08-04 21:27:53 UTC,"Cresol, para-",Organic Compound;Solvent;Disinfectant;Aromatic Hydrocarbon,"1-Hydroxy-4-methylbenzene1-Methyl-4-hydroxybenzene4-(Pentafluorosulfanyl)phenol4-Cresol4-Hydroxytoluene4-Methylphenol4-Methylphenol (p-cresol)Aluminum p-cresoxideCresolCresol (m-/p- mixture)Cresol, all isomersCresol, p-Cresol, p-isomerCresol, paraCresol, para-Cresol,p-CresolsFEMA No. 2337FEMA Number 2337M,p-cresol mixtureP-cresol for synthesisP-cresylateP-cresylic acidP-hydroxytolueneP-kresolP-kresol [german]P-methyl phenolP-methylhydroxybenzeneP-methylphenolP-oxytolueneP-toluolP-tolyl alcoholPCRPara-cresolPara-cresylic acidParacresolParamethyl phenolPhenol, 4-methyIPhenol, 4-methyl-Phenol, 4-methyl-, aluminum saltPhenol, methyl-Rcra waste number U052TOLUENE,4-HYDROXY (PARA-CRESOL)TricresolWLN: QR D1p-Cresol (4-methylphenol)p-Cresol 98+ %p-Cresol Hydrate 90 %p-Cresol [UN2076] [Poison, Corrosive]p-cresol (ACD/Name 4.0)","p-Cresol is an isomer of cresol. Cresols are organic methylphenol compounds that may occur naturally or be manufactured. Cresols have an odor characteristic to that of other simple phenols, reminiscent to some of a ""medicine"" smell. Cresols are used as solvents, disinfectants and deodorizers, as well as to make other chemicals. They may be formed normally in the body from other compounds. Cresols are found in many foods and in wood and tobacco smoke, crude oil, coal tar, and in chemical mixtures used as wood preservatives. Small organisms in soil and water produce cresols when they break down materials in the environment. p-Cresol is a major component in pig odor. (R781, R835)",,106-44-5,2879,,C01468,"",17847,CPD-108,,C032538,"Cresol, para-",1807,,,http://en.wikipedia.org/wiki/p-Cresol,"InChI=1/C7H8O/c1-6-2-4-7(8)5-3-6/h2-5,8H,1H3",4-methylphenol,http://www.biospider.ca/saved_files/mol/594bee687c94e1e678141ce61d230e40_1237952786.mol,CC1=CC=C(O)C=C1,CC1=CC=C(O)C=C1,C7H8O,108.057510,Colorless solids or liquids. ,35.5 °C,,,"21.5 mg/mL at 25 °C [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral 
Inhalation 
Dermal 
(R835)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2C19 (P33261) 
Cytochrome P450 2D6 (P10635) 
Cytochrome P450 2E1 (P05181) 
Tyrosinase (P14679) 
Thyroid peroxidase (P07202) 
(R835) ","p-Cresol is the most toxic of the three cresol isomers. Target organs of ingested cresols in humans are the blood, kidneys, lungs, liver, heart, and central nervous system. Cresols impair the stratum corneum and produce coagulation necrosis by denaturating and precipitating proteins. They may also induce changes in neurotransmitter levels, affect the activities of some enzymes, increase lipid peroxidation, and change membrane fluidity in the brain. (R835)  ","Cresols can be absorbed following inhalation, oral, and dermal exposure. Once in the body they can distribute rapidly into many organs and tissues. Cresols undergo oxidative metabolism in the liver and are rapidly eliminated, mostly in the urine, as sulfate or glucuronide conjugates. The activation of cresols by oxidation involves tyrosinase and thyroid peroxidase, forming a reactive quinone methide. Experiments with recombinant P-450s demonstrated cresol metabolism was mediated by several P-450s including CYP2D6, 2C19, 1A2, 1A1, and 2E1. (R835, R836, R837, R839)  ","LD50: 207 mg/kg (Oral, Rat) (R261) 
LD50: 301 mg/kg (Dermal, Rabbit) (R8261)
LD50: 25 mg/kg (Intraperitoneal, Mouse) (R261)","",,"Cresols are used as solvents, disinfectants and deodorizers, as well as to make other chemicals. They may be formed normally in the body from other compounds. Cresols are found in many foods and in wood and tobacco smoke, crude oil, coal tar, and in chemical mixtures used as wood preservatives. Small organisms in soil and water produce cresols when they break down materials in the environment. Breathing air containing cresols is the primary source of exposure. Exposure may also result from drinking contaminated water, eating contaminated food and coming into contact with liquids containing cresols. (R835)  ","Intermediate Oral: 0.1 mg/kg/day (R260) 
Chronic Oral: 0.1 mg/kg/day (R260)","Cresols breathed, ingested, or applied to the skin at very high levels can be very harmful because they are corrosive substances. Ingestion of high levels results in mouth and throat burns, abdominal pain, vomiting, kidney problems, and effects on the blood and nervous system. Tachycardia, respiratory failure, unconsciousness and death may occur. Many of these effects may not be caused directly by cresols, but may be a result of secondary reactions to shock caused by external and internal burns. (R782, R835) ","Ingestion of p-cresol results in burning of the mouth and throat, abdominal pain, and vomiting. Inhalation or dermal exposure of animals to p-cresol can produce irritation and corrosion at the site of contact. (R782)","Following oral exposure, immediately dilute with 4 to 8 ounces (120 to 240 mL) of water or milk (not to exceed 4 ounces/120 mL in a child). Observe patients with ingestion carefully for the possible development of esophageal or gastrointestinal tract irritation or burns. If signs or symptoms of esophageal irritation or burns are present, consider endoscopy to determine the extent of injury. In case of hypotension, infuse isotonic fluid. If hypotension persists, administer dopamine or norepinephrine. In case of hypertension, monitor vital signs regularly. For mild/moderate asymptomatic hypertension (no end organ damage), pharmacologic treatment is generally not necessary. Following inhalation, move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with inhaled beta2 agonist and oral or parenteral corticosteroids. In case of acture lung injury, maintain ventilation and oxygenation and evaluate with frequent arterial blood gas or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed. Following eye exposure, irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes. Following dermal exposure, remove contaminated clothing and wash exposed area thoroughly with soap and water. Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines. (R624)",P09172;P22079;P05164
173,T3D0172,2009-03-06 18:58:13 UTC,2009-08-04 21:27:53 UTC,"1,2-Dichlorobenzene",Organic Compound;Solvent;Industrial Precursor/Intermediate;Aromatic Hydrocarbon;Organochloride,"1,2-Dichlorbenzene1,2-Dichlorobenzene1,2-Dichlorobenzene (o-dichlorobenzene)1,2-Dichlorobenzene solution1,2-dichlorobenzene (ACD/Name 4.0)1,3-Cyclohexadien-5-yne, 1,2-dichloro-1,3-Cyclohexadien-5-yne,1,2-dichloro-2-dichlorobenzeneBENZENE,1,2-DICHLOROBenzene, 1, 2-dichloro-Benzene, dichloro-Benzene, o-dichloro-Caswell No. 301ChlorobenChlorodenClorobenDCBDichloricideDichlorobenzeneDichlorobenzene (all isomers)Dichlorobenzene (mixed isomers)Dichlorobenzene (mixed)Dichlorobenzene, 1,2-Dichlorobenzene, o-Dichlorobenzene, orthoDichlorobenzene, ortho, liquidDichlorobenzolDilantin DBDilatin DBDilatin dbiDizeneDowtherm eMott-exMottenschutzmittel evau pO,p-dichlorobenzene mixtureO-dichlor benzolO-dichlorbenzeneO-dichlorbenzolO-dichlorobenzeneO-dichlorobenzolODBODCBOrtho-dichlorobenzeneOrthodichlorobenzeneOrthodichlorobenzolRCRA waste no. U070RotamottSpecial termite fluidTermitkilWLN: GR BGYANo-Dichlorobenzene [UN1591] [Keep away from food]","1,2-Dichlorobenzene (1,2-DCB), or ortho-dichlorobenzene, is an organic compound with the formula C6H4Cl2. This colourless liquid is poorly soluble in water but miscible with most organic solvents. 1,2-Dichlorobenzene contains two chlorine atoms connected to one benzene molecule. Most of the 1,2-DCB released into the environment is present as a vapor. 1,2-DCB can burn, but they do not burn easily. (R677, R872)",,95-50-1,7239,,C14328,"",35290,CPD-1125,,C004726,"1,2-Dichlorobenzene",433,,,,InChI=1/C6H4Cl2/c7-5-3-1-2-4-6(5)8/h1-4H,"1,2-dichlorobenzene",http://www.biospider.ca/saved_files/mol/bec5de7e7ea336b47d9dafac1484cc02_1237952906.mol,C1=CC=C(C(=C1)Cl)Cl,C1=CC=C(C(=C1)Cl)Cl,C6H4Cl2,145.969010,,-16.7 °C,,,"0.156 mg/mL at 25 °C [BANERJEE,S et al. (1980)]",,,,"Inhalation
Oral
Dermal
(R873)","Cytochrome P450 1A1 (P04798)
Cytochrome P450 1A2 (P05177)
Cytochrome P450 2D6 (P10635)
Cytochrome P450 2E1 (P05181)
(R687)","1,2-DCB was found to covalently bind to DNA, RNA, and proteins of liver, kidney, lung, and stomach. (R677)","After absorption, 1,2-DCB ist distributed in blood, the urinary bladder, kidney, fat, and liver. The initial step in the metabolism of 1,2-DCB is metabolism by cytochrome P-450 isozymes, mainly P4502E1, to an active epoxide. This epoxide can either react directly with cellular components, be conjugated to glutathione or glucuronic acid, or be hydrolyzed to form 2,3-dichlorophenol or 3,4-dichlorophenol. The dichlorophenol metabolites can be further metabolized by conjugation with glutathione, glucuronic acid, or sulfate, or further oxidized to catechols. An additional oxidation to form dichlorohydroquinone metabolites has also been proposed. Microsomal studies have implicated cytochrome P-450, and particularly P4502E1, as a major component of 1,2-DCB metabolism, resulting in the formation of dichlorophenols, dichlorocatechols, and dichlorohydroquinones. 1,2-DCB is eliminated primarily in the urine as metabolites rather than as the parent compound. (R677)","LD50: 500 mg/kg (Oral, Rat) (R677)","","3, not classifiable as to its carcinogenicity to humans. (R264)","Exposure may result from breathing contaminated air, drinking contaminated water or eating contaminated food, and skin contact. (R677)","Acute Oral: 0.7 mg/kg/day (Rat and mice) (R260) 
Intermediate Oral: 0.6 mg/kg/day (Rat and mice) (R260) 
Chronic Oral: 0.3 mg/kg/day (Rat and mice) (R260)","Inhaling the vapor or dusts of 1,2-DCB at very high concentrations could be very irritating to eyes and nose and cause burning and tearing of the eyes, coughing, difficult breathing, and an upset stomach. Ingestion of 1,2-DCB can cause effects in the kidneys and blood, and that 1,3-DCB caused thyroid and pituitary effects. (R677)","Cough, drowsiness, sore throat and unconsciousness can result from inhalation. Burning sensation, diarrhoea, nausea and vomiting can follow ingestion. In case of dermal or eye exposure, redness and pain of the exposed surface can occur. Moreover, skin exposure can cause skin dryness. (R873)","Following oral exposure, administer charcoal as a slurry; administer oxygen to all cyanotic or symptomatic patients. In case of methemoglobinemia, administer 1 to 2 mg/kg of 1% methylene blue slowly IV in symptomatic patients; also consider adjunctive therapy. In case of inhalation exposure, move patient to fresh air; monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis; administer oxygen and assist ventilation as required. Treat bronchospasm with inhaled beta2 agonist and oral or parenteral corticosteroids. Following eye exposure, irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes. Following dermal exposure, skin should be thoroughly washed with soap and water; contaminated clothing and shoes should be discarded; seek medical attention. Administer 100 percent humidified supplemental oxygen with assisted ventilation as required. Treat for methemoglobinemia and sequelae. Signs and symptoms of methemoglobinemia may be delayed. (R624)",P09211;DNA;RNA;P98194;O75185;P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P78334;Q8N1C3;P18507;Q99928;O00591;P24046;P28476;A8MPY1;Q9UN88;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;P54710;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P03372;Q92731
174,T3D0173,2009-03-06 18:58:13 UTC,2009-08-04 21:27:53 UTC,"1,2-Dichloroethene, trans-",Organic Compound;Solvent;Organochloride,"(E)-1,2-Dichloroethene(E)-1,2-Dichloroethylene(e)-CHCL=CHCL1,2-Dichlor-aethen [German]1,2-Dichloraethen1,2-Dichloroethene1,2-Dichloroethene, trans-1,2-Dichloroethylene1,2-Dichloroethylene (trans)1,2-Dichloroethylene, all isomers1,2-Dichloroethylene, mixture of cis and trans1,2-dichloroethylene (ACD/Name 4.0)1,2-trans-Dichloroethene1,2-trans-Dichloroethylene1,trans-2-DichloroetheneAcetylene dichlorideAcetylene dichloride, trans-CIS & TRANS 1,2-DICHLOROETHYLENECIS-1,2-DICHLOROETHYLENEDichloro-1,2-ethylene [French]Dichloroethylene, trans-Dichloroethylene-transDioformETHENE,1,2-DICHLORO (CIS)Ethene, 1, 2-dichloro-, (E)-Ethene, 1,2-dichloro-Ethene, 1,2-dichloro-, (1E)-Ethene, 1,2-dichloro-, (E)- (9CI)Ethylene, 1,2-dichloro-Ethylene, 1,2-dichloro-, (E)-Ethylene, 1,2-dichloro-, trans-RCRA waste no. U079Rcra waste number U079SYM-dichloroethyleneTrans-acetylene dichlorideTrans-dichloroetheneTrans-dichloroethyleneWLN: G1U1G-Ttrans-1, 2-Dichloroethenetrans-1,2-DCEtrans-1,2-Dichloroethenetrans-1,2-Dichloroethylenetrans-Di-1, 2-chloroethylenetrans-Di-1,2-Chloroethylene","Trans-1,2-dichloroethene (1,2-DCE) is one of two isomers of 1,2-dichloroethene. It is a highly flammable, colorless liquid with a sharp, harsh odor. 1,2-DCE is used as a solvent for waxes, resins, acetylcellulose, perfumes, dyes, lacquers, thermoplastics, fats, and phenols. It is also used as an intermediate in the preparation of other chlorinated solvents. (R913, R914)",,156-60-5,638186,,C06791,"",29027,11-DCE,,,"1,2-Dichloroethene, trans-",3719,,,,InChI=1/C2H2Cl2/c3-1-2-4/h1-2H/b2-1+,"(E)-1,2-dichloroethene",http://www.biospider.ca/saved_files/mol/c83c66e5f6c54583229c41164bc1948b_1237953041.mol,C(=C/Cl)\Cl,C(=CCl)Cl,C2H2Cl2,95.953360,Colorless liquid.,-49.8 °C,"47.2 °C at 745 mm Hg
48.0 - 48.5 °C at 760 mm Hg",1.2565,"6.41 mg/mL at 25 °C [HORVATH,AL et al. (1999)]",,2-4 °C,,"Inhalation
Oral
Dermal and eye contact 
(R913)","","Trans-1,2-dichloroethene is a volatile, lipophilic molecule that easily moves through the respiratory and gastrointestinal systems. It has a high affinity for lipids and blood, but little accumulation in tissues. 1,2-Dichloroethene isomers inhibit liver enzymes involved in metabolism and may increase the “toxic” response to other chemicals. Reactive metabolites of trans-1,2-dichloroethene modify the heme moiety of hepatic microsomal cytochrome P-450, resulting in a loss of both cytochrome P-450 and heme. Trans-1,2-dichloroethene can also mixed-function oxidase activities. Metabolism of trans-1,2-dichloroethene can lead to dose-related decrease in the levels of serum glutamicoxaloacetic transaminase (SGOT) and serum glutamic-pyruvic transaminase (SGPT). (R913)","Metabolism of trans-1,2-dichloroethene is initially catalyzed by hepatic microsomal cytochrome P-450. This metabolism is believed to involve epoxidation of the ethylene double bond, forming dichlorinated epoxides. Dichlorinated epoxides, in turn, can undergo a non-enzymatic rearrangement. Studies on the metabolism of 1,2-dichloroethene by hepatic microsomes and hepatocytes provide evidence to suggest that dichloroacetaldehyde is the predominant metabolite of microsomal cytochrome P-450 and that it, in turn, is extensively converted to dichloroethanol and dichloroacetate by cytosolic and/or mitochondrial aldehyde and alcohol dehydrogenases present in hepatocytes. (R913)","LD50: 1,300-10,000 mg/kg/day (Inhalation, Rat) (R913)","","3, not classifiable as to its carcinogenicity to humans. (R264)","Trans-1,2-DCE is used as a solvent for waxes, resins, acetylcellulose, perfumes, dyes, lacquers, thermoplastics, fats, and phenols. It is also used as an intermediate in the preparation of other chlorinated solvents. One may be exposed by breathing contaminated air, eating, or drinking the substance, or by skin contact (R913, R914).","Acute Inhalation: 0.2 ppm (Rat) (R913)
Acute Oral: 1 mg/kg/day (Rat) (R913)
Intermediate Oral: 0.3 mg/kg/day (R913)","Breathing trans-1,2-DCE can cause sever liver and kidney damages, pulmonary capillary hyperemia, as well as alveolar septal distention; depression of the central nervous sustem can occur; moderate iritis and conjunctivitis can follow eye exposure; dermatitis and irritation of mucous membranes can follow dermal exposure. Symptoms associated with lethal oral doses included decreased activity, ataxia, suppressed or total loss of righting reflex, and depressed respiration. (R913)","Symptoms of trans-1,2-DCE exposure include nausea, dowiness, and tiredness. Mild or moderate erythema may follow dermal exposure, and skin or eye irritation can follow dermal/eye contact. (R913)","Following inhalation exposure, move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with inhaled beta2 agonist and oral or parenteral corticosteroids. In case of seizures, administer a benzodiazepine IV. Irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes in case of eye exposure. Following dermal exposure, remove contaminated clothing and wash exposed area thoroughly with soap and water. Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines. (R624) ",P05181;P03372;Q92731
175,T3D0174,2009-03-06 18:58:13 UTC,2009-08-04 21:27:53 UTC,"Indeno(1,2,3-cd)pyrene",Organic Compound;Industrial By-product/Pollutant;Aromatic Hydrocarbon;Polycyclic Aromatic Hydrocarbon,"1,10-(1,2-Phenylene)pyrene1,10-(o-Phenylene)pyrene1,10-(ortho-Phenylene)pyrene2,3-(o-Phenylene)pyrene2,3-Phenylenepyrene2,3-o-PhenylenepyreneIPIndeno(1,2,3-cd)pyreneIndeno(1,2,3-cd)pyrene [Polycyclic aromatic compounds]Indeno(1,2,3-cd)pyrene [Polycyclic aromatic hydrocarbons]IndenopyreneO-phenylenepyreneRCRA waste no. U137Rcra waste number U137","Indeno(1,2,3-cd)pyrene is one of over 100 different polycyclic aromatic hydrocarbons (PAHs). PAHs are chemicals that are formed during the incomplete burning of organic substances, such as fossil fuels. They are usually found as a mixture containing two or more of these compounds. (R028)",,0193-39-5,9131,,"","","","",,,"Indeno(1,2,3-cd)pyrene",,,,,InChI=1/C22H12/c1-2-7-17-16(6-1)18-11-10-14-9-8-13-4-3-5-15-12-19(17)22(18)21(14)20(13)15/h1-12H,"",http://www.biospider.ca/saved_files/mol/,C1=CC=C2C(=C1)C3=C4C2=CC5=CC=CC6=C5C4=C(C=C6)C=C3,C1=CC=C2C(=C1)C3=C4C2=CC5=CC=CC6=C5C4=C(C=C6)C=C3,C22H12,276.093900,Yellow crystals.,163.6 °C,"","","1.9e-07 mg/mL at 25 °C [PEARLMAN,RS et al. (1984)]","","","","Oral 
Inhalation 
(R028)","Serum albumin (P02768) 
Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 1B1 (Q16678) 
(R060)","The ability of PAH's to bind to blood proteins such as albumin allows them to be transported throughout the body. Many PAH's induce the expression of cytochrome P450 enzymes, especially CYP1A1, CYP1A2, and CYP1B1, by binding to the aryl hydrocarbon receptor or glycine N-methyltransferase protein. These enzymes metabolize PAH's into their toxic intermediates. The reactive metabolites of PAHs (epoxide intermediates, dihydrodiols, phenols, quinones, and their various combinations) covalently bind to DNA and other cellular macromolecules, initiating mutagenesis and carcinogenesis. (R028, R060, R068, R073)","PAH metabolism occurs in all tissues, usually by cytochrome P-450 and its associated enzymes. PAHs are metabolized into reactive intermediates, which include epoxide intermediates, dihydrodiols, phenols, quinones, and their various combinations. The phenols, quinones, and dihydrodiols can all be conjugated to glucuronides and sulfate esters; the quinones also form glutathione conjugates. (R028)","","","2B, possibly carcinogenic to humans. (R264)","PAHs are released into the environment via the combustion of fossil fuels, coke oven emissions and vehicle exhausts, as well as naturally from forest fires and volcanic eruptions. PAHs from these sources may contaminate nearly water systems. They are also found in coal tar and charbroiled food. (R028)","","PAHs are carcinogens and have been associated with the increased risk of skin, respiratory tract, bladder, stomach, and kidney cancers. They may also cause reproductive effects and depress the immune system. (R028)","Acute exposure to PAHs causes irritation and inflammation of the skin and lung tissue. (R034)
",There is no known antidote for PAHs. Exposure is usually handled with symptomatic treatment. (R028),P35869;Q14749;DNA
177,T3D0176,2009-03-06 18:58:13 UTC,2009-08-04 21:27:54 UTC,Carbon disulfide,Organic Compound;Solvent,"Alcohol of sulfurCarbon bisulfideCarbon bisulfuretCarbon bisulphideCarbon disulfide [UN1131] [Flammable liquid]Carbon disulfide [bsi:iso]Carbon disulfide cationCarbon disulphideCarbon disulphide [bsi:iso]Carbon sulfideCarbon sulfide (CS2)Carbon sulphideCarbon-12C disulfideCarbon-disulphide-CarboneCarbone (sulfure de) [french]Carboneum sulfuratumCarboneum sulphuratumCarbonioCarbonio (solfuro di) [italian]Caswell No. 162Disulfide, carbonDisulfidocarbonDithiocarbonic anhydrideDithioxomethaneHSDB 52KohlendisulfidKohlendisulfid (schwefelkohlenstoff) [german]KoolstofdisulfideKoolstofdisulfide (zwavelkoolstof) [dutch]Methyl disulfideRCRA waste no. P022Rcra waste number P022SchwefelkohlenstoffSchwefelkohlenstoff [german]Solfuro di carbonioSolfuro di carbonio [italian]Sulfocarbonic anhydrideSulfure de carbone [iso-french]Sulphocarbonic anhydrideSulphuret of carbonWeeviltoxWegla dwusiarczekWegla dwusiarczek [polish]","Pure carbon disulfide is a colorless liquid with a pleasant sweet odor. The impure carbon disulfide that is usually used in most industrial processes, however, is a yellowish liquid with an unpleasant odor like that of rotting radishes. Carbon disulfide evaporates at room temperature, and the vapor is more than twice as heavy as air. It easily explodes in air and also catches fire very easily. In nature, small amounts of carbon disulfide are found in gases released to the earth’s surface. Commercial carbon disulfide is made by combining carbon and sulfur at very high temperatures. Several industries use carbon disulfide as a raw material to make such things as rayon, cellophane, and carbon tetrachloride. (R922)",,075-15-0,6348,,"","",23012,CPD-844,,,Carbon disulfide,,,,http://en.wikipedia.org/wiki/Carbon disulfide,InChI=1/CS2/c2-1-3,methanedithione,http://www.biospider.ca/saved_files/mol/,C(=S)=S,C(=S)=S,CS2,75.944140,,−111.6 °C (161.6 K),,,"1.18 mg/mL at 25 °C [SEIDELL,A (1941)]",,,,"Inhalation
Ingestion
Skin and eye exposure 
(R923)","Hemooglobin subunit alpha (P69905) 
Hemoglobin subunit beta (P68871) 
Hemoglobin subunit gamma-1 (P69891) 
Hemoglobin subunit gamma-2 (P69892) 
Hemoglobin subunit delta (P02042) 
Hemoglobin subunit epsilon (P02100) 
Hemoglobin subunit theta-1 (P09105) 
Hemoglobin subunit zeta (P02008) 
Hemoglobin subunit mu (Q6B0K9) 
Serum albumin (P02768) 
Carbonic anhydrase 2 (P00918)
(R937, R958, R595, R960)","Carbon disulfide is a potent nerve toxin and also affect liver enzymes, particularly those related to lipid metabolism. The increases in serum cholesterol that are sometimes seen following carbon disulfide exposure may be a result of increased hepatic cholesterol synthesis. The primary target of carbon disulfide appears to be the nervous system. Neurophysiological and behavioral effects as well as pathomorphology of peripheral nervous system structures have been reported in humans. Moreover, carbon disulfide metabolites of the thiocarbamate type inhibit aldehyde anhydrase. (R922, R968)","Nitrogenase reduces carbon disulfide and can also be inhibited by this toxin. Carbon disulfide binds (in the form of AL CS2) mainly to hemoglobin and to a small extent to other blood proteins, such as albumin and gamma-globulin. Carbon disulfide is bioactivated by cytochrome P-450 to an unstable oxygen intermediate. The intermediate may either spontaneously degrade to atomic sulfur and carbonyl sulfide or hydrolyze to form atomic sulfur and monothiocarbonate. The atomic sulfur generated in these reactions may either covalently bind to macromolecules or be oxidized to products such as sulfate. The carbonyl sulfide formed may be converted to monothiocarbonate by carbonic anhydrase. Monothiocarbonate may further spontaneously degrade, regenerating carbonyl sulfide or forming carbon dioxide and sulfide bisulfide ion (HS-). The HS- formed can subsequently be oxidized to sulfate or other nonvolatile metabolites. Dithiocarbamates are the products of the reaction of carbon disulfide with amino acids. Most of the carbon disulfude absorbed is metabolized. Small traces of unchanged can be found in the urine. Carbon disulfide or carbonyl sulfide can conjugate with endogenous glutathione to yield thiazolidine-2-thione-4-carboxylic acid and 2-oxythiazolidine-4-carboxylic acid, respectively. Carbonic anhydrase 2 mediates the metabolism of carbon disulfide. (R922, R937, R952, R958, R959, R960)","LD50: 3,020 mg/kg/day (Oral, Mouse) (R922)","",,"Several industries use carbon disulfide as a raw material to make such things as rayon, cellophane, and carbon tetrachloride. Exposure to carbon disulfide can results from breathing air, drinking water, or eating foods that contain it. One can also be exposed by skin contact with soil, water, or other substances that contain it. (R922)","Chronic Inhalation: 0.3 ppm (R922)
 Acute Oral: 0.01 mg/kg/day (R922)","Following inhalation, subtle and transient changes in pulmonary function can be manifested as reduced vital capacity and decreased partial pressure of arterial oxygen. Patients can developed normochromic and normocytic anemia, eosinopenia, and an increase in reticulocyte cell numbers after oral exposure . Carbon disulfide poisoning can result in central nervous system depression, coma, respiratory paralysis, and death. It also may accelerate coronary artery disease. Peripheral neuropathies, cranial nerve dysfunction, and neuropsychiatric changes are present in over 70% of chronic carbon sulfide victims. (R922)","Dizziness, headache, nausea, shortness of breath, vomiting, weakness, irritability and hallucination can result from inhalation, ingestion or skin exposure to carbon disultfide. Skin and eye exposure can lead to pain, redness. Moreover, dermal exposure can lead to dryness of the skin; the carbon disulfide may be absorbed. Weak pulse, palpitations, fatigue, weakness in the legs, unsteady gait, vertigo, hyperesthesia, agitation, mania, hallucinations of sight, hearing, taste, and smell in acute are other symtoms of carbon disulfide poisoning. (R923, R324)","Following oral exposure, administer charcoal as a slurry (240 mL water/30 g charcoal). Consider gastric lavage after ingestion of a potentially life-threatening amount of poison if it can be performed soon after ingestion (generally within 1 hour). Intravenous urea (0.5 to 1.5 g/kg) has been recommended to inactivate free carbon disulfide in the blood. The efficacy of this treatment is unknown. Following inhalation exposure, move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with inhaled beta2 agonist and oral or parenteral corticosteroids. If the exposure ocuured through eye exposure, irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes. If the exposure occured trhough dermal contact, remove contaminated clothing and wash exposed area thoroughly with soap and water. (R624)",P09172;P04798;P05181
178,T3D0177,2009-03-06 18:58:13 UTC,2009-08-04 21:27:54 UTC,"2,3,4,5-Tetrachlorophenol",Organic Compound;Aromatic Hydrocarbon;Organochloride,"2,3,4,5-Tetrachlorophenate2,3,4,5-TetrachlorophenolCaswell No. 832Phenol, 2,3,4,5-tetrachloro-Phenol, tetrachloro-TetrachlorophenolTetrachlorophenol, isomerTetrachlorophenol, isomer unspecifiedTetrachlorophenols","2,3,4,5-Tetrachlorophenol is one of several chlorophenol isomers. It is a solid with a strong medicinal taste and odor, and small amounts can be tasted in water. (R970)",,25167-83-3,21013,,"","","","",,C009408,"2,3,4,5-Tetrachlorophenol",,,,,"InChI=1/C6H2Cl4O/c7-2-1-3(11)5(9)6(10)4(2)8/h1,11H","2,3,4,5-tetrachlorophenol",http://www.biospider.ca/saved_files/mol/,C1=C(C(=C(C(=C1Cl)Cl)Cl)Cl)O,C1=C(C(=C(C(=C1Cl)Cl)Cl)Cl)O,C6H2Cl4O,229.885980,,"",,,"",,,,"Inhalation
Ingestion
Skin or eye contact 
(R970)",No interacting proteins found.,"Tetrachlorophenols decrease or block ATP production without blocking the electron transport chain. Thus the poisons uncouple phosphorylation from oxidation. Free energy from the electron transport chain then converts to more body heat. As body temp rises, heat-dissipating mechanisms are overcome and metabolism is speeded. More ADP and other substrates accumulate, and these substrates stimulate the electron transport chain further. The electron transport chain responds by using up more and more available oxygen (increasing oxygen demand) in an effort to produce ATP, but much of the free energy generated is liberated as still more body heat. Oxygen demand quickly overcomes oxygen supply, and energy reserves become depleted. (R974)","Tetrachlorophenols are rapidly absorbed and excreted following occupational exposure, which involves both the inhalation and dermal routes. Most of the 2,3,4,5-tetrachlorophenol is excreted unchanged in the urine; trichlorohydroquinone has been identified as one of its metabolites. (R970)","LD50: > 2000 mg/kg (Dermal, Rabbit) (R970)
LD50: 400 mg/kg/day (Oral, Mouse) (R970)","","2B, possibly carcinogenic to humans. (R264)","Exposure may result from breathing contaminated air, ingesting contaminated water or foods, and skin or eye contact, particularly while treating wood. (R970)","Acute Oral: 0.01 mg/kg/day (Rat) (R970) 
Intermediate Oral: 0.003 mg/kg/day (Rat) (R970)",Dermal exposure can cause corrosive skin damage. (R970),"Dust has been found irritating to the nose and throat. Skin or eye contact can cause irritation of the exposed surface. Clinical signs preceding death for all tetrachlorophenol isomers included initial hyperactivity followed by hypoactivity, neuromuscular weakness, and convulsions. Headache can also result from exposure to 2,3,4,5-tetrachlorophenol. (R970)","In case of oral exposure, dilution may enhance absorption of phenol and should be avoided, but charcoal may be administered. If methemoglobinemia occurs, administer 1 to 2 mg/kg of 1% methylene blue slowly IV in symptomatic patients. Additional doses may be required. If hypotension occurs, infuse 10 to 20 mL/kg isotonic fluid. If hypotension persists, administer dopamine or norepinephrine. Following inhalation exposure, move patient to fresh air; monitor for respiratory distress; if cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with inhaled beta2 agonist and oral or parenteral corticosteroids. Irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes following eye exposure. Following dermal exposure, remove phenol with undiluted polyethylene glycol 300 to 400 or isopropyl alcohol prior to washing, if readily available. Wash exposed areas twice or for at least 10 minutes with large quantities of SOAPY water. Water alone may be harmful. (R624)",P03372;Q92731
179,T3D0178,2009-03-06 18:58:13 UTC,2009-08-25 16:03:04 UTC,Americium,Inorganic Compound;Metal;Americium Compound,"AMAmericioAmericium(III)Americium, ion(3+)Amerizium","Americium is a synthetic element that has the symbol Am and atomic number 95. It is a radioactive metallic element of the actinide series. Eighteen radioisotopes of americium, with mass number from 231 to 249, have been characterized. The most stable isotopes are Am-243 (half-life of 7370 years) and Am-241 (half-life of 432.2 years). The most used isotope is Am-241 because it is easiest to produce. Americium is widely used in commercial ionization-chamber smoke detectors as well as in neutron sources and industrial gauges. Americium emits alpha and gamma radiation, which represents a serious health hazard. (S530)",,7440-35-9,23966,,"","",33389,"",,D000576,Americium,,,,http://en.wikipedia.org/wiki/Americium,InChI=1/Am,americium,http://www.biospider.ca/saved_files/mol/,[Am],[Am],Am,0.000000,"Americium is a silvery-white solid metal, which tarnishes in dry air at room temperature. (S530)","1449 K (1176 °C, 2149 °F )","2880 K (2607 °C, 4725 °F)",12 g·cm−3 (room temperature),"",,,,"Oral
Inhalation
(W516)",,"Americium toxicity results primarily from the damage done by the alpha particle emitted during radioactive decay. This alpha particle has very limited penetration in tissue, and hence, the cellular damage occurs only in the immediate vicinity of the sequestered americium. The ionizing radiation produced by americium causes cellular damage that includes DNA breakage, accurate or inaccurate repair, apoptosis, gene mutations, chromosomal change, and genetic instability. This leads to loss of normal cell and tissue homeostasis, and development of malignancy. Ionizing radiation that does not directly damage DNA can produce reactive oxygen intermediates that directly affect the stability of p53, an important enzyme in cell-cycle regulation, and produce oxidative damage to individual bases in DNA and point mutations by mispairing during DNA replication. (W510)","Americium can be absorbed following ingestion, inhalation, and dermal exposure. In the body it distributes primarily to the liver, as well as to the bone and skeletal muscle. The metabolism of americium involves binding interactions with proteins and probably complex formation with various inorganic anions, such as carbonate and phosphate, and carboxylic acids, such as citrate and lactate. Americium is excreted in faeces and urine. (W516)",,,,Americium is widely used in commercial ionization-chamber smoke detectors as well as in neutron sources and industrial gauges. (S530),"Acute Radiation: 4 mSv (R260)
Chronic Radiation: 1 mSv/yr (R260)","Americium's radioactivity can cause cancer, especially of the bone, where it is known to accumulate. Exposure to large amount of americium may also damage the lungs, liver, and thyroid. (W516)","Exposure to high doses of ionizing radiation results in acute radiation syndrome, which can cause skin burns, hair loss, nausea, vomiting, dizziness, disorientation, low blood pressure, headache, fatigue, weakness, fever, birth defects, illness, infection, and death. (W510, W525)","Treatment reversing the effects of irradiation is currently not possible. Anaesthetics and antiemetics are administered to counter the symptoms of exposure, as well as antibiotics for countering secondary infections due to the resulting immune system deficiency. (W525)",DNA
180,T3D0179,2009-03-06 18:58:14 UTC,2009-08-25 16:03:12 UTC,Uranium-233,Inorganic Compound;Metal;Uranium Compound;Radioactive Isotope,"Uranium, isotope of mass 233Uranium-233","Uranium-233 is an artificial isotope of uranium. Uranium is a chemical element with the symbol U and atomic number 92. It is a normal part of rocks, soil, air, and water, and occurs in nature in the form of minerals. Natural uranium is a mixture of three radioactive isotopes called uranium-234, uranium-235, and uranium-238. Uranium-233 is used as a fuel for nuclear reactors and nuclear weapons.  Uranium is also used as a colorant in uranium glass, producing orange-red to lemon yellow hues. (R465, R466)",,13968-55-3,61707,,"","","","",,,Uranium-233,,,,,InChI=1/U/i1-5,uranium-233,http://www.biospider.ca/saved_files/mol/,[233U],[233U],U,238.050780,Silver metallic solid.,"",,,"",,,,"Oral 
Inhalation 
Dermal 
Radiation 
(R466)","Serotransferrin (P02787) 
Serum albumin (P02768) 
Ceruloplasmin (P00450) 
Hemopexin (P02790) 
Complement C3 (P01024) 
Complement C4-A (P0C0L4) 
Complement C4-B (P0C0L5) 
(R465, R468)","Uranium is combined with either bicarbonate or a plasma protein in the blood but once in the kidney, it is released and forms complexes with phosphate ligands and proteins in the tubular wall, causing damage. Uranium may also inhibit both sodium transport-dependent and independent ATP utilization and mitochondrial oxidative phosphorylation in the renal proximal tubule. Uranium causes respiratory diseases by damaging alveolar epithelium type II cells in the lungs. Uranium induces c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (p38 MAPK) activation, which in turn induces tumor necrosis factor alpha (TNF-alpha) secretion and generates an inflammatory response in the lungs. Studies have shown that the more soluble the uranium salt, the more toxic it is. Ionizing radiation produced by uranium damages the DNA, resulting in gene mutations and chromosomal aberrations. This can both initiate and promote carcinogenesis, and interfere with reproduction and development. (R466, R467)","Uranium is absorbed in low amounts via oral, inhalation, and dermal routes. Uranium in body fluids generally exists as the uranyl ion (UO2)2+ complexed with anions, such as citrate and bicarbonate, or plasma proteins. Uranium preferentially distributes to bone, liver, and kidney. The large majority of uranium that enters the body is not absorbed and is eliminated from the body via the urine and faeces. (R465)",,,,"Uranium-233 is used as a fuel for nuclear reactors and nuclear weapons.  Uranium is also used as a colorant in uranium glass, producing orange-red to lemon yellow hues. (R465, R466)","Intermediate Inhalation: 0.0004 mg/m3 (Soluble salts) (R260)
Chronic Inhalation: 0.0003 mg/m3 (Soluble salts) (R260)
Intermediate Oral: 0.002 mg/kg/day (Soluble salts) (R260)
Intermediate Inhalation: 0.008 mg/m3 (Insoluble compounds) (R260)","Uranium primarily damages the kidney, but may also damage the lungs, central nervous system, and immune system. Uranium's radioactivity is believed to damage the DNA, resulting in carcinogenic effects and reproductive and developmental damage. (R465, R466)","Ingestion of uranium may cause vomiting and diarrhea. Exposure to high doses of ionizing radiation results in acute radiation syndrome, which can cause skin burns, hair loss, nausea, vomiting, dizziness, disorientation, low blood pressure, headache, fatigue, weakness, fever, birth defects, illness, infection, and death. (W510, W525, R465)","Treatment reversing the effects of irradiation is currently not possible. Anaesthetics and antiemetics are administered to counter the symptoms of exposure, as well as antibiotics for countering secondary infections due to the resulting immune system deficiency. (W525)",DNA
181,T3D0180,2009-03-06 18:58:14 UTC,2009-08-04 21:27:54 UTC,Palladium,Inorganic Compound;Metal;Palladium Compound,"PALLADIUM, 10% ON CALCIUM CARBONATEPALLADIUM, 10% ON SrCO<V>3<D>PALLADIUM, 5% ON CHARCOALPALLADIUM, WIRE,0.05"""" DIAMPDPaladioPalladex 600Palladium Metallicum 4-30chPalladium atomic absorption standard solutionPalladium blackPalladium elementPalladium metallicumPalladium on activated aluminaPalladium on activated charcoalPalladium on aluminaPalladium on barium sulfatePalladium on carbonPalladium, elementPalladium, spongePrecipitated palladium","Palladium is a chemical element with the symbol Pd and atomic number 46. It is found as a free metal alloyed with gold and other platinum group metals and in the rare minerals cooperite and polarite. The unique properties of palladium and other platinum group metals account for their widespread use. One in four goods manufactured today either contain platinum group metals or had platinum group metals play a key role during their manufacturing process. Palladium is found mainly in catalytic converters and jewelry. It is also found in many electronics including computers, mobile phones, multi-layer ceramic capacitors, component plating, low voltage electrical contacts, and SED/OLED/LCD televisions. Palladium is also used in dentistry, medicine, hydrogen purification, chemical applications, and groundwater treatment. Palladium plays a key role in the technology used for fuel cells, which combines hydrogen and oxygen to produce electricity, heat and water. (S058)",,7440-05-3,23938,,"","",33363,"",,D010165,Palladium,,,,http://en.wikipedia.org/wiki/Palladium,InChI=1/Pd,palladium,http://www.biospider.ca/saved_files/mol/,[Pd],[Pd],Pd,105.903480,Silver-white metal.,10.38  g·cm −3,,10.38  g·cm −3,"",,,,"Oral 
Inhalation
Dermal 
(R062)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
(S062)","Palladium ions are able to inhibit most major cellular fuctions. They form strong complexes with both inorganic and organic ligands, substitute essential ions, bind to amino acids and various enzymes including creatine kinase and prolyl hydroxylase, and interact with functional groups of other macromolecules such as DNA leading to strand breakage. (S062)","Palladium may be absorbed through oral, dermal, and inhalation exposure. Once in the body it distributes to the kidney, liver, spleen, lymph nodes, adrenal gland, lung and bone. Palladium and its metabolites are excreted in the urine and faeces. (R062)",,,,"Palladium is found mainly in catalytic converters and jewelry. It is also found in many electronics including computers, mobile phones, multi-layer ceramic capacitors, component plating, low voltage electrical contacts, and SED/OLED/LCD televisions. Palladium is also used in dentistry, medicine, hydrogen purification, chemical applications, and groundwater treatment. Palladium plays a key role in the technology used for fuel cells, which combines hydrogen and oxygen to produce electricity, heat and water. (S058)",,Contact with palladium may cause palladium sensitivity and allergy. Animal studies have shown that palladium may damage the liver and kidney. (S062),"Skin contact with palladium may cause contact dermatitis, erythema, and oedema. (S062)","",P06732;Q9NXG6;P13674;O15460;Q7Z4N8
182,T3D0181,2009-03-06 18:58:14 UTC,2009-08-25 16:16:58 UTC,Hexachlorodibenzofuran,Organic Compound;Industrial By-product/Pollutant;Aromatic Hydrocarbon;Organochloride;Dibenzofuran,"1,2,3,4,8,9-HEXACHLORODIBENZOFURANDibenzofuran, 1,2,3,4,8,9-hexachloroDibenzofuran, 1,2,3,4,8,9-hexachloro-Dibenzofuran, hexachloro-Hexachlorodibenzofuran","Chlorinated dibenzofurans (CDFs) are a family of chemical that contain one to eight chlorine atoms attached to the carbon atoms of the parent chemical, dibenzofuran. The CDF family contains 135 individual compounds (known as congeners) with varying harmful health and environmental effects. Of these 135 compounds, those that contain chlorine atoms at the 2,3,7,8-positions of the parent dibenzofuran molecule are especially harmful. Other than for laboratory use of small amounts of CDFs for research and development purposes, these chemicals are not deliberately produced by industry. Most CDFs are produced in very small amounts as unwanted impurities of certain products and processes utilizing chlorinated compounds. Only a few of the 135 CDF compounds have been produced in large enough quantities so that their properties, such as color, smell, taste, and toxicity could be studied. (S290)",,55684-94-1,41522,,"","","","",,,Hexachlorodibenzofuran,,,,,InChI=1/C12H2Cl6O/c13-3-1-2-4-5(7(3)14)6-8(15)9(16)10(17)11(18)12(6)19-4/h1-2H,"1,2,3,4,8,9-hexachlorodibenzofuran",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C2=C1OC3=C2C(=C(C(=C3Cl)Cl)Cl)Cl)Cl)Cl,C1=CC(=C(C2=C1OC3=C2C(=C(C(=C3Cl)Cl)Cl)Cl)Cl)Cl,C12H2Cl6O,371.823680,Colorless crystals.,"",,,"",,,,"Occupational exposure to dibenzofuran may occur through inhalation and dermal contact, particularly at sites where coal tar, coal tar derivatives, and creosote are produced and used. Consumption of contaminated water and food are the primary sources of exposure for the general population. (S290)",,"Dibenzofurans bind the aryl hydrocarbon receptor, which increases its ability to activate transcription in the XRE promoter region. This alters the expression of a number of genes. (S285)","No information on the metabolism of dibenzofuran in mammalian organisms was found in the available literature. The bacteria Sphingomonas, Brevibacterium, Terrabacter, and Staphylococcus auricularis degrade dibenzofuran to 2,2',3-trihydroxybiphenyl via dibenzofuran 4,4a-dioxygenase. (S290)",,,"3, not classifiable as to its carcinogenicity to humans. (R264)","CDFs are created from production of coal tar and during incineration. They are used as insecticides, in the production of PVC, and in industrial bleaching. (S290)",,"CDFs cause vomiting and diarrhea, anemia, more frequent lung infections, numbness and other effects on the nervous system, and mild changes in the liver. However, there were no permanent liver changes or definite liver damage found in  people who ingested CDFs. (S290)","Skin and eye irritations, especially severe acne, darkened skin color, and swollen eyelids with discharge are the most obvious health effects of the CDF poisoning. (S290)",,P03372;Q92731;P35869
183,T3D0182,2009-03-06 18:58:14 UTC,2009-08-04 21:27:55 UTC,Phenol,Organic Compound;Antiseptic;Aromatic Hydrocarbon,"(14C)PhenolAcid, carbolicAcide carboliqueAcide carbolique [french]Acide carbolique(french)Acide pheniqueAnbesolAntiseptic Salve 1.2%Baker's p & s liquid & ointmentBaker's p &amp; s liquid &amp; ointmentBaker's p and sBaker's p and s liquid and ointmentBenzene, hydroxy-BenzenolBenzophenolCampho-phenique cold sore gelCampho-phenique gelCampho-phenique liquidCarbolic acidCarbolic acid liquidCarbolic acid, liquidCarbolic acid, liquid (dot)Carbolic oilCarbolicum acidumCarbolsaeureCarbolsaureCarbolsaure [german]Caswell No. 649Cepastat lozengesChloraseptic Cherry Spray 1.4%Chloraseptic Menthol Spray 1.4%Chloraseptic sore throat spray kids grape flavorCuticura pain relieving ointmentFEMA No. 3223FenolFenol [dutch, polish]Fenol(dutch, polish)FenoloFenolo [italian]Fenolo(italian)FenosmolinFenosmolineHydroxy-benzeneHydroxybenzeneIPHIZALKarbolsaeureLiquefied phenolLiquefied phenol (JP15)Liquefied phenol (TN)Liquid phenolLiquified phenolM-cresolMixture nameMonohydroxy benzeneMonohydroxybenzeneMonophenolOxybenzeneP&S Liquid Phenol 4.95mg/MlP6471_SIGMAPHOHPaosclePaoscle (TN)Petro Carbo Salve-Ont 1.5%PhenicPhenic acidPhenic alcoholPhenol (JP15/USP)Phenol (TN)Phenol (liquid)Phenol (or solutions with 5% or more phenol)Phenol 6%Phenol [jan]Phenol alcoholPhenol for disinfectionPhenol for disinfection (JP15)Phenol for disinfection (TN)Phenol homopolymerPhenol liquidPhenol moltenPhenol polymer-boundPhenol reage NTPhenol reagentPhenol solutionPhenol solutions [UN2821] [Poison]Phenol syntheticPhenol, chlorinatedPhenol, chloro derivs.Phenol, labeled with carbon-14Phenol, liquefiedPhenol, liquefied (usp)Phenol, liquidPhenol, liquid (dot)Phenol, moltenPhenol, molten [UN2312] [Poison]Phenol, polymer-boundPhenol, purePhenol, sodium saltPhenol, solidPhenol, solid [UN1671] [Poison]Phenol, sulfuratedPhenol, syntheticPhenol-UL-14CPhenolated waterPhenolated water for disinfectionPhenolePhenole [german]Phenole(german)PhenosmolinPhenyl alcoholPhenyl hydratePhenyl hydroxidePhenylalcoholPhenylic acidPhenylic acid, phenyl hydroxidePhenylic alcoholRCRA waste no. U188Rcra waste number U188Sodium salt phenolSynthetic phenolTea polyphenolUN 1671 (solid)UN 2312 (molten)Un 2812 (solution)WLN: QRphenol (ACD/Name 4.0)","Phenol is a colorless-to-white solid when pure. It has a distinct odor that is sickeningly sweet and tarry. Commercial phenol is a liquid that evaporates more slowly than water. Phenol is both a manufactured chemical and produced naturally. Large amounts of phenol are produced in the United States. Phenol is used to make plastics. Phenol is also used as a disinfectant in household cleaning products and in consumer products such as mouthwashes, gargles, throat sprays. (R983)",,108-95-2,996,,C00146,"147450
147460
171150
191740
600641
601292",15882,24-DICHLOROPHENOL,,D019800,Phenol,1148,,,http://en.wikipedia.org/wiki/Phenol,"InChI=1/C6H6O/c7-6-4-2-1-3-5-6/h1-5,7H",phenol,http://www.biospider.ca/saved_files/mol/09c1124689402c7c7c3b2e04ec66284a_1237954034.mol,OC1=CC=CC=C1,OC1=CC=CC=C1,C6H6O,94.041870,"",40.9 °C,,,"82.8 mg/mL at 25 °C [SOUTHWORTH,GR & KELLER,JL (1986)]",,,,"Inhalation
Ingestion
Dermal or eye contact 
(R970)","Sulfotransferase 1A1 (P50225)
Sulfotransferase 1A3/1A4 (P50224) 
Sulfotransferase family cytosolic 1B member 1 (O43704) 
Tyrosinase (P14679)
UDP-glucuronosyltransferase 1-6 (19224) 
(R986, R993, R984, R992)","Phenol is irritating and corrosive at high concentrations. Phenol impairs the stratum corneum and produces coagulation necrosis by denaturing and precipitating proteins. It is suggested that dermal application of phenol increases the formation of free radicals in the skin, and that the redox cycling of these radicals reduces antioxidant capacity, leading to significant oxidative damage of protein, DNA, and lipids. Phenol also act as a cyclooxygenase inhibitor. (R998, R983)","When it is absorbed through the lungs, gut, or skin, phenol conjugated at the portal-of-entry and free phenol enter the bloodstream where it can then be distributed throughout the body. The dilution of phenol in water enhances the dermal absorption of phenol. Three different enzymes systems catalyze the reactions that transform phenol. Cytosolic phenol sulfotransferases catalyze the transfer of inorganic sulfur from the activated 3'-phosphoadenosine-5'phosphosulfate donor molecule to the hydroxyl group on phenol. Microsomal membrane-located uridine diphosphate (UDP) glucuronosyltransferases catalyze the transfer of an activated glucuronic acid molecule to the hydroxyl moiety of phenol to form an O-glucuronide conjugate. Cytochrome P4502E1, also microsomally located, catalyzes the hydroxylation of phenol to form hydroquinone (and to a much lesser extent, catechol), which is then acted upon by the phase II enzymes. Hydroquinone can, in turn, form conjugates, undergo peroxidation to form benzoquinone, or undergo further oxidation to form trihydroxybenzene. All three enzyme systems that metabolize phenol are found in multiple tissues and there is competition among them not only for phenol, but also for subsequent oxidative products, like hydroquinone. As a consequence, the relative amount of the products formed can vary based on species, dose and route of administration. Cytochromes other than CYP2E1, such as CYP2F2 are suggested to participate in the phenol metabolism in the liver. Tyrosinase also catalyzes the oxidation of phenols. The gastrointestinal tract, liver, lung, and kidney appear to be the major sites of phenol sulfate and glucuronide conjugation of simple phenols. Phenol, in its free and conjugated forms, is a normal constituent of human urine. (R983, R986, R993, R984, R992)","LD50: 400 mg/kg/day (Oral, Rat) (R983) 
LD50: 669 mg/cm2/day (Dermal, Rat) (R983) 
LD50: 1,400 mg/cm2/day (Dermal, Rabbit) (R983)","",,"Phenol is used to make plastics. Phenol is also used as a disinfectant in household cleaning products and in consumer products such as mouthwashes, gargles, throat sprays. Exposure may result from breathing air containing phenol and drinking contaminated water or eating food contaminated with phenol. Exposure also occurs through dermal contact with contaminated air or by skin contact with products containing phenol. Dermal contact can occur through the use of general disinfectants and ointments containing phenol. Ingestion can occur through the use of products such as throat lozenges or sore throat sprays that contain phenol. (R983)",Acute Oral: 1 mg/kg/day (Rat) (R983),"Long-term exposure to phenol at work has been associated with cardiovascular disease, irritation of the respiratory tract and muscle twitching depedning of the route of exposure. Ingestion of liquid products containing concentrated phenol can cause serious gastrointestinal damage and even death. Application of concentrated phenol to the skin can cause severe skin damage. Longer-term exposure to high levels of phenol caused damaged to the heart, kidneys, liver, and lungs. Liver effects, as judged by increased serum activities of alanine aminotransferase (ALT) and aspartate amino transferase (AST), were also reported in a case of prolonged inhalation exposure to phenol. (R983)","Burning pain in mouth and throat; white necrotic lesions in mouth; abdominal pain, vomiting, bloody diarrhea, pallor, sweating, weakness, headache, dizziness, tinnitus can result from phenol poisoning. Phenol absorption can lead to weak irregular pulse, hypotension, shallow respirations, cyanosis, pallor, a profound fall in body temperature, muscle tremors, and difficulty walking. Possibly fleeting excitement and confusion, followed by unconsciousness. (R321, R983)","",P00918;P00915;P07451;P22748;Q16790;O43570;Q9ULX7;Q8N1Q1;P35218;Q9Y2D0;P23280;P43166
184,T3D0183,2009-03-06 18:58:14 UTC,2009-08-04 21:27:55 UTC,Chloroethane,Organic Compound;Industrial Precursor/Intermediate;Organochloride,"1-CHLORO-ETHANE1-ChloroethaneAethylII chloridumAethylchloridAethylchlorid [german]Aethylchloride [german]AethylisAethylis chloridumAethylisaethylis chloridumAnodynonC2H5ClChelenChloorethaanChloorethaan [dutch]ChloraethanChloreneChlorethylChloridumChlorinated ethane byproduct residuesChloroaethanChloroaethan [german]ChloroethaneChloroethane solutionChloroethyl groupChlorure d'ethyleChlorure d'ethyle [french]ChlorylChloryl anestheticChloryle anestheticCloretiloCloroetanoCloroetano [italian]Cloruro di etileCloruro di etile [italian]DublofixETCLEthane, chloro derivs.Ethane, chloro-Ethane, chloro- (8CI,9CI)Ether chloratusEther chloridumEther hydrochloricEther muriaticEthyl chloride (chloroethane)Ethyl chloride (usp)Ethyl chloride [UN1037] [Flammable gas]Ethyl hloride (c hloroethaneEthyl hloride (chloroethaneEthyl, 1-chloro-Etylu chlorekEtylu chlorek [polish]Hydrochloric etherInChI=1/C2H5Cl/c1-2-3/h2H2,1HKeleneMCEMonochlorethaneMonochloroethaneMuriatic etherNarcotilePolychlorinated ethanes","Chloroethane, also called ethyl chloride, is a colorless gas at room temperature and pressure, with a characteristically sharp odor. People can smell chloroethane in the air at levels above 4 parts chloroethane in a million parts of air by volume (ppm). It can be smelled in water at levels above 0.02 parts chloroethane in a million parts of water (ppm). In pressurized containers, chloroethane exists as a liquid. However, the liquid evaporates quickly when exposed to air. It catches fire easily and is very dangerous when exposed to heat or flame. Chloroethane does not occur naturally in the environment. It is present in the environment as a result of human activity. In the past, the largest single use for chloroethane was for the production of tetraethyl lead, which is a gasoline additive. However, production of chloroethane has decreased dramatically as a result of stricter government regulations controlling lead in gasoline. Other applications include use in the production of ethyl cellulose, dyes, medicinal drugs, and other commercial chemicals, and use as a solvent and refrigerant. It is used to numb skin prior to medical procedures such as ear piercing and skin biopsies, and it is used in the treatment of sports injuries. (N001)",,75-00-3,6337,,"","",47554,CPD-4521,,D005018,Chloroethane,304,,,http://en.wikipedia.org/wiki/Ethyl chloride,"InChI=1/C2H5Cl/c1-2-3/h2H2,1H3",chloroethane,http://www.biospider.ca/saved_files/mol/,CCCl,CCCl,C2H5Cl,64.007980,,-138.7 °C,,,"6.71 mg/mL at 25 °C [HORVATH,AL et al. (1999)]",,,,"Inhalation, dermal or eye contact, ingestion. (N001)","Cytochrome P450 2E1 (P05181)
Glutathione S-transferase theta-1 (P30711)
Gamma-glutamyltranspeptidase 1 (P19440)
Gamma-glutamyltranspeptidase 2 (P36268)
Putative gamma-glutamyltranspeptidase 3 (A6NGU5)
Gamma-glutamyltranspeptidase 5 (P36269)
Gamma-glutamyltranspeptidase 6 (Q6P531)
Gamma-glutamyltranspeptidase 7 (Q9UJ14)
Arylamine N-acetyltransferase 1 (P18440)
Arylamine N-acetyltransferase 2 (P11245)
N-acetyltransferase 5 (P61599)
N-acetyltransferase 6 (Q93015)
Probable N-acetyltransferase 8 (Q9UHE5)
N-acetyltransferase 8-like protein (Q8N9F0)
Probable N-acetyltransferase 8B (Q9UHF3)
N-acetyltransferase 9 (Q9BTE0)
N-acetyltransferase 10 (Q9H0A0)
N-acetyltransferase 11 (Q86UY6)
N-acetyltransferase MAK3 homolog (Q147X3)
N-acetyltransferase 13 (Q9GZZ1)
N-acetyltransferase 14 (Q8WUY8)
N-acetyltransferase 15 (Q9H7X0)
(N001, N003)","Chloroethane targets the central nervous system and the heart. The lipophilicity of chloroethane suggests it acts upon the lipid layer of cellular membrane or the hydrophobic areas of specific membrane-bound cellular proteins. Euphoria and excitement resulting from the effects of chloroethane on the central nervous system induice catecholamine release. At levels adequate to induce anesthesia, chloroethane sensitizes the heart to the effects of catecholamines.  This sensitization, along with asphyxia and hypoxia, can cause arrhythmias, and death. (N001)","Because chloroethane is a small lipophilic compound, simple diffusion accounts for its absorption across membranes, and its higher affinity for lipids determines its distribution. Metabolism of chloroethane is believed to occur exclusively in the liver. The two major pathways are the production of acetaldehyde by cytochrome P450, and conjugation of chloroethane with glutathione to form S-ethyl-glutathione (catalyzed by glutathione S-transferase). The P450 enzyme CYP2El is responsible for chloroethane metabolism. The latter reaction is catalyzed by glutathione-S-transferase enzymes. Acetaldehyde is rapidly metabolized to acetic acid by aldehyde dehydrogenase. S-ethyl-glutathione can be furhter metabolized to S-ethyl-N-acety-L-cysteine (by γ-glutamyltranspeptidase, cysteinyl glycinase, and N-acetyltransferase, NAT) or S-ethyl-L-cysteine (by γ-glutamyltranspeptidase and cysteinyl glycinase). Chloroethane is eliminated from the body by pulmonary exhalation. (N001)",,,"3, not classifiable as to its carcinogenicity to humans. (R264)","In the past, the largest single use for chloroethane was for the production of tetraethyl lead, which is a gasoline additive. However, production of chloroethane has decreased dramatically as a result of stricter government regulations controlling lead in gasoline. Other applications include use in the production of ethyl cellulose, dyes, medicinal drugs, and other commercial chemicals, and use as a solvent and refrigerant. It is used to numb skin prior to medical procedures such as ear piercing and skin biopsies, and it is used in the treatment of sports injuries. Exposure may result from breathing air containing chloroethane vapor, drinking water containing chloroethane, and through skin or eye contact. (N001)",Acute Inhalation: 15 ppm (Mice) (N001),"Chloroethane poisoning may cause liver and kidney damage. Decreased defensive responses against illness, neurological effects following inhalation, effects on the nervous system, and cardiac depression can result from the exposure to this toxin. Moreover, respiratory paralysis and toxic injury to the heart have been reported following anesthesia with chloroethane. (N001)","Several sypmtoms can be manifested after inhalation of chloroethane, such as Jerking eye movements, an inability to control muscles in voluntary movements, difficulty in speaking clearly, an inability to perform finger tapping exercises, sluggish lower limb reflexes, seizures, difficulties in walking, disorientation, short-term memory loss, and hallucinations affecting sight and hearing. Moreover, dizziness, headache, feelings of drunkenness, nausea, vomiting, and abdominal cramps can occur. Redness, pain, and blurred vision can result from eye exposure. Long time skin exposure to chloroethane can cause frostbite. (N001, N002)","If the exposure occured through inhalation, move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis; administer oxygen and assist ventilation as required. Treat bronchospasm with inhaled beta2 agonist and oral or parenteral corticosteroids; in case of seizures, administer a benzodiazepine IV, diazepam or lorazepam; consider phenobarbital or propofol if seizures recur after diazepam; monitor for hypotension, dysrhythmias, respiratory depression, and need for endotracheal intubation; evaluate for hypoglycemia, electrolyte disturbances, hypoxia. Irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes if the expousre cuured through eye contact. Following dermal exposure, remove contaminated clothing and wash exposed area thoroughly with soap and water; treat dermal irritation or burns with standard topical therapy; patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines. (R624)",P03372;Q92731
185,T3D0184,2009-03-06 18:58:14 UTC,2009-08-04 21:27:55 UTC,Acetone,Organic Compound;Solvent;Industrial Precursor/Intermediate;Ketone,"&beta;-ketopropane(CH3)2CO.beta.-ketopropane2-propanoneACNAcetonAceton (german, dutch, polish)Aceton [german, dutch, polish]Acetone (NF)Acetone (TN)Acetone (natural)Acetone [UN1090] [Flammable liquid]Acetone oilAcetonumAzetonB-ketopropaneBeta-ketopropaneCaswell No. 004Chevron acetoneDimethyl formaldehydeDimethyl ketoneDimethylcetoneDimethylformaldehydeDimethylketalDimethylketonDimethylketoneFEMA No. 3326HSDB 41InChI=1/C3H6O/c1-3(2)4/h1-2HKetone propaneKetone, dimethylKetone, dimethyl-Methyl ketonePropanonPropanonePyroacetic acidPyroacetic etherRCRA waste no. U002Rcra waste number U002SasetoneWLN: 1V1acetone (ACD/Name 4.0)propan-2-one","Acetone is a chemical naturally found in the environment or produced by industries. Acetone is a colorless liquid with a distinct smell and taste; it evaporates readily into the air and is highly water soluble. Acetone naturally occurs in many fruits and vegetables. Low levels of acetone are produced by the body from the breakdown of fat. Most acetone industrially produced is used for other chemicals production that make plastics, fibers, and drugs. Acetone is also used as a dissolvant. (N004)",,67-64-1,180,,C00207,"182270
240600",15347,1-ACYL-GLYCERONE-3-PHOSPHATE,,D000096,Acetone,1512,,,http://en.wikipedia.org/wiki/Acetone,InChI=1/C3H6O/c1-3(2)4/h1-2H3,Acetone,http://www.biospider.ca/saved_files/mol/63f14e3e34565cc98258656ee658ed6e_1237954231.mol,CC(C)=O,CC(C)=O,C3H6O,58.041870,,-94.8 °C,,,"1000 mg/mL at 25 °C [RIDDICK,JA et al. (1986)]",,,,"Inhalation, ingestion, skin and eye contact. (N005)",Cytochrome P450 2E1 (P05181),"Since acetone is highly water soluble, it is readily taken up by the blood and widely distributed to body tissues. Acetone may interfere with the composition of the membranes, altering their permeability to ions. Systemically, acetone is moderately toxic to the liver and produces hematological effects. The renal toxicity may be due to the metabolite, formate, which is known to be nephrotoxic and is excreted by the kidneys. One of the major effects of acetone is the potentiation of the toxicity of other chemicals. Pretreatment with acetone has been shown to potentiate the hepatotoxicity and nephrotoxicity of carbon tetrachloride and chloroform by inducing particular forms of cytochrome P-450, especially cytochrome P-45OIIE1, and associated enzyme activities. (N004)","The metabolic fate of acetone is independent of route of administration and involves three separate gluconeogenic pathways, with ultimate incorporation of carbon atoms into glucose and other products and substrates of intermediary metabolism with generation of carbon dioxide. The primary (major) pathway involves hepatic metabolism of acetone to acetol and hepatic metabolism of acetol to methylglyoxal, while two secondary (minor) pathways are partially extrahepatic, involving the extrahepatic reduction of acetol to L-1,2-propanediol. Subsequent conversion of acetol to methylglyoxal in microsomes is catalyzed by acetol monooxygenase (also called acetol hydroxylase), an activity also associated with cytochrome P-450IIE1, and also requires oxygen and NADPH. Methylglyoxal can then be converted to D-glucose by an unidentified pathway, and/or possibly by catalysis by glyoxalase I and II and glutathione to D-lactate, which is converted to D-glucose. Some of exogenous acetone is unmetabolized and is excreted primarily in the expired air with little acetone excreted in urine. (N004)","LD50: 2,400 mg/kg/day (Oral, Mouse) (N004)","","3, not classifiable as to its carcinogenicity to humans. (R264)","Most acetone produced is used to make other chemicals that make plastics, fibers, and drugs. Acetone is also used to dissolve other substances. Exposure may occur from breathing air, drinking water and eating food with acetone, and through dermal and eye contact. (N004)","Acute Inhalation: 26 ppm (N004)
Intermediate Inhalation: 13 ppm (N004) 
Chronic Inhalation: 13 ppm (N004)","Pulmonary congestion and edema can follow inhalation of acetone, which irritates the mucosa. Gastrointestinal hemorrhage caused by repeated vomiting of blood has been reported. Neurobehavioral effects, indicative of narcosis, sedation, respiratory depression, ataxia, paresthesia and renal lesions can also result from acetone poisoning. (N004, N006)","Sore throat, cough, confusion, headache, dizziness, drowsiness, and unconsciousness are some signs observed after acetone poisoning. Moreover, ingestion of the product can cause nausea and vomiting. Redness, pain, blurred vision as well as corneal damage can result from eye exposure. A dry skin can be the result of dermal contact. Irritation of the nose, throat, lungs, and eyes can also occur depending on the route of exposure. (N005)","Following oral exposure to acetone, consider insertion of a nasogastric tube to aspirate stomach contents only after recent, large acetone ingestions; symptomatic and supportive treatment is generally all that is required. Following inhalation exposure, move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with inhaled beta2 agonist and oral or parenteral corticosteroids. Irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes in case of eye exposure to acetone. In case of dermal exposure, remove contaminated clothing and wash exposed area thoroughly with soap and water. A physician may need to examine the area if irritation or pain persists. (R624)",""
186,T3D0185,2009-03-06 18:58:14 UTC,2009-08-04 21:27:55 UTC,"Xylene, para-",Organic Compound;Solvent;Aromatic Hydrocarbon,"1, 4-Xylene1,4-Dimethylbenzene1,4-Xylene1,4-dimethyl-benzene ( p-xylene)4-Methyltoluene4-XyleneBenzene, 1,4-dimethyl-Benzene, p-dimethyl-ChromarP-dimethylbenzeneP-methyltolueneP-xyleneP-xylolScintillarXylene, p-Xylene, p-isomerp-Xylene [UN1307] [Flammable liquid]p-xylene (ACD/Name 4.0)","p-Xylene is an aromatic hydrocarbon based on benzene with two methyl substituents. It is an isomer of xylene. Xylene occurs naturally in petroleum and coal tar, and is a major component of gasoline and fuel oil. Xylene is used mainly as a solvent and in the printing, rubber, and leather industries. p-Xylene is used on a large scale for the manufacture of terephthalic acid for polyester. Its polymer is known as parylene. p-Xylene is produced by catalytic reforming and separated in a series of distillation and reaction processes from m-xylene, o-xylene and ethylbenzene. Its melting point is the highest among this series of isomers, but simple crystallization does not allow easy purification due to the formation of eutectic mixtures. (N007, R029, R319) ",,106-42-3,7809,,C06756,"",27417,CPD-1422,,C031286,"Xylene, para-",1806,,,,"InChI=1/C8H10/c1-7-3-5-8(2)6-4-7/h3-6H,1-2H3","1,4-dimethylbenzene",http://www.biospider.ca/saved_files/mol/7574a69cc9d64ffb3c0b9d65313265e3_1237954394.mol,CC1=CC=C(C=C1)C,CC1=CC=C(C=C1)C,C8H10,106.078250,Colorless liquid. ,13.2 °C,,,"0.162 mg/mL at 25 °C [SANEMASA,I et al. (1982)]",,,,"Oral 
Inhalation 
Dermal 
(R319)","Serum albumin (P02768)
Cytochrome P450 2E1 (P05181) 
Cytochrome P450 1A2 (P05177) 
(R319)","Xylene binds to serum proteins and accumulates primarily in the adipose tissue. Xylene dissolves lipid membranes and is responsible for irritant effects on eyes, mucous membranes and skin. Interaction of xylene with neuronal cell membranes affects transmission of nerve impulses having narcotic and anaesthetic consequences. Acute-duration oral or intermediate-duration inhalation exposures to high concentrations of xylene may result in death of cochlear hair cells and hearing loss. Experiments suggest that renal toxicity of xylene may be related to its metabolism by CYP2E1, which generates the production of oxidative intermediates and subsequent necrosis. Nephrotoxicity from xylene may involve induction of apoptosis through the activation of mitochondrial caspase-9 and caspase-3. (N009)","Xylenes are well absorbed by the inhalation and oral routes, and to a much lesser extent by dermal route. Xylene is rapidly distributed throughout the body via the systemic circulation. Its metabolites are excreted in urine. Methylhippuric acid, the primary metabolite of xylenes, is formed from conjugation with glycine and oxidation of a methyl group. Xylenol is a minor metabolite obtained from aromatic hydroxylation of xylene. Other minor metabolites found in urine include methylbenzyl alcohol and glucuronic acid conjugates of the oxidized xylene. In humans, hepatic microsomal CYP2E1 is the primary enzyme involved in metabolisation of xylene to methylbenzylalcohol, intermediate in the methylhippuric acid pathway. Unmetabolized xylene is also found in urine, and can also be exhalated. (N009)","LC50: 4740 ppm (Inhalation, Rat) (N009) 
LC50: 3907 ppm (Inhalation, Mouse) (N009)",,"3, not classifiable as to its carcinogenicity to humans. (R264)","Xylene is used as a solvent and in the printing, rubber, and leather industries. It is also used as a cleaning agent, a thinner for paint, and in paints and varnishes. It is found in small amounts in airplane fuel and gasoline. Exposure to xylene may occur from breathing it in contaminated air, drinking or eating xylene-contaminated water or food, and through dermal and eye contact with xylene containing products. (N009, R319)","Acute Inhalation: 2 ppm (N009) 
Intermediate Inhalation: 0.6 ppm (N009) 
Chronic Inhalation: 0.05 ppm (N009) 
Acute Oral: 1 mg/kg/day (N009) 
Intermediate Oral: 0.4 mg/kg/day (N009) 
Chronic Oral: 0.2 mg/kg/day (N009)","Xylene mainly affects the nervous system. Exposure may cause delayed reaction time, impaired short-term memory, and changes in sense of balance. High levels of exposure can result in coma, respiratory depression and death from cerebral anoxia. Xylene may also damage the liver, kidney, and lungs. Effects on fetal body weight and delay of skeletal ossification can occur in pregnant women. (N009, R319, R320)","Inhalation and ingestion can lead to dizziness, drowsiness, headache, and nausea. Burning sensations and abdominal pain can also result from ingestion. Dermal and eye exposure can cause skin dryness, redness, and pain. Conjunctivitis, dermatitis, respiratory tract irritation, dyspnea, anorexia, vomiting, fatigue, vertigo, incoordination, irritation, gangrene and anemia are other symptoms following xylene poisoning. (N010)","Gastric lavage is generally NOT indicated following oral exposure, as it is likely to increase the risk of aspiration. Activated charcoal may induce vomiting and increase pulmonary aspiration risk, and is generally NOT indicated. It should be limited to rare situations when there is a toxic coingestant. Following inhalation exposure, move patient to fresh air. Monitor for respiratory distress, if cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with inhaled beta2 agonist and oral or parenteral corticosteroids. The development of pulmonary edema from extreme vapor inhalation may be delayed up to 72 hours. If symptomatic, obtain chest x-ray, if severe, monitor arterial blood gases or pulse oximetry. Supplemental oxygen, PEEP, or CPAP may be necessary. Do not administer excessive fluids. Irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes in case of eye exposure. Following dermal exposure, remove contaminated clothing and wash exposed area thoroughly with soap and water. A physician may need to examine the area if irritation or pain persists. (R264) ",P05181;P13584
188,T3D0187,2009-03-06 18:58:14 UTC,2009-08-04 21:27:55 UTC,Aluminum,Inorganic Compound;Metal;Aluminum Compound,"AD1MADOADOMAEALALNALUMALUMINUM (SEE ALSO ALUMINUM OXIDE 1344-28-1)ALUMINUM, 99.999%AO A1AQUANAL-plus aluminum (Al) 0.02-0.2 mg/LActive roll-on anti-perspirant deodorantAdidas Action 3 TechAdidas active anti-perspirant for women cool gelAl alloyAlaunAlaun [german]Allbri aluminum paste and powderAlloyAlugelAlum (potassium)AlumenAlumen crudumAluminaAlumina 3ch-30chAlumina 6x - TabAlumina Drops 5chAlumina Drops D3-C1000Alumina Tablet (S No.37)Alumina fibreAluminioAluminiumAluminium bronzeAluminium flakeAluminium metallicumAluminium muriaticumAluminium powderAluminium, elementarAluminum (dust or fume)Aluminum (fume or dust)Aluminum (metal)Aluminum 27Aluminum A00Aluminum Oligosol Liq 4mg/2mlAluminum Potassium Sulfate (S#253)Aluminum alloyAluminum atomic absorption standard solutionAluminum dehydratedAluminum dustAluminum metalAluminum metal, alkylsAluminum metal, pyro powdersAluminum metal, respirable fractionAluminum metal, soluble saltsAluminum metal, total dustAluminum metal, welding fumesAluminum powderAluminum powder, coated [UN1309] [Flammable solid]Aluminum powder, uncoated [UN1396] [Dangerous when wet]Aluminum productionAluminum pyro powdersAluminum soluble saltsAluminum welding fumesAluminum, atomizedAluminum, elementalAluminum, molten [NA9260] [Class 9]Aluminum, pyro powdersAluminum, soluble saltsAluminum, welding fumesAmmonium iodatumAmphojel Suspension - 320mg/5mlAmphojel Tablets - 600mgAngel - caresse d'ange - deodorant roll-on antiperspirantAnti-Perspirant Deodorant Liquid Roll-On 20%Anti-perspirant pump sprayAnti-perspirant roll-onAo alArm & hammer advance clear gelArm & hammer advance invisible solidArm & hammer advance solidArm & hammer advance wide stick clear gelArrid extra DRY aerosolArrid extra DRY clear gel transparentArrid extra DRY invisible solidArrid extra DRY roll-on regular scentArrid extra DRY roll-on unscentedArrid total - soft solidArrid total - solidAvon On Duty 24 PlusAvon roll on antipersp deodAvon roll-on antiperspirant deodorantAvon roll-on antiperspirant deodorant cool confidenceAvon roll-on antiperspirant deodorant feelin' freshAvon skin so soft roll-on antiperspirant deodorantAvon skin-so-soft roll-on anti-perspirant deodorantAxe DRY gel anti-perspirant and deodorantAxe DRY invisible solid antiperspirant & deodorantBan invisible solid anti-perspirantBan roll-on antiperspirantBasaljel-capBody Series Deodorant/Antiperspirant Roll-On - 25%Body satin antiperspirant and deodorantBrut aerosol anti-perspirantBrut antiperspirantC-Pigment 1 [German]Caswell No. 028ACedre bleu antiperspirant roll-on deodorantCertain dri anti-perspirantChantilly Creme Desodorisante a Bille-20Clarins men-antiperspirant deo stick sans alcoolClinique skin supplies for men antiperspirant - deodorantCreme deodorant multi-soin anti-perspirantDR. scholl's DRY antiperspirant foot aerosol powderDRY idea anti-perspirant roll-onDegree aerosol antiperspirantDegree body heat activated gelDegree men ultra DRYDegree women invisibleDegree women soft solid anti-perspirantDeo douceur creme anti-transpiranteDeo douceur roll-on anti-transpirantDonna karan cashmere mist deodorant/anti-perspirantDove invisible solid antiperspirantDove roll-on antiperspirantDove soft solid antiperspirantEmanay atomized aluminum powderExpasylFor men roll-on antiperspirant deodorantFraicheur bambou deo bille antiperspirantFraicheur chevrefeuille deo bille antiperspirantFraicheur the vert deo bille antiperspirantGel - Cord - 25%Gillette clear gel antiperspirantGillette invisible solid antiperspirantGillette power beads antiperspirantGillette series clear stick antiperspirantGillette series invisible solid antiperspirantGillette series power caps clear gel antiperspirantGillette series power stripe antiperspirantGingibraid W Alum Pot Sulf 0a 0.25mg/2.5cmGingibraid W Alum Pot Sulf 1a 0.35mg/2.5cmGingibraid W Alum Pot Sulf 2a 0.65mg/2.5cmGingibraid W Alum Pot Sulf 3a 1.15mg/2.5cmGingigel Gel 200mg/GmHemoban Liq 25%Hemodent 25%IRMM523A_FLUKAIRMM523B_FLUKAIRMM523C_FLUKAIRMM527RA_FLUKAIRMM527RB_FLUKAIRMM527RC_FLUKAIRMM528RA_FLUKAIRMM528RB_FLUKAIRMM528RC_FLUKAIRMM530RA_FLUKAIRMM530RC_FLUKAIRMM532A_FLUKAIRMM532B_FLUKAIRMM532C_FLUKAIRMM533A_FLUKAIRMM533B_FLUKAIRMM533C_FLUKAIRMM534A_FLUKAIRMM534B_FLUKAIRMM534C_FLUKAInvisible lady speed stickInvisible solid antiperspirant & deodorant stickL'homme essentiel antiperspirantLadies antiperspirant invisibleLadies antiperspirant stick - powder freshLadies antiperspirant stick - unscentedLady Speed Stick 24/7Lady Speed Stick 24/7 GelLady mitchum anti-perspirant clear gelLady mitchum ap super DRY roll-on lotionLady mitchum clear roll-on anti-perspirant powder freshLady mitchum wide solid ap - powder freshLady speed stickLady speed stick clean glideMen's a/P Stk 22%MetanaMetana aluminum pasteMitchum Ap Super Dry Roll-On Lotion 25%Mitchum Wide Solid Anti-Perspirant 25%Mitchum clear gel a.p. & deod. - gel STKMitchum clear gel a.p. and deod.supersportMitchum clear roll-on anti-perspirant unscentedMitchum cool DRYNoral aluminiumNoral aluminumNoral extra fine lining gradeNoral ink grade aluminiumNoral ink grade aluminumNoral non-leafing gradeNu skin for men anti-perspirant deodorantOld spice high endurance antiperspirantOld spice high endurance clear gel antiperspirantOld spice high endurance invisible solid antiperspirantOld spice high endurance red zone antiperspirant soft solidOld spice red zone clear gel antiperspirantOld spice red zone invisible solidOld spice red zone soft solid antiperspirantOligostim Aluminium - Tab 6dhOscar de la renta pour lui antipers.deod.STKOscar de la renta, so de la renta antiperspirant deodorantOscar for men, oscar de la rentaPAP-1Pascord No 10Pascord No 8Pascord No 9Perfumed anti-perspirant deodorant STKPigment metal 1ProtegelRight guard antiperspirant aerosol (fresh)Right guard antiperspirant aerosol (scented)Right guard clear gel antiperspirant (active, fresh)Right guard sportRight guard sport invisible solid antiperspirantRight guard sport power caps clear gel antiperspirantRight guard xtreme sport power caps clear gelRight guard xtreme sport power caps clear gel antiperspirantRoll-on anti-perspirant deodorantRoll-on deodorant multi-soin anti-perspirantSecret Clean Antipersp Aer 12%Secret antiperspirant DRY roll-onSecret antiperspirant soft solidSecret antiperspirant solidSecret invisible antiperspirantSecret platinum clear gel antiperspirantSecret platinum invisible antiperspirantSecret platinum soft solid antiperspirantSecret platinum soft solid baby powder antiperspirantSecret renew antiperspirant soft solidSecret roll-on antiperspirantSecret sheer DRY antiperspirant invisible solidSecret sheer DRY antiperspirant invisible solid baby powderShaklee roll-on anti-perspirantSil Trax As No 10Sil Trax As No 8Sil Trax As No 9Siltrax A.S. 7 0.48mg/2.54cmSoft & dri - dri gel clear gelSoft & dri - dri gel with microbeadsSoft & dri anti-perspirant roll-onSoft & dri antiperspirant aerosol (baby powder)Soft & dri antiperspirant aerosol (soft scent)Soft & dri clear glide invisible solidSoft & dri dri gel with microbeads antiperspirantSoft & dri invisible solid antiperspirantSoft & dri power stripe antiperspirantSpeed Stick 24/7Speed Stick 24/7 GelSpeed Stick Gel (4 Variants) - 22%Speed Stick Plus (20% Active - Not Part of Product Name)Speed Stick Plus - 22%Speed stick clearSpeed stick ultimateStat dental hemostatic solnStick deodorant multi-soin anti-perspirantStyptic pencil / crayon styptiqueTissue gooTommy girl antiperspirant deodorant stickaluminium(0)","Aluminum is the most abundant metal in the earth’s crust. It is always found combined with other elements such as oxygen, silicon, and fluorine. Aluminium is extracted from aluminum-containing minerals such as bauxite ore. Small amounts of aluminum can be found dissolved in water. It is often mixed with small amounts of other metals to form aluminum alloys, which are stronger and harder. Aluminum compounds have many different uses, for example, as alums in water-treatment and alumina in abrasives and furnace linings. They are also found in consumer products such as antacids, astringents, buffered aspirin, food additives, cosmetics, and antiperspirants. Aluminum is used for beverage cans, pots and pans, airplanes, siding and roofing, and foil. (R1128, R1129)",,7429-90-5,5359268,,C06264,"103180
104300
105500
108730
155140
211900
601924",28984,"",,D000535,Aluminum,7939,,,http://en.wikipedia.org/wiki/Aluminum,InChI=1/Al/q+3,aluminum,http://www.biospider.ca/saved_files/mol/,[Al+3],[Al+3],[Al]3+,26.981541,Silvery white metallic solid.,660 °C,,,"",,,,"Oral 
Inhalation 
(R1128)",,"The main targets of aluminum are the central nervous system and bones. Aluminum binds to dietary phosphorus and impairs gastrointestinal absorption of phosphorus. The decreased phosphate body burden results in osteomalacia and rickets. Aluminum's neurotoxicity is believed to involve different mechanisms. Changes in cytoskeletal protein functions as a result of altered phosphorylation, proteolysis, transport, and synthesis are believed to be one cause. Aluminum may induce neurobehavioral effects by affecting permeability of the blood-brain barrier, cholinergic activity, signal transduction pathways, lipid peroxidation, and impair neuronal glutamate nitric oxide-cyclic GMP pathway, as well as interfere with metabolism of essential trace elements because of similar coordination chemistries and consequent competitive interactions. Aluminum can also interact with estrogen receptors, increasing the expression of estrogen-related genes and contributing to the progression of breast cancer. Certain aluminum salts induce immune responses by activating inflammasomes. (R1128, R1130, R1132)","Aluminum is poorly absorbed following oral or inhalation exposure and is essentially not absorbed dermally. The bioavailability of aluminum is strongly influenced by the aluminum compound and the presence of dietary constituents which can complex with aluminum and enhance or inhibit its absorption. Aluminum binds to various ligands in the blood and distributes to every organ, with highest concentrations found in bone and lung tissues. In living organisms, aluminum is believed to exist in four different forms: as free ions, as low-molecular-weight complexes, as physically bound macromolecular complexes, and as covalently bound macromolecular complexes. Absorbed aluminum is excreted principally in the urine and, to a lesser extent, in the bile, while unabsorbed aluminum is excreted in the faeces. (R1128)",,,,"Aluminum is used for beverage cans, pots and pans, airplanes, siding and roofing, and foil. It is often mixed with small amounts of other metals to form aluminum alloys, which are stronger and harder. Aluminum compounds have many different uses, for example, as alums in water-treatment and alumina in abrasives and furnace linings. They are also found in consumer products such as antacids, astringents, buffered aspirin, food additives, cosmetics, and antiperspirants. (R1128, R1129)","Intermediate Oral: 1.0 mg/kg/day (R260)
Chronic Oral: 1.0 mg/kg/day (R260)","Aluminum targets the nervous system and causes decreased nervous system performance and is associated with altered function of the blood-brain barrier. The accumulation of aluminum in the body may cause bone or brain diseases. High levels of aluminum have been linked to Alzheimer’s disease. A small percentage of people are allergic to aluminium and experience contact dermatitis, digestive disorders, vomiting or other symptoms upon contact or ingestion of products containing aluminium. (R1128, R1129)","Inhalating aluminum dust causes coughing and abnormal chest X-rays. A small percentage of people are allergic to aluminium and experience contact dermatitis, digestive disorders, vomiting or other symptoms upon contact or ingestion of products containing aluminium. (R1128, R1129)","",Phosphorus;P03372;Q96P20
190,T3D0189,2009-03-06 18:58:15 UTC,2009-08-04 21:27:56 UTC,Carbon monoxide,Organic Compound;Industrial By-product/Pollutant,"C#oCMOCOCarbon monooxideCarbon monoxide 10% by volume or moreCarbon monoxide, compressed [UN1016] [Poison gas]Carbon oxideCarbon oxide (co)Carbon(II) oxideCarboneCarbone (oxyde de) [french]Carboneum oxygenisatumCarbonic oxideCarbonioCarbonio (ossido di) [italian]Exhaust gasFLHFlue gasFlue gasnideHEMKohlenmonoxidKohlenmonoxid [german]KohlenoxydKohlenoxyd [german]KoolmonoxydeKoolmonoxyde [dutch]MonoxideMonoxide, carbonOxyde de carboneOxyde de carbone [french]Wegla tlenekWegla tlenek [polish]ZN[co]","Carbon monoxide is a colorless, odorless, tasteless, and highly toxic gas. It is produced from the partial oxidation of carbon-containing compounds in limited oxygen availability conditions. Carbon monoxide has significant fuel value. It is a major atmospheric pollutant in urban areas, chiefly from exhaust of internal combustion engines, but also from improper burning of various other fuels. (S311)",,630-08-0,281,,C00237,"141250
172460
259900
266500",17245,CARBON-MONOXIDE,,D002248,Carbon monoxide,3844,,,http://en.wikipedia.org/wiki/Carbon monoxide,InChI=1/CO/c1-2,carbon monoxide,http://www.biospider.ca/saved_files/mol/f80feece61040ddb88effad70cbcbe25_1237954954.mol,[C]#[O],[C]#[O],CO,27.994910,Colorless gas.,-56.5 °C,,,"",,,,"Inhalation
(S311)",,"Carbon monoxide possesses a higher affinity than oxygen for hemoglobin, leading to the formation of carboxyhemoglobin, this provoking anoxemia. Carbon monoxide also binds to myoglobin, impairing its ability to utilize oxygen. It can also bind to cytochrome c oxidase, though with a lesser affinity than oxygen. This interferes with aerobic metabolism and efficient ATP synthesis. As a result, cells switch to anaerobic metabolism, causing anoxia, lactic acidosis, and eventual cell death. Carbon monoxide also causes endothelial cell and platelet release of nitric oxide, and the formation of oxygen free radicals. This results in lipid peroxidation, leading to edema and necrosis within the brain. (S312)","",,5000 ppm over 5 minutes for an adult human. (R293),,"Carbon monoxide is a major atmospheric pollutant in urban areas, chiefly from exhaust of internal combustion engines, but also from improper burning of various other fuels. (S311)",,"Chronic exposure to low levels of carbon monoxide may cause persistent headaches, lightheadedness, depression, confusion, memory loss, and nausea and vomiting. (S312)","Early symptoms of acute carbon monoxide poisoning are nonspecific and include headaches, nausea, and fatigue. Symptoms may progress to tachycardia and hypertension. The central nervous system is one of the organ systems most sensitive to poisoning and symptoms displayed include dizziness, ataxia, confusion, convulsions, unconsciousness, respiratory arrest, and even death. (S312)","Carbon monoxide poisoning is first treated by immediate removal from the source of exposure. High-flow or 100% oxygen should then be administered by a nonrebreather reservoir oxygen mask. Oxygen hastens the dissociation of carbon monoxide from hemoglobin, improving tissue oxygenation by reducing carbon monoxides biological half-life. Hyperbaric oxygen may also be used, as it increases carboxyhemoglobin dissociation to a greater extent than normal oxygen. (S312)",P69905;P68871;P02042;P02100;P69891;P69892;Q6B0K9;P09105;P02008;P02144;P24310;P14406;P00395;P00403;P00414;P13073;Q96KJ9;P20674;P10606;P12074;Q02221;P14854;Q6YFQ2;P09669;O60397;P24311;Q8TF08;P15954;P10176;Q7Z4L0
192,T3D0191,2009-03-06 18:58:15 UTC,2009-08-04 21:27:56 UTC,Hydrogen sulfide,Inorganic Compound;Industrial Precursor/Intermediate,"A thiolAcide sulfhydriqueAcide sulfhydrique [french]Acide sulphhydriqueAcnomelAgri-sulAn-sulfur colloid kitAquiliteAsulfa-supraAtomic sulfurBMEBensulfoidBensulfoid (TN)BrimstoneCaswell No. 812Colloidal sulfurColloidal-sCollokitColsulCorosul d and sCosanCosan 80CrystexDevisulphurDihydridosulfurDihydrogen disulfideDihydrogen monosulfideDihydrogen sulfideDihydrogen(sulfide)ElosalFEMA No. 3779Flour sulfurFlour sulphurFlowers of sulfurFlowers of sulphurFostrilGofrativGround vocle sulfurGround vocle sulphurHSHepatateHepatic acidHepatic gasHexasulHydrogen Sulfide (H2(Sx))Hydrogen Sulfide (H2S2)Hydrogen Sulfide (H2S3)Hydrogen monosulfideHydrogen sulfide (H2S)Hydrogen sulfide H2SHydrogen sulfide [UN1053] [Poison gas]Hydrogen sulfure [french]Hydrogen sulfuric acidHydrogen sulphideHydrogen-sulfideHydrogen-sulphide-Hydrogene sulfureHydrogene sulfure [french]Hydrogene sulphureHydrosulfurateHydrosulfuric acidIdrogeno solforatoIdrogeno solforato [italian]Kolloidschwefel 95KolofogKolosprayKristexKumulusKumulus FLLiquamatMagnetic 6Magnetic 70, 90, and 95MercaptanMercaptansMerkaptanMicowetsulfMicroflotoxMicrothiolMixture nameNetzschwefelPernoxPolsulkol extraPrecipitated sulfurRC-schwefel extraRCRA waste no. U135RSHRcra waste number U135RezamidSalicylic acid & sulfur soapSastidSastid (TN)Schwefel, feinverteilterSchwefelwasserstoffSchwefelwasserstoff [german]SebulexSewer gasShreesulSiarkowodorSiarkowodor [polish]SofrilSolfaSoufre [iso-french]Sour gasSperlox-sSpersulSpersul thiovitStink dampSublimed sulfurSublimed sulphurSuffaSufranSufran dSulfaneSulfexSulfidalSulfideSulfide (HS1-)Sulfide, hydrogenSulforcinSulforonSulfosporSulfoxylSulfurSulfur (JP15)Sulfur (molten)Sulfur [NA1350] [Class 9]Sulfur [UN1350] [Flammable solid]Sulfur atomSulfur donorSulfur hydrideSulfur hydroxideSulfur ointmentSulfur soapSulfur vaporSulfur, colloidal, metastable technetium-99 labeledSulfur, molten [NA2448] [Class 9]Sulfur, molten [UN2448] [Flammable solid]Sulfur, monoclinicSulfur, pharmaceuticalSulfur, precipitatedSulfur, precipitated (usp)Sulfur, precipitated [usp]Sulfur, rhombicSulfur, solidSulfur, sublimedSulfur, sublimed (usp)Sulfur, sublimed [usp]Sulfure d'hydrogeneSulfureted hydrogenSulfuretted hydrogenSulikolSulkolSulphurSulphur [iso]Sulphur, precipitated, sublimed or colloidalSulsolSultafSuper cosanSuper sixSvovlTechnecollTesuloidThiolThiolsThioluxThionThiovitThiovit sThiozolTransactUltra sulfurWettasulZolvisZwavelwaterstofZwavelwaterstof [dutch]","Hydrogen sulfide is the chemical compound with the formula H2S. This colorless gas is partially responsible for the foul odor of rotten eggs and flatulence. It often results from the bacterial break down of sulfites in nonorganic matter in the absence of oxygen, such as in swamps and sewers (anaerobic digestion). It also occurs in volcanic gases, natural gas and some well waters. Hydrogen sulfide is a highly toxic and flammable gas; its toxicity is comparable with that of hydrogen cyanide. (S579)",,7783-06-4,402,,C00283,176790,16136,HS,,D006862,Hydrogen sulfide,,,,http://en.wikipedia.org/wiki/Hydrogen_sulfide,InChI=1/H2S/h1H2,hydrogen sulfide,http://www.biospider.ca/saved_files/mol/da107a5e3f3870f92bde89b64c34e1d0_1237955181.mol,S,S,H2S,33.987720,Colorless gas. (S579),-82.30 °C (190.85 K),-60.28 °C (212.87 K),1.363 g/L,"3.74 mg/mL at 21 °C [VENABLE,CS & FUWA,T (1922)]",,"",,Oral. Inhalation. Dermal.,,"Although very pungent at first, hydrogen sulfide quickly deadens the sense of smell, so potential victims may be unaware of its presence until it is too late. Hydrogen sulfide forms a complex bond with iron in the mitochondrial cytochrome enzymes, thereby blocking oxygen from binding and stopping cellular respiration. (S579)",,,,,"Volcanoes and hot springs emit some hydrogen sulfide, where it probably arises via the hydrolysis of sulfide minerals. Hydrogen sulfide can be present naturally in well water; it can be removed using ozone or a filter with manganese dioxide. About 10% of total global emissions of H2S is due to human activity. By far the largest industrial route to hydrogen sulfide occurs in petroleum refineries. Other anthropogenic sources of hydrogen sulfide include coke ovens, paper mills, and tanneries. H2S arises from virtually anywhere where elemental sulfur comes into contact with organic material, especially at high temperatures. Being heavier than air, H2S tends to accumulate at the bottom of poorly ventilated spaces. (S579)",,"Hydrogen sulfide is a highly toxic and flammable gas. Hydrogen sulfide is considered a broad-spectrum poison, meaning that it can poison several different systems in the body, although the nervous system is most affected. The toxicity of hydrogen sulfide is comparable with that of hydrogen cyanide. (S579)","Exposure to lower concentrations can result in eye irritation, a sore throat and cough, nausea, shortness of breath, and fluid in the lungs; these symptoms usually go away in a few weeks. Long-term, low-level exposure may result in fatigue, loss of appetite, headaches, irritability, poor memory, and dizziness. Higher concentrations of 700-800 ppm tend to be fatal. (S579)","Treatment involves immediate inhalation of amyl nitrite, injections of sodium nitrite, inhalation of pure oxygen, administration of bronchodilators to overcome eventual bronchospasm, and in some cases hyperbaric oxygen therapy (HBO). HBO therapy has anecdotal support and remains controversial. (S579)",""
193,T3D0192,2009-03-06 18:58:15 UTC,2009-08-25 16:16:30 UTC,Pentachlorodibenzofuran,Organic Compound;Industrial By-product/Pollutant;Aromatic Hydrocarbon;Organochloride;Dibenzofuran,"1,2,4,6,9-PENTACHLORODIBENZOFURANDibenzofuran, 1,2,4,6,9-pentachloroDibenzofuran, 1,2,4,6,9-pentachloro-Dibenzofuran, pentachloro-Pentachlorodibenzofuran","Chlorinated dibenzofurans (CDFs) are a family of chemical that contain one to eight chlorine atoms attached to the carbon atoms of the parent chemical, dibenzofuran. The CDF family contains 135 individual compounds with varying damaging health and environmental effects; those 2,3,7,8-substitued being particularly harmful. Most CDFs are produced in very small amounts as unwanted impurities after use of chlorinated compounds. Only a few of these 135 compounds have been produced and their properties (color, smell, taste, and toxicity) studied. (S290)",,30402-15-4,35332,,"","","","",,,Pentachlorodibenzofuran,,,,,InChI=1/C12H3Cl5O/c13-4-1-2-5(14)11-8(4)9-10(17)6(15)3-7(16)12(9)18-11/h1-3H,"1,2,4,6,9-pentachlorodibenzofuran",http://www.biospider.ca/saved_files/mol/,C1=CC(=C2C(=C1Cl)C3=C(O2)C(=CC(=C3Cl)Cl)Cl)Cl,C1=CC(=C2C(=C1Cl)C3=C(O2)C(=CC(=C3Cl)Cl)Cl)Cl,C12H3Cl5O,337.862650,Colorless crystals.,"",,,"",,,,"Occupational exposure to dibenzofuran may occur through inhalation and dermal contact, particularly at sites where coal tar, coal tar derivatives, and creosote are produced and used. Consumption of contaminated water and food are the primary sources of exposure for the general population. (S290)",,"Dibenzofurans bind the aryl hydrocarbon receptor, which increases its ability to activate transcription in the XRE promoter region. This alters the expression of a number of genes. (S285)","No information on the metabolism of dibenzofuran in mammalian organisms was found in the available literature. The bacteria Sphingomonas, Brevibacterium, Terrabacter, and Staphylococcus auricularis degrade dibenzofuran to 2,2',3-trihydroxybiphenyl via dibenzofuran 4,4a-dioxygenase. (S290)",,,"3, not classifiable as to its carcinogenicity to humans. (R264)","CDFs are created from production of coal tar and during incineration. They are used as insecticides, in the production of PVC, and in industrial bleaching. (S290)",,"CDFs cause vomiting and diarrhea, anemia, more frequent lung infections, numbness and other effects on the nervous system, and mild changes in the liver. However, there were no permanent liver changes or definite liver damage found in  people who ingested CDFs. (S290)","Skin and eye irritations, especially severe acne, darkened skin color, and swollen eyelids with discharge are the most obvious health effects of the CDF poisoning. (S290)",,P03372;Q92731;P35869
197,T3D0196,2009-03-06 18:58:15 UTC,2009-08-04 21:27:57 UTC,"Cresol, ortho-",Organic Compound;Solvent;Disinfectant;Aromatic Hydrocarbon,"1-Hydroxy-2-methylbenzene1-Methyl-2-hydroxybenzene2-Cresol2-Hydroxytoluene2-Methylphenol2-hydroxy-1-methylbenzeneCresol, all isomersCresol, o-Cresol, o-isomerCresol, ortho-Cresylic acidFEMA No. 3480O-cresylic acidO-hydroxytolueneO-kresolO-kresol (german)O-kresol [german]O-methylphenolO-methylphenylolO-oxytolueneO-toluolOrtho-cresolOrthocresolOrthocresol [NF v]Para-cresolPhenol, 2-methyl-Rcra waste number U052TOLUENE,2-HYDROXY (ORTHO-CRESOL)WLN: QR B1o-Cresol [UN2076] [Poison, Corrosive]o-cresol (ACD/Name 4.0)","o-Cresol is an isomer of cresol. Cresols are organic methylphenol compounds that may occur naturally or be manufactured. Cresols have an odor characteristic to that of other simple phenols, reminiscent to some of a ""medicine"" smell. Cresols are used as solvents, disinfectants and deodorizers, as well as to make other chemicals. They may be formed normally in the body from other compounds. Cresols are found in many foods and in wood and tobacco smoke, crude oil, coal tar, and in chemical mixtures used as wood preservatives. Small organisms in soil and water produce cresols when they break down materials in the environment. (R835) ",,95-48-7,335,,C01542,"",28054,CPD-109,,C034047,"Cresol, ortho-",1760,,,http://en.wikipedia.org/wiki/o-Cresol,"InChI=1/C7H8O/c1-6-4-2-3-5-7(6)8/h2-5,8H,1H3",2-methylphenol,http://www.biospider.ca/saved_files/mol/afca22560ea490b5bdd32a14eee455de_1237955721.mol,CC1=CC=CC=C1O,CC1=CC=CC=C1O,C7H8O,108.057510,Colorless solids or liquids. ,29.8 °C,,,"25.9 mg/mL at 25 °C [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral 
Inhalation 
Dermal 
(R835)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2C19 (P33261) 
Cytochrome P450 2D6 (P10635) 
Cytochrome P450 2E1 (P05181) 
Tyrosinase (P14679) 
Thyroid peroxidase (P07202) 
(R835) ","Target organs of ingested cresols in humans are the blood, kidneys, lungs, liver, heart, and central nervous system. Cresols impair the stratum corneum and produce coagulation necrosis by denaturating and precipitating proteins. They may also induce changes in neurotransmitter levels, affect the activities of some enzymes, increase lipid peroxidation, and change membrane fluidity in the brain. (R835)  ","Cresols can be absorbed following inhalation, oral, and dermal exposure. Once in the body they can distribute rapidly into many organs and tissues. Cresols undergo oxidative metabolism in the liver and are rapidly eliminated, mostly in the urine, as sulfate or glucuronide conjugates. The activation of cresols by oxidation involves tyrosinase and thyroid peroxidase, forming a reactive quinone methide. Experiments with recombinant P-450s demonstrated cresol metabolism was mediated by several P-450s including CYP2D6, 2C19, 1A2, 1A1, and 2E1. (R835, R836, R837, R839)  ","LD50: 344 mg/kg (Oral, Mouse) (R261)
LD50: 179 mg/m3 (Inhalation, Mouse) (R261)
LD50: 620 mg/kg (Dermal, Mouse) (R261)",,,"Cresols are used to as solvents, disinfectants and deodorizers, as well as to make other chemicals. They may be formed normally in the body from other compounds. Cresols are found in many foods and in wood and tobacco smoke, crude oil, coal tar, and in chemical mixtures used as wood preservatives. Small organisms in soil and water produce cresols when they break down materials in the environment. Breathing air containing cresols is the primary source of exposure. Exposure may also result from drinking contaminated water, eating contaminated food and coming into contact with liquids containing cresols. (R835)  ","Intermediate Oral: 0.1 mg/kg/day (R260) 
Chronic Oral: 0.1 mg/kg/day (R260)","Cresols breathed, ingested, or applied to the skin at very high levels can be very harmful because they are corrosive substances. Ingestion of high levels results in mouth and throat burns, abdominal pain, vomiting, kidney problems, and effects on the blood and nervous system. Skin contact with high levels of cresols can burn the skin and damage the kidneys, liver, blood, lungs, and brain. Tachycardia, respiratory failure, unconsciousness and death may occur in both cases. Many of these effects may not by caused directly by cresols, but may be a result of secondary reactions to shock caused by external and internal burns. (R782, R835) ","Ingestion of cresols results in burning of the mouth and throat, abdominal pain, and vomiting. Inhalation or dermal exposure to cresols can produce irritation and corrosion at the site of contact. (R782)  ","Following oral exposure, immediately dilute with 4 to 8 ounces (120 to 240 mL) of water or milk (not to exceed 4 ounces/120 mL in a child). Observe patients with ingestion carefully for the possible development of esophageal or gastrointestinal tract irritation or burns. If signs or symptoms of esophageal irritation or burns are present, consider endoscopy to determine the extent of injury. In case of hypotension, infuse isotonic fluid. If hypotension persists, administer dopamine or norepinephrine. In case of hypertension, monitor vital signs regularly. For mild/moderate asymptomatic hypertension (no end organ damage), pharmacologic treatment is generally not necessary. Following inhalation, move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with inhaled beta2 agonist and oral or parenteral corticosteroids. In case of acture lung injury, maintain ventilation and oxygenation and evaluate with frequent arterial blood gas or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed. Following eye exposure, irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes. Following dermal exposure, remove contaminated clothing and wash exposed area thoroughly with soap and water. Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines. (R624) ",P23219;P35354 
199,T3D0198,2009-03-06 18:58:16 UTC,2009-08-04 21:27:58 UTC,Vanadium,Inorganic Compound;Metal;Vanadium Compound,"Ammonium (meta)vanadate solutionVANADIUM, 99%, 200 MESHVNVanadioVanadium (fume or dust)Vanadium 5+Vanadium Liquid (S#207)-LiqVanadium acid solutionVanadium atomic absorption standard solutionVanadium atomic spectroscopy standard concentrate 1.00- g VVanadium cationVanadium dustVanadium ionVanadium ion(3+)Vanadium ion(5+)Vanadium metallicumVanadium standard for aasVanadium standard for icpVanadium(1+)Vanadium(1+), ionVanadium(I) cationVanadium(III)Vanadium(III) cationVanadium(IV) oxide sulfate solutionVanadium(v) cationVanadium, elementalVanadium, ion(V1+)vanadium(0)vanadium(1+) ionvanadium(3+)vanadium(3+) ionvanadium(5+)vanadium(5+) ionvanadium, ion (V5+)vanadium, ion(3+)","Vanadium is a transition metal with the chemical symbol V and atomic number 23. Vanadium usually combines with other elements such as oxygen, sodium, sulfur, or chloride, and occurs naturally in about 65 different minerals and in fossil fuel deposits. It may be produced from steel smelter slag, the flue dust of heavy oil, or as a byproduct of uranium mining. Vanadium is mainly used to produce specialty steel alloys such as high speed tool steels. Vanadium is found in many organisms, and is used by some life forms as an active center of enzymes. (S107, S108)",,7440-62-2,23990,,C06267,"",27698,"",,D014639,Vanadium,8184,,,http://en.wikipedia.org/wiki/Vanadium,InChI=1/V/q+3,vanadium,http://www.biospider.ca/saved_files/mol/,[V+3],[V+3],[V]3+,50.943958,Grey metallic solid.,1910 °C,,,"",,,,"Oral
Inhalation
Dermal
(S107)",,"Vanadium damages alveolar macrophages by decreasing the macrophage membrane integrity, thus impairing the cell's phagocytotic ability and viability. The pentavalent form of vanadium, vanadate, is a potent inhibitor of the Ca+-ATPase and Na+,K+-ATPase of plasma membranes, which decreases intracellular ATP concentration. Vanadium is also believed to induce the production of reactive oxygen species. This may damage DNA and also cause oxidative stress, which can damage the reproductive system. Vanadium also inhibits protein tyrosine phosphatases, producing insulin-like effects. (S107, S109, S110, S111, S112, S113)","Vanadium is absorbed mainly via inhalation, though small amounts can be absorbed through the skin and gastrointestional tract. It is rapidly distributed in the plasma, mainly to the kidney, liver, lungs, heart, bone, where it tends to accumulate. With the help of cytochrome P-450 enzymes, it can interconvert between its two oxidation states, vanadyl (V+4) and vanadate (V+5). Both states of vanadium can reversibly bind to transferrin protein in the blood and then be taken up into erythrocytes. Vanadium is excreted mainly in the urine. (S107)",,,,"Vanadium is mainly used to produce specialty steel alloys such as high speed tool steels. It is also mixed with iron to make important parts for aircraft engines, and small amounts are used in making rubber, plastics, ceramics, and other chemicals. (S107, S108)","Acute Inhalation: 0.0002 mg/m3 (R260)
Intermediate Oral: 0.003 mg/kg/day (R260)","Breathing high levels of vanadium affects the lungs, throat, and eyes. Ingestion of vanadium may cause kidney and liver damage, birth defects, or death. (S107)","Inhalation of vanadium causes lung irritation, coughing, wheezing, chest pain, runny nose, and a sore throat. (S107)","",P54710;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;Q93096;Q12974;O75365;Q8WUK0;P18433;P23467;P23468;P23469;Q12913;P10586;P23470;Q9HD43;Q15262;P28827;Q92932;Q16827;Q15256;Q13332;O14522;Q92729 ;P23471;Q16849;P18031;Q06124;Q05209;Q12923;Q15678;Q99952;P17706;Q4JDL3;Q16825;Q9Y2R2;Q9H3S7;P29074;P54829;P29350;P35236;P43378;P26045
200,T3D0199,2009-03-06 18:58:16 UTC,2009-08-04 21:27:58 UTC,n-Nitrosodimethylamine,Organic Compound;Industrial By-product/Pollutant;Amine;Nitrite,"(CH3)2NNO1,1-Dimethyl-2-oxohydrazine1,1-dimethyl-2-oxohydrazine (ACD/Name 4.0)DMNDMNADimethylamine, n-nitroso-DimethylnitrosaminDimethylnitrosamin (german)Dimethylnitrosamin [german]DimethylnitrosamineDimethylnitrosoamineMethamine, n-methyl-n-nitroso-Methanamine, n-methyl-n-nitroso-N nitrosodimethylamineN, n-dimethylnitrosamineN,n-dimethylnitrosamineN-dimethyl-nitrosamineN-dimethylnitrosoamineN-methyl-n-nitroso-methanamineN-methyl-n-nitrosomethanamineN-nitroaodimethylamineN-nitroso-n,n-dimethylamineN3632_SIGMAN7756_SIGMANDMANdma nitrosodimethylamineNitrosamine, dimethyl-NitrosodimethylamineNitrosodimethylamine, ndmaNitrous dimethylamideRCRA waste no. P082Rcra waste number P082WLN: ONN1&1","n-Nitrosodimethylamine (commonly known as NDMA) is produced by industry only in small amounts for research. It was used to make rocket fuel, but this use was stopped after unusually high levels of this chemical were found in air, water, and soil samples collected near a rocket fuel manufacturing plant. It is used in some cosmetic and toiletry products and in cleansers. NDMA is toxic to the liver. (S725)",,62-75-9,6124,,C14704,"",35807,"",,D004128,n-Nitrosodimethylamine,1050,,,http://en.wikipedia.org/wiki/N-Nitrosodimethylamine,InChI=1/C2H6N2O/c1-4(2)3-5/h1-2H3,"N,N-dimethylnitrous amide",http://www.biospider.ca/saved_files/mol/fbb9ff5aab34758bd4952d4458ccfe94_1237956222.mol,CN(C)N=O,CN(C)N=O,C2H6N2O,74.048010,Yellow liquid. (S725),< 25 °C,154 °C,1.005 g/cm3,29 g/100 ml (at 20 °C),,61 °C,,Oral. Inhalation. Dermal. (S725),,The mechanism of NDMAinduced liver toxicity is not clearly understood but may be related to alkylation of cellular protein. (S725),"Evidence from in vitro and in vivo studies with rodents indicates that NDMA is metabolized by hydroxylation of the alpha-carbon, followed by formation of formaldehyde, molecular nitrogen and a methylating agent, which is considered to be the carcinogenic form. Recent evidence suggests that a significant proportion of NDMA is metabolized via a denitrosation mechanism. (S725)",,,,"The general population might be exposed to NDMA from a wide variety of sources, including environmental, consumer, and occupational sources. The primary sources of human exposure to NDMA are tobacco smoke, chewing tobacco, diet (cured meats [particularly bacon], beer, fish, cheese, and other food items), toiletry and cosmetic products (for example, shampoos and cleansers), interior air of cars, and various other household goods, such as detergents and pesticides.  In addition, NDMA can form in the stomach during digestion of alkylamine-containing foods.  Alkylamines are naturally occurring compounds which are found in some drugs and in a variety of foods. Infants may be exposed to NDMA from the use of rubber baby bottle nipples and pacifiers which may contain very small amounts of NDMA, from ingestion of contaminated infant formulas, and from breast milk of some nursing mothers.  Very low levels of NDMA have been found in some samples of human breast milk. Occupational exposure may happen in a large number of places including industries such as tanneries, pesticide manufacturing plants, rubber and tire manufacturing plants, alkylamine manufacture/use industries, fish processing industries, foundries, and dye manufacturing plants.  Researchers making or handling NDMA may also be exposed to this compound if it passes through the rubber gloves they wear during laboratory work.  (S725)",,"NDMA is very harmful to the liver of animals and humans. Moreover, although there are no reports of NDMA causing cancer in humans, it is reasonable to expect that exposure to NDMA by eating, drinking, or breathing could also cause cancer in humans. (S725)",,"",""
201,T3D0200,2009-03-06 18:58:16 UTC,2009-08-04 21:27:58 UTC,"1,2,4-Trichlorobenzene",Organic Compound;Solvent;Aromatic Hydrocarbon;Organochloride,"1,2, 4-Trichlorobenzene1,2,4-Trichlorbenzol1,2,4-Trichlorobenzene1,2,4-Trichlorobenzene-UL-14C1,2,4-Trichlorobenzol1,2,4-trichlorobenzene (ACD/Name 4.0)1,2,5-Trichlorobenzene1,3,4-TrichlorobenzeneAs-trichlorobenzeneHipochem GMHostetex l-pecT0396_SIGMATrichlorobenzene aTrichlorobenzolTrojchlorobenzenTrojchlorobenzen [polish]Trojchlorobenzen(polish)Unsym-trichlorobenzeneWLN: GR bg DGghl.PD_Mitscher_leg0.137","1,2,4-Trichlorobenzene is an organochloride aromatic compound and one of the three isomeric forms of trichlorobenzene. Trichlorobenzene is used as a solvent. (R428)",,120-82-1,13,,C06594,"",28222,CPD-1125,,C009947,"1,2,4-Trichlorobenzene",1878,,,,InChI=1/C6H3Cl3/c7-4-1-2-5(8)6(9)3-4/h1-3H,"1,2,4-trichlorobenzene",http://www.biospider.ca/saved_files/mol/86f63a208a77ddd5c2e2cac9c3209e66_1237956394.mol,C1=CC(=C(C=C1Cl)Cl)Cl,C1=CC(=C(C=C1Cl)Cl)Cl,C6H3Cl3,179.930030,White crystals.,17 °C,,,"0.049 mg/mL at 25 °C [SOUTHWORTH,GR & KELLER,JL (1986)]",,,,Oral Inhalation Dermal (R430),,"Trichlorobenzene may uncouple mitochondrial oxidative phosphorylation, inducing potassium ion release and inhibiting respiratory control. It's metabolites may covalently bind to cellular proteins and alkylate DNA. (R432, R433)","Trichlorobenzene is absorbed via oral, inhalation, and dermal routes. It is believed to be metabolized via cytochrom p-450 enzymes into metabolites that include phenols, mercapturic acid, and catechols.(R430)","LD50: 756 mg/kg (Oral, Rat) (R287)",,,"Trichlorobenzene is used as a solvent in chemical manufacturing, as well as in dyes, dielectric fluid, synthetic transformer oils, lubricants, heat-transfer medium, and insecticides. (R431)",,"High levels of trichlorobenzene may damage the liver, kidney, and thyroid. (R429)",Trichlorobenzene irritates the eyes and respiratory tract. (R285),"",P98194;O75185;P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P78334;Q8N1C3;P18507;Q99928;O00591;P24046;P28476;A8MPY1;Q9UN88;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;P54710;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P03372;Q92731
203,T3D0202,2009-03-06 18:58:16 UTC,2009-08-25 19:31:15 UTC,Tetrachlorodibenzo-p-dioxin,Organic Compound;Industrial By-product/Pollutant;Chlorinated Dibenzo-p-dioxin;Aromatic Hydrocarbon;Organochloride,"","Tetrachlorodibenzo-p-dioxins are chlorinated dibenzo-p-dioxin (CDD) congeners. CDDs are a class of manufactured chemicals that consist of dioxin skeletel structures with chlorine substituents. They are also persistent organic pollutants (POPs), thus their production is regulated in most areas. Dioxins occur as by-products from the manufacture of organochlorides, the bleaching of paper, chlorination by waste and drinking water treatment plants, municipal solid waste and industrial incinerators, and natural sources such as volcanoes and forest fires. (R346, R347)",,41903-57-5,"",,"","","","",,,Tetrachlorodibenzo-p-dioxin,,,,,"","",http://www.biospider.ca/saved_files/mol/,"",Clc1cc2Oc3cc(Cl)c(Cl)cc3Oc2cc1Cl,"","",Colorless solid.,"",,,"3.5e-07 mg/mL at 25 °C [SHIU,WY et al. (1988)]",,,,"Oral 
Inhalation 
Dermal 
(R346)",,"CDDs cause their toxic effects by binding to the aryl hydrocarbon receptor and subsequently altering the transcription of certain genes. The affinity for the Ah receptor depends on the structure of the specific CDD. The change in gene expression may result from the direct interaction of the Ah receptor and its heterodimer-forming partner, the aryl hydrocarbon receptor nuclear translocator, with gene regulatory elements or the initiation of a phosphorylation/dephosphorylation cascade that subsequently activates other transcription factors. The affected genes include several oncogenes, growth factors, receptors, hormones, and drug-metabolizing enzymes. The change in transcription/translation of these genes is believed to be the cause of most of the toxic effects of CDDs. (R346)","CDDs are absorbed through oral, inhalation, and dermal routes of exposure. CDDs are carried in the plasma by serum lipids and lipoproteins, distributing mainly to the liver and adipose tissue. CDDs are very slowly metabolized by the microsomal monooxygenase system to polar metabolites that can undergo conjugation with glucuronic acid and glutathione. They may increase the rate of their own metabolism by inducing both phase I and phase II enzymes. The major routes of excretion of CDDs are the bile and the faeces, though smaller amounts are excreted in the urine and via lactation. (R346)",,,"3, not classifiable as to its carcinogenicity to humans. (R264) ","Dioxins occur as by-products from the manufacture of organochlorides, the bleaching of paper, chlorination by waste and drinking water treatment plants, municipal solid waste and industrial incinerators, and natural sources such as volcanoes and forest fires. (R346, R347) ","Acute Oral: 0.0002 ug/kg/day (R260) 
Intermediate Oral: 0.00002 ug/kg/day (R260) 
Chronic Oral: 0.000001 ug/kg/day (R260) ","Exposure to large amounts of CDDs causes chloracne, a severe skin disease with acne-like lesions that occur mainly on the face and upper body. CDDs may also cause liver damage and induce long-term alterations in glucose metabolism and subtle changes in hormonal levels. In addition, studies have shown that CDDs may disrupt the endocrine system and weaken the immune system, as well as cause reproductive damage and birth defects, central and peripheral nervous system pathology, thyroid disorders, endometriosis, and diabetes. (R346, R347) ","In addition to chloracne, CDD exposure causes skin rashes, discoloration, and excessive body hair. (R346) ","Treatment of CDD exposure may include washing the area of contact, GI decontamination, administering an IV, or forced alkaline diuresis. (R622) ",P35869;P03372;Q92731
205,T3D0204,2009-03-06 18:58:16 UTC,2009-08-25 18:00:17 UTC,Pentachlorodibenzo-p-dioxin,Organic Compound;Industrial By-product/Pollutant;Chlorinated Dibenzo-p-dioxin;Aromatic Hydrocarbon;Organochloride,K-strophanthosideK-strophantosideStrophanthoside-k,"Pentachlorodibenzo-p-dioxins are chlorinated dibenzo-p-dioxin (CDD) congeners. CDDs are a class of manufactured chemicals that consist of dioxin skeletel structures with chlorine substituents. They are also persistent organic pollutants (POPs), thus their production is regulated in most areas. Dioxins occur as by-products from the manufacture of organochlorides, the bleaching of paper, chlorination by waste and drinking water treatment plants, municipal solid waste and industrial incinerators, and natural sources such as volcanoes and forest fires. (R346, R347)",,36088-22-9,222159,,"","","","",,,Pentachlorodibenzo-p-dioxin,,,,,"InChI=1/C42H64O19/c1-19-36(61-38-35(51)33(49)31(47)27(60-38)17-56-37-34(50)32(48)30(46)26(15-43)59-37)25(54-3)13-29(57-19)58-21-4-9-40(18-44)23-5-8-39(2)22(20-12-28(45)55-16-20)7-11-42(39,53)24(23)6-10-41(40,52)14-21/h12,18-19,21-27,29-38,43,46-53H,4-11,1","5,14-dihydroxy-3-[4-methoxy-6-methyl-5-[3,4,5-trihydroxy-6-[[3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxymethyl]oxan-2-yl]oxyoxan-2-yl]oxy-13-methyl-17-(5-oxo-2H-furan-3-yl)-2,3,4,6,7,8,9,11,12,15,16,17-dodecahydro-1H-cyclopenta[a]phenanthrene-10-carba",http://www.biospider.ca/saved_files/mol/,"",COC1CC(OC2CCC3(C=O)C4CCC5(C)C(CCC5(O)C4CCC3(O)C2)C2=CC(=O)OC2)OC(C)C1OC1OC(COC2OC(CO)C(O)C(O)C2O)C(O)C(O)C1O |t:32|,C42H64O19,872.404180,Colorless solid.,220 °C,,,"1.2e-07 mg/mL at 20 °C [FISCHER,J et al. (1992)]",,,,"Oral 
Inhalation 
Dermal 
(R346)",,"CDDs cause their toxic effects by binding to the aryl hydrocarbon receptor and subsequently altering the transcription of certain genes. The affinity for the Ah receptor depends on the structure of the specific CDD. The change in gene expression may result from the direct interaction of the Ah receptor and its heterodimer-forming partner, the aryl hydrocarbon receptor nuclear translocator, with gene regulatory elements or the initiation of a phosphorylation/dephosphorylation cascade that subsequently activates other transcription factors. The affected genes include several oncogenes, growth factors, receptors, hormones, and drug-metabolizing enzymes. The change in transcription/translation of these genes is believed to be the cause of most of the toxic effects of CDDs. (R346)","CDDs are absorbed through oral, inhalation, and dermal routes of exposure. CDDs are carried in the plasma by serum lipids and lipoproteins, distributing mainly to the liver and adipose tissue. CDDs are very slowly metabolized by the microsomal monooxygenase system to polar metabolites that can undergo conjugation with glucuronic acid and glutathione. They may increase the rate of their own metabolism by inducing both phase I and phase II enzymes. The major routes of excretion of CDDs are the bile and the faeces, though smaller amounts are excreted in the urine and via lactation. (R346)",,,"3, not classifiable as to its carcinogenicity to humans. (R264) ","Dioxins occur as by-products from the manufacture of organochlorides, the bleaching of paper, chlorination by waste and drinking water treatment plants, municipal solid waste and industrial incinerators, and natural sources such as volcanoes and forest fires. (R346, R347) ","Acute Oral: 0.0002 ug/kg/day (R260) 
Intermediate Oral: 0.00002 ug/kg/day (R260) 
Chronic Oral: 0.000001 ug/kg/day (R260) ","Exposure to large amounts of CDDs causes chloracne, a severe skin disease with acne-like lesions that occur mainly on the face and upper body. CDDs may also cause liver damage and induce long-term alterations in glucose metabolism and subtle changes in hormonal levels. In addition, studies have shown that CDDs may disrupt the endocrine system and weaken the immune system, as well as cause reproductive damage and birth defects, central and peripheral nervous system pathology, thyroid disorders, endometriosis, and diabetes. (R346, R347) ","In addition to chloracne, CDD exposure causes skin rashes, discoloration, and excessive body hair. (R346) ","Treatment of CDD exposure may include washing the area of contact, GI decontamination, administering an IV, or forced alkaline diuresis. (R622) ",P35869;P03372;Q92731
208,T3D0207,2009-03-06 18:58:17 UTC,2009-08-04 21:27:59 UTC,"2,3,7,8-Tetrachlorodibenzofuran",Organic Compound;Industrial By-product/Pollutant;Aromatic Hydrocarbon;Organochloride;Dibenzofuran,"2,3,7,8-Tetrachloro-dibenzofuran2,3,7,8-Tetrachlorodibenzo[b,d]furan2,3,7,8-Tetrapolychlorinated dibenzofuranDibenzofuran, 2,3,7,8-tetrachloro-TCDFTcdbf","Chlorinated dibenzofurans (CDFs) are a family of chemical that contain one to eight chlorine atoms attached to the carbon atoms of the parent chemical, dibenzofuran. The CDF family contains 135 individual compounds with varying damaging health and environmental effects; those 2,3,7,8-substitued being particularly harmful. Most CDFs are produced in very small amounts as unwanted impurities after use of chlorinated compounds. Only a few of these 135 compounds have been produced and their properties (color, smell, taste, and toxicity) studied. (S290)",,51207-31-9,39929,,"","","","",,C014211,"2,3,7,8-Tetrachlorodibenzofuran",8003,,,,InChI=1/C12H4Cl4O/c13-7-1-5-6-2-8(14)10(16)4-12(6)17-11(5)3-9(7)15/h1-4H,"2,3,7,8-tetrachlorodibenzofuran",http://www.biospider.ca/saved_files/mol/,C1=C2C3=CC(=C(C=C3OC2=CC(=C1Cl)Cl)Cl)Cl,C1=C2C3=CC(=C(C=C3OC2=CC(=C1Cl)Cl)Cl)Cl,C12H4Cl4O,303.901630,Colorless crystals.,227 °C,,,"6.92e-07 mg/mL at 26 °C [FRIESEN,KJ & WEBSTER,GRB (1990)]",,,,"Occupational exposure to dibenzofuran may occur through inhalation and dermal contact, particularly at sites where coal tar, coal tar derivatives, and creosote are produced and used. Consumption of contaminated water and food are the primary sources of exposure for the general population. (S290)",,"Dibenzofurans bind the aryl hydrocarbon receptor, which increases its ability to activate transcription in the XRE promoter region. This alters the expression of a number of genes. (S285)","No information on the metabolism of dibenzofuran in mammalian organisms was found in the available literature. The bacteria Sphingomonas, Brevibacterium, Terrabacter, and Staphylococcus auricularis degrade dibenzofuran to 2,2',3-trihydroxybiphenyl via dibenzofuran 4,4a-dioxygenase. (S290)",,,"3, not classifiable as to its carcinogenicity to humans. (R264)","CDFs are created from production of coal tar and during incineration. They are used as insecticides, in the production of PVC, and in industrial bleaching. (S290)",,"CDFs cause vomiting and diarrhea, anemia, more frequent lung infections, numbness and other effects on the nervous system, and mild changes in the liver. However, there were no permanent liver changes or definite liver damage found in  people who ingested CDFs. (S290)","Skin and eye irritations, especially severe acne, darkened skin color, and swollen eyelids with discharge are the most obvious health effects of the CDF poisoning. (S290)",,P35869;P03372;Q92731
210,T3D0209,2009-03-06 18:58:17 UTC,2009-08-04 21:27:59 UTC,"2,4-Dichlorophenol",Organic Compound;Industrial Precursor/Intermediate;Aromatic Hydrocarbon;Organochloride,"1,3-Dichloro-4-hydroxybenzene1-Hydroxy-2,4-dichlorobenzene2,4-Dichlorohydroxybenzene2,4-Dichlorophenate2,4-Dichlorophenic acid2,4-Dichlorophenol-UL-14C2,4-dichloro-Phenol2,4-dichlorophenol (ACD/Name 4.0)2,4-dichlorophenol potassium2,4-dichlorophenol sodium2,4-dichlorophenol, 14C-labeled cpd4, 6-Dichlorophenol4,6-DichlorophenolC6H4Cl2ODCPDichlorophenol, 2,4-IsobacPhenol, 2,4-dichloro-RCRA waste no. U081Rcra waste number U081WLN: QR bg DG","2,4-Dichlorophenol (2,4-DCP) is a chlorinated derivative of phenol. It is a chlorophenol and one of six dichlorophenol isomers. 2,4-DCP is used primarily as intermediate in the preparation of the herbicide 2,4-dichlorophenoxyacetic acid (2,4-D). 2,4-DCP is readily absorbed through the skin and contact with large amounts may be fatal. (R970)",,120-83-2,8449,,C02625,"",16738,24-DICHLOROPHENOL,,C004762,"2,4-Dichlorophenol",444,,,"http://en.wikipedia.org/wiki/2,4-Dichlorophenol","InChI=1/C6H4Cl2O/c7-4-1-2-6(9)5(8)3-4/h1-3,9H","2,4-dichlorophenol",http://www.biospider.ca/saved_files/mol/75efa76af51cf698fe0352cb00d6e05b_1237957455.mol,OC1=CC=C(Cl)C=C1Cl,OC1=CC=C(Cl)C=C1Cl,C6H4Cl2O,161.963920,White solid. (R970),45 °C,210 °C,1.383 at 60 °C/25 °C,"4.5 mg/mL at 20 °C [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,121 °C,,Oral. Dermal. (R970),,"Chlorophenols have moderately high lipophilicity. Absorption through the gastrointestinal tract is by simple diffusion and is expected to be both rapid and virtually complete. The chlorophenols are also readily absorbed after dermal exposure. Chlorophenols uncouple mitochondrial oxidative phosphorylation and produce convulsions. At low concentrations, uncoupling produces stimulation of state 4 (resting state) respiration as a result of increased adenosine triphosphatase (ATPase) activity in the absence of a phosphate acceptor. Inhibition of state 3 (active) respiration is also observed. At moderate concentrations, resting respiration is neither stimulated nor inhibited. Significant inhibition of respiration, associated with a breakdown of the electron transport process and decreased ATPase activity, occurs at very high concentrations. (R970)","After inhalation and dermal routes, 2,4-DCP is rapidly absorbed and excreted. Data on absorption following oral route are limited to animal studies. When administered intravenously to rats, 2,4-DCP rapidly distributes to the kidney, liver, fat, and brain, with the highest concentrations in the kidney and liver. 2,4-DCP strongly bind to serum proteins, including albumin and globulin. Both human and animal studies indicate that sulfation and glucuronidation are the main metabolic pathways of chlorophenols. 2,4-DCP has been shown to be metabolized into two major metabolites identified as 2-chloro-1,4-hydroxyquinone and 2-chloro-1,4-benzoquinone by microsomal fractions and whole cells of yeast Saccharomyces cerevisiae expressing human cytochrome P-450 3A4. Another metabolite, 1,2,4-hydroxybenzene, was also detected during biotransformation by whole cells but was not observed in microsomal fractions. (R970)",,,,"Chlorophenols are used as intermediates in the production of dyes and chlorinated pesticides. Exposed pesticide production workers may be at increased risk for soft tissue sarcoma, Hodgkin’s disease, and non-Hodgkin’s lymphoma. Most people are exposed to very low levels of chlorophenols from chlorinated drinking water. (R970)",,"Dermally absorbed doses of chlorophenols are potentially more toxic than orally absorbed doses. Within 20 minutes of being accidentally splashed with 2,4-DCP on his right arm and leg, a worker experienced seizures, collapsed, and died shortly thereafter. Lethargy, tremors, convulsions, and/or central nervous system depression have been reported in chlorophenol-exposed animals. (R970)",,"",P03372;Q92731
212,T3D0211,2009-03-06 18:58:17 UTC,2009-08-04 21:28:00 UTC,Fluorine,Inorganic Compound;Halogen,"BifluoridenDiatomic fluorineDifluorineFluorFluorideFluoride ionFluorine 19Fluorine atomFluorine radicalFluorine(.)Fluorine, compressedFluoroFluorures acideFluoruri acidiMolecular fluorineMonofluorineOral-b minute gelRcra waste number P056Saeure fluoride","Fluorine is a halogen with the chemical symbol F and atomic number 9. At standard conditions for temperature and pressure, fluorine is found as difluorine F2, a supremely reactive and toxic, pale, yellowish brown gas. Difluorine is the most chemically reactive and electronegative of all the elements. Fluorine-containing compounds have various uses. Difluorine is mainly used for the production of two compounds of commercial interest, uranium hexafluoride and sulfur hexafluoride. Inorganic compounds of fluoride, the reduced form of fluorine, are used in toothpaste to prevent dental cavities, while organofluorides may be used in pharmaceuticals. Elemental fluorine, fluoride ions, and some organofluorides are toxic. (S319)",,7782-41-4,5360525,,C00742,"173395
177400",30236,"",,D005461,Fluorine,6447,,,http://en.wikipedia.org/wiki/Fluorine,InChI=1/FH/h1H/p-1,fluorine,http://www.biospider.ca/saved_files/mol/9f77b9710699ee55e2574784db898303_1237957762.mol,[F-],[F-],[F]-,18.998400,,-219.61 °C,,,"0.00169 mg/mL at 25 °C [MCCRADY,JK et al. (1985)]",,,,"Oral
Inhalation
Dermal
(S318)",,"Fluoride ions are incorporated into bone by substituting for hydroxyl groups in the carbonate-apatite structure to produce hydroxyfluorapatite, thus altering the mineral structure of the bone. Alteration in mineralization increases hardness and bone mass, but also decreases mechanical strength. A portion of the circulating inorganic fluoride acts as an enzyme inhibitor because it forms metalfluoride-phosphate complexes that interfere with the activity of those enzymes requiring a metal ion cofactor. In addition, fluoride may interact directly with the enzyme or the substrate. It is a general inhibitor of the energy production system of the cell. Fluorine may bind calcium and decrease its concentration. This is thought to indirectly inhibit amelogeninase activity, resultin in altered crystal growth and subsequently dental fluorosis. (S318)","Fluoride ions are incorporated into bone by substituting for hydroxyl groups in the carbonate-apatite structure to produce hydroxyfluorapatite, thus altering the mineral structure of the bone. Alteration in mineralization increases hardness and bone mass, but also decreases mechanical strength. A portion of the circulating inorganic fluoride acts as an enzyme inhibitor because it forms metalfluoride-phosphate complexes that interfere with the activity of those enzymes requiring a metal ion cofactor. In addition, fluoride may interact directly with the enzyme or the substrate. It is a general inhibitor of the energy production system of the cell. Fluorine may bind calcium and decrease its concentration. This is thought to indirectly inhibit amelogeninase activity, resulting in altered crystal growth and subsequently causing dental fluorosis. (S318)",,25 ppm over 5 minutes for an adult human. (R270),,"Elemental fluorine is mainly used for the production of two compounds of commercial interest, uranium hexafluoride and sulfur hexafluoride. Inorganic compounds of fluoride are used in toothpaste to prevent dental cavities, while organofluorides may be used in pharmaceuticals. Elemental fluorine, fluoride ions, and some organofluorides are toxic. (S319)",Acute Inhalation: 0.01 ppm (R260),"Exposure to high levels of fluoride can result in denser bones. However, if exposure is high enough, these bones may be more fragile and brittle and there may be a greater risk of fracture. Chronic exposure may also cause dental fluorosis, which alters the appearance of children's teeth during tooth development. (S318, S325)","Fluorine is very irritating to the skin, eyes, and respiratory tract. Symptoms of fluoride exposure include abdominal pain, diarrhea, dysphagia, hypersalivation, mucosal injury, nausea, vomiting. Electrolyte abnormalities including hyperkalemia, hypocalcemia, hypoglycemia, and hypomagnesemia may occur. Neurological symptoms include headache, muscle weakness, hyperactive reflexes, muscular spasms, paresthesia seizures, tetanic contractions, and tremors. In severe cases, multiorgan failure will occur. Death typically results from cardiac arrest, shock, widening of QRS, and various arrhythmias occur. (S318, S325)","Oral exposure to fluoride compounds should be treated by giving milk, calcium carbonate, or milk of magnesia to slow absorption. Eye or skin contact should be treated by removing any contaminated clothing and flushing with water. (S325)",Calcium
213,T3D0212,2009-03-06 18:58:17 UTC,2009-08-05 14:37:04 UTC,Nitrite,Inorganic Compound;Nitrite,"Dioxonitrate(III)NitritNitrite (NO2-)Nitrite anionNitrite ionNitrite ion (NO2-)Nitrogen dioxideNitrogen dioxide ionNitrogen dioxide ion(1-)Nitrogen oxide, ionNitrogen peroxide ionNitrogen peroxide ion(1-)Nitrogen protoxideOno-dioxidonitrate(1-)dioxonitrate(1-)nitrite(1-)nitrous acid, ion(1-)","Nitrate (NO3-) and nitrite (NO2-) are naturally occurring inorganic ions that are part of the nitrogen cycle. Microbial action in soil or water decomposes wastes containing organic nitrogen into ammonia, which is then oxidized to nitrite and nitrate. Because nitrite is easily oxidized to nitrate, nitrate is the compound predominantly found in groundwater and surface waters. Contamination with nitrogen‑containing fertilizers (e.g. potassium nitrate and ammonium nitrate), or animal or human organic wastes, can raise the concentration of nitrate in water. Nitrate‑containing compounds in the soil are generally soluble and readily migrate with groundwater. Nitrite is a toxic compound known to cause methemoglobinemia. While nitrate is not toxic, it can be metabolized into nitrite once in the body, resulting in toxic effects. (S575)",,14797-65-0,946,,C00088,"",16301,NITRITE,,,Nitrite,6495,,,http://en.wikipedia.org/wiki/Nitrite,"InChI=1/HNO2/c2-1-3/h(H,2,3)",Nitrite,http://www.biospider.ca/saved_files/mol/4a3294d2acd251504ae463c2f1ccb5b3_1237957859.mol,[O-]N=O,[O-]N=O,[NO2]-,45.992901,,"",,,"",,,,"Oral
Inhalation
(S575)",,"Nitrite causes the autocatalytic oxidation of oxyhemoglobin to hydrogen peroxide and methemoglobin. This elevation of methemoglobin levels is a condition known as methemoglobinemia, and is characterized by tissue hypoxia, as methemoglobin cannot bind oxygen. (V305, V306)","Intake of some amount of nitrates and nitrites is a normal part of the nitrogen cycle in humans. In vivo conversion of nitrates to nitrites can occur in the gastrointestional tract under the right conditions, significantly enhancing nitrates' toxic potency. The major metabolic pathway for nitrate is conversion to nitrite, and then to ammonia. Nitrites, nitrates, and their metabolites are excreted in the urine. (S575)",,10 to 100 mg/kg for an adult human. (V311),"2A, probably carcinogenic to humans. (R264)","Nitrates and nitrites are naturally produced and may also be found in pesticides. Exposure usually occurs from contact with contaminated soil, food water. Nitrates may also be found in certain drugs. (S575)",,Nitrite poisoning causes methemoglobinemia. Nitrites may cause pregnancy complications and developmental effects. They may also be carcinogenic. (S575),"Nitrite poisoning causes methemoglobinemia. Symptoms include cyanosis, cardiac dysrhythmias and circulatory failure, and progressive central nervous system (CNS) effects. CNS effects can range from mild dizziness and lethargy to coma and convulsions. (S575)",Methemoglobinemia can be treated with supplemental oxygen and methylene blue 1% solution administered intravenously slowly over five minutes followed by IV flush with normal saline. Methylene blue restores the iron in hemoglobin to its normal (reduced) oxygen-carrying state. (V306),P69905;P68871;P02042;P02100;P69891;P69892;Q6B0K9;P09105;P02008
214,T3D0213,2009-03-06 18:58:17 UTC,2009-08-25 19:51:59 UTC,Cesium-137,Inorganic Compound;Metal;Radioactive Isotope,"(137Cs)caesiumCESIUM 137Caesium-137Cesium, Isotope Of Mass 137Cesium-137","Cesium is the chemical element with the symbol Cs and atomic number 55. Cesium-137 is a radioactive isotope of cesium with a half-life of 30.07 years. It is produced from the detonation of nuclear weapons and is produced in nuclear power plants. Cesium-137 was released to the atmosphere most notably from the 1986 Chernobyl meltdown. It is commonly used as a gamma-emitter in industrial applications such as moisture and density gauges, leveling gauges, flow meters, and other sensor equipment. Cesium-137 is water-soluble and extremely toxic in minute amounts. (S540, S555)",,10045-97-3,5486527,,"","","","",,,Cesium-137,,,,http://en.wikipedia.org/wiki/Caesium-137,InChI=1/Cs/i1+4,cesium-137,http://www.biospider.ca/saved_files/mol/,[137Cs],[137Cs],Cs,132.905450,Cesium is a silvery gold metal. It is liquid at room temperature. (S555),"301.59 K (28.44 °C, 83.19 °F)","944 K (671 °C, 1240 °F)",1.93  g·cm−3 (room temperature) and 1.843  g·cm−3 (melting point),"",,,,"Oral 
Inhalation
Dermal
(S558)",,"Highly penetrating gamma rays are the major cause of damage to tissues and internal organs following external overexposure to radioactive cesium. Once radioactive cesium is taken internally, cells of nearby tissues are at highest risk for damage due to the emission of beta particles. The ionizing radiation produced by cesium-137 causes cellular damage that includes DNA breakage, accurate or inaccurate repair, apoptosis, gene mutations, chromosomal change, and genetic instability. This leads to loss of normal cell and tissue homeostasis, and development of malignancy. Ionizing radiation that does not directly damage DNA can produce reactive oxygen intermediates that directly affect the stability of p53, an important enzyme in cell-cycle regulation, and produce oxidative damage to individual bases in DNA and point mutations by mispairing during DNA replication. (W510, W523)","Cesium can be absorbed following ingestion, inhalation, or dermal exposure. Cesium behaves in a manner similar to potassium and distributes uniformly throughout the body. Gastrointestinal absorption from food or water is the principal source of internally deposited cesium in the general population.  Essentially all cesium that is ingested is absorbed into the bloodstream through the intestines. Cesium tends to concentrate in muscles because of their relatively large mass. Cesium has been shown to compete
with potassium for transport through potassium channels and can also substitute for potassium in
activation of the sodium pump and subsequent transport into the cell. Like potassium, cesium is excreted from the body fairly quickly, mainly in the urine. In an adult, 10% is excreted with a biological half-life of 2 days, and the rest leaves the body with a biological half-life of 110 days. This means that if someone is exposed to radioactive cesium and the source of exposure is removed, much of the cesium will readily clear the body along the normal pathways for potassium excretion within several months. (S558' W523)",,,,"Cesium-137 is produced from the detonation of nuclear weapons and is produced in nuclear power plants. Cesium-137 was released to the atmosphere most notably from the 1986 Chernobyl meltdown. It is commonly used as a gamma-emitter in industrial applications such as moisture and density gauges, leveling gauges, flow meters, and other sensor equipment. Cesium-137 is also used in brachytherapy to treat various types of cancer. (S540, S558)","Acute Radiation: 4 mSv (R260)
Chronic Radiation: 1 mSv/yr (R260)","Cesium-137 presents external as well as internal health hazard, both from beta and gamma radiation. Cesium-137 is water-soluble and extremely toxic in minute amounts. The radioactivity of Cesium-137 can damage cells and cause cancer 10, 20 or 30 years from the time of ingestion, inhalation or absorption, provided sufficient material enters the body. Radioactive cesium overexposure can result in adverse effects such as reduced fertility, abnormal neurological development, genotoxicity, and damage to blood-forming organs(S540, S558, W523)","Large amounts of cesium can cause hyperirritability and spasms. Exposure to high doses of ionizing radiation results in acute radiation syndrome, which can cause skin burns, hair loss, nausea, vomiting, dizziness, disorientation, low blood pressure, headache, fatigue, weakness, fever, birth defects, illness, infection, and death. (W510, W525, S555, W523)","Treatment reversing the effects of irradiation is currently not possible. Anaesthetics and antiemetics are administered to counter the symptoms of exposure, as well as antibiotics for countering secondary infections due to the resulting immune system deficiency. (W525)",DNA
215,T3D0214,2009-03-06 18:58:18 UTC,2009-08-04 21:28:00 UTC,Silver,Inorganic Compound;Metal;Silver Compound,"AGAGNAg+AlgaedynAmalgumArgentArgent. nit.ArgentumArgentum Met.Praep.D8(D10 D12 D15 D20 D30)Argentum Metallicum (Silver Metallicum 6x)Argentum Metallicum 4ch - 30chArgentum Mettallicum Gtte 4ch-30chArgentum Nitricum 3ch-30chArgentum Nitricum Drops D3-C1000Argentum Nitricum Gtte 5ch-15chArgentum colloidaleArgentum cyanatumArgentum metallicumArgentum nitricumArgentum nitricum homaccordArgentum phosphoricumAstroflake 5Carey lea silverCaswell No. 735Col silColloidal silverCollosol argentumD 25 (metal)Degussa 67Degussa 80Dermazin Crm 1%Dotite XA 208EpinallFA 2 (metal)Flamazine Crm 1%G 12 (metal)Germany: C-Pigment 2Jelcon SH 1KS (metal)L-3 (element)Lead refinery silver bullionLiquid silverMetz 25BPekana - argentum metallicumPekana - argentum nitricumPlataShell silverSilberSilber [german]Silflake 135Silpowder 130SilvadeneSilver Liquid (S#107)-LiqSilver Nitrate Liquid (S#106)-LiqSilver atomSilver atomic absorption standard solutionSilver atomic spectroscopy standard concentrate 1.00 g AgSilver colloidalSilver elementalSilver iodideSilver ion standard solutionSilver metalSilver metal and soluble compoundsSilver nanoparticlesSilver nitrate solutionSilver preparationSilver standard for aasSilver standard for icpSilver(II)Silver, colloidalSilver, elementalSilver, metal and soluble compoundsSsd (1% Silver Sulfadiazine Cream Usp)TCG 7rsilver(0)","Silver is a metallic element with the chemical symbol Ag and atomic number 47. It occurs naturally in its pure, free form, as an alloy with gold and other metals, and in minerals such as argentite and chlorargyrite. Most silver is produced as a by-product of copper, gold, lead, and zinc refining. Silver is a precious metal used to make ornaments, jewelry, silverware, and currency coins. It is also used in electrical equipment, mirrors, dental fillings, and brazing alloys and solders. Silver compounds are used in photographic film and as antibacterial agents. (S074, S075)",,7440-22-4,23954,,C06710,"155550
180860
224410
270685
312780",9141,AG%2b,,D012834,Silver,6532,,,http://en.wikipedia.org/wiki/Silver,InChI=1/Ag,silver,http://www.biospider.ca/saved_files/mol/16daed060334a872095fea2c8b748ece_1237958016.mol,[Ag+],[Ag+],[Ag]+,106.905098,White metallic solid.,960.5 °C,,,"",,,,"Oral
Inhalation
Dermal
(S074)",,"Metallic silver is oxidized and may deposit in the tissues, causing arygria. The silver ion is known to inhibit glutathione peroxidase and NA+,K+-ATPase activity, respectively disrupting selenium-catalyzed sulfhydryl oxidation-reduction reactions and intracellular ion concentrations. Silver nanoparticles are believed to disrupt the mitochondrial respiratory chain, causing oxidative stress, reduced ATP synthesis, and DNA damage. (S074, S077, S078, S079, S080)","Silver and its compounds can be absorbed via inhalation, orally and dermally. It distributes throughout the body, particularily to the liver. Insoluble silver salts are transformed into soluble silver sulfide albuminates, bind to amino or carboxyl groups in RNA, DNA, and proteins, or are reduced to metallic silver by ascorbic acid or catecholamines. Metallic silver is oxidized and may deposit in the tissues, causing arygria. Silver is eliminated primarily in the faeces. (S074)","LD50: 100 mg/kg (Oral, Mouse) (R371)",,,"Most silver is produced as a by-product of copper, gold, lead, and zinc refining. Silver is a precious metal used to make ornaments, jewelry, silverware, and currency coins. It is also used in electrical equipment, mirrors, dental fillings, and brazing alloys and solders. Silver compounds are used in photographic film and as antibacterial agents. (S074, S075)",,"Exposure to high levels of silver for a long period of time may result in a condition called arygria, a blue-gray discoloration of the skin and other body tissues. Argyria is a permanent effect but does not appear to be harmful to health. While silver itself is not toxic, most silver salts are, and may damage the liver, kidney, and central nervous system, as well as be carcinogenic. (S074, S075, S076)","Exposure to high levels of silver for a long period of time may result in a condition called arygria, a blue-gray discoloration of the skin and other body tissues. Argyria is a permanent effect but does not appear to be harmful to health. Exposure to high levels of silver in the air has resulted in breathing problems, lung and throat irritation, and stomach pains. Skin contact with silver can cause mild allergic reactions such as rash, swelling, and inflammation in some people. (S074)","",P54710;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P07203;P18283;P22352;P59796;Q96SL4;P36969;O75715;Q8TED1 
216,T3D0215,2009-03-06 18:58:18 UTC,2009-08-04 21:28:00 UTC,Chromic acid,Inorganic Compound;Chromium Compound,Acide chromique [french]Caswell No. 221Chromic acidChromic acid (H2CrO4)Chromic(vi) acidChromium hydroxide oxideDihydrogen(tetraaoxidochromate)DihydroxidodioxidochromiumH2CrO4Tetraoxochromic acid[CrO2(OH)2],"Chromic acid generally refers to a collection of compounds generated by the acidification of solutions containing chromate and dichromate anions or the dissolving of chromium trioxide in sulfuric acid. Chromic acid contains hexavalent chromium. Hexavalent chromium refers to chromium in the +6 oxidation state, and is more toxic than other oxidation states of the chromium atom because of its greater ability to enter cells and a higher redox potential. (R189)",,7738-94-5,24425,,"","",33143,"",,,Chromic acid,7935,,,,InChI=1/Cr.2H2O.2O/h;2*1H2;;/q+2;;;;/p-2,dihydroxy(dioxo)chromium,http://www.biospider.ca/saved_files/mol/,O[Cr](=O)(=O)O,O[Cr](=O)(=O)O,CrH2O4,117.935820,Red solid.,"","","","","","","","Oral 
Inhalation 
Dermal 
(R042)","Sulfate transporter (P50443) 
Sulfate anion transporter 1 (Q9H2B4) 
(R041)","Hexavalent chromium's carcinogenic effects are caused by its metabolites, pentavalent and trivalent chromium. The DNA damage may be caused by hydroxyl radicals produced during reoxidation of pentavalent chromium by hydrogen peroxide molecules present in the cell. Trivalent chromium may also form complexes with peptides, proteins, and DNA, resulting in DNA-protein crosslinks, DNA strand breaks, DNA-DNA interstrand crosslinks, chromium-DNA adducts, chromosomal aberrations and alterations in cellular signaling pathways. It has been shown to induce carcinogenesis by overstimulating cellular regulatory pathways and increasing peroxide levels by activating certain mitogen-activated protein kinases. It can also cause transcriptional repression by cross-linking histone deacetylase 1-DNA methyltransferase 1 complexes to CYP1A1 promoter chromatin, inhibiting histone modification. Chromium may increase its own toxicity by modifying metal regulatory transcription factor 1, causing the inhibition of zinc-induced metallothionein transcription. (R041, R042, R075, R076, R077)","Chromium is absorbed from oral, inhalation, or dermal exposure and distributes to nearly all tissues, with the highest concentrations found in kidney and liver. Bone is also a major storage site and may contribute to long-term retention. Hexavalent chromium's similarity to sulfate and chromate allow it to be transported into cells via sulfate transport mechanisms. Inside the cell, hexavalent chromium is reduced first to pentavalent chromium, then to trivalent chromium by many substances including ascorbate, glutathione, and nicotinamide adenine dinucleotide. Chromium is almost entirely excreted with the urine. (R041, R042)","LD50: 330 mg/kg (Oral, Dog) (R1102)",1 to 3 grams for an adult human (hexavalent chromium). (R869),"1, carcinogenic to humans. (R264)","Chromic acid is an intermediate in chromium plating, and is also used in ceramic glazes, and colored glass. (R198)","Intermediate Oral: 0.005 mg/kg/day (R260)  
Chronic Oral: 0.001 mg/kg/day (R260)",Hexavalent chromium is a known carcinogen. Chronic inhalation especially has been linked to lung cancer. Hexavalent chromium is also known to cause reproductive and developmental defects. (R041),"Breathing hexavalent chromium can cause irritation to the lining of the nose, nose ulcers, runny nose, and breathing problems, such as asthma, cough, shortness of breath, or wheezing. Ingestion of hexavalent chromium causes irritation and ulcers in the stomach and small intestine, as well as anemia. Skin contact can cause skin ulcers. (R042)",There is no known antidote for chromium poisoning. Exposure is usually handled with symptomatic treatment. (R042) ,P28482;P27361;Q13547;Q14872;DNA
217,T3D0216,2009-03-06 18:58:18 UTC,2009-08-05 15:58:37 UTC,Nitrate,Inorganic Compound;Nitrate,"Econazole nitrateFemstat 3GaniteGynazole-1IsordilIsosorbide dinitrateNitrate ionNitratesNitrates, inorganic, n.o.s.Nitrates, inorganic, n.o.s. [UN1447] [Oxidizer]Nitric acidSorbitrateTrioxidonitrateTrioxonitrateTrioxonitrate(v)nitrate(1-)trioxidonitrate(1-)trioxonitrate(1-)","Nitrate (NO3-) and nitrite (NO2-) are naturally occurring inorganic ions that are part of the nitrogen cycle. Microbial action in soil or water decomposes wastes containing organic nitrogen into ammonia, which is then oxidized to nitrite and nitrate. Because nitrite is easily oxidized to nitrate, nitrate is the compound predominantly found in groundwater and surface waters. Contamination with nitrogen‑containing fertilizers (e.g. potassium nitrate and ammonium nitrate), or animal or human organic wastes, can raise the concentration of nitrate in water. Nitrate‑containing compounds in the soil are generally soluble and readily migrate with groundwater. While nitrate is not toxic, it can be metabolized into nitrite once in the body. Nitrite is a toxic compound known to cause methemoglobinemia. (S575)",,14797-55-8,943,,C00244,"109270
125853
163729",17632,CPD-144,,,Nitrate,6494,,,http://en.wikipedia.org/wiki/Nitrate,"InChI=1/HNO3/c2-1(3)4/h(H,2,3,4)",nitrate,http://www.biospider.ca/saved_files/mol/7fb600ae7a2e9fda9213b24866958c2d_1237958264.mol,[O-][N+]([O-])=O,[O-][N+]([O-])=O,[NO3]-,61.987820,,"",,,"",,,,"Oral
Inhalation
(S575)",,"Nitrate's toxicity is a result of it's conversion to nitrite once in the body. Nitrite causes the autocatalytic oxidation of oxyhemoglobin to hydrogen peroxide and methemoglobin. This elevation of methemoglobin levels is a condition known as methemoglobinemia, and is characterized by tissue hypoxia, as methemoglobin cannot bind oxygen. (V305, V306)","Intake of some amount of nitrates and nitrites is a normal part of the nitrogen cycle in humans. In vivo conversion of nitrates to nitrites can occur in the gastrointestional tract under the right conditions, significantly enhancing nitrates' toxic potency. The major metabolic pathway for nitrate is conversion to nitrite, and then to ammonia. Nitrites, nitrates, and their metabolites are excreted in the urine. (S575)",,"","2A, probably carcinogenic to humans. (R264)","Nitrates and nitrites are naturally produced and may also be found in pesticides. Exposure usually occurs from contact with contaminated soil, food water. Nitrates may also be found in certain drugs. (S575)",,Nitrate and nitrite poisoning causes methemoglobinemia. Nitrites may cause pregnancy complications and developmental effects. They may also be carcinogenic. (S575),"Nitrate and nitrite poisoning causes methemoglobinemia. Symptoms include cyanosis, cardiac dysrhythmias and circulatory failure, and progressive central nervous system (CNS) effects. CNS effects can range from mild dizziness and lethargy to coma and convulsions. (S575)",Methemoglobinemia can be treated with supplemental oxygen and methylene blue 1% solution administered intravenously slowly over five minutes followed by IV flush with normal saline. Methylene blue restores the iron in hemoglobin to its normal (reduced) oxygen-carrying state. (V306),P69905;P68871;P02042;P02100;P69891;P69892;Q6B0K9;P09105;P02008
218,T3D0217,2009-03-06 18:58:18 UTC,2009-08-25 19:52:00 UTC,Potassium-40,Inorganic Compound;Metal;Radioactive Isotope,"Potassium, isotope of mass 40Potassium-40","Potassium-40 is a naturally occurring radioactive isotope of potassium. Potassium is the chemical element with the symbol K and atomic number 19. Potassium is widely distributed in nature and is present in all plant and animal tissues. Potassium-40 comprises about 0.012% of naturally occurring potassium. It is the predominant radioactive component in human tissues and in most food. Potassium-40 has a half-life of 1.3 billion years and emits beta and gamma radiation. (S571, W524)",,13966-00-2,6328542,,"","","","",,,Potassium-40,,,,,InChI=1/K/i1+1,potassium-40,http://www.biospider.ca/saved_files/mol/,[40K],[40K],K,38.963710,Silvery-white metal.,"",,,"",,,,"Oral 
Inhalation
(S571)",,"The ionizing radiation produced by potassium causes cellular damage that includes DNA breakage, accurate or inaccurate repair, apoptosis, gene mutations, chromosomal change, and genetic instability. This leads to loss of normal cell and tissue homeostasis, and development of malignancy. Ionizing radiation that does not directly damage DNA can produce reactive oxygen intermediates that directly affect the stability of p53, an important enzyme in cell-cycle regulation, and produce oxidative damage to individual bases in DNA and point mutations by mispairing during DNA replication. (W510)","Potassium-40 behaves in the body in the same manner as other potassium isotopes. Potassium is almost completely absorbed upon ingestion, moving quickly from the gastrointestinal tract to the bloodstream. The potassium-40 that enters the bloodstream after ingestion or inhalation is quickly distributed to all organs and tissues. Potassium-40 is eliminated from the body with a biological half-life of 30 days. The potassium content of the body is under strict homeostatic control (in which the amount retained is actively regulated by the body to achieve the normal range required for system functions), and it is not influenced by variations in environmental levels. Hence, the potassium-40 content in the body is constant, with an adult male having about 0.1 microcurie or 100,000 pCi. Each year this isotope delivers doses of about 18 millirem (mrem) to soft tissues of the body and 14 mrem to bone. Potassium cations are important in neuron function, influencing osmotic balance between cells and the interstitial fluid, allowing muscle contraction and the sending of all nerve impulses through action potentials, and maintaining fluid and electrolyte balance in the body. (S571, W524)",,,,There are no specific commercial or medical uses associated with the radioactive properties of potassium-40. (S571),,"Potassium-40 presents external as well as internal health hazard. The strong gamma radiation makes external exposure to this isotope a concern. While in the body, potassium-40 poses a health hazard from both the beta particles and gamma rays. The health hazard of  potassium-40 is associated with cell damage caused by the ionizing radiation that results from radioactive decay, with the general potential for subsequent cancer induction. (S571)","Exposure to high doses of ionizing radiation results in acute radiation syndrome, which can cause skin burns, hair loss, nausea, vomiting, dizziness, disorientation, low blood pressure, headache, fatigue, weakness, fever, birth defects, illness, infection, and death. (W510, W525)","Treatment reversing the effects of irradiation is currently not possible. Anaesthetics and antiemetics are administered to counter the symptoms of exposure, as well as antibiotics for countering secondary infections due to the resulting immune system deficiency. (W525)",DNA
219,T3D0218,2009-03-06 18:58:18 UTC,2009-08-06 21:37:37 UTC,Dinitrotoluene,Organic Compound;Explosive;Plasticizer;Aromatic Hydrocarbon;Nitrite,"1-Methyl-2,4-dinitrobenzene2,4-Dinitro-1-methylbenzene2,4-Dinitromethylbenzene2,4-Dinitrotoluene2,4-Dinitrotoluene (containing 0.5% 2,6-dinitrotoluene)2,4-Dinitrotoluene (containing 1.0-1.5% 2,6-dinitrotoluene)2,4-Dinitrotoluene, practical grade2,4-Dinitrotoluol4-Methyl-1,3-dinitrobenzeneBenzene, 1-methyl-2,4-dinitro-Benzene, 1-methyl-2,4-dinitro-, sulfurizedBenzene, methyldinitro-CHEBI:920DNTDinitrophenylmethaneDinitrotolueneDinitrotoluene, technical grade (2,4 (77%)- and 2,6 (19%)-)Dinitrotoluene-MethyldinitrobenzeneRCRA waste no. U105RCRA waste number U105Toluene, 2,4-dinitro-Toluene, ar,ar-dinitro-Toluene, dinitro-WLN: WNR B1 ENWnchembio882-comp9","Dinitrotoluene (DNT) is a high explosive. It is one of the precursors for trinitrotoluene (TNT), which is synthesized through three separate nitrations of toluene. The first product is mononitrotoluene, DNT is the second, and TNT is the third and final product. There are 6 possible isomers of dinitrotolulene. The most common is 2,4-dinitrotoluene. (S606)",,25321-14-6,8461,,"","","","",,,Dinitrotoluene,540,,,http://en.wikipedia.org/wiki/Dinitrotoluene,"InChI=1/C7H6N2O4/c1-5-2-3-6(8(10)11)4-7(5)9(12)13/h2-4H,1H3","1-methyl-2,4-dinitrobenzene",http://www.biospider.ca/saved_files/mol/,CC1=C(C=C(C=C1)[N+](=O)[O-])[N+](=O)[O-],CC1=C(C=C(C=C1)[N+](=O)[O-])[N+](=O)[O-],C7H6N2O4,182.032760,At room temperature it is a pale yellow to orange crystalline solid. (S606),"",,,"0.27 mg/mL at 22 °C [SEIDELL,A (1941)]",,,,"Exposure to skin and eyes, inhalation, or ingestion. (R502)","","Dinitrotoluene may cause conversion of oxyhemoglobin to methemoglobin via oxidation of iron(II) to iron(III) by its metabolites. High levels of methemoglobin are removed by catabolism, leading to the development of anemia. Some metabolites of dinitrotoluene  are also transported back from the bile to the liver, where the amine group is N-hydroxylated by cytochrome P-450 to form an unstable sulfate conjugate. The sulfate conjugate is degraded into carbonium or nitrenium ions. These ions covalently bind to hepatic macromolecules (DNA, RNA), leading to mutations and subsequently liver tumors. They also bind to DNA of the lung and the intestine. (R511)","Dinitrotoluene can be absorbed following inhalation, ingestion, or skin contact. Metabolism occurs in the liver and also in the intestine by microflora. DNT appears to be first metabolized by the liver by cytochrome P-450 enzymes, with the metabolites being excreted into the bile. The biliary metabolites are hydrolyzed and further metabolized in the intestine, then after reabsorption and circulation back to the liver they are activated and bound to macromolecules. The main urinary metabolites of dinitrotoluene are the corresponding dinitrobenzyl alcohol glucuronide, dinitrobenzoic acid, and aminonitrobenzoic acid. (R511)",,,"2B, possibly carcinogenic to humans. (R264)","It is a high explosive and one of the precursors for trinitrotoluene (TNT), which is synthesized through three separate nitrations of toluene. Dinitrotoluene can affect the body if it is inhaled, comes in contact with the eyes or skin, is swallowed, or is absorbed through the skin. Even a small amount absorbed from clothes or shoes may cause toxic symptoms. It is assumed that oral ingestion could be a secondary route for occupationally exposed humans. (R502, S606)",,"Dinitrotoluene poisoning may cause methemoglobinemia, anemia, leukopenia, and liver necrosis. Liver injury may be more common than cyanosis. (R511)","Symptoms of dinitrotoluene poisoning include blue lips or finger nails, blue skin, vertigo, fatigue, dizziness, weakness, nausea, vomiting, dyspnea, arthralgia, insomnia, tremor, paralysis, unconsciousness, chest pain, shortness of breath, palpitation, anorexia, and loss of weight. (R504, R505)","Following oral exposure, immediately dilute with 4 to 8 ounces (120 to 240 mL) of water or milk (not to exceed 4 ounces/120 mL in a child). Administer charcoal as a slurry. Gastric lavage and oxygen administration is recommended. Following inhalation exposure, move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with inhaled beta2 agonist and oral or parenteral corticosteroids. Following eyes exposure, irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes. Following dermal exposure, remove contaminated clothing and wash exposed area thoroughly with soap and water, and administer a benzodiazepine IV in case of irritation. In all those cases, a physician may need to examine the area if irritation or pain persists. (R624)",DNA;RNA;P69905;P68871;P02042;P02100;P69891;P69892;Q6B0K9;P09105;P02008
220,T3D0219,2009-03-06 18:58:18 UTC,2009-08-04 21:28:01 UTC,Antimony,Inorganic Compound;Metalloid;Antimony Compound,"Antimonium Crudum 3ch - 30chAntimonium Crudum Drops D3-C1000Antimonium Crudum Gtte 5ch-15chAntimonium Crudum Liquid (S No. 38)Antimonium Tartaricum 2ch - 30chAntimonium Tartaricum Drops D3-C1000Antimonium crudumAntimonium crudum homaccordAntimonium iodatumAntimonium muriaticumAntimonium sulfuratum aureumAntimonium sulphuratum aureumAntimonium tartaricumAntimonium tartaricum homaccordAntimony 4x PwrAntimony Potassium Tartrate Liquid (S#312)Antimony and compoundsAntimony blackAntimony elementAntimony powder [UN2871] [Poison]Antimony, elementalAntimony, metallicAntimony, regulusAntymonAntymon [polish]DiantimonyGrey antimonyPekana - antimonium tartaricumRegulus of antimonySBSB#SBStibiumStibium metallicumThermoguard cpa","Antimony is a metallic element with the chemical symbol Sb and atomic number 51. It is a silvery white metal of medium hardness that breaks easily. Small amounts of antimony are found in the earth's crust. Antimony ores are mined and then either changed into antimony metal or combined with oxygen to form antimony oxide. Antimony enters the environment during the mining and processing of its ores and in the production of antimony metal, alloys, antimony oxide, and combinations of antimony with other substances. (R1131)",,7440-36-0,23967,,"","",30304,"",,D000965,Antimony,6363,,,http://en.wikipedia.org/wiki/Antimony,InChI=1/Sb/q+3,Antimony,http://www.biospider.ca/saved_files/mol/,[Sb+3],[Sb+3],[Sb]3+,120.903809,,630 °C,,,"",,,,"Inhalation
Ingestion
Skin or dermal contact 
(R1131)","","The inhalation data suggests that the myocardium is a target of antimony toxicity. It is possible that antimony affects circulating glucose by interfering with enzymes of the glycogenolysis and gluconeogenesis pathways. The mechanism of action of antimony remains unclear. However, some studies suggest that antimony combines with sulfhydryl groups including those in several enzymes important for tissue respiration. The antidotal action of BAL (2,3-dimercaptopropanol) depends on its ability to prevent or break the union between antimony and vital enzymes. Moreover, the cause of death is believed to be essentially the same as that in acute arsenic poisoning. (R276, R1131, S004)","Absorbed antimony is transported to various tissue compartments of the body via the blood; the highest levels are found in the hair and skin; the adrenal glands, lung, large intestine, trachea, cerebellum, and kidneys also contain relatively high levels of antimony. Antimony can covalently interact with sulfhydryl groups and phosphate, as well as numerous reversible binding interactions with endogenous ligands (e.g., proteins). It is not known if these interactions are toxicologically significant. Antimony is a metal and, therefore, does not undergo catabolism. Antimony is excreted via the urine and feces. Some of the fecal antimony may represent unabsorbed antimony that is cleared from the lung via mucociliary action into the esophagus to the gastrointestinal tract. (R1131)",Not available.,,"2B, possibly carcinogenic to humans. (R264)","Antimony enters the environment during the mining and processing of its ores and in the production of antimony metal, alloys, antimony oxide, and combinations of antimony with other substances. Exposure usually occurs from breathing air, drinking water, and eating foods that contain antimony. Exposure can also occur through dermal or skin contact. (R1131)",Not available.,"Dermal exposure to antimony can cause antimony spots (papules and pustules around sweat and sebaceous glands). Antimony poisoning can also lead to pneumoconiosis. Alterations in pulmonary function and other effects including chronic bronchitis, chronic emphysema, inactive tuberculosis, pleural adhesions, and irritation can result from inhalation of antimony. Increased blood pressure can also result from antimony poisoning. Myocardial depression, vasodilation and fluid loss may cause shock with hypotension, electrolyte disturbances and acute renal failure. Cerebral oedema, coma, convulsions, and death are possible. (R1131)","Abdominal pain, vomiting, diarrhea can result from inhalation of antimony. Dyspnea, headache, vomiting,cough, conjunctivitis, and bloody purulent discharge from nose can result from inhalation exposure. Skin or eye contact can cause pain and redness of the exposed surface. (R692, R1131)","Following oral exposure to antimony, administer charcoal as a slurry (240 mL water/30 g charcoal). Following inhalation exposure, move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with inhaled beta2 agonist and oral or parenteral corticosteroids. In case of eye exposure, irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes. Following dermal exposure, remove contaminated clothing and wash exposed area thoroughly with soap and water. A physician may need to examine the area if irritation or pain persists. (R624)",P08263;P09210;Q16772;Q03013;Q7RTV2;Q9Y2Q3;P09488;P28161;P21266;P46439;P78417;Q9H4Y5;P09211;P30711;P30712;A8MPT4;P10620;Q99735;O14880;O43708
222,T3D0221,2009-03-06 18:58:18 UTC,2009-08-25 19:52:01 UTC,Thorium-227,Inorganic Compound;Metal;Thorium Compound;Radioactive Isotope,"Thorium, isotope of mass 227Thorium-227","Thorium is the chemical element of symbol Th and atomic number 90. It is a naturally occurring radioactive metal of the actinide series. In the environment, thorium exists in combination with other minerals, such as silica. Small amounts of thorium are present in all rocks, soil, water, plants, and animals. Twenty-seven radioactive isotopes of thorium, with mass number from 210 to 236, have been characterized. Naturally occurring thorium is composed mainly of one isotope: 232Th. The most abundant and/or stable isotopes are: 232Th (half-life of 14.05 billion years), 230Th (half-life of 75,380 years), 229Th (half-life of 7340 years), and 228Th (half-life of 1.92 years). Thorium is used to make ceramics, gas lantern mantles, and metals used in the aerospace industry and in nuclear reactions. Thorium can also be used as a fuel for generating nuclear energy. Thorium has been linked to increased risk of liver cancer. (S521, W511)",,15623-47-9,61806,,"","","","",,,Thorium-227,,,,http://en.wikipedia.org/wiki/Thorium-227,InChI=1/Th/i1-5,thorium-227,http://www.biospider.ca/saved_files/mol/,[227Th],[227Th],Th,232.038050,,"",,,"",,,,"Oral
Inhalation
Dermal
(W511)","Serotransferrin (P02787)
(W511)","The ionizing radiation produced by thorium causes cellular damage that includes DNA breakage, accurate or inaccurate repair, apoptosis, gene mutations, chromosomal change, and genetic instability. This leads to loss of normal cell and tissue homeostasis, and development of malignancy. Ionizing radiation that does not directly damage DNA can produce reactive oxygen intermediates that directly affect the stability of p53, an important enzyme in cell-cycle regulation, and produce oxidative damage to individual bases in DNA and point mutations by mispairing during DNA replication. (W510)","Exposure to thorium can occur following inhalation, ingestion, or dermal exposure. Once in the body thorium accumulates mainly in the liver, spleen, lymph nodes, lungs, and bone. Transferrin plays a major role in the transport and cellular uptake of thorium. Thorium may combine with oxygen to form thorotrast (thorium dioxide), a colloid which may affect protein uptake. Thorium and thorotrast are excreted mainly in the faeces. (W511)",,,"1, carcinogenic to humans. (R264)","Thorium can also be used as a fuel for generating nuclear energy. Thorium is used as an alloying element in magnesium, used in aircraft engines, imparting high strength and creep resistance at elevated temperatures. Thorium is also used as an alloying agent in gas tungsten arc welding (GTAW) to increase the melting temperature of tungsten electrodes and improve arc stability. Thorium is used to coat tungsten wire used in electronic equipment, improving the electron emission of heated cathodes. Thorium is used as a fertile material for producing nuclear fuel. Thorium is a very effective radiation shield, although it has not been used for this purpose as much as lead or depleted uranium. Uranium-thorium age dating has been used to date hominid fossils. (S521)",,"Lungs and other internal organs can be penetrated by the alpha radiation produced by thorium. As a result, exposure to an aerosol of thorium can lead to increased risk of cancers of the lung, pancreas and blood. Exposure to thorium internally leads to increased risk of liver diseases. (S521)","Exposure to high doses of ionizing radiation results in acute radiation syndrome, which can cause skin burns, hair loss, nausea, vomiting, dizziness, disorientation, low blood pressure, headache, fatigue, weakness, fever, birth defects, illness, infection, and death. (W510, W525)","Treatment reversing the effects of irradiation is currently not possible. Anaesthetics and antiemetics are administered to counter the symptoms of exposure, as well as antibiotics for countering secondary infections due to the resulting immune system deficiency. (W525)",DNA
223,T3D0222,2009-03-06 18:58:19 UTC,2009-08-04 21:28:01 UTC,"2,4,5-Trichlorophenol",Organic Compound;Aromatic Hydrocarbon;Organochloride,"2,4, 5-Trichlorophenol2,4,5-Trichlorophenol2,4,5-trichlorophenol (ACD/Name 4.0)CollunosolDowcide 2Dowicide 2Dowicide bNurellePS9_SUPELCOPreventol IRCRA waste no. U230Rcra waste number U230TCPTCP (van)WLN: QR bg CG eg","2,4,5-Trichlorophenol is a chlorinated phenol that has been used as a fungicide, herbicide, insecticide, antiseptic, defoliant, and glue preservative. The chemical 2,4,5-trichlorophenol serves as a raw material for making the herbicides Silvex and 2,4,5-T (2,4,5-trichlorophenoxyacetic acid) (R970).",,95-95-4,7271,,C07101,"",28520,CPD-10489,,C009534,"2,4,5-Trichlorophenol",6559,,,,"InChI=1/C6H3Cl3O/c7-3-1-5(9)6(10)2-4(3)8/h1-2,10H","2,4,5-trichlorophenol",http://www.biospider.ca/saved_files/mol/dbe1184d635c1991bf6ca445808a14c1_1237959001.mol,C1=C(C(=CC(=C1Cl)Cl)Cl)O,C1=C(C(=CC(=C1Cl)Cl)Cl)O,C6H3Cl3O,195.924950,,69 °C,,,"1.2 mg/mL at 25 °C [LEUENBERGER,C et al. (1985A)]",,,,"Oral, inhalation, dermal, and eye exposure (R970).",,"2,4,5-TCP acts as an uncoupler of oxidative phosphorylation. (R970)","2,4,5-TCP can be metabolized to 3,4,6-trichlorocatechol, 2,5-dichlorohydroquinone, and a dihydroxydichlorobenzene. Metabolites can also be dimerized to a dihydroxyhexachlorobiphenyl, a dihydroxypentachlorodiphenyl ether, two hydroxypentachlorodiphenyl ethers, a hydoxyhexachlorodiphenyl ether, and a hydroxyhexachlorodioxin or hydroxyhexachlorodiphenoquinone. The metabolites are excreted in urine (R970).","LD50: 820 mg/kg (oral, rat) (R1113).",,"2B, possibly carcinogenic to humans. (R264)","Exposure may occur from drinking water that has been disinfected with chlorine and breathing air contaminated by 2,4,5-trichlorophenol. Dermal and eye contact with the toxin are also sources of exposure (R970).","0.003 mg/kg/day (intermediate, oral, human) (R1114).","Exposure through the skin can lead to acne and mild injury of the liver. Major effects after ingestion of 2,4,5-trichlorophenol affect the liver and the immune system. Toxic manifestations include central nervous system depression followed by increased respiration, hyperthermia, a blood pressure rise, progressive euromuscular weakness, and cyanosis (R970).","Inhalation of 2,4,5-trichlorophenol may cause coughing and sore throat. Eye or skin contact causes redness and pain at the site of contact. Convulsions, diarrhoea, dizziness, headache, shortness of breath, vomiting, weakness, and ataxia may occur after ingestion (R970). ","Avoid dilution following oral exposure; instead, administer charcoal as a slurry. Following inhalation, move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with inhaled beta2 agonist and oral or parenteral corticosteroids. In case the exposure occurs through eye contact, irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes. Following dermal exposure, remove phenol with undiluted polyethylene glycol 300 to 400 or isopropyl alcohol prior to washing, if readily available. Wash exposed areas twice or for at least 10 minutes with large quantities of SOAPY water. Water alone may be harmful (R624). ",P22303;P03372;Q92731
224,T3D0223,2009-03-06 18:58:19 UTC,2009-08-04 21:28:01 UTC,Arsenic acid,Inorganic Compound;Arsenic Compound,"Acide arsenique liquide [french]ArsenateArsenate, dihydrogenArsenic acidArsenic acid (H3AsO4)Arsenic acid (H3AsO4), trilithium saltArsenic acid H3AsO4Arsenic acid, hemihydrateArsenic acid, liquidArsenic acid, liquid [UN1553] [Poison]Arsenic acid, solid [UN1554] [Poison]Arsoric acidCaswell No. 056Crab grass killerDesiccant L-10Dessicant L-10H3AsO4HI-Yield desiccant H-10Lithium arsenateLithium arsenate (Li3AsO4)Orthoarsenic acidRCRA waste no. P010RCRA waste number P010ScorchTetraoxoarsenic acidTrihydrogen tetraoxoarsenateTrihydroxidooxidoarsenicZotoxZotox crab grass killer[AsO(OH)3]",Arsenic acid is a highly toxic chemical compound of arsenic. It is an analog of phosphoric acid and capable of oxidizing. (R1103),,7778-39-4,234,,C01478,"",18231,ARSENATE,,C025657,Arsenic acid,7936,,,,"InChI=1/AsH3O4/c2-1(3,4)5/h(H3,2,3,4,5)",arsoric acid,http://www.biospider.ca/saved_files/mol/51d0b82cdeb78bb691b1c7428bc688db_1237959110.mol,O[As](=O)(O)O,O[As](=O)(O)O,AsH3O4,141.924730,White crystals.,"","","","590 mg/mL [SHIU,WY et al. (1990)]","","","","Oral 
Inhalation 
Dermal 
(R009)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Arsenite methyltransferase (Q9HBK9) 
(R164)","Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase. By competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carginogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (R001, R054)","Arsenic is mainly absorbed by inhalation or ingestion, and to a lesser extent by dermal exposure. It is then distributed throughout the body, where it is reduced into arsenite, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant. (R055)","LD50: 48 mg/kg (Oral, Rat) (R263)
LD50: 8 mg/kg (Intravenous, Rabbit) (R1104)",,"1, carcinogenic to humans. (R264)","Arsenic acid is used as a wood preservative, broad-spectrum biocide, and finishing agent for glass and metal. (R1103)","Acute Oral: 0.005 mg/kg/day (R260) 
Chronic Oral: 0.0003 mg/kg/day (R260) 
Chronic Inhalation: 0.01 mg/m3 (R260)","Arsenic poisoning can lead to death from multi-system organ failure, probably from necrotic cell death and not apoptosis. Arsenic is also a known carcinogen, especially in skin, liver, bladder and lung cancers. (R001, R055)","Exposure to lower levels of arsenic can cause nausea and vomiting, decreased production of red and white blood cells, abnormal heart rhythm, and damage to blood vessels.","Arsenic poisoning can be treated by chelation therapy, using chelating agents such as dimercaprol, EDTA or DMSA. Charcoal tablets may also be used for less severe cases. In addition, maintaining a diet high in sulfur helps eliminate arsenic from the body. (R055)",P29803;P68871;P69905;P00738;P03372;P04150;P00390;Q14145;P09874;P07437;P60709;P63261;Q9NNW7;Q86VQ6;P68032;P68133;P62736;P63267;P10515;P23025;P08559;P11177;A6NKZ8 ;Q99867;Q9H853;O00330;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2
225,T3D0224,2009-03-06 18:58:19 UTC,2009-08-04 21:28:02 UTC,Arsenic trioxide,Inorganic Compound;Arsenic Compound,"2,4,5-trioxa-1,3-diarsabicyclo[1.1.1]pentaneAcide arsenieuxAcide arsenieux [french]Anhydride arsenieuxAnhydride arsenieux [french]Arseni trioxydumArsenic (III) trioxideArsenic Trioxide [UN1561] [Poison]Arsenic blancArsenic blanc [french]Arsenic oxideArsenic oxide (3)Arsenic oxide (As2O3)Arsenic oxidearsenous trioxideArsenic sesquioxideArsenic(III) oxideArsenic, whiteArsenicum Album 3ch-30ch GranulesArsenicum albumArsenigen saureArsenigen saure [german]Arsenious acidArsenious acid anhydrideArsenious oxideArsenious trioxideArseniteArsenoliteArsenous acidArsenous acid anhydrideArsenous anhydrideArsenous oxideArsenous oxide anhydrideArsentrioxideArsodentClaudeliteClaudetiteCrude arsenicDi-arsenic trioxideDiarsenic trioxideDiarsonic trioxideOxyde arsenieux [iso-french]Poison flourRcra waste number P012TrisenoxWhite arsenic",Arsenic trioxide is a chemical compound of arsenic found naturally in the minerals arsenolite and claudetite. It is the most important commercial compound of arsenic and the main starting material for arsenic chemistry. (R1105),,1327-53-3,518740,,"","",30621,CPD-763,,C006632,Arsenic trioxide,104,,,http://en.wikipedia.org/wiki/Arsenic trioxide,InChI=1/2As.3O/q2*+3;3*-2,"2,4,5-trioxa-1,3-diarsabicyclo[1.1.1]pentane",http://www.biospider.ca/saved_files/mol/7cecc8a957de9a56f2dbbed2f1f63ec4_1237959214.mol,O1[As]2O[As]1O2,O1[As]2O[As]1O2,As2O3,197.827940,White solid.,465 °C,"","","17 mg/mL at 16 °C [SHIU,WY et al. (1990)]","","","","Oral 
Inhalation 
Dermal 
(R009)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Arsenite methyltransferase (Q9HBK9) 
(R164)","Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carginogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (R001, R054)","Arsenic is mainly absorbed by inhalation or ingestion, and to a lesser extent by dermal exposure. It is then distributed throughout the body, where it is reduced into arsenite if necessary, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant. (R055)","LD50: 871 mg/kg (Intraperitoneal, Rat) (R263)
LD50: 31 500 ug/kg (Oral, Mouse) (R263)
LD50: 9800 ug/kg (Subcutaneous, Mouse) (R263)
LD50: 10 700 ug/kg (Intravenous, Mouse) (R263)",200 mg for an adult human. (R273),"1, carcinogenic to humans. (R264)","Arsenic trioxide is a byproduct of certain kinds of ore processing. It is the starting point for the manufacture of many arsenic-based products, including pesticides, pharamaceuticals, alloys, and semiconductors. It is also used as a wood preservative and decolorizing agent. (R1105)","Acute Oral: 0.005 mg/kg/day (R260) 
Chronic Oral: 0.0003 mg/kg/day (R260) 
Chronic Inhalation: 0.01 mg/m3 (R260)","Arsenic poisoning can lead to death from multi-system organ failure, probably from necrotic cell death, not apoptosis. Arsenic is also a known carcinogen, especially in skin, liver, bladder and lung cancers. (R001, R055)","Exposure to lower levels of arsenic can cause nausea and vomiting, decreased production of red and white blood cells, abnormal heart rhythm, and damage to blood vessels. ","Arsenic poisoning can be treated by chelation therapy, using chelating agents such as dimercaprol, EDTA or DMSA. Charcoal tablets may also be used for less severe cases. In addition, maintaining a diet high in sulfur helps eliminate arsenic from the body. (R055)",P29803;P68871;P69905;P00738;P03372;P04150;P00390;Q14145;P09874;P07437;P60709;P63261;Q16881;Q9NNW7;Q86VQ6;P68032;P68133;P62736;P63267;P10515;P23025;P08559;P11177;A6NKZ8 ;Q99867;Q9H853;O00330;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2
226,T3D0225,2009-03-06 18:58:19 UTC,2009-08-04 21:28:02 UTC,Phorate,Organic Compound;Pesticide;Organophosphate,"AastarAgrimetAmerican Cyanamid 3,911CHIMCaswell No. 660Dithiophosphate de o,o-diethyle et d'ethylthiomethyleExperimental Insecticide 3911ForaatForaat [dutch]ForateGeometGranutoxO,o-diaethyl-s-(aethylthio-methyl)-dithiophosphatO,o-diaethyl-s-(aethylthio-methyl)-dithiophosphat [german]O,o-diethyl ethylthiomethyl phosphorodithioateO,o-diethyl s-(ethylthio)methyl phosphorodithioateO,o-diethyl s-(ethylthiomethyl) phosphorodithioateO,o-diethyl s-[(ethylsulfanyl)methyl] dithiophosphateO,o-diethyl s-[(ethylsulfanyl)methyl] phosphorodithioateO,o-diethyl s-[(ethylthio)methyl] phosphorodithioateO,o-diethyl s-ethylmercaptomethyl dithiophosphateO,o-diethyl s-ethylmercaptomethyl dithiophosphonateO,o-diethyl s-ethylthiomethyl dithiophosphateO,o-diethyl s-ethylthiomethyl dithiophosphonateO,o-diethyl s-ethylthiomethyl thiothionophosphateO,o-diethyl-s-((ethylthio)methyl)phosphorodithioateO,o-diethyl-s-(ethylthio-methyl)-dithiofosfaatO,o-diethyl-s-(ethylthio-methyl)-dithiofosfaat [dutch]O,o-dietil-s-(etiltio-metil)-ditiofosfatoO,o-dietil-s-(etiltio-metil)-ditiofosfato [italian]PS654_SUPELCOPhoratPhorat [german]Phorate 10GPhorate [ansi:bsi:iso]Phorate-10GRCRA waste no. P094RampartRcra waste number P094TerrathionThimateThimenoxThimetThimet 10 GThimet 10-GThimet 10GThimet gTimetVUAgT 182VegfruVegfru foratoxVergfru foratoxVolphor","Phorate is an organophosphate insecticide and acaricide that controls pests by systemic, contact, and fumigant action. It is used against sucking and chewing insects, leafhoppers, leafminers, mites, some nematodes and rootworms. Phorate is used in pine forests and on root and field crops, including corn, cotton, coffee, some ornamental and herbaceous plants and bulbs. Phorate is extremely toxic; it is a Restricted Use Pesticide (RUP) and is among the most poisonous chemicals commonly used for pest control. (S681)",,298-02-2,4790,,"","",38764,"",,D010702,Phorate,7903,,,,"InChI=1/C7H17O2PS3/c1-4-8-10(11,9-5-2)13-7-12-6-3/h4-7H2,1-3H3",diethoxy-(ethylsulfanylmethylsulfanyl)-sulfanylidene-$l^{5}-phosphane,http://www.biospider.ca/saved_files/mol/,CCOP(=S)(OCC)SCSCC,CCOP(=S)(OCC)SCSCC,C7H17O2PS3,260.012830,Phorate is a clear pale-yellow liquid with a skunk-like odor. (S681),-43.7 °C,"188 °C at 2 torr
118-120 °C at 0.8 torr",1.167,"0.05 mg/mL at 25 °C [MARTIN,H & WORTHING,CR (1977)]",,,,Oral. Inhalation. Dermal. (S681),,"Phorate and its metabolites are cholinesterase inhibitors; they affect the normal functioning of the nervous system. Phorate metabolites are even more toxic and have greater anticholinesterase activity than phorate. (S681)
","Phorate is readily absorbed from the gastrointestinal tract, through dermal or inhalation exposure. Phorate does not accumulate in body tissues. Phorate is metabolized into phorate sulphoxide and phorate sulphone and the oxygenated analogues (phoratoxon, phoratoxone sulphoxide and phoratoxone sulphone) which are excreted as diethyl phosphoric acid, O-O-diethyl phosphorothioic and O-O-diethylphosphorodithioic acid. In rats, less than 40% of a high oral dose of phorate was excreted in urine and feces in six days. (S682)","LD50: 1.0 mg/kg (Oral, Rat) (S681)
LD50: 3.5 to 6.59 mg/kg (Oral, Mouse) (S681)
LD50: 20 mg/kg (Oral, Guinea pig) (S681)
LD50: 5.7 mg/kg (Dermal, Rat) (S681)
LD50: 5.2 mg/kg (Dermal, Rabbit) (S681)
LD50: 20-30 mg/kg (Dermal, Guinea pig) (S681)
LC50: 11 mg/m3 (Inhalation, Rat) (S681)",,,,,Phorate affects the normal functioning of the nervous system. (S681),"Symptoms of acute oral exposure may include blurred vision, headache, inability to concentrate, fatigue, nausea, diarrhea, irregular heart and respiration rates, tremors, excessive sweating, confusion and convulsions. Death can occur at high doses due to respiratory arrest or lung constriction. Symptoms resulting from phorate inhalation or skin contact may occur from a few minutes up to 12 hours after exposure. Workers chronically exposed to organophosphates have shown slow thinking, memory defects, irritability, delayed reaction time, and anxiety. Symptoms included a lowering of the heart rate. (S681)","Atropine sulfate is the principal antidote, repeated doses may be necessary. Pralidoxime chloride (2-PAM or protopam chloride) may be effective as an adjunct to atropine treatment. Artificial respiration also may be needed. (S682)",""
227,T3D0226,2009-03-06 18:58:19 UTC,2009-08-04 21:28:02 UTC,Benzo[e]pyrene,Organic Compound;Industrial By-product/Pollutant;Aromatic Hydrocarbon;Polycyclic Aromatic Hydrocarbon,"1,2-Benzopyrene1,2-Benzopyrene (VAN)1,2-Benzpyrene1,2-Benzpyrene (VAN)1,2-benzo(e)pyrene4,5-Benzopyrene4,5-Benzpyrene9,10-BenzpyreneB(e)pBCR050_FLUKABENZO(E)PYRENE (SEE ALSO: BENZ(A)PYRENE (CAS 50-32-8))Benz(e)pyreneBenzo(e)pyreneBenzo(l)pyreneBenzo[e]pyreneBenzo[e]pyrene solutionBenzopyrene","Benzo[e]pyrene is one of over 100 different polycyclic aromatic hydrocarbons (PAHs). PAHs are chemicals that are formed during the incomplete burning of organic substances, such as fossil fuels. They are usually found as a mixture containing two or more of these compounds. (R028)",,192-97-2,9128,,"","","","",,C026487,Benzo[e]pyrene,,,,,InChI=1/C20H12/c1-2-8-16-15(7-1)17-9-3-5-13-11-12-14-6-4-10-18(16)20(14)19(13)17/h1-12H,benzo[e]pyrene,http://www.biospider.ca/saved_files/mol/,C1=CC=C2C(=C1)C3=CC=CC4=C3C5=C(C=CC=C25)C=C4,C1=CC=C2C(=C1)C3=CC=CC4=C3C5=C(C=CC=C25)C=C4,C20H12,252.093900,Colorless solid.,177.5 oC,"","","6.3e-06 mg/mL at 25 oC [PEARLMAN,RS et al. (1984)]","","","","Oral 
Inhalation 
(R028)","Serum albumin (P02768) 
Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 1B1 (Q16678) 
(R060)","The ability of PAH's to bind to blood proteins such as albumin allows them to be transported throughout the body. Many PAH's induce the expression of cytochrome P450 enzymes, especially CYP1A1, CYP1A2, and CYP1B1, by binding to the aryl hydrocarbon receptor or glycine N-methyltransferase protein. These enzymes metabolize PAH's into their toxic intermediates. The reactive metabolites of PAHs (epoxide intermediates, dihydrodiols, phenols, quinones, and their various combinations) covalently bind to DNA and other cellular macromolecules, initiating mutagenesis and carcinogenesis. (R028, R060, R068, R073)","PAH metabolism occurs in all tissues, usually by cytochrome P-450 and its associated enzymes. PAHs are metabolized into reactive intermediates, which include epoxide intermediates, dihydrodiols, phenols, quinones, and their various combinations. The phenols, quinones, and dihydrodiols can all be conjugated to glucuronides and sulfate esters; the quinones also form glutathione conjugates. (R028)",,,"3, not classifiable as to its carcinogenicity to humans. (R264)","PAHs are released into the environment via the combustion of fossil fuels, coke oven emissions and vehicle exhausts, as well as naturally from forest fires and volcanic eruptions. PAHs from these sources may contaminate nearly water systems. They are also found in coal tar and charbroiled food. (R028)",,"PAHs are carcinogens and have been associated with the increased risk of skin, respiratory tract, bladder, stomach, and kidney cancers. They may also cause reproductive effects and depress the immune system. (R028)",Acute exposure to PAHs causes irritation and inflammation of the skin and lung tissue. (R034),There is no known antidote for PAHs. Exposure is usually handled with symptomatic treatment. (R028),P35869;Q14749;DNA
228,T3D0227,2009-03-06 18:58:19 UTC,2009-08-04 21:28:03 UTC,Cresols,Organic Compound;Solvent;Disinfectant;Aromatic Hydrocarbon,"1-Hydroxy-4-methylbenzene1-Methyl-4-hydroxybenzene4-(Pentafluorosulfanyl)phenol4-Cresol4-Hydroxytoluene4-Methylphenol4-methylphenol (p-cresol)Aluminum p-cresoxideCresolCresol (m-/p- mixture)Cresol, all isomersCresol, p-Cresol, p-isomerCresol, paraCresol, para-CresolsFEMA No. 2337FEMA Number 2337M,p-cresol mixtureO(m and p)-cresolP-cresol for synthesisP-cresylateP-cresylic acidP-hydroxytolueneP-kresolP-kresol [german]P-methyl phenolP-methylhydroxybenzeneP-methylphenolP-oxytolueneP-toluolP-tolyl alcoholPCRPara-cresolPara-cresylic acidParacresolParamethyl phenolPhenol, 4-methyl-Phenol, 4-methyl-, aluminum saltPhenol, methyl-RCRA waste number U052TOLUENE,4-HYDROXY (PARA-CRESOL)TricresolWLN: QR D1p-Cresol 98+ %p-Cresol Hydrate 90 %p-Cresol [UN2076] [Poison, Corrosive]","Cresols are organic methylphenol compounds that may occur naturally or be manufactured. Cresols can be solid or liquid because they have melting points not far from room temperature, and have an odor characteristic to that of other simple phenols, reminiscent to some of a ""medicine"" smell. Cresols are used as solvents, disinfectants and deodorizers, as well as to make other chemicals. They may be formed normally in the body from other compounds. Cresols are found in many foods and in wood and tobacco smoke, crude oil, coal tar, and in chemical mixtures used as wood preservatives. Small organisms in soil and water produce cresols when they break down materials in the environment. (R835)",,1319-77-3,2879,,C01468,"",25399,CPD-108,,C077977,Cresols,3936,,,http://en.wikipedia.org/wiki/p-Cresol,"InChI=1/C7H8O/c1-6-2-4-7(8)5-3-6/h2-5,8H,1H3",4-methylphenol,http://www.biospider.ca/saved_files/mol/9c46deb32b89f8733b161ac893178150_1237959660.mol,CC1=CC=C(O)C=C1,CC1=CC=C(O)C=C1,C7H8O,108.057510,Colorless solids or liquids.,35.5 °C,,,"",,,,"Oral
Inhalation
Dermal
(R835)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2C19 (P33261) 
Cytochrome P450 2D6 (P10635) 
Cytochrome P450 2E1 (P05181) 
Tyrosinase (P14679) 
Thyroid peroxidase (P07202) 
(R835) ","Target organs of ingested cresols in humans are the blood, kidneys, lungs, liver, heart, and central nervous system. Cresols impair the stratum corneum and produce coagulation necrosis by denaturating and precipitating proteins. They may also induce changes in neurotransmitter levels, affect the activities of some enzymes, increase lipid peroxidation, and change membrane fluidity in the brain. (R835) ","Cresols can be absorbed following inhalation, oral, and dermal exposure. Once in the body they can distribute rapidly into many organs and tissues. Cresols undergo oxidative metabolism in the liver and are rapidly eliminated, mostly in the urine, as sulfate or glucuronide conjugates. The activation of cresols by oxidation involves tyrosinase and thyroid peroxidase, forming a reactive quinone methide. Experiments with recombinant P-450s demonstrated cresol metabolism was mediated by several P-450s including CYP2D6, 2C19, 1A2, 1A1, and 2E1. (R835, R836, R837, R839) ","LD50: 1454 mg/kg (Oral, Rat) (R263)",,,"Cresols are used as solvents, disinfectants and deodorizers, as well as to make other chemicals. They may be formed normally in the body from other compounds. Cresols are found in many foods and in wood and tobacco smoke, crude oil, coal tar, and in chemical mixtures used as wood preservatives. Small organisms in soil and water produce cresols when they break down materials in the environment. Breathing air containing cresols is the primary source of exposure. Exposure may also result from drinking contaminated water, eating contaminated food and coming into contact with liquids containing cresols. (R835) ","Intermediate Oral: 0.1 mg/kg/day (R260) 
Chronic Oral: 0.1 mg/kg/day (R260)","Cresols breathed, ingested, or applied to the skin at very high levels can be very harmful because they are corrosive substances. Ingestion of high levels results in mouth and throat burns, abdominal pain, vomiting, kidney problems, and effects on the blood and nervous system. Skin contact with high levels of cresols can burn the skin and damage the kidneys, liver, blood, lungs, and brain. Tachycardia, respiratory failure, unconsciousness and death may occur in both cases. Many of these effects may not by caused directly by cresols, but may be a result of secondary reactions to shock caused by external and internal burns. (R782, R835)","Ingestion of cresols results in burning of the mouth and throat, abdominal pain, and vomiting. Inhalation or dermal exposure to cresols can produce irritation and corrosion at the site of contact. (R782) ","Following oral exposure, immediately dilute with 4 to 8 ounces (120 to 240 mL) of water or milk (not to exceed 4 ounces/120 mL in a child). Observe patients with ingestion carefully for the possible development of esophageal or gastrointestinal tract irritation or burns. If signs or symptoms of esophageal irritation or burns are present, consider endoscopy to determine the extent of injury. In case of hypotension, infuse isotonic fluid. If hypotension persists, administer dopamine or norepinephrine. In case of hypertension, monitor vital signs regularly. For mild/moderate asymptomatic hypertension (no end organ damage), pharmacologic treatment is generally not necessary. Following inhalation, move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with inhaled beta2 agonist and oral or parenteral corticosteroids. In case of acture lung injury, maintain ventilation and oxygenation and evaluate with frequent arterial blood gas or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed. Following eye exposure, irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes. Following dermal exposure, remove contaminated clothing and wash exposed area thoroughly with soap and water. Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines. (R624) ",P09172;P05164;P22079;P23219;P35354 
229,T3D0228,2009-03-06 18:58:19 UTC,2009-08-04 21:28:03 UTC,"Chlordane, technical",Organic Compound;Pesticide;Organochloride,".gamma.-chlordan1,3,4,7,8,9,10,10-octachlorotricyclo[5.2.1.0(2,6)]dec-8-ene:chlordaneAlpha-, gamma-chlordaneAlpha-chlordanAlpha-chlordaneAspon-chlordaneBELTC orodaneC-chlordaneCHLORDANE (TECHNICAL GRADE) (SEE ALSO 57-74-9)Caswell No. 174Caswell No. 174EChloordaanChloordaan [dutch]Chlor kilChlor killChlordanChlordaneChlordane (alpha and gamma isomers)Chlordane (analytical grade)Chlordane (avg cis-,trans-)Chlordane (technical grade)Chlordane (technical mixture and metabolites)Chlordane (technical mixture)Chlordane (trans)Chlordane , purChlordane, alpha & gamma isomersChlordane, liquidChlordane, technicalChlordane, technical gradeChlordane, technically gradeChlordane-technicalChlorindanChlorodaneChlorotoxChlortoxCis-chlordaneCis-photochlordaneClordanClordan [italian]ClordanoCompound kCompound k (fda)CorodaneCortilan-neuDichlorochlordeneDow-klorDowchlorGold crestIntoxIntox (insecticide)Intox 8Kilex lindaneKypchlorLatka 1068 [Czech]NiranOcta-klorOctach lorohexahydromethanoindeneOctachlorOctachlordaneOctachloro-4,7-methanohydroindaneOctachloro-4,7-methanotetrahydroindaneOctachlorodihydrodicyclopentadieneOctachlorohexahydromethanoindeneOindaneOktaterrOrtho-klorPhotochlordaneRCRA waste no. U036RCRA waste number U036StarchlorSydaneSyndaneSynklorT-chlordaneTat chlor 4Technical chlordaneTermexTermi-dedTopiclorToxichlorTrans-chlordanTrans-chlordaneUnexan-koederVelsicol 1068WLN: L C555 A IUTJ AG AG BG DG EG HG IG JGshell sd-5532topichlor 20topiclor 20","Chlordane is a manufactured chemical that was used as a pesticide in the United States from 1948 to 1988. Chlordane occurs in two isomers, called cis-chlordane (alpha-chlordane) and trans-chlordane (gamma-chlordane). (R158)",,12789-03-6,5993,,"","",25520,"",,D002706,"Chlordane, technical",6398,,,http://en.wikipedia.org/wiki/Literature,"InChI=1/C10H6Cl8/c11-3-1-2-4(5(3)12)9(16)7(14)6(13)8(2,15)10(9,17)18/h2-5H,1H2","",http://www.biospider.ca/saved_files/mol/,C1C2C(C(C1Cl)Cl)C3(C(=C(C2(C3(Cl)Cl)Cl)Cl)Cl)Cl,C1C2C(C(C1Cl)Cl)C3(C(=C(C2(C3(Cl)Cl)Cl)Cl)Cl)Cl,C10H6Cl8,405.797770,Colorless to amber liquid.,"",,,"",,,,"Oral 
Inhalation 
(R259)","Glutathione S-transferase P (P09211) 
Glutathione S-transferase Mu 1 (P09488) 
Glutathione S-transferase A1 (P08263) 
Glutathione S-transferase theta-2 (P30712) 
Glutathione S-transferase Mu 4 (Q03013) 
Glutathione S-transferase theta-1 (P30711) 
Glutathione S-transferase A4 (O15217) 
Glutathione S-transferase A2 (P09210) 
Glutathione S-transferase A3 (Q16772) 
Glutathione S-transferase Mu 3 (P21266) 
Glutathione S-transferase omega-1 (P78417) 
Glutathione S-transferase kappa 1 (Q9Y2Q3) 
Glutathione S-transferase Mu 2 (P28161) 
Glutathione S-transferase omega-2 (Q9H4Y5) 
Glutathione S-transferase A5 (Q7RTV2) 
Glutathione S-transferase Mu 5 (P46439) 
Glutathione S-transferase theta-4 (A8MPT4) 
Maleylacetoacetate isomerase (O43708) 
Microsomal glutathione S-transferase 1 (P10620) 
Microsomal glutathione S-transferase 2 (Q99735) 
Microsomal glutathione S-transferase 3 (O14880) 
(R159)","Chlordane is believed to bind irreversibly to DNA, leading to cell death or altered cellular function. It also affects transcription by antagonizing estrogen-related receptors. Chlordane induces hepatic cytochrome P-450, causing a large increase in the volume of the smooth endoplasmic reticulum, which results in hepatocellular enlargement and hypertrophy. Chlordane has also been shown to bind and activate retinoic acid receptor, causing various developmental defects, and inhibit alkaline phosphatases in hepatic and renal tissues. (R159, R162, R163, R205, R206)","Chlordane is highly lipophilic and is thus easily absorbed by ingestion, inhalation, and dermal exposure, then stored mainly in the fat. Chlordane is metabolized mainly in the liver and kidney. Metabolism is slow, and is believed to occur by multiple pathways involving cytochrome P-450 enzymes, glutathione-S-transferase type enzymes, and microsomal mixed-function oxidase systems. The metabolites are generally less toxic and include chlordene chlorohydrin, monohydroxylated dihydrochlordene, and oxychlordane. They are excreted in the urine and faeces. (R159)","LD50: 200 mg/kg (Oral, Rat) (R261) 
LD50: 343 mg/kg (Intraperitoneal, Rat) (R261) 
LD50: 10 mg/kg (Intravenous, Mouse) (R263) 
LD50: 780 mg/kg (Dermal, Rat) (R263) 
LC50: 100 mg/m3 over 4 hours (Inhalation, Cat) (R263)",100 mg/kg for an adult human. (R265),"2B, possibly carcinogenic to humans. (R264)",Chlordane was used as a pesticide. (R158),"Intermediate Inhalation: 0.0002 mg/m3 (R260) 
Chronic Inhalation: 0.00002 mg/m3 (R260) 
Acute Oral: 0.001 mg/kg/day (R260) 
Intermediate Oral: 0.0006 mg/kg/day (R260) 
Chronic Oral: 0.0006 mg/kg/day (R260)","Chlordane is a central nervous system stimulant, and can also damage the digestive system and the liver. Large doses are known to cause convulsions, respiratory failure, and death. Chlordane is also known to have adverse reproductive and developmental effects. (R159)","Ingestion and inhalation of chlordane cause headaches, irritability, confusion, weakness, vision problems, vomiting, stomach cramps, diarrhea, and jaundice. (R159)","Treatment is symptomatic. It is aimed at controlling convulsions, coma, and respiratory depression. Gastric lavage, followed by the administration of activated charcoal, may be performed following ingestion. (R282)",P05186;P20813;P08684;Q9HB55;P20815;P24462;DNA;P62508;P10826;P13631;P11474;O95718;P98194;O75185;P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P78334;Q8N1C3;P18507;Q99928;O00591;P24046;P28476;A8MPY1;Q9UN88;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;P54710;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P03372;Q92731
230,T3D0229,2009-03-06 18:58:19 UTC,2009-08-04 21:28:03 UTC,Dimethoate,Organic Compound;Pesticide;Organophosphate,"2-Dimethoxyphosphinothioylthio-N-methylacetamideAadimethoalAmerican Cyanamid 12,880BI 58 ECCaswell No. 358CekuthoateCygonCygon 2-ECygon 400Cygon 4ECygon insecticideDapheneDe-fendDefendDemos-L40DevigonDimate 267DimetateDimethoaat [dutch]Dimethoat Tech 95%Dimethoat [german]Dimethoate 30 ECDimethoate [ansi:bsi:iso]Dimethoate bayerDimethoate solutionDimethogenDimethyl s-((methylcarbamoyl)methyl) phosphorodithioateDimethyl s-(n-(methylcarbamoyl)methyl) phosphorodithioateDimetonDimevurExperimental Insecticide 12,880FIPFerkethionFortion NMFosfamidFosfamid (ussr)Fosfatox rFosfotoxFosfotox R 35Fosfotox rFostion MMFostion m mLurgoMaxima phlanzenschutzO,O-Dimethyl-S-(2-oxo-3-aza-butyl)-dithiophosphat [German]O,o-dimethyl methylcarbamoylmethyl phosphorodithioateO,o-dimethyl s-((methylcarbamoyl)methyl)phosphorodithioateO,o-dimethyl s-(n-methylcarbamoylmethyl) dithiophosphateO,o-dimethyl s-(n-methylcarbamoylmethyl) phosphorodithioateO,o-dimethyl s-(n-methylcarbamylmethyl) thiothionophosphateO,o-dimethyl s-methylcarbamoylmethyl phosphorodithioatePS659_SUPELCOPerfecthionPerfekthionPhosphamidPhosphamideRCRA waste no. P044RCRA waste number P044RacusanRebelateRogodanRogorRogor 20 LRogor 20LRogor 40Rogor lRogor pRoxionRoxion uaS-methylcarbamoylmethyl o,o-dimethyl phosphorodithioateSalutSevigorSinoratoxSisteminSolutSystemic insecticideSysteminSystoateTARATrimetionTurbairo,o-Dimethyl S-[2-(methylamino)-2-oxoethyl] dithiophosphate","Dimethoate is an organophosphate insecticide used to kill mites and insects systemically and on contact. It is used against a wide range of insects, including aphids, thrips, planthoppers and whiteflies on ornamental plants, alfalfa, apples, corn, cotton, grapefruit, grapes, lemons, melons, oranges, pears, pecans, safflower, sorghum, soybeans, tangerines, tobacco, tomatoes, watermelons, wheat and other vegetables. It is also used as a residual wall spray in farm buildings for house flies. Dimethoate has been administered to livestock for control of botflies. Dimethoate is moderately toxic and severe poisoning affects the central nervous system. (S683)",,60-51-5,3082,,C14326,"",34714,"",,D004117,Dimethoate,487,,,http://en.wikipedia.org/wiki/Dimethoate,"InChI=1/C5H12NO3PS2/c1-6-5(7)4-12-10(11,8-2)9-3/h4H2,1-3H3,(H,6,7)",2-dimethoxyphosphinothioylsulfanyl-N-methylacetamide,http://www.biospider.ca/saved_files/mol/818387433735d925dc285a8f07854e72_1237959862.mol,CNC(=O)CSP(=S)(OC)OC,CNC(=O)CSP(=S)(OC)OC,C5H12NO3PS2,228.999620,Dimethoate is a colorless crystalline solid with a camphor-like odor. (S683),52 °C,117 °C (390 K) at 10 Pa,1.3 g/cm3,"25 mg/mL at 21 °C [MARTIN,H & WORTHING,CR (1977)]",,107 °C,,Oral. Inhalation. Dermal. (S683),,Dimethoate is a cholinesterase inhibitor. (S683),,"LD50: 60 to 387 mg/kg (Oral, Rat)
LD50: 60 mg/kg (Oral, Mouse)
LD50: 400 mg/kg (Oral, Dog) 
LD50: 200 mg/kg (Oral, Hamster)
LD50: 300 mg/kg (Oral, Rabbit)
LD50: 350 mg/kg (Oral, Guinea pig)
LD50: 100 mg/kg (Oral, Cat)
LD50: 1,000 mg/kg (Dermal, Rabbit)
LD50: 353 mg/kg (Dermal, Rat)
LC50: 1.2 mg/l (Rat)",,,"Dimethoate is an organophosphate insecticide used to kill mites and insects systemically and on contact. It is used against a wide range of insects, including aphids, thrips, planthoppers and whiteflies on ornamental plants, alfalfa, apples, corn, cotton, grapefruit, grapes, lemons, melons, oranges, pears, pecans, safflower, sorghum, soybeans, tangerines, tobacco, tomatoes, watermelons, wheat and other vegetables. It is also used as a residual wall spray in farm buildings for house flies. Dimethoate has been administered to livestock for control of botflies. (S683)",,"Dimethoate is moderately toxic by ingestion, inhalation and dermal absorption. Severe eye irritation has occurred in workers manufacturing dimethoate. Severe poisoning affects the central nervous system. (S683)","The first symptoms include bloody or runny nose, coughing, chest discomfort, difficult or short breath, and wheezing due to constriction or excess fluid in the bronchial tubes. Skin contact may cause localized sweating and involuntary muscle contractions. Eye contact will cause pain, bleeding, tears, pupil constriction, and blurred vision. Other symptoms following any way of exposure may include pallor, nausea, vomiting, diarrhea, abdominal cramps, headache, dizziness, eye pain, blurred vision, constriction or dilation of the eye pupils, tears, salivation, sweating, and confusion. Severe poisoning will affect the central nervous system, producing incoordination, slurred speech, loss of reflexes, weakness, fatigue, involuntary muscle contractions, twitching, tremors of the tongue or eyelids, and eventually paralysis of the body extremities and the respiratory muscles. In severe cases there may also be involuntary defecation or urination, psychosis, irregular heart beats, unconsciousness, convulsions and coma. Death may be caused by respiratory failure or cardiac arrest. (S683)
","",""
231,T3D0230,2009-03-06 18:58:20 UTC,2009-08-25 19:52:05 UTC,Actinium-227,Inorganic Compound;Metal;Radioactive Isotope,"Actinium, isotope of mass 227Actinium-227","Actinium is a radioactive chemical element with the symbol Ac and atomic number 89. Actinium-227 is the naturally occurring radioactive isotope of actinium and has a half-life of 21.772 years. Actinium-227 is also produced in milligram amounts by the neutron irradiation of 226Ra in nuclear reactors. Actinium-227  is an alpha and beta emitter. It is extremely radioactive, and is even more dangerous than plutonium. Ingesting even small amounts would be fatal. (S565)",,14952-40-0,105152,,"","","","",,,Actinium-227,,,,,InChI=1/Ac/i1+0,actinium-227,http://www.biospider.ca/saved_files/mol/,[227Ac],[227Ac],Ac,0.000000,"Actinium is a silvery solid metal. Due to its intense radioactivity, actinium glows in the dark with a pale blue light. (S565)","1323 K (1050 °C, 1922 °F)","3471 K (3198 °C, 5788 °F)",10 g·cm−3 (room temperature),"",,,,"Oral
Inhalation
(W510)",,"The ionizing radiation produced by actinium causes cellular damage that includes DNA breakage, accurate or inaccurate repair, apoptosis, gene mutations, chromosomal change, and genetic instability. This leads to loss of normal cell and tissue homeostasis, and development of malignancy. Ionizing radiation that does not directly damage DNA can produce reactive oxygen intermediates that directly affect the stability of p53, an important enzyme in cell-cycle regulation, and produce oxidative damage to individual bases in DNA and point mutations by mispairing during DNA replication. (W510)",,,,,Actinium's radioactivity make it a valuable as a neutron source for energy. (S565),,Actinium is extremely radioactive and thus poses a dangerous cancer risk. It can also cause acute radiation syndrome. (S565),"Exposure to high doses of ionizing radiation results in acute radiation syndrome, which can cause skin burns, hair loss, nausea, vomiting, dizziness, disorientation, low blood pressure, headache, fatigue, weakness, fever, birth defects, illness, infection, and death. (W510, W525)","Treatment reversing the effects of irradiation is currently not possible. Anaesthetics and antiemetics are administered to counter the symptoms of exposure, as well as antibiotics for countering secondary infections due to the resulting immune system deficiency. (W525)",DNA
233,T3D0232,2009-03-06 18:58:20 UTC,2009-08-10 17:34:56 UTC,4-Aminobiphenyl,Organic Compound;Industrial Precursor/Intermediate;Aromatic Hydrocarbon;Amine,"(1,1'-Biphenyl)-4-amine(4-phenyl-phenyl)-amine4-Amino-1,1'-biphenyl4-Aminobifenyl4-Aminobifenyl [Czech]4-Aminodifenil4-Aminodifenil (spanish)4-Aminodifenil [Spanish]4-Aminodiphenyl4-Bifenylamin4-Bifenylamin [Czech]4-Biphenylamine4-Biphenylylamine4-Phenylaniline4-biphenylamine hydrochloride4-biphenylnitrenium ionA2898_SIGMAAminobiphenylAniline, p-phenyl-BiphenylamineP-aminobiphenylP-aminodiphenylP-biphenylamineP-phenylanilineP-xenylamineParaaminodiphenylWLN: ZR DRXenylaminXenylamin (czech)Xenylamin [czech]Xenylamine[1,1'-Biphenyl]-4-amine[1,1'-biphenyl]-4-amine (ACD/Name 4.0)[1,1'-biphenyl]-4-ylamine (ACD/Name 4.0)biphenyl-4-aminebiphenyl-4-ylamine{[1,1'-Biphenyl]-4-amine}","4-Aminobiphenyl is a derivative of biphenyl used to manufacture azo dyes. As it is a known human carcinogen, it has been largely replaced by less toxic compounds. However, 4-aminobiphenyl may still be found in tobacco smoke. (V357, V359)",,92-67-1,7102,,C10998,"",1784,N-HYDROXY-4-AMINOBIPHENYL,,C006757,4-Aminobiphenyl,70,,,http://en.wikipedia.org/wiki/4-Aminobiphenyl,"InChI=1/C12H11N/c13-12-8-6-11(7-9-12)10-4-2-1-3-5-10/h1-9H,13H2",4-phenylaniline,http://www.biospider.ca/saved_files/mol/4ac959e079062767ae3e5e9a77277c83_1237960103.mol,C1=CC=C(C=C1)C2=CC=C(C=C2)N,C1=CC=C(C=C1)C2=CC=C(C=C2)N,C12H11N,169.089150,,53.5 °C,,,"",,,,"Oral
Inhalation
Dermal
(R624)","Cytochrome P450 1A2 (P05177)
Sulfotransferase 1A1 (P50225)
Arylamine N-acetyltransferase 2 (P11245)
Hemoglobin subunit alpha (P69905)
Hemoglobin subunit beta	(P68871)
Hemoglobin subunit delta (P02042)
Hemoglobin subunit epsilon (P02100)
Hemoglobin subunit gamma-1 (P69891)
Hemoglobin subunit gamma-2 (P69892)
Hemoglobin subunit mu (Q6B0K9)
Hemoglobin subunit theta-1(09105)
Hemoglobin subunit zeta	(P02008)
(V358, V359, V360, V361)","4-Aminobiphenyl requires metabolic activation in order to exert its toxicity. This is catalyzed by N-hydroxylation via cytochrome P450 1A2, then followed by O-sulfation and O-acetylation by sulfotransferase 1A1 and arylamine N-acetyltransferase 2. The metabolites of 4-aminobiphenyl may form adducts with DNA, inducing mutations. 4-Aminobiphenyl and its metabolites may also cross the placenta and have fetal effects. (V358, V359, V360, V361)","4-Aminobiphenyl exposure can be assayed by measuring the extent of adduct formation with hemoglobin. 4-Aminobiphenyl metabolism is catalyzed by N-hydroxylation via cytochrome P450 1A2. It is then followed by O-sulfation and O-acetylation by sulfotransferase 1A1 and arylamine N-acetyltransferase 2. The urinary metabolites of 4-aminobiphenyl include 4-acetylaminobiphenyl, 4'-hydroxy-4-aminobiphenyl, 2'-hydroxy-4-acetylaminobiphenyl, 4'-hydroxy-4-acetylaminobiphenyl, 3'-hydroxy, 4'-methoxy-4-acetylaminobiphenyl, 4'-hydroxy, 3'-methoxy-4-acetylaminobiphenyl, and 3',4'-dihydroxy-4-acetylaminobiphenyl. (R624, V361)","LD50: 205 mg/kg (Oral, Mouse) (R263)",,"1, carcinogenic to humans. (R264)","4-Aminobiphenyl is used to manufacture azo dyes and is also found in tobacco smoke. (V357, V359)",,"4-Aminobiphenyl is a known human carcinogen. It may also cause methemoglobinemia. (R264, R624)","Symptoms of 4-aminobiphenyl may include dyspnea, headache, dizziness, lethargy, and ataxia. (R624)","",DNA
234,T3D0233,2009-03-06 18:58:20 UTC,2009-08-04 21:28:04 UTC,Pyrethrum,Organic Compound;Pesticide;Pyrethroid,"(+)-pyrethronyl (+)-pyrethrateBuhachCaswell No. 716Chrysanthemum cinerareaefoliumChrysanthemumdicarboxylic acid monomethyl ester pyrethrolone esterCinerin I or IIDalmatian insect powderDalmation insect flowersFirmotoxInsect powderInsecticides, pyrethrinsJasmolin I or IIPersian insect powderPrentox pyrethrum extractPyrenonePyrethres [iso-french]PyrethrinPyrethrin I or IIPyrethrin IIPyrethrin II [bsi:iso]Pyrethrine II [iso-french]PyrethrinsPyrethrins [bsi:iso]Pyrethrins and pyrethroidsPyrethroidsPyrethrolone ester of chrsanthemumdicarboxylic acid monomethyl esterPyrethrumPyrethrum (insecticide)Pyrethrum powder other than pyrethrinsPyretrin IIPyrocidePyronylTrieste flowers","A pyrethroid is a synthetic chemical compound similar to the natural chemical pyrethrins produced by the flowers of pyrethrums (Chrysanthemum cinerariaefolium and C. coccineum). Pyrethroids are common in commercial products such as household insecticides and insect repellents. In the concentrations used in such products, they are generally harmless to human beings but can harm sensitive individuals. They are usually broken apart by sunlight and the atmosphere in one or two days, and do not significantly affect groundwater quality except for being toxic to fish. (S081)",,8003-34-7,6433155,,C14941,"",39098,"",,,Pyrethrum,8193,,,http://en.wikipedia.org/wiki/Pyrethrum,"InChI=1/C22H28O5/c1-7-8-9-10-15-14(3)18(12-17(15)23)27-21(25)19-16(22(19,4)5)11-13(2)20(24)26-6/h7-9,11,16,18-19H,1,10,12H2,2-6H3/b9-8+,13-11+/t16-,18+,19+/m1/s1","[(1S)-2-methyl-4-oxo-3-[(2E)-penta-2,4-dienyl]cyclopent-2-en-1-yl] (1R,3R)-3-[(E)-3-methoxy-2-methyl-3-oxoprop-1-enyl]-2,2-dimethylcyclopropane-1-carboxylate",http://www.biospider.ca/saved_files/mol/,CC1=C(C(=O)C[C@@H]1OC(=O)[C@@H]2[C@H](C2(C)C)/C=C(\C)/C(=O)OC)C/C=C/C=C,CC1=C(C(=O)CC1OC(=O)C2C(C2(C)C)C=C(C)C(=O)OC)CC=CC=C,C22H28O5,372.193670,,76 °C,,,"",,,,"Oral
Inhalation
Dermal
(S135)",,"Both type I and type II pyrethroids exert their effect by prolonging the open phase of the sodium channel gates when a nerve cell is excited. They appear to bind to the membrane lipid phase in the immediate vicinity of the sodium channel, thus modifying the channel kinetics. This blocks the closing of the sodium gates in the nerves, and thus prolongs the return of the membrane potential to its resting state. The repetitive (sensory, motor) neuronal discharge and a prolonged negative after potential produce effects quite similar to those produced by DDT, leading to hyperactivity of the nervous system which can result in paralysis and/or death. Other mechanisms of action of pyrethroids include antagonism of gamma-aminobutyric acid (GABA)-mediated inhibition, modulation of nicotinic cholinergic transmission, enhancement of noradrenaline release, and actions on calcium ions. They also inhibit calcium channels and Ca2+, Mg2+-ATPase. (R029, R276, S135)","Following ingestion, pyrethriods are hydrolysed by various digestive enzymes in the gastro-intestinal tract. However, a small portion of the insecticidally active compounds or its derivatives are absorbed, as shown by their toxicity and their effect on the liver. Pyrethriods may also be absorbed following inhalation or dermal contact. They are rapidly distributed to most tissues, particularly to those with a high lipid content, and are concentrated in central and peripheral nervous tissues. Pyrethriods or their metabolites are not known to be stored in the body or to be excreted in the milk, but no study of the matter has employed modern methods. The major metabolic pathways for pyrethriods are hydrolysis of the central ester bond, oxidative attacks at several sites, and conjugation reactions, to produce a complex array of primary and secondary water-soluble metabolites that undergo urinary excretion. Metabolism is believed to involve nonspecific microsomal carboxyesterases and microsomal mixed function oxidases, which are located in nearly all tissue types, with particularly high activities in the liver. Metabolites are excreted in the urine and faeces. (S135, S189)",,,,Pyrethroids are used as insecticides. (S135),,"Pyrethroid effects typically include rapid onset of aggressive behavior and increased sensitivity to external stimuli, followed by fine tremor, prostration with coarse whole body tremor, elevated body temperature, coma, and death. Paresthesia, severe corneal damage, hypotension and tachycardia, associated with anaphylaxis, can also occur following pyrethriod poisoning. (S135)","Spilling on the head, face and eyes can result in  pain, lacrimation, photophobia, congestion, and edema of the conjunctiva and eyelids. Ingestion causes epigastric pain, nausea, vomiting, headache, dizziness, anorexia, fatigue, tightness in chest, blurred vision, paresthesia, palpitations, coarse muscular fasciculations, and disturbances of conciousness. In severe poisonings, convulsive attacks with opisthotonos and loss of conciousness have occurred. (R029)","Following oral exposure, the treatment is symptomatic and supportive and includes monitoring for the development of hypersensitivity reactions with respiratory distress. Provide adequate airway management when needed. Gastric decontamination is usually not required unless the pyrethrin product is combined with a hydrocarbon. Following inhalation exposure, move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with inhaled beta2 agonist and oral or parenteral corticosteroids. In case of eye exposure, irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist, the patient should be seen in a health care facility. If the contamination occurs through dermal exposure, remove contaminated clothing and wash exposed area thoroughly with soap and water. A physician may need to examine the area if irritation or pain persists. Vitamin E topical application is highly effective in relieving paresthesias. (R624) ",P35498;Q9Y5Y9;Q9UI33;Q99250;Q9NY46;P35499;Q14524;Q01118;Q9UQD0;Q15858;Q07699;O60939;Q9NY72;Q8IWT1;Q96D31;Q12791;P98194;O75185;P16615;O14983
235,T3D0234,2009-03-06 18:58:20 UTC,2009-08-26 14:28:22 UTC,Arsine,Inorganic Compound;Arsenic Compound,"ARSARSENIC, 99.999%ASAgent saArsenArsen [german,polish]Arsenic [UN1558] [Poison]Arsenic and arsenic compoundsArsenic and certain arsenic compoundsArsenic and compoundsArsenic atomic absorption standard solutionArsenic blackArsenic compoundsArsenic elementalArsenic hydridArsenic hydrideArsenic hydride (AsH3)Arsenic trihydrideArsenic, elementalArsenic, inorganicArsenic, organic compoundsArsenic, water-soluble compounds, n.o.sArsenic, water-soluble compounds, n.o.s.Arsenic-75ArsenicalsArsenicoArsenicumArsenicum Album 3ch-30ch GranulesArsenicum Drops D3-C1000Arsenicum Iodatum 3ch-30chArseniuretted hydrogenArsenous hydrideArsenowodorArsenowodor [polish]ArsenwasserstoffArsenwasserstoff [german]ArsineArsine [UN2188] [Poison gas]AsH3CACColloidal arsenicCompounds, arsenicGray arsenicGrey arsenicHydrogen arsenideMetallic arsenicTrisenox","Arsine is a highly toxic gas formed when arsenic-containing materials react with hydrogen in water or acids. It is nonirritating and colorless, with a slight garlic odor. (R030)",,7784-42-1,5359596,,C06269,"",47217,CPD-763,,C006633,Arsine,6368,,,http://en.wikipedia.org/wiki/Arsenic,InChI=1S/AsH3/h1H3,arsane,"",[AsH3],[AsH3],AsH3,74.921600,Colorless gas.,> 615 °C,−62.5 °C,"4.93 g/l, gas; 1.640 g/mL","","","","",Inhalation,"","Arsine enters the bloodstream and crosses the alveolo-capillary membrane into red blood cells. Here it preferentially binds to hemoglobin and is oxidized to an arsenic dihydride intermediate and elemental arsenic, both of which are hemolytic agents. Arsine also depletes the reduced glutathione content of the red blood cells, resulting in the oxidation of sulfhydryl groups in hemoglobin and red cell membranes. These effects produce membrane instability, resulting in hemolysis. Arsine may also inhibit catalase, which leads to the accumulation of hydrogen peroxide. This destroys red cell membranes and may contribute to arsine-induced conversion of Fe+2 to Fe+3, which also impairs oxygen transport. (R030)","Arsine is gradually converted to arsenite (As3+), then methylated into monomethylarsonic and dimethylarsinic acids. It is primarily excreted in the urine. (R286)","LC50: 390 mg/m3 (Inhalation, Rat)",250 ppm or 25 to 50 ppm over a half-hour period for adult humans.,"1, carcinogenic to humans. (R264)","Exposure to arsine usually occurs in an industrial setting, as it is often produced as a byproduct during the smelting and refining of metals. It is also used in the manufacture of semiconductors and crystals for fiberoptics and computer chips.",Chronic Inhalation: 0.016 mg/m3,"Arsine exposure causes haemolytic anaemia, polyneuropathy, hypotension, and damage to the lungs, kidneys, liver, nervous system, heart, and blood-forming organs. (R030)","The first signs of arsine exposure are difficultly breathing, headaches, vertigo, nausea, vomiting, abdominal pain, skin discoloration, and haemoglobinuria. (R030)","There is no antidote for arsine. Treatment is symptomatic and consists of measures to support respiratory, vascular, and renal function. Whole blood transfusions may be effective if significant haemolysis has occured. (R030)",P69905;P68871;P69891;P69892;P02042;P02100;P09105;P02008;P04040;Q6B0K9
236,T3D0235,2009-03-06 18:58:20 UTC,2009-08-04 21:28:04 UTC,Naled,Organic Compound;Pesticide;Organochloride;Organobromide;Organophosphate,"1,2-Dibromo-2,2-Dichloroethyl dimethyl phosphate1,2-Dibromo-2,2-dichloroethyl dimethyl phosphatic acidAlvoraArthodibromBRPBromchlophosBromexBromex (insecticide)Bromex 50C4H7Br2Cl2O4PCaswell No. 586DibromDibromfosDimethyl 1,2-dibromo-2,2-dichloroethyl phosphateEthanol, 1,2-dibromo-2,2-dichloro-, dimethyl phosphateFlibol exFosbromHibromNaledNaled [ansi:bsi:iso]Naled dibromo-Naledu [polish]NikabromO,O-Dimethyl-O-(1,2-dibromo-2,2-dichloroethyl)phosphateO,O-dimethyl O-2,2-dichloro-1,2-dibromoethyl phosphateOrtho Dibrom 8EOrtho-dibromOrthodibromodimethyl-1,2-dibromo-2,2-dichloroethyl phosphateo-Dibrom 8E","Naled is an organophosphate insecticide registered since 1959 for use in the United States. Naled is used primarily to control adult mosquitoes but also is used on food and feed crops and in greenhouses. The mode of action of naled is as a nonsystemic contact and stomach poison. State and local authorities apply naled by truck-mounted or aircraft-mounted sprayers. Because of the very small quantities of pesticide applied, naled does not pose a moderate or serious health risk if applied according to the guidelines for use. One of the degradation products of naled is dichlorvos, another registered organophosphate. (S689)",,300-76-5,4420,,"","",38729,5-TERT-BUTYLAMINOL-2-HYDROXYPRO-1234-TET,,D009267,Naled,6490,,,,"InChI=1/C4H7Br2Cl2O4P/c1-10-13(9,11-2)12-3(5)4(6,7)8/h3H,1-2H3","(1,2-dibromo-2,2-dichloroethyl) dimethyl phosphate",http://www.biospider.ca/saved_files/mol/,COP(=O)(OC)OC(C(Cl)(Cl)Br)Br,COP(=O)(OC)OC(C(Cl)(Cl)Br)Br,C4H7Br2Cl2O4P,377.782580,Colorless solid or straw-colored liquid with a slightly pungent odor. (S689),27 °C,110 °C at 5 mm Hg (technical) ,,0.0015 mg/mL [USDA PESTICIDE PROP DATABASE],1.96,,,Oral. Inhalation. Dermal. (S689),,Naled is a cholinesterase inhibitor. (S689),"Naled can be absorbed into the body by inhalation, dermal contact, and ingestion. It does not accumulate in body tissues, but repeated exposure may have a cumulative effect on cholinesterase levels. Naled is hydrolysed rapidly in the body to produce a number of metabolites, including dichlorvos, dichlorobromoacetaldehyde, dimethyl phosphate, and an amino acid conjugate of degraded naled. (S689)",,,,"Major routes of exposure are by application from fog and mist sprayers. The use of application by aircraft increases the potential for exposure of humans and nontarget organisms to naled. Human exposure to naled during mixing, handling, application, and reentry operations can be minimized by use of approved respirators and other protective clothing. (S689)",,"Naled primarily affects the nervous system through cholinesterase inhibition, by which there is a deactivation of cholinesterase, an enzyme required for proper nerve functioning. Lab studies have shown liver damage in rats. (S691)","If inhaled, effects on the respiratory system and the eyes are the first to appear. (S689)","",P03372;Q92731
237,T3D0236,2009-03-06 18:58:20 UTC,2009-08-25 16:18:02 UTC,Chlorinated dibenzofurans,Organic Compound;Industrial By-product/Pollutant;Aromatic Hydrocarbon;Organochloride;Dibenzofuran,"1-CHLORODIBENZOFURANDibenzofuran, 1-chloroDibenzofuran, chloro-Dibenzofurans, chlorinatedMonochlorodibenzofuran","Chlorinated dibenzofurans (CDFs) are a family of chemicals that contain one to eight chlorine atoms attached to the carbon atoms of the parent chemical, dibenzofuran. The CDF family contains 135 individual compounds (known as congeners) with varying harmful health and environmental effects. Of these 135 compounds, those that contain chlorine atoms at the 2,3,7,8-positions of the parent dibenzofuran molecule are especially harmful. Other than for laboratory use of small amounts of CDFs for research and development purposes, these chemicals are not deliberately produced by industry. Most CDFs are produced in very small amounts as unwanted impurities of certain products and processes utilizing chlorinated compounds. Only a few of the 135 CDF compounds have been produced in large enough quantities so that their properties, such as color, smell, taste, and toxicity could be studied. (S290)",,"42934-53-2

",55293,,"","","","",,,Chlorinated dibenzofurans,,,,,InChI=1/C12H7ClO/c13-9-5-3-7-11-12(9)8-4-1-2-6-10(8)14-11/h1-7H,1-chlorodibenzofuran,http://www.biospider.ca/saved_files/mol/,C1=CC=C2C(=C1)C3=C(O2)C=CC=C3Cl,C1=CC=C2C(=C1)C3=C(O2)C=CC=C3Cl,C12H7ClO,202.018540,Colorless crystals.,"",,,"",,,,"Occupational exposure to dibenzofuran may occur through inhalation and dermal contact, particularly at sites where coal tar, coal tar derivatives, and creosote are produced and used. Consumption of contaminated water and food are the primary sources of exposure for the general population. (S290)",,"Dibenzofurans bind the aryl hydrocarbon receptor, which increases its ability to activate transcription in the XRE promoter region. This alters the expression of a number of genes. (S285)","No information on the metabolism of dibenzofuran in mammalian organisms was found in the available literature. The bacteria Sphingomonas, Brevibacterium, Terrabacter, and Staphylococcus auricularis degrade dibenzofuran to 2,2',3-trihydroxybiphenyl via dibenzofuran 4,4a-dioxygenase. (S290)",,,"3, not classifiable as to its carcinogenicity to humans. (R264)","CDFs are created from production of coal tar and during incineration. They are used as insecticides, in the production of PVC, and in industrial bleaching. (S290)",,"CDFs cause vomiting and diarrhea, anemia, more frequent lung infections, numbness and other effects on the nervous system, and mild changes in the liver. However, there were no permanent liver changes or definite liver damage found in  people who ingested CDFs. (S290)","Skin and eye irritations, especially severe acne, darkened skin color, and swollen eyelids with discharge are the most obvious health effects of the CDF poisoning. (S290)",,P03372;Q92731;P35869
238,T3D0237,2009-03-06 18:58:20 UTC,2009-08-10 17:53:01 UTC,Ethoprop,Organic Compound;Pesticide;Organophosphate,"Caswell No. 434CEthopropEthoprop [ansi]Ethoprophos [bsi:iso]JOLTMOBIL V-C 9-104MocapMocap 10gO-Ethyl S,S-dipropyl phosphorodithioate (8CI)O-Ethyl S,S-dipropyl phosphorodithioate (8CI)(9CI)O-ethyl s,s-dipropyl dithiophosphateO-ethyl s,s-dipropyl phosphorodithioateO-ethyl s,s-dipropylphosphorodithioateO-ethyl-s,s-dipropyl phosphorodiothioateO-ethyl-s,s-dipropyl phosphorodithionatePS672_SUPELCOPhophosPhosethopropPhosphorodithioic acid o-ethyl s,s-dipropyl esterPhosphorodithioic acid, o-ethyl s,s-dipropyl esterProphosRovokilS,s-dipropyl o-ethyl phosphorodithioateV-C Chemical V-C 9-104Virginia-carolina vc 9-104","Ethoprop is an organophosphate acetylcholinesterase inhibitor used as an insecticide. It is extremely toxic to mammals. (S697, V362)",,13194-48-4,3289,,"","",38665,"",,C001182,Ethoprop,7765,,,http://en.wikipedia.org/wiki/Ethoprop,"InChI=1/C8H19O2PS2/c1-4-7-12-11(9,10-6-3)13-8-5-2/h4-8H2,1-3H3",1-[ethoxy(propylsulfanyl)phosphoryl]sulfanylpropane,http://www.biospider.ca/saved_files/mol/,CCCSP(=O)(OCC)SCCC,CCCSP(=O)(OCC)SCCC,C8H19O2PS2,242.056410,Ethoprop is a clear yellow-tinted liquid with a strong mercaptan odor. (S697),-13 °C,86-91 °C at 0.2 mmHg. ,,"0.75 mg/mL at 25 °C [WAUCHOPE,RD et al.(1991A)]",,,,"Oral
Inhalation 
Dermal 
(V362)",,"Ethoprop inhibits acetylcholinesterase. This results in the accumulation of acetylcholine in the nerve synapses, causing overstimulation of the nervous system. (V362)","The urinary metabolites of ethoprop include O-ethyl-S-propyl phosphorothioic acid, O-ethyl-phosphoric acid, and desethyl ethoprophos. (V362)","LD50: 56.2 mg/kg (Oral, Male Rat) (S697)
LD50: 30.2 mg/kg (Oral, Female Rat) (S697)
LD50: 23.7 ul/kg (Dermal, Rabbit) (S697)
LD50: 60 mg/kg  (Percutaneous, Rat) (R263)
LC50: 250 mg/L over 4 hours (Inhalation, Rat) (V362)",,,Ethoprop is used as an insecticide. (V362),,Ethoprop affects the central nervous system and can also cause respiratory difficulties. (V362),"Early symptoms of poisoning may include excessive sweating, headache, weakness, giddiness, nausea, vomiting, hypersalivation, stomach pains, blurred vision, slurred speech and muscle twitching. Later, there may be convulsions and coma. (V362)
","If the pesticide has been ingested, rapid gastric lavage should be performed using 5% sodium bicarbonate. For skin contact, the skin should be washed with soap and water. If the compound has entered the eyes, they should be washed with large quantities of isotonic saline or water. In serious cases, atropine and/or pralidoxime should be administered. (V362)",P22303
241,T3D0240,2009-03-06 18:58:21 UTC,2009-08-13 22:20:00 UTC,Dichlorvos,Organic Compound;Pesticide;Organochloride;Organophosphate,"(2, 2-Dichlor-vinyl)-dimethyl-phosphat(2, 2-Dichlor-vinyl)-dimethyl-phosphat (GERMAN)(2, 2-Dichloro-vinil)dimetil-fosfato(2, 2-Dichloro-vinil)dimetil-fosfato (ITALIAN)(2,2-Dichloor-vinyl)-dimethyl-fosfaat(2,2-Dichloor-vinyl)-dimethyl-fosfaat (Dutch)(2,2-Dichloor-vinyl)-dimethyl-fosfaat [Dutch](2,2-Dichlor-vinyl)-dimethyl-phosphat(2,2-Dichlor-vinyl)-dimethyl-phosphat [German](2,2-Dichloro-vinil)dimetil-fosfate(2,2-Dichloro-vinil)dimetil-fosfato(2,2-Dichloro-vinil)dimetil-fosfato [Italian](2,2-Dichlorovinyl)-dimethyl-fosfate0, 0-Dimethyl 0-2,2-dichlorovinyl phosphate0,0-Dimethyl 0-2,2-dichlorovinyl phosphate2,2-Dichloroethenyl dimethyl phosphate2,2-Dichlorovinyl dimethyl phosphate2,2-Dichlorovinyl-O,O- dimethyl phosphate2,2-Dichlorovinyl-O,O-dimethyl phosphate2,2-Dimethyldichlorovinyl phosphate2,2-dichloroethenol dimethyl phosphate2,2-dichloroethenyl phosphoric acid dimethyl ester2,2-dichlorovinyl alcohol dimethyl phosphate2,2-dichlorovinyl dimethyl phosphate (ACD/Name 4.0)2,2-dichlorovinyl dimethyl phosphoric acid ester:dichlorvosAlgardApavapAstrobotAtgardAtgard (TN)Atgard cAtgard vBenfosBibesolBrevinylBrevinyl E 50Brevinyl E-50C4H7Cl2O4PCanogardCaswell No. 328CekusanChlorvinphosCyanophosCyponaDDVFDDVPDDVP (insecticide)De devapDedevapDelevapDenkaveponDeribanDerribanDerribanteDes (phosphate)DethlacDevikolDichlo rvos [dimethyl dichlorvinyl phosphate]DichlofosDichloorvoDichloorvo [dutch]Dichloorvo(dutch)DichlorfosDichlorfos [polish]Dichlorfos(polish)DichlormanDichloroethenyl dimethyl phosphateDichlorophosDichlorovasDichlorovosDichlorphosDichlorvosDichlorvos (DDVP)Dichlorvos (usan/inn)Dichlorvos (vapona)Dichlorvos [bsi:iso]Dichlorvos [dimethyl dichlorvinyl phosphate]Dichlorvos [usan:ban:inn]Dichlorvos [usan:inn:ban]Dichlorvos solutionDichlorvos(usan)Dichlorvosum [inn-latin]DiclorvosDiclorvos [inn-spanish]DihlorvosDimethyl 2,2-dichloroethenyl phosphateDimethyl 2,2-dichlorovinyl phosphateDimethyl O, O-dichlorovinyl-2,2-phosphateDimethyl O,O-dichlorovinyl-2,2-phosphateDimethyl dichlorovinyl phosphateDimethyldichlorovinyl phosphateDivipanDuo-killDuravosEquigandEquigardEquigelEquiguardEstroselEstrosolEthenol, 2, 2-dichloro-, dimethyl phosphateEthenol, 2,2-dichloro-, dimethyl phosphateFLY fighterFLY-dieFecamaFekamaHerkaHerkalHerkolInsectigas dKrecalvinLindanLindanmafuMAFUMafu stripMarvexMopariNUVANefrafosNerkolNo-pestNo-pest stripNogosNogos 50Nogos 50 ECNogos gNovotoxNuvanNuvan 100 ECNuvan 7Nuvan top aerosolNuvanolO, o-dimethyl dichlorovinyl phosphateO,O-DIMETHYL-O(2,2-DICHLOROVINYL)-PHOSPHATEO,O-Dimethyl-O-(2, 2-dichlor-vinyl)-phosphatO,O-Dimethyl-O-(2, 2-dichlor-vinyl)-phosphat (GERMAN)O,O-Dimethyl-O-(2,2-dichlor-vinyl)-phosphatO,O-Dimethyl-O-(2,2-dichlor-vinyl)-phosphat [German]O,O-dimethyl 2,2-dichlorovinyl phosphateO,O-dimethyl O-2,2-dichlorovinyl phosphateO,o-di methyl dichlorovinyl phosphateO,o-dimethyl dichlorovinyl phosphateO,o-dwumetylo-o-dwuchlorowinylofosforan [polish]O-(2,2-Dichlorvinyl)-O,O-dimethylphosphat [German]O-(2,2-Dichlorvinyl)-O,O-dimethylphosphateO-O-Dimethyl-O(2,2-dichlorovinyl)phosphateOKOPS89_SUPELCOPanaplatePho sphoric acid 2,2-dichloroethenyl dimethyl esterPhosphate de dimethyle et de 2,2-dichlorovinylePhosphate de dimethyle et de 2,2-dichlorovinyle (FRENCH)Phosphate de dimethyle et de 2,2-dichlorovinyle [French]Phosphate, 2-2-dichlorovinyl dimethylPhosphoric acid 2,2 dichloroethenyl dimethyl esterPhosphoric acid 2,2-dichloroethenyl dimethyl esterPhosphoric acid 2,2-dichlorovinyl dimethyl esterPhosphoric acid, 2,2-dichloroethenyl dimethyl esterPhosphoric acid, 2,2-dichlorovinyl dimethyl esterPhosvitPrentoxSzklarniakTAP 9VPTASKTask tabsTenacTenox BHTTetravosTopanolUDVFUnifosUnifos (pesticide)Unifos 50 ECUniphosUnitoxVaponaVapona insecticideVaponiteVapora IIVerdicanVerdiporVerdisolVinyl alcohol, 2,2-dichloro-, dimethyl phosphateVinylofosVinylophosWLN: GYGU1OPO&O1&O1Winylophosbrevinyl e50nuvan 100eco-(2, 2-Dichlorvinyl)-O,O-dimethylphosphato-(2, 2-Dichlorvinyl)-O,O-dimethylphosphat (GERMAN)o-(2,2-Dichlorvinyl)-O,O-dimethylphosphat","Dichlorvos or 2,2-dichlorovinyl dimethyl phosphate (DDVP) is a highly volatile organophosphate insecticide, widely used as a fumigant, which acts as both a contact and a stomach poison. Many organophosphates are potent nerve agents, functioning by inhibiting the action of acetylcholinesterase (AChE). Organophosphates are one of the most common causes of poisoning worldwide, and are frequently intentionally used in suicides in agricultural areas. The United States Environmental Protection Agency first considered a ban on DDVP in 1981. Since then it has been close to being banned on several occasions, but continues to be available. Major concerns are over acute and chronic toxicity. There is no conclusive evidence of carcinogenicity to date. (S654)(S657)",,62-73-7,3039,,C14430,"",34690,PANTOYL-LACTONE,,D004006,Dichlorvos,454,,,http://en.wikipedia.org/wiki/Dichlorvos,"InChI=1/C4H7Cl2O4P/c1-8-11(7,9-2)10-3-4(5)6/h3H,1-2H3","2,2-dichloroethenyl dimethyl phosphate",http://www.biospider.ca/saved_files/mol/0027d0cfc8e66a2e10b420f2dacbe55b_1237961158.mol,COP(=O)(OC)OC=C(Cl)Cl,COP(=O)(OC)OC=C(Cl)Cl,C4H7Cl2O4P,219.945900,Colorless liquid.,< 25 °C,> 184°C (363°F ),,8 mg/mL at 20 °C [USDA PESTICIDE PROP DATABASE],0.825 g/mL (20°C),,,Oral. Inhalation. Dermal. (S660),,Organophosphates apparently share a common mechanism of cholinesterase inhibition and cause similar symptoms. Organophosphates poison insects and mammals primarily by phosphorylation of the acetylcholinesterase enzyme (AChE) at nerve endings. The result is a loss of available AChE so that the effector organ becomes overstimulated by the excess of acetylcholine (Ach) in the nerve ending. (S660),,"LD50: 56 mg/kg (Oral, Rat) (S659)
LC50: 198 mg/m3 (Inhalation, Rat) (S659)
LD50: 205 mg/kg (Dermal, Rabbit) (S659)",,,"Organophosphates are used in agriculture, in the home, in gardens, and in veterinary practice. (S660)",,Dichlorvos is neurotoxic. (S660),"The effects of organophosphate poisoning are recalled using the mnemonic SLUDGEM (Salivation, Lacrimation, Urination, Diaphoresis (or Defecation), Gastrointestinal motility, Emesis, Miosis). (S657)","Atropine can be used as an antidote in conjunction with pralidoxime. Atropine blocks the parasympathetic nervous system, both vagal effects on the heart. (S657)",P03372;Q92731
242,T3D0241,2009-03-06 18:58:21 UTC,2009-08-04 21:28:05 UTC,Calcium arsenate,Inorganic Compound;Arsenic Compound,"Arseniate de calcium (french)Arsenic acid (H3AsO4), calcium salt (2:3)Arsenic acid, calcium saltArsenic acid, calcium slt (2:3)Calcium arsenateCalcium arsenate (Ca3(AsO4)2)Calcium arsenate [UN1573] [Poison]Calcium arsenate [arsenic and certain arsenic compounds]Calcium orthoarsenateCalcium-o-arsenateChip-cal granularCucumber dustKalziumarseniat (german)PencalSpra-calTricalcium arsenate","Calcium arsenate is a chemical compound or arsenic, made especially toxic by its high solubility in water. (R1106)",,7778-44-1,24501,,"","","","",,C045817,Calcium arsenate,,,,,"InChI=1/2AsH3O4.3Ca/c2*2-1(3,4)5;;;/h2*(H3,2,3,4,5);;;/q;;3*+2/p-6",tricalcium diarsorate,http://www.biospider.ca/saved_files/mol/,[O-][As](=O)([O-])[O-].[O-][As](=O)([O-])[O-].[Ca+2].[Ca+2].[Ca+2],[O-][As](=O)([O-])[O-].[O-][As](=O)([O-])[O-].[Ca+2].[Ca+2].[Ca+2],As2Ca3O8,397.690280,Colorless solid.,"","","","","","","","Oral 
Inhalation 
Dermal 
(R009)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Arsenite methyltransferase (Q9HBK9) 
(R164)","Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carginogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (R001, R054)","Arsenic is absorbed mainly by inhalation or ingestion, as to a lesser extent, dermal exposure. It is then distributed throughout the body, where it is reduced into arsenite if necessary, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant. (R055)","LD50: 20 mg/kg (Oral, Rat) (R263)
LD50: 2400 mg/kg (Dermal, Rat) (R263)",,"1, carcinogenic to humans. (R264)",Calcium arsenate is used as a pesticide. (R1106),"Acute Oral: 0.005 mg/kg/day (R260) 
Chronic Oral: 0.0003 mg/kg/day (R260) 
Chronic Inhalation: 0.01 mg/m3 (R260)","Arsenic poisoning can lead to death from multi-system organ failure, probably from necrotic cell death, not apoptosis. Arsenic is also a known carcinogen, especially in skin, liver, bladder and lung cancers. (R001, R055)","Exposure to lower levels of arsenic can cause nausea and vomiting, decreased production of red and white blood cells, abnormal heart rhythm, damage to blood vessels. ","Arsenic poisoning can be treated by chelation therapy, using chelating agents such as dimercaprol, EDTA or DMSA. Charcoal tablets may also be used for less severe cases. In addition, maintaining a diet high in sulfur helps eliminate arsenic from the body. (R055)",P29803;P68871;P69905;P00738;P03372;P04150;P00390;Q14145;P09874;P07437;P60709;P63261;Q16881;Q9NNW7;Q86VQ6;P68032;P68133;P62736;P63267;P10515;P23025;P08559;P11177;A6NKZ8 ;Q99867;Q9H853;O00330;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2
243,T3D0242,2009-03-06 18:58:21 UTC,2009-08-05 21:38:45 UTC,Mercuric chloride,Inorganic Compound;Mercury Compound,"Abavit bAgrosanBichloride of mercuryBichloride, mercuryBichlorure de mercureBichlorure de mercure (french)Bichlorure de mercure [french]Calo-clorCalochlorCalocureCaswell No. 544Chlorid rtutnatyChlorid rtutnaty (czech)Chlorid rtutnaty [czech]Chloride, mercuricChlorure mercuriqueChlorure mercurique (french)Chlorure mercurique [french]Chlorure mercurique [iso-french]ClhgclCloruro di mercurioCloruro di mercurio [italian]Corrosive mercury chlorideCorrosive sublimateDichloride, mercuryDichloromercuryDichlorure de mercureEmisan 6FungchexHSDB 33HgCl2Hydraargyrum bichloratumHydrargyrum bichloratumMCMercuric bichlorideMercuric chlorideMercuric chloride (jan)Mercuric chloride [UN1624] [Poison]Mercuric chloride [iso]Mercuric chloride [jan]Mercuric chloride [mercury and mercury compounds]Mercuric chloride, solidMercuric chloride, solid (dot)Mercuric perchlorideMercury (II ) chlorideMercury (II) chlorideMercury bichlorideMercury chlorideMercury chloride (2)Mercury chloride (HgCl(2))Mercury chloride (HgCl2)Mercury perchlorideMercury(I) chlorideMercury(II) chloridePerchloride of mercuryPerchloride, mercuricPerchloride, mercuryQuecksilber chloridQuecksilber chlorid (german)Quecksilber chlorid [german]Quecksilber(II)-chloridSublimatSublimat (czech)Sublimat [czech]SublimateSublimate, corrosiveSulemSulemaSulema [russian]WLN: HG G2dichloromercury (ACD/Name 4.0)mercury(2+) chloridemercury(2+) dichloride","Mercuric chloride is one of the most toxic chemical compounds of mercury, due to its high solubility in water. It is most often used as a laboratory reagent, and occasionally used to form amalgams with metals.",,7487-94-7,24085,,C13377,"",31823,"",,D008627,Mercuric chloride,826,,,,InChI=1/2ClH.Hg/h2*1H;/q;;+2/p-2,dichloromercury,http://www.biospider.ca/saved_files/mol/b8abd2c7cacd32e791f4e74a6c442707_1237961398.mol,Cl[Hg]Cl,Cl[Hg]Cl,Cl2Hg,271.908330,White crystals.,277 °C,"","","69 mg/mL at 20 °C [SHIU,WY et al. (1990)]","","","","Oral 
Inhalation 
Dermal 
(R022)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Catalase (P04040) 
Hemoglobin subunit alpha (P69905) 
Hemoglobin subunit beta (P68871) 
Hemoglobin subunit gamma-1 (P69891) 
Hemoglobin subunit gamma-2 (P69892) 
Hemoglobin subunit delta (P02042) 
Hemoglobin subunit epsilon (P02100) 
Hemoglobin subunit theta-1 (P09105) 
Hemoglobin subunit zeta (P02008) 
Hemoglobin subunit mu (Q6B0K9) 
(R022, R164) ","High-affinity binding of the divalent mercuric ion to thiol or sulfhydryl groups of proteins is believed to be the major mechanism for the activity of mercury. Through alterations in intracellular thiol status, mercury can promote oxidative stress, lipid peroxidation, mitochondrial dysfunction, and changes in heme metabolism. Mercury is known to bind to microsomal and mitochondrial enzymes, resulting in cell injury and death. For example, mercury is known to inhibit aquaporins, halting water flow across the cell membrane. It also inhibits the protein LCK, which causes decreased T-cell signalling and immune system depression. Mercury is also believed to inhibit neuronal excitability by acting on the postsynaptic neuronal membrane. It also affects the nervous system by inhibiting protein kinase C and alkaline phosphatase, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Mercury also produces an autoimmune response, likely by modification of major histocompatibility complex (MHC) class II molecules, self peptides, T-cell receptors, or cell-surface adhesion molecules. (R022, R025, R066, R067)","Mercury is absorbed mainly via ingestion and inhalation, then distributed throughout the body via the bloodstream, where a portion binds to sulfhydryl groups on haemoglobin. Mercury can undergo oxidation to mercuric mercury, which takes place via the catalase-hydrogen peroxide pathway. The mercury atom is able to diffuse down the cleft in the catalase enzyme to reach the active site where the heme ring is located. Oxidation most likely occurs in all tissue, as the catalase hydrogen peroxide pathway is ubiquitous. Following oxidation, mercury tends to accumulate in the kidneys. Mercury is excreted mainly by exhalation and in the faeces. (R021, R022)","LD50: 1 mg/kg (Oral, Rat) (R1108)
LD50: 5 mg/kg (Intraperitoneal, Mouse) (R1108)
LD50: 14 mg/kg (Subcutaneous, Rat) (R1108)",1 gram for an adult human (average for inorganic mercurials). (R273),"3, not classifiable as to its carcinogenicity to humans. (R264)","Mercuric chloride is most often used as a laboratory reagent, and occasionally used to form an amalgam with metals. (R1107)",Chronic Inhalation: 0.0002 mg/m3 (R260),"Mercury mainly affects the nervous system. Exposure to high levels of metallic, inorganic, or organic mercury can permanently damage the brain, kidneys, and developing fetus. Effects on brain functioning may result in irritability, shyness, tremors, changes in vision or hearing, and memory problems. Acrodynia, a type of mercury poisoning in children, is characterized by pain and pink discoloration of the hands and feet. Mercury poisoning can also cause Hunter-Russell syndrome and Minamata disease. (R022)","Common symptoms include peripheral neuropathy (presenting as paresthesia or itching, burning or pain), skin discoloration (pink cheeks, fingertips and toes), edema (swelling), and desquamation (dead skin peels off in layers). (R020)","Mercury poisoning is treated by immediate decontamination and chelation therapy using DMSA, DMPS, DPCN, or dimercaprol. (R023)",P06239;P68363;Q13748;P68366;P07437;Q13885;P68371;Q13509;P04350;P23258;P29972;P41181;Q92482;P55087;P55064;Q13520;O14520;O94778;O43315;Q96PS8;Q8NBQ7;Q8IXF9;Q71U36;Q9BQE3;Q6PEY2;Q9NY65;Q9H4B7;Q9BVA1;Q9BUF5;Q3ZCM7;Q9UJT1;Q9UJT0;Q9NRH3;P05186;P30301;P17252;P05771;Q05655;Q02156;P24723;P05129;P41743;Q04759;Q05513;A6NM10;A6NKZ8 ;Q99867;Q9H853;A6NHL2;A6NNZ2
244,T3D0243,2009-03-06 18:58:21 UTC,2009-08-25 18:00:34 UTC,Sodium arsenite,Inorganic Compound;Arsenic Compound,"Arsenenous acid, sodium saltArsenious acid, monosodium saltArsenious acid, sodium saltArsenite de sodium [french]Arsenite, sodiumAtlas ""a""Caswell No. 744Chem pels cChem-Sen 56Kill-allPeniteProdalumnolProdalumnol doubleRat death liquidS7400_SIGMASodanitSodium (meta)arseniteSodium (meta)arsenite solutionSodium arsenite solutionSodium arsenite, techSodium dioxoarsenateSodium metaarsenite",Sodium arsenite is a chemical compound derived from arsenous acid. Arsenous acid is the hydrolyzed form of arsenic trioxide and is found in aqueous solutions. (R658),,7784-46-5,443495,,C11906,"",29678,CPD0-1496,,,Sodium arsenite,,,,http://en.wikipedia.org/wiki/sodium arsenite,"InChI=1/AsHO2.Na/c2-1-3;/h(H,2,3);/q;+1/p-1","",http://www.biospider.ca/saved_files/mol/77764c8103f9c8e1c8a921d90ad17fac_1237961563.mol,[O-][As]=O.[Na+],[Na]O[As]=O,AsNaO2,129.901200,White or grey solid.,"","","","","","","","Oral 
Inhalation 
Dermal 
(R009)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Arsenite methyltransferase (Q9HBK9) 
(R164)","Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carginogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (R001, R054)","Arsenic is absorbed mainly by inhalation or ingestion, as to a lesser extent, dermal exposure. It is then distributed throughout the body, where it is reduced into arsenite if necessary, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant. (R055)","LD50: 41 mg/kg (Oral, Rat) (R263) 
LD50: 150 mg/kg (Dermal, Rat) (R263) 
LD50: 1170 ug/kg (Intraperitoneal, Mouse) (R263) 
LD50: 14 mg/kg (Intramuscular Mouse) (R263)
LD50: 7600 ug/kg (Intravenous, Rabbit) (R263)",,"1, carcinogenic to humans. (R264)",,"Acute Oral: 0.005 mg/kg/day (R260) 
Chronic Oral: 0.0003 mg/kg/day (R260) 
Chronic Inhalation: 0.01 mg/m3 (R260)","Arsenic poisoning can lead to death from multi-system organ failure, probably from necrotic cell death, not apoptosis. Arsenic is also a known carcinogen, especially in skin, liver, bladder and lung cancers. (R001, R055)","Exposure to lower levels of arsenic can cause nausea and vomiting, decreased production of red and white blood cells, abnormal heart rhythm, damage to blood vessels.","Arsenic poisoning can be treated by chelation therapy, using chelating agents such as dimercaprol, EDTA or DMSA. Charcoal tablets may also be used for less severe cases. In addition, maintaining a diet high in sulfur helps eliminate arsenic from the body. (R055)",P29803;P68871;P69905;P00738;P03372;P04150;P00390;Q14145;P09874;P07437;P60709;P63261;Q16881;Q9NNW7;Q86VQ6;P68032;P68133;P62736;P63267;P10515;P23025;P08559;P11177;A6NKZ8 ;Q99867;Q9H853;O00330;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2
245,T3D0244,2009-03-06 18:58:21 UTC,2009-08-25 19:52:11 UTC,Formaldehyde,Organic Compound;Industrial Precursor/Intermediate;Aldehyde,"AldacideAldehyd mravenciAldehyd mravenci [czech]Aldehyde formiqueAldehyde formique (french)Aldehyde formique [french]Aldehyde formique [iso-french]Aldeide formicaAldeide formica (italian)Aldeide formica [italian]BFVCH2OCMOCarbon monoxideCarbon oxideCarbon oxide (co)Caswell No. 465Caswell No. 633CetoneChloditanChlodithanChlodithaneDialkyl ketoneDialkyl ketonesDormolDurineDyna-formF-genFAFORFYDEFannoformFlo-morFloguard 1015FordorFormageneFormaldehydFormaldehyd (czech, polish)Formaldehyd [czech, polish]Formaldehyde (gas)Formaldehyde (usp)Formaldehyde [bsi:iso]Formaldehyde polymerFormaldehyde solutionFormaldehyde, 37%, methanol-freeFormaldehyde, as formalin solutionFormaldehyde, as formalin solution (dot)Formaldehyde, gasFormaldehyde, solutionFormaldehyde, solution (37% to 50%)Formaldehyde, solution, flammableFormaldehyde, solutions (formalin) (corrosive)FormalinFormalin (JP15)Formalin 40Formalin-loesungenFormalin-loesungen (german)Formalin-loesungen [german]FormalinaFormalina (italian)Formalina [italian]FormalineFormaline (german)Formaline [german]FormalithFormic aldehydeFormolFormyl groupH2COHCHOHOCHHercules 37M6-8HyperbandHyperband (TN)IvalonKarsanKetonKetoneKetonesLysoformMelamine-formaldehyde resinMethaldehydeMethan 21MethanalMethyl aldehydeMethylene glycolMethylene oxideMitotanMitotaneMorbicidOilstop, halowaxOplossingenOplossingen (dutch)Oplossingen [dutch]OxomethaneOxomethyleneOxymethyleneParaformParaform (van)ParaformaldehydeParaformaldehyde (JP15)Paraformaldehyde [UN2213] [Flammable solid]Paraformaldehyde [jan]Paraformaldehyde, polymerParaformaldehydumParaformic aldehydePoly(oxymethylene)PolyformaldehydePolymerised formaldehydePolyoxymethylenePolyoxymethylene glycolPolyoxymethylene glycolsR-co-r'RCRA waste no. U122RFPDT@Rcra waste number U122SuperlysoformUN 2209 (formalin)VeracurWLN: VHHformaldehyde (ACD/Name 4.0)nchembio.123-comp9nchembio.146-comp5","Formaldehyde is a colorless gas that is naturally produced in small amounts in our bodies. Formaldehyde is used in the production of fertilizer, paper, plywood, and urea-formaldehyde resins. It is also also used as a preservative in some foods and in many products used around the house, such as antiseptics, medicines, and cosmetics. (S313)",,50-00-0,712,,C00067,"",16842,FORMALDEHYDE,,D005557,Formaldehyde,647,,,http://en.wikipedia.org/wiki/Formaldehyde,InChI=1/CH2O/c1-2/h1H2,formaldehyde,http://www.biospider.ca/saved_files/mol/c61a75e5cc84f84f32a31a3d0882ccfe_1237961834.mol,C=O,C=O,CH2O,30.010560,,-92 °C,,,"400 mg/mL at 20 °C [PICKRELL,JA et al. (1983)]",,,,"Oral
Inhalation
Dermal
(R313)",Alcohol dehydrogenase class-3 (P11766) (S313),"It is likely that formaldehyde toxicity occurs when intracellular levels saturate formaldehyde dehydrogenase activity, allowing the unmetabolized intact molecule to exert its effects. Formaldehyde is known to form cross links between protein and DNA and undergo metabolic incorporation into macromolecules (DNA, RNA, and proteins). (R313)","Formaldehyde may be absorbed following inhalation, oral, or dermal exposure. It is an essential metabolic intermediate in all cells and is produced during the normal metabolism of serine, glycine, methionine, and choline and also by the demethylation of N-, S-, and O-methyl compounds. Exogenous formaldehyde is metabolized to formate by the enzyme formaldehyde dehydrogenase at the initial site of contact. After oxidation of formaldehyde to formate, the carbon atom is further oxidized to carbon dioxide or incorporated into purines, thymidine, and amino acids via tetrahydrofolatedependent one-carbon biosynthetic pathways. Formaldehyde is not stored in the body and is excreted in the urine (primarily as formic acid), incorporated into other cellular molecules, or exhaled as carbon dioxide. (S313)","LD50: 300 mg/kg (Subcutaneous, Mouse) (R261)
LD50: 42 mg/kg (Oral, Mouse) (R261)
LD50: 87 mg/kg (Intravenous, Rat) (R261)
LD50: 16 mg/kg (Intraperitoneal, Mouse) (R327)
LC50: 0.414 mg/L over 4 hours (Inhalation, Mouse) (R317)",,"1, carcinogenic to humans. (R264)","Formaldehyde is used in the production of fertilizer, paper, plywood, and urea-formaldehyde resins. It is also also used as a preservative in some foods and in many products used around the house, such as antiseptics, medicines, and cosmetics. (S313)","Acute Inhalation: 0.04 ppm (R260)
Intermediate Inhalation: 0.03 ppm (R260)
Chronic Inhalation: 0.008 ppm (R260)
Intermediate Oral: 0.3 mg/kg/day (R260)
Chronic Oral: 0.2 mg/kg/day (R260)","Drinking large amounts of formaldehyde can cause severe pain, vomiting, coma, and possible death. Formaldehyde is also a known human carcinogen. (S313)","Low levels of formaldehyde can cause irritation of the eyes, nose, throat, and skin. (S313)","",DNA;RNA
246,T3D0245,2009-03-06 18:58:21 UTC,2009-08-04 21:28:06 UTC,2-Chlorophenol,Organic Compound;Disinfectant;Aromatic Hydrocarbon;Organochloride,"1-Chloro-2-hydroxybenzene1wbo2-Chloro-1-hydroxybenzene2-Hydroxychlorobenzene2-chlorophenol (ACD/Name 4.0)Caswell No. 203ChlorophenolChlorophenolsChlorophenols, liquidChlorophenols, solidO-chlorophenic acidO-chlorophenolO-chlorphenolO-chlorphenol (german)O-chlorphenol [german]O-monochlorophenolOrtho-chlorophenolOrtho-monochlorophenolP-chlorfenol [czech]PHENOL,2-CHLOROPhenol, 2-chloro-Phenol, chloro-Phenol, o-chloro-Pine-o disinfectantRCRA waste no. U048Rcra waste number U048Septi-kleenWLN: QR BGo-Chlorophenol, liquid [UN2021] [Keep away from food]o-Chlorophenol, solid [UN2020] [Keep away from food]","2-Chlorophenol or ortho-chlorophenol is a monochlorophenol isomer that has a chlorine atom in the ortho position. It has a medicinal taste and smell, and is a slightly acidic liquid. 2-Chlorophenol is used as a disinfectant agent (R1109).",,95-57-8,7245,,C14219,"",47083,CPD-10866,,C030683,2-Chlorophenol,1557,,,http://en.wikipedia.org/wiki/2-Chlorophenol,"InChI=1/C6H5ClO/c7-5-3-1-2-4-6(5)8/h1-4,8H",2-chlorophenol,http://www.biospider.ca/saved_files/mol/53f963787309000d58c4135f56d1171c_1237961958.mol,C1=CC=C(C(=C1)O)Cl,C1=CC=C(C(=C1)O)Cl,C6H5ClO,128.002890,,9.8 °C,,,"11.3 mg/mL at 25 °C [BANERJEE,S et al. (1980)]",,,,"Inhalation, ingestion, dermal and skin contact (R1110).",No interacting proteins found.,"2-chlorophenol works as a weak uncoupler of oxidative phosphorylation and inhibitors of cellular respiration. The ability of chlorophenols to uncouple oxidative phosphorylation increases with increasing chlorination. In fact, studies indicate a concentration-dependent triphasic effect of chlorophenols on phosphorylation and cellular respiration. At low concentrations, uncoupling produces stimulation of the resting state respiration as a result of increased adenosine triphosphatase (ATPase) activity in the absence of a phosphate acceptor.Inhibition of active respiration is also observed. At moderate concentrations, resting respiration is neither stimulated nor inhibited. Significant inhibition of respiration, associated with a breakdown of the
electron transport process and decreased ATPase activity, occurs at very high concentrations. Uncoupling activity has been attributed to a protonophoric effect (a disruption of the energy gradient across the mitochondrial membrane resulting from distribution of chlorophenols in the phospholipid bilayer of the membrane), whereas inhibition of cellular respiration has been attributed to a direct action on intracellular proteins (R970).",Absorption of 2-chlorophenol is favored in the stomach and the intestine. Absorption through the gastrointestinal tract is by simple diffusion and is expected to be both rapid and virtually complete.The metabolism of the 2-chlorophenol is principally via conjugation. The principal metabolite excreted is the glucuronide. Other metabolites are sulfate conjugates such as the ethereal sulfate. The metabobites are excreted in urine (R970). ,"LD50: 1,000-1,580 mg/kg (dermal, rabbit) (R1111).",,"2B, possibly carcinogenic to humans. (R264)",Breathing in contaminated air; drinking contaminated water; dermal and eye exposure  (R970).,Not avaliable.,"2-chlorophenol is corrosive to epithelial tissue. It produce effects ranging from slight hyperemia to severe corrosion when applied to the corneas. Acute inhalation exposure may lead to hemorrhage in the lungs and tachypnea. Oral exposure to 2-chlorophenol can produce a variety of neurological effects,
including tremors, myoclonic convulsions, a hunched posture, dyspnea, collapse, and coma (R970). ","Cough, shortness of breath and sore throat can result from inhalation of 2-chlorophenol. These symptoms may be delayed. Abdominal pain, drowsiness, weakness, and convulsions can result from ingestion as well as inhalation. Moreover, ingestion of 2-chlorophenol can cause restlessness, tremors, or central nervous system depression to occur. Eye exposure to 2-chlorophenol can lead to redness, pain, and blurred vision, while dermal contact can lead to redness and pain of the skin. Moreover, the substance can be rapidily absorbed after derma exposure (R1110).","Avoid dilution following oral exposure; instead, administer charcoal as a slurry. Following inhalation, move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with inhaled beta2 agonist and oral or parenteral corticosteroids. In case the exposure occurs through eye contact, irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes. Following dermal exposure, remove phenol with undiluted polyethylene glycol 300 to 400 or isopropyl alcohol prior to washing, if readily  available. Wash exposed areas twice or for at least 10 minutes with large quantities of SOAPY water. Water alone may be harmful (R624).
 ",P03372;Q92731
247,T3D0246,2009-03-06 18:58:21 UTC,2009-08-04 21:28:06 UTC,Phenanthrene,Organic Compound;Industrial By-product/Pollutant;Aromatic Hydrocarbon;Polycyclic Aromatic Hydrocarbon,"9,10-DehydrophenanthreneCoal tar pitch volatiles: phenanthrenePEYPhenanthracenePhenanthrenPhenanthren (german)Phenanthren [german]Phenanthrene solutionPhenanthrene, purePhenanthrene-ringPhenanthrinPhenantrinRavatiteWLN: L B666Jphenanthrene (ACD/Name 4.0)","Phenanthrene is one of over 100 different polycyclic aromatic hydrocarbons (PAHs). PAHs are chemicals that are formed during the incomplete burning of organic substances, such as fossil fuels. They are usually found as a mixture containing two or more of these compounds. (R028)",,85-01-8,995,,C11422,"",28851,CPD-1904,,C031181,Phenanthrene,6508,,,http://en.wikipedia.org/wiki/Phenanthrene,InChI=1/C14H10/c1-3-7-13-11(5-1)9-10-12-6-2-4-8-14(12)13/h1-10H,phenanthrene,http://www.biospider.ca/saved_files/mol/363d89ab2694beeb3c0067ac66cec25b_1237962133.mol,C1=CC=C2C(=C1)C=CC3=CC=CC=C32,C1=CC=C2C(=C1)C=CC3=CC=CC=C32,C14H10,178.078250,Colorless solid.,99.2 °C,"","","0.00115 mg/mL at 25 °C [SCHWARZ,FP (1977)]","","","","Oral 
Inhalation 
(R028)","Serum albumin (P02768) 
Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 1B1 (Q16678) 
(R060)","The ability of PAH's to bind to blood proteins such as albumin allows them to be transported throughout the body. Many PAH's induce the expression of cytochrome P450 enzymes, especially CYP1A1, CYP1A2, and CYP1B1, by binding to the aryl hydrocarbon receptor or glycine N-methyltransferase protein. These enzymes metabolize PAH's into their toxic intermediates. The reactive metabolites of PAHs (epoxide intermediates, dihydrodiols, phenols, quinones, and their various combinations) covalently bind to DNA and other cellular macromolecules, initiating mutagenesis and carcinogenesis. (R028, R060, R068, R073)","PAH metabolism occurs in all tissues, usually by cytochrome P-450 and its associated enzymes. PAHs are metabolized into reactive intermediates, which include epoxide intermediates, dihydrodiols, phenols, quinones, and their various combinations. The phenols, quinones, and dihydrodiols can all be conjugated to glucuronides and sulfate esters; the quinones also form glutathione conjugates. (R028)","LD50: 700 mg/kg (Oral, Mouse) (S218)
LD50: 700 mg/kg (Intraperitoneal, Mouse) (S218)
LD50: 56 mg/kg (Intravenousm, Mouse) (S218)",,"3, not classifiable as to its carcinogenicity to humans. (R264)","PAHs are released into the environment via the combustion of fossil fuels, coke oven emissions and vehicle exhausts, as well as naturally from forest fires and volcanic eruptions. PAHs from these sources may contaminate nearly water systems. They are also found in coal tar and charbroiled food. (R028)",,"PAHs are carcinogens and have been associated with the increased risk of skin, respiratory tract, bladder, stomach, and kidney cancers. They may also cause reproductive effects and depress the immune system. (R028)",Acute exposure to PAHs causes irritation and inflammation of the skin and lung tissue. (R034),There is no known antidote for PAHs. Exposure is usually handled with symptomatic treatment. (R028),P35869;Q14749;DNA
248,T3D0247,2009-03-06 18:58:22 UTC,2009-08-04 21:28:06 UTC,Hydrogen fluoride,Inorganic Compound;Industrial By-product/Pollutant;Industrial Precursor/Intermediate;Fluoride Compound,"Acide fluorhydriqueAcide fluorhydrique [french]Acido fluorhidrico [spanish]Acido fluoridricoAcido fluoridrico [italian]Acidum Fluor-Injeel Forte Liq (D4-D200)Anhydrous hydrofluoric acidAntisal 2BBoron tribromideCaswell No. 484FluorFluorhydric acidFluoric Acid Gtte 4ch-30chFluoric acidFluoricum Acidum 4ch-30chFluoricum acidumFluorineFluorowodorFluorowodor [polish]FluorumFluorure d'hydrogene anhydre [french]Fluoruro de hidrogeno anhidro [spanish]FluorwasserstoffFluorwasserstoff [german]FluorwaterstofFluorwaterstof [dutch]HFHydrofluoric acidHydrofluoric acid 70% by weight or more HFHydrofluoric acid gasHydrofluoricum acidumHydrofluorideHydrogen fluoride (HF)Hydrogen fluoride, anhydrous [UN1052] [Corrosive]Hydrogen fluoride/Hydrofluoric acid (conc 50% or greater)RCRA waste no. U134Rcra waste number U134RubigineUN 1052 (anhydrous)UN 1790 (solution)","Hydrogen fluoride is a chemical compound of fluorine and hydrogen. Fluorine is a halogen with the chemical symbol F, and the atomic number 9. Hydrogen fluoride dissolves in water to form hydrofluoric acid. Hydrofluoric acid is used for etching glass. (S318)",,7664-39-3,14917,,C16487,"",29228,"",,D006858,Hydrogen fluoride,7949,,,http://en.wikipedia.org/wiki/Hydrogen fluoride,InChI=1/FH/h1H,hydrogen fluoride,http://www.biospider.ca/saved_files/mol/9c10fa6d4820b54724ff97086b88200e_1237962263.mol,F,F,FH,20.006230,,-83.36 °C,,,"0.922 mg/mL at 0 °C [DEAN,JA (1985)]",,,,"Oral
Inhalation
Dermal
(S318)",,"Fluoride ions are incorporated into bone by substituting for hydroxyl groups in the carbonate-apatite structure to produce hydroxyfluorapatite, thus altering the mineral structure of the bone. Alteration in mineralization increases hardness and bone mass, but also decreases mechanical strength. A portion of the circulating inorganic fluoride acts as an enzyme inhibitor because it forms metalfluoride-phosphate complexes that interfere with the activity of those enzymes requiring a metal ion cofactor. In addition, fluoride may interact directly with the enzyme or the substrate. It is a general inhibitor of the energy production system of the cell. Fluorine may bind calcium and decrease its concentration. This is thought to indirectly inhibit amelogeninase activity, resultin in altered crystal growth and subsequently dental fluorosis. (S318)","Fluoride ions are incorporated into bone by substituting for hydroxyl groups in the carbonate-apatite structure to produce hydroxyfluorapatite, thus altering the mineral structure of the bone. Alteration in mineralization increases hardness and bone mass, but also decreases mechanical strength. A portion of the circulating inorganic fluoride acts as an enzyme inhibitor because it forms metalfluoride-phosphate complexes that interfere with the activity of those enzymes requiring a metal ion cofactor. In addition, fluoride may interact directly with the enzyme or the substrate. It is a general inhibitor of the energy production system of the cell. Fluorine may bind calcium and decrease its concentration. This is thought to indirectly inhibit amelogeninase activity, resulting in altered crystal growth and subsequently causing dental fluorosis. (S318)","LC50: 500 ppm over 1 hours (Inhalation, Mouse) (R555)","50 to 250 ppm over 5 minutes (Inhalation) or 1.5 grams (Oral) for an adult human. (R411, S323)",,Hydrofluoric acid is used mainly for etching glass. It is also used in oil refining and as a precursor to other fluoride compounds. (S318),,"Hydrogen fluoride is extremely corrosive. It may penetrate the skin and weaken the bones, as well as interfere with nerve function and react with blood calcium, causing cardiac arrest. (S324)","Hydrogen fluoride is very irritating to the skin, eyes, and respiratory tract. (S318)","Hydrogen fluoride burns can be treated with a water wash and 2.5% calcium gluconate gel or special rinsing solutions. However, because it is absorbed, further medical treatment is necessary. (R324)",Calcium
250,T3D0249,2009-03-06 18:58:22 UTC,2009-08-04 21:28:06 UTC,Dibromochloromethane,Organic Compound;Reagent;Organobromide;Organochloride,"CDBMCHClBr2ChlorobromoformChlorodibromomethaneDBCMDibromo(chloro)methaneDibromochloromethaneDibromomonochloromethaneInChI=1/CHBr2Cl/c2-1(3)4/h1Methane, chlorodibromo-Monochlorodibromomethane","Dibromochloromethane (and bromoform also known as tribromomethane) are colorless to yellow, heavy, nonburnable liquids with a sweetish odor. These chemicals are possible contaminants of drinking water that has been chlorinated. Bromoform and dibromochloromethane may form when chlorine reacts with other naturally occurring substances in water, such as decomposing plant material. Plants in the ocean also produce small amounts of these chemicals. (S662)",,124-48-1,31296,,C14692,"","",CPD-10560,,C032707,Dibromochloromethane,302,,,http://en.wikipedia.org/wiki/Dibromochloromethane,InChI=1/CHBr2Cl/c2-1(3)4/h1H,dibromo(chloro)methane,http://www.biospider.ca/saved_files/mol/9633ecd56cfe09a0cbe485ce6db61205_1237962567.mol,C(Cl)(Br)Br,C(Cl)(Br)Br,CHBr2Cl,205.813350,Colorless to pale yellow liquid. (S662),-20 °C,120 °C,2.451 g/cm3 (at 20 °C),"2.7 mg/mL at 20 °C [HEIKES,DL (1987)]",,,,Oral. Inhalation. Dermal. (S662),,"Dibromochloromethane is oxidized into trihalomethanol by the cytochrome P-450 mixed function oxidase system of liver. Trihalomethanol then decomposes by loss of hydrogen and halide ions to yield the dihalocarbonyl (an analogue of phosgene), which is a highly reactive molecule, and may undergo a number of reactions, including direct reaction with cellular nucleophiles to yield covalent adducts, reaction with two moles of glutathione (GSH) to yield CO and oxidized glutathione (GSSG), and hydrolysis to yield CO2. The fraction of the dose converted to carbon monoxide has not been quantified, but dramatically increased levels of carboxyhemoglobin have been reported following oral exposure of rats to bromoform. (S662)","In humans and laboratory animals, dibromochloromethane (and bromoform) are generally absorbed quickly. Dibromochloromethane (and bromoform) are thought to be metabolized by at least two route-independent pathways: oxidation by cytochrome P-450 mixed function oxidase system and conjugation via glutathione S-transferase. After ingestion, excretion occurs primarily by exhalation of the compound or of CO2. (S662)",,,,"Dibromochloromethane exposition occurs by drinking water that has been treated with chlorine, at a swimming pool, by breathing bromoform or dibromochloromethane that has evaporated into the air, or by uptake from the water through the skin. Neither dibromochloromethane nor bromoform are likely to be found in food. (S662)",,"Exposure to dibromochloromethane leads to central nervous system depression, which is probably the chief  cause of death in acute exposures. Some studies in animals indicate that exposure to high doses of dibromochloromethane may also lead to liver and the kidney injury within a short period of time. (S662)",,"",P03372;Q92731
253,T3D0252,2009-03-06 18:58:22 UTC,2009-08-11 03:29:56 UTC,Dimethyl formamide,Organic Compound;Solvent;Amide,"Caswell No. 366AD4551_SIGMADMFDMF (amide)DMF (dimethylformamide)DMF (van)DMFADimethyl formamideDimethyl-formamideDimethylamid kyseliny mravenciDimethylamid kyseliny mravenci [czech]DimethylforamideDimethylformamidDimethylformamid (german)Dimethylformamid [german]DimethylformamideDimethylformamide, n,n-DimetilformamideDimetilformamide (italian)Dimetilformamide [italian]DimetylformamiduDimetylformamidu [czech]DwumetyloformamidDwumetyloformamid (polish)Dwumetyloformamid [polish]Dynasolve 100Formamide, dimethyl-Formamide, n,n-dimethyl-Formamide, n,n-dimethyl- ( )Formic acid, amide, n,n-dimethyl-Formin acid,amide,n,n-dimethylFormyldimethylamineHCON(CH3)2HSDB 78InChI=1/C3H7NO/c1-4(2)3-5/h3H,1-2HN, n-dimethylmethanamideN,N-Dimethylformamide [UN2265] [Flammable liquid]N,n'-dimethylformamideN,n- dimethyl formamideN,n- dimethylformamideN,n-dimethyl formamideN,n-dimethyl-formamideN,n-dimethylmethanamideN,n-dimetilformamida [spanish]N-formyldimethylamineWLN: VHN1&1dimethylformamide (ACD/Name 4.0)",Dimethyl formamide (DMF) is an organic compounds commonly used as a solvent for chemical reactions. (V366),,68-12-2,6228,,C03134,"",17741,CPD-581,,,Dimethyl formamide,523,,,"http://en.wikipedia.org/wiki/N,N-Dimethylformamide","InChI=1/C3H7NO/c1-4(2)3-5/h3H,1-2H3","N,N-dimethylformamide",http://www.biospider.ca/saved_files/mol/c9d4c68ea6b82d34511a4651ba0c9672_1237962946.mol,CN(C)C=O,CN(C)C=O,C3H7NO,73.052760,,-60.4 oC,,,1000 mg/mL at 25 oC [ISHOW (NA--) @2ND],,,,"Oral
Inhalation
Dermal
(V368)",,"While the mechanism of action of dimethyl formamide has not bee fully elucidated, thiocarbamate pesticides have been shown to inhibit aldehyde dehydrogenases. (V369)","Dimethyl formamide may be absorbed following ingestion, inhalation, and dermal exposure, and is distributed evenly throughout the body. Metabolism takes place in the liver via microsomal enzyme systems, producing N-hydroxymethyl- N-methylformamide (DMF-OH) as the main urinary metabolite. (V368)","LD50: 2800 mg/kg (Oral, Rat) (R263)
LD50: 1400 mg/kg (Intraperitoneal, Rat) (R263)
LD50: 3800 mg/kg (Subcutaneous, Rat) (R263)
LD50: 2000 mg/kg (Intravenous, Rat) (R263)",10 grams for an adult human. (R624),"3, not classifiable as to its carcinogenicity to humans. (R264)",Dimethyl formamide (DMF) is commonly used as a solvent for chemical reactions. (V366),,"Dimethyl formamide is a known hepatatotoxin. It may also cause birth defects, kidney damage, and temporary alcohol intolerance. (V366)","Symptoms of dimethyl formamide exposure may include abdominal pain, nausea, vomiting, dizziness, fatigue, headache, loss of appetite, and temporary alcohol intolerance. (V366)","As there is no antidote for dimethyl formamide poisoning, treatment is mainly supportive and symptomatic. (R624)",P05091
254,T3D0253,2009-03-06 18:58:22 UTC,2009-08-04 21:28:07 UTC,Pyrene,Organic Compound;Industrial By-product/Pollutant;Aromatic Hydrocarbon;Polycyclic Aromatic Hydrocarbon,"&beta;-pyrene.beta.-pyreneBCR177R_FLUKABenzo(def)phenanthreneBenzo[def]phenanthreneBeta-pyreneCoal tar pitch volatiles: pyreneCoal tar pitch volatiles:pyreneP4185_SIGMAP6805_SIGMAP8712_SIGMAP9712_SIGMAPyrenPyren [german]Pyren(german)Pyrene solutionPyrene, reagPyrene[def]phenanthreneWLN: L666 B6 2AB PJpyrene (ACD/Name 4.0){benzo[def]phenanthrene}","Pyrene is one of over 100 different polycyclic aromatic hydrocarbons (PAHs). PAHs are chemicals that are formed during the incomplete burning organic substances, such as fossil fuels. They are usually found as a mixture containing two or more of these compounds. (R028)",,000129-00-0,31423,,C14335,"",39106,"",,,Pyrene,,,,http://en.wikipedia.org/wiki/Pyrene,InChI=1/C16H10/c1-3-11-7-9-13-5-2-6-14-10-8-12(4-1)15(11)16(13)14/h1-10H,pyrene,http://www.biospider.ca/saved_files/mol/7d167e022e29b3ce5f71d3e5b9080e42_1237963003.mol,C1=CC2=C3C(=C1)C=CC4=CC=CC(=C43)C=C2,C1=CC2=C3C(=C1)C=CC4=CC=CC(=C43)C=C2,C16H10,202.078250,Colorless solid.,151.2 oC,"","","0.000135 mg/mL at 25 oC [MILLER,MM et al. (1985)]","","","","Oral 
Inhalation 
(R028)","Serum albumin (P02768) 
Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 1B1 (Q16678) 
(R060)","The ability of PAH's to bind to blood proteins such as albumin allows them to be transported throughout the body. Many PAH's induce the expression of cytochrome P450 enzymes, especially CYP1A1, CYP1A2, and CYP1B1, by binding to the aryl hydrocarbon receptor or glycine N-methyltransferase protein. These enzymes metabolize PAH's into their toxic intermediates. The reactive metabolites of PAHs (epoxide intermediates, dihydrodiols, phenols, quinones, and their various combinations) covalently bind to DNA and other cellular macromolecules, initiating mutagenesis and carcinogenesis. (R028, R060, R068, R073)","PAH metabolism occurs in all tissues, usually by cytochrome P-450 and its associated enzymes. PAHs are metabolized into reactive intermediates, which include epoxide intermediates, dihydrodiols, phenols, quinones, and their various combinations. The phenols, quinones, and dihydrodiols can all be conjugated to glucuronides and sulfate esters; the quinones also form glutathione conjugates. (R028)","LD50: 2700 mg/kg (Oral, Rat) (S219)",,"3, not classifiable as to its carcinogenicity to humans. (R264)","PAHs are released into the environment via the combustion of fossil fuels, coke oven emissions and vehicle exhausts, as well as naturally from forest fires and vocanic eruptions. PAHs from these sources may contaminate nearly water systems. They are also found in coal tar and charbroiled food. (R028)",,"PAHs are carcinogens and have been associated with the increased risk of skin, respiratory tract, bladder, stomach, and kidney cancers. They may also cause reproductive effects and depress the immune system. (R028)",Acute exposure to PAHs causes irritation and inflammation of the skin and lung tissue. (R034),There is no know antidote for PAHs. Exposure is usually handled with symptomatic treatment. (R028),P35869;Q14749;DNA
256,T3D0255,2009-03-06 18:58:22 UTC,2009-08-11 03:31:01 UTC,Ethyl ether,Organic Compound;Solvent;Ether,"1,1'-Oxybisethane1,1'-oxydiethane1-Ethoxyethane1-ethoxyethane (ACD/Name 4.0)3-OxapentaneAetherAnaesthetic etherAnesthesia etherAnesthetic etherDiaethylaetherDiaethylaether (german)Diaethylaether [german]Diethyl etherDiethyl ether [anaesthetics, volatile]Diethyl ether or ethyl ether [UN1155] [Flammable liquid]Diethyl oxideDwuetylowy eterDwuetylowy eter (polish)Dwuetylowy eter [polish]Etere etilicoEtere etilico (italian)Etere etilico [italian]Ethane, 1,1'-oxybis-EtherEther [jan]Ether ethyliqueEther ethylique (french)Ether ethylique [french]Ether, diethylEther, ethylEther, ethyl (dot)EthoxyethaneEthyl etherEthyl ether anhydrous a.c.s.Ethyl ether usp/acsEthyl ether, techEthyl ether, tech.Ethyl oxideHSDB 70Oxyde d'ethyleOxyde d'ethyle (french)Oxyde d'ethyle [french]PronarcolRCRA waste no. U117Rcra waste number U117Solvent etherSulfuric etherSulfuric ether, anesthetic etherdiethyl ether (ACD/Name 4.0)","Diethyl ether, also known as ether and ethoxyethane, is a clear, colorless, and highly flammable liquid with a low boiling point and a characteristic odor. It is the most common member of a class of chemical compounds known generically as ethers. Diethyl ether is used as a common solvent and has been used as a general anesthetic. It can also be found in recreational drug use. (V371)",,60-29-7,3283,,C13240,"",35702,CPD-5702,,,Ethyl ether,1704,,,,"InChI=1/C4H10O/c1-3-5-4-2/h3-4H2,1-2H3",ethoxyethane,http://www.biospider.ca/saved_files/mol/61e58597df151cb3988f19c6b2142629_1237963257.mol,CCOCC,CCOCC,C4H10O,74.073170,,-116.3 oC,,,"60.4 mg/mL at 25 oC [RIDDICK,JA et al. (1986)]",,,,"Oral
Inhalation
(R624)",,"Diethyl ether inhibits alcohol dehydrogenase. This slows down the metabolism of ethanol and also inhibits the metabolism of other drugs requiring oxidative metabolism. (V371, V375)","Diethyl ether can be absorbed following ingestion and inhalation, and is then rapidly distributed to the brain and fatty tissues. Diethyl ether is not metabolized in humans and is excreted mainly in expired air. (R624)","LD50: 996 mg/kg (Intravenous, Mouse) (V372)
LD50: 2420 mg/kg (Intraperitoneal, Mouse) (V372)
LD50: 1213 mg/kg (Oral, Rat) (V374)
LC50: 186 mg/L (Inhalation, Mouse) (V373)",30 mL for an adult human. (R624),,Diethyl ether is used as a common solvent and has been used as a general anesthetic. It can also be found in recreational drug use. (V371),,Diethyl ether causes CNS depression. Death due to respiratory depression may result from severe and prolonged exposure. (R624),"Inhalation may result in dizziness, giddiness, euphoria, drowsiness, salivation, and CNS depression. Diethyl ether is also a skin and eye irritant. (R624)","There is no antidote for diethyl ether poisoning, thus treatment is symptomatic and supportive. (R624)",P07327;P00325;P00326;P08319;P28332;P40394;P11766
258,T3D0257,2009-03-06 18:58:23 UTC,2009-08-25 18:00:42 UTC,4-Nitrophenol,Organic Compound;Industrial Precursor/Intermediate;Aromatic Hydrocarbon;Nitrite,"1-Hydroxy-4-nitrobenzene4-(hydroxy(oxido)amino)phenol (ACD/Name 4.0)4-Nitrofenol4-Nitrofenol [Dutch]4-Nitrofenol(DUTCH)4-Nitrophenol solution4-Nitrophenol-UL-14C4-Notrophenol4-hydroxynitrobenzene4-nitrophenol, (18)O-labeled cpd4-nitrophenol, 1-(13)C-labeled cpd4-nitrophenol, 14C-labeled cpd4-nitrophenol, 2,6-(13)C2-labeled cpd4-nitrophenol, 2,6-(14)C2-labeled cpd4-nitrophenol, 2-(14)C-labeled cpd4-nitrophenol, aluminum salt4-nitrophenol, ammonium salt4-nitrophenol, cesium salt4-nitrophenol, copper(1+) salt4-nitrophenol, ion(1-)4-nitrophenol, ion(1-) hydride4-nitrophenol, iron(3+) salt4-nitrophenol, lithium salt4-nitrophenol, manganese (2+) salt4-nitrophenol, manganese salt4-nitrophenol, potassium salt4-nitrophenol, silver(2+) salt4-nitrophenol, sodium salt4-nitrophenol, sodium salt, (2:1), dihydrate4-nitrophenol, tin (2+) salt4-nitrophenol, tin (4+) salt4-nitrophenol, zinc saltCaswell No. 603MononitrophenolN2767_SIGMANPONiphenP-hydroxynitrobenzeneP-nitrofenolP-nitrofenol [czech]P-nitrophenolP-nitrophenol solutionPHENOL,4-NITROPNPPNP, p-nitrophenolParanitrofenolParanitrofenol [dutch]Paranitrofenol(dutch)ParanitrofenoloParanitrofenolo [italian]Paranitrofenolo(italian)ParanitrophenolParanitrophenol [french,german]Paranitrophenol(french,german)Phenol, 4-nitro-Phenol, p-nitro-RCRA waste no. U170RPNRcra waste number U170WLN: WNR DQp-Nitrophenol [UN1663] [Poison]","4-Nitrophenol is a phenolic compound that is used mainly to make fungicides and dyes, and to darken leather. It is also used in the synthesis of drugs such as paracetamol, phenetidine, and acetophenetidine. (V376, V377)",,100-02-7,980,,C00870,168820,16836,P-NITROPHENOL,,,4-Nitrophenol,1778,,,http://en.wikipedia.org/wiki/4-Nitrophenol,"InChI=1/C6H5NO3/c8-6-3-1-5(2-4-6)7(9)10/h1-4,8H",4-nitrophenol,http://www.biospider.ca/saved_files/mol/333da5e50240933f0c4de6a9c6095d94_1237963577.mol,OC1=CC=C(C=C1)[N+]([O-])=O,Oc1ccc(cc1)[N+]([O-])=O,C6H5NO3,139.026940,Colorless to light yellow solid.,113.8 oC,,,"11.6 mg/mL at 20 oC [SCHWARZENBACH,RP et al.(1988)]",,,,"Oral
Inhalation
Dermal
(V376)","Cytochrome P450 2E1 (P05181)
(V378)","The nitrite in nitrophenols causes the autocatalytic oxidation of oxyhemoglobin to hydrogen peroxide and methemoglobin. This elevation of methemoglobin levels is a condition known as methemoglobinemia, and is characterized by tissue hypoxia, as methemoglobin cannot bind oxygen. (V305, V306)","Nitrophenol may be absorbed following ingestion, inhalation, or dermal exposure. The major metabolic route for nitrophenols is conjugation, with the resultant formation of either glucuronide or sulfate conjugates. Conjugates are more polar than the parent compounds and therefore are easier to excrete in the urine. (V376)","LD50: 380 mg/kg (Oral, Mouse) (R263)
LD50: 75 mg/kg (Intraperitoneal, Mouse) (R263)",,,"4-Nitrophenol is used mainly to make fungicides and dyes, and to darken leather. It is also used in the synthesis of drugs such as paracetamol, phenetidine, and acetophenetidine. (V376, V377)",,"Nitrophenols may cause methemoglobinemia. This is a disorder in which there is an abnormally high level of methemoglobin in the blood, resulting in a decrease in the amount of oxygen that can be carried to the tissues and organs. (V376, V306)","Symptoms of methemoglobinemia include shortness of breath, cyanosis, mental status changes, headache, fatigue, exercise intolerance, dizziness and loss of consciousness. Severe methemoglobinemia may cause dysrhythmias, seizures, coma and death. (V306)",Methemoglobinemia can be treated with supplemental oxygen and methylene blue 1% solution at 1-2mg/kg administered intravenously slowly over five minutes followed by an IV flush with normal saline. Methylene blue restores the iron in hemoglobin to its normal (reduced) oxygen-carrying state. (V306),P69905;P68871;P02042;P02100;P69891;P69892;Q6B0K9;P09105;P02008
260,T3D0259,2009-03-06 18:58:23 UTC,2009-08-04 21:28:08 UTC,Phosphine,Inorganic Compound;Pesticide,"Amgard CPCAmgard CPC 405Black phosphorusBonide blue death rat killerCaswell No. 663CelphosCommon sense cockroach and rat preparationsDeliciaDetiaDetia gas ex-bECO2FUMEExolit 385Exolit 405Exolit LPKNExolit LPKN 275Exolit RP 605Exolit RP 650Exolit RP 652Exolit RP 654Exolit VPK-n 361FR-T 2 (element)FosforowodorFosforowodor [polish]Gas-ex-bGelber phosphor [german]HishigadoHishigado CPHishigado NP 10Hishigado PLHishigado apHostaflam RP 602Hostaflam RP 614Hostaflam RP 622Hostaflam RP 654Hydrogen phosphideNova Sol R 20Novaexcel 140Novaexcel 150Novaexcel F 5Novaexcel ST 100Novaexcel ST 140Novaexcel ST 300Novared 120UFNovared 120UFANovared 120VFANovared 140Novared 280Novared C 120Novared F 5PHOSPHORUS METAL, 99.999%, REDPhosphanePhosphenePhosphine (fumigant)Phosphine [UN2199] [Poison gas]Phosphoretted hydrogenPhosphorusPhosphorus (red)Phosphorus hydridePhosphorus trihydridePhosphorus, amorphous [UN1338] [Flammable solid]Phosphorus, redPhosphorus, whitePhosphorus-31PhosphorwasserstoffPhosphorwasserstoff [german]RCRA waste no. P096Rat-nipRcra waste number P096Red phosphorusTrihydrogen phosphideViolet phosphorusWhite phosphorushydrogen phosphorus, PH3","Phosphine is a colorless, flammable, and explosive gas. Pure phosphine is odourless, but technical grade phosphine has a highly unpleasant odor like garlic or rotting fish. Small amounts occur naturally from the break down of organic matter. It is slightly soluble in water. Phosphine is used in semiconductor and plastics industries, in the production of a flame retardant, and as a pesticide in stored grain. (S342, S343)",,007803-51-2,24404,,"","",30278,CPD-3703,,,Phosphine,,,,http://en.wikipedia.org/wiki/Phosphine,InChI=1/H3P/h1H3,phosphane,http://www.biospider.ca/saved_files/mol/,P,P,H3P,33.997240,,-133 oC,,,"",,,,"Oral
Inhalation
(S345)",,"Phosphine inhibits cytochrome c oxidase, preventing mitochondrial oxidative phosphorylation. This non-competitive inhibition prevents cellular respiration and leads to multi-organ dysfunction. Phosphine can also react with hydrogen peroxide to form the highly reactive hydroxyl radical, which can cause lipid peroxidation. (S346, S347)","Phosphine and metal phosphides may be absorbed following ingestion or inhalation, then distribute to the nervous system, liver, and kidney. In the body, metal phosphides are hydrolysed to phosphine, and phosphine is oxidized to hypophosphite and phosphite. Metabolites are excreted in the urine, while unchanged phosphine is exhaled. (S345)","LC50: 11 ppm over 4 hours (Inhalation, Rat) (S344)",,,"Phosphine is used in semiconductor and plastics industries, in the production of a flame retardant, and as a pesticide in stored grain. (S342)",,"Inhalation of phosphine may cause severe pulmonary irritation leading to acute pulmonary oedema, cardiovascular dysfunction, CNS excitation, coma and death. Gastrointestinal disorders, renal damage and leukopenia may also occur. Chronic exposure to phosphine can result in anemia, bronchitis, gastrointestinal effects, and visual, speech and motor problems. (S342, S345)","Early symptoms of acute phosphine intoxication include pain in the diaphragm, nausea, vomiting, excitement, and a phosphorus smell on the breath. Higher levels can cause weakness, bronchitis, pulmonary edema, shortness of breath, convulsions, and death. Some effects, such as pulmonary edema, convulsions, and liver injury, may appear or continue to be present days after an exposure. Liquid phosphine on your skin can cause frostbite. Ingestion of metal phosphides results in release of phosphine in your stomach which can cause nausea, vomiting, abdominal pain, and diarrhea. (S342)","As there is no antidote for phosphine poisoning, treatment is mainly symptomatic. Artificial respiration, gastric lavage, and/or administration of activated charcoal may be necessary. (S345)",P24310;P14406;P00395;P00403;P00414;P13073;Q96KJ9;P20674;P10606;P12074;Q02221;P14854;Q6YFQ2;P09669;O60397;P24311;Q8TF08;P15954;P10176;Q7Z4L0
261,T3D0260,2009-03-06 18:58:23 UTC,2009-08-04 21:28:08 UTC,Trichlorobenzene,Organic Compound;Solvent;Aromatic Hydrocarbon;Organochloride,"*chlorobenzens1,2,3-Trichlorbenzol1,2,3-Trichlorobenzene1,2,6-TrichlorobenzeneBenzene, 1,2,3-trichloro-Invalon TCPyranol 1478TCBTrichlorbenzeneTrichlorobencenos [spanish]TrichlorobenzeneTrichlorobenzenesVic-trichlorobenzene",Trichlorobenzene is an organochloride aromatic compound and may refer to any of its three isomeric forms. It is used as a solvent. (R428),,012002-48-1,6895,,"","","",CPD-1125,,,Trichlorobenzene,,,,,InChI=1/C6H3Cl3/c7-4-2-1-3-5(8)6(4)9/h1-3H,"1,2,3-trichlorobenzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C(=C1)Cl)Cl)Cl,C1=CC(=C(C(=C1)Cl)Cl)Cl,C6H3Cl3,179.930030,,"",,,"0.03 mg/mL at 25 oC [TALIAN,SF et al. (1986)]",,,,"Oral 
Inhalation 
Dermal 
(R430)",,"Trichlorobenzene may uncouple mitochondrial oxidative phosphorylation, inducing potassium ion release and inhibiting respiratory control. It's metabolites may covalently bind to cellular proteins and alkylate DNA. (R432, R433)","Trichlorobenzene is absorbed via oral, inhalation, and dermal routes. It is believed to be metabolized via cytochrom p-450 enzymes into metabolites that include phenols, mercapturic acid, and catechols.(R430)",,,,"Trichlorobenzene is used as a solvent in chemical manufacturing, as well as in dyes, dielectric fluid, synthetic transformer oils, lubricants, heat-transfer medium, and insecticides. (R431)",,"High levels of trichlorobenzene may damage the liver, kidney, and thyroid. (R429)",Trichlorobenzene irritates the eyes and respiratory tract. (R285),"",P98194;O75185;P14867;P47869;P34903;P48169;P31644;Q16445;P18505;P47870;P28472;O14764;P78334;Q8N1C3;P18507;Q99928;O00591;P24046;P28476;A8MPY1;Q9UN88;P20020;Q01814;Q16720;P23634;O14983;P16615;Q93084;P54710;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P03372;Q92731
262,T3D0261,2009-03-06 18:58:23 UTC,2009-08-11 03:29:56 UTC,"2,6-Dinitrotoluene",Organic Compound;Explosive;Plasticizer;Aromatic Hydrocarbon;Nitrite,"1,3-Dinitro 2-methyl benzene1-Methyl-2,6-dinitrobenzene2,4-/2,6-Dinitrotoluene mixture2,6-Dinitrotoluene2,6-dinitromethylbenzene2-Methyl-1,3-dinitro-benzene2-methyl-1,3-dinitrobenzeneCHEBI:957DNTRCRA waste no. U106Rcra waste number U106Toluene, 2,6-dinitro-","2,6-Dinitrotoluene is one of the six dinitrotoluene isomers. Dinitrotoluene (DNT) or Dinitro is an explosive with the formula C6H3(CH3)(NO2)2. At room temperature it is a pale yellow to orange crystalline solid. It is a high explosive and one of the precursors for trinitrotoluene (TNT), which is synthesized through three separate nitrations of toluene. The first product is mononitrotoluene, DNT is the second, and TNT is the third and final product. (R501)",,606-20-2,11813,,C11008,"",957,CPD-1125,,,"2,6-Dinitrotoluene",538,,,,"InChI=1/C7H6N2O4/c1-5-6(8(10)11)3-2-4-7(5)9(12)13/h2-4H,1H3","2-methyl-1,3-dinitrobenzene",http://www.biospider.ca/saved_files/mol/394b9de1c34894e1abfc914cc4eaad0a_1237964060.mol,CC1=C(C=CC=C1[N+](=O)[O-])[N+](=O)[O-],CC1=C(C=CC=C1[N+](=O)[O-])[N+](=O)[O-],C7H6N2O4,182.032760,,66 oC,,,"",,,,"Exposure to skin and eyes, inhalation, or ingestion. (R502)","","Dinitrotoluene may cause conversion of oxyhemoglobin to methemoglobin via oxidation of iron(II) to iron(III) by its metabolites. High levels of methemoglobin are removed by catabolism, leading to the development of anemia. Some metabolites of dinitrotoluene  are also transported back from the bile to the liver, where the amine group is N-hydroxylated by cytochrome P-450 to form an unstable sulfate conjugate. The sulfate conjugate is degraded into carbonium or nitrenium ions. These ions covalently bind to hepatic macromolecules (DNA, RNA), leading to mutations and subsequently liver tumors. They also bind to DNA of the lung and the intestine. (R511)","The metabolism of 2,6-DNT occurs in the liver and also in the intestine by microflora. Both oxidized and reduced metabolites are excreted in the urine after oral administration of the compound. Oxidative metabolism by cytochrome P450 predominates in the liver, leading to the formation of dinitrobenzyl alcohol which is either converted to glucuronide conjugate or further oxidized to dinitrobenzoic acid. Dinitrobenzyl alcohol glucuronide is partially excreted into the bile, followed by metabolism by gut microflora and enterohepatic cycling (nitroreductase). Thus, 2,6-DNT appears to be first metabolized by the liver with the metabolites being excreted into the bile; the biliary metabolites are hydrolyzed and further metabolized in the intestine; after reabsorption and circulation back to the liver, a portion of the metabolites (2-amino-6-nitrobenzyl) are oxidized to a hydroxylamine by hepatic enzymes. The hydroxylamine is then conjugated with sulfate by hepatic sulfotransferase. The unstable N-sulfate decomposes to form an electrophilic nitrenium ion, which can react with cellular nucleophiles such as DNA. 2,6-Dinitrobenzyl alcohol glucuronide, 2-amino-6-nitrotoluene, and 2,6-dinitrobenzaldehyde can be detected in the bile. Some amounts of 2,6-dinitrobenzylalcohol and 2-amino-6nitrobenzyl alcohol can also be found. (R511)","LD50: 180-795 mg/kg/day (Oral, Rat) (R511)","","2B, possibly carcinogenic to humans. (R264)","It is a high explosive and one of the precursors for trinitrotoluene (TNT), which is synthesized through three separate nitrations of toluene. 2,6-Dinitrotoluene can affect the body if it is inhaled, comes in contact with the eyes or skin, is swallowed, or is absorbed through the skin. Even a small amount absorbed from clothes or shoes may cause toxic symptoms. It is assumed that oral ingestion could be a secondary route for occupationally exposed humans. (R501, R502)",Intermediate Oral: 0.004 mg/kg/day (Dog) (511),"2,6-Dinitrotoluene poisoning may cause methemoglobinemia, anemia, leukopenia, and liver necrosis. Liver injury may be more common than cyanosis. (R511)","Symptoms of 2,4-dinitrotoluene poisoning include blue lips or finger nails, blue skin, vertigo, fatigue, dizziness, weakness, nausea, vomiting, dyspnea, arthralgia, insomnia, tremor, paralysis, unconsciousness, chest pain, shortness of breath, palpitation, anorexia, and loss of weight. (R504, N014)","Following oral exposure, immediately dilute with 4 to 8 ounces (120 to 240 mL) of water or milk (not to exceed 4 ounces/120 mL in a child). Administer charcoal as a slurry. Gastric lavage and oxygen administration is recommended. Following inhalation exposure, move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with inhaled beta2 agonist and oral or parenteral corticosteroids. Following eyes exposure, irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes. Following dermal exposure, remove contaminated clothing and wash exposed area thoroughly with soap and water, and administer a benzodiazepine IV in case of irritation. In all those cases, a physician may need to examine the area if irritation or pain persists. (R624)",DNA;RNA;P69905;P68871;P02042;P02100;P69891;P69892;Q6B0K9;P09105;P02008
263,T3D0262,2009-03-06 18:58:23 UTC,2009-08-04 21:28:08 UTC,Fluoride ion,Inorganic Compound;Fluoride Compound,"BifluoridenDiatomic fluorineDifluorineDrinking water, fluoride treatedDrinking water,fluoride treatedFluorideFluoride as dustFluoride compounds, inorganic, n.o.s.Fluoride dustFluoride ionFluoride ion(1-)Fluoride ion(f-)Fluoride(1-)FluoridesFluorides (inorganic, used in drinking-water)Fluorides, inorganicFluorine 19Fluorine anionFluorine atomFluorine ionFluorine ion(1-)Fluorine radicalFluorine(.)Fluorine, ionMolecular fluorineMonofluorineOral-b minute gelPerfluoride","Fluorine is a halogen with the chemical symbol F, and the atomic number 9. Fluoride compounds are used in making steel, chemicals, ceramics, lubricants, dyes, plastics, and pesticides. Fluorides are often added to drinking water supplies and to a variety of dental products, including toothpaste and mouth rinses, to prevent dental cavities. (S318)",,016984-48-8,28179,,C00742,"173395
177400",17051,"",,,Fluoride ion,,,,http://en.wikipedia.org/wiki/Fluorine,InChI=1/FH/h1H/p-1,fluorine,http://www.biospider.ca/saved_files/mol/179cd71cffb07fc7ae518c0085ed37ca_1237964165.mol,[F-],[F-],[F]-,18.998400,,-219.61 oC,,,"",,,,"Oral
Inhalation
Dermal
(S318)",,"Fluoride ions are incorporated into bone by substituting for hydroxyl groups in the carbonate-apatite structure to produce hydroxyfluorapatite, thus altering the mineral structure of the bone. Alteration in mineralization increases hardness and bone mass, but also decreases mechanical strength. A portion of the circulating inorganic fluoride acts as an enzyme inhibitor because it forms metalfluoride-phosphate complexes that interfere with the activity of those enzymes requiring a metal ion cofactor. In addition, fluoride may interact directly with the enzyme or the substrate. It is a general inhibitor of the energy production system of the cell. Fluorine may bind calcium and decrease its concentration. This is thought to indirectly inhibit amelogeninase activity, resulting in altered crystal growth and subsequently causing dental fluorosis. (S318)","Fluorides may be absorbed following inhalation, oral, or dermal exposure. Once in the body, the fluoride ion is transported in the blood and accumulates in the bones and teeth. Fluoride is believed to replace the hydroxyl ion (OH-) and possibly the bicarbonate ion (HCO3-) associated with hydroxyapatite—a mineral phase during formation of bone. The resultant material is hydroxyfluorapatite. Once absorbed, a portion of the fluoride is deposited in the skeleton, and most of the remainder is excreted in the urine, with smaller amounts in feces, and sweat, and saliva. (S318)",,,"3, not classifiable as to its carcinogenicity to humans. (R264)","Fluoride compounds are used in making steel, chemicals, ceramics, lubricants, dyes, plastics, and pesticides. Fluorides are often added to drinking water supplies and to a variety of dental products, including toothpaste and mouth rinses, to prevent dental cavities. (S318)",,"Exposure to high levels of fluoride can result in denser bones. However, if exposure is high enough, these bones may be more fragile and brittle and there may be a greater risk of breaking the bone. Chronic exposure may also cause dental fluorosis, which alters the appearance of children's teeth during tooth development. (S318, S325)","Symptoms of fluoride exposure include abdominal pain, diarrhea, dysphagia, hypersalivation, mucosal injury, nausea, vomiting. Electrolyte abnormalities including hyperkalemia, hypocalcemia, hypoglycemia, and hypomagnesemia may occur. Neurological symptoms include headache, muscle weakness, hyperactive reflexes, muscular spasms, paresthesia seizures, tetanic contractions, and tremors. In severe cases, multiorgan failure will occur. Death typically results from cardiac arrest, shock, widening of QRS, and various arrhythmias occur. (S325)","Oral exposure to fluoride compounds should be treated by giving milk, calcium carbonate, or milk of magnesia to slow absorption. Eye or skin contact should be treated by removing any contaminated clothing and flushing with water. (S325)",Calcium
265,T3D0264,2009-03-06 18:58:24 UTC,2009-08-04 21:28:09 UTC,Methyl parathion,Organic Compound;Pesticide;Aromatic Hydrocarbon;Organophosphate,"A-groAzofosAzophosBladan mBladan-mC8H10NO5PSCaswell No. 372CekumethionDALFDalifDemethylfenitrothionDevithionDimethyl 4-nitrophenyl phosphorothionateDimethyl o-p-nitrophenyl thioph osphateDimethyl o-p-nitrophenyl thiophosphateDimethyl p-nitrophenyl monothiophosphateDimethyl p-nitrophenyl phosphorothionateDimethyl p-nitrophenyl thionophosphateDimethyl p-nitrophenyl thiophosphateDimethyl parathionDimethyl-p-nitrophenyl thionphosphateDrexel methyl parathion 4EFolid ol-mFolidol 600Folidol M 50Folidol M-40Folidol mFolidol-mFosferno M 50FulkilKilex parathionLiquidM-parathionMe-parathionMepatonMeptoxMetacid 50MetacideMetacide (insecticide)MetafosMetafos (pesticide)MetaphorMetaphosMethyl 1605Methyl fosfernoMethyl niranMethyl parathionMethyl parathion, liquid [NA3018] [Poison]Methyl parathion, solid [NA2783] [Poison]Methyl-E 605Methyl-bladanMethylparathionMethylparathioneMethylthiophosMetilparation (hungarian)MetronMetron (pesticide)Metyloparation [polish]Metylparation [czech]NitroxNitrox 80O,O-Dimethyl O-(4-nitrophenyl) phosphorothioateO,O-Dimethyl O-4-nitrophenyl phosphorothioateO,O-Dimethyl-O-(4-nitro-fenyl)-monothiofosfaat [Dutch]O,O-Dimethyl-O-(4-nitro-phenyl)-monothiophosphat [German]O,O-Dimethyl-O-(4-nitrophenyl) phosphorothioateO,O-Dimethyl-O-(4-nitrophenyl)-thionophosphat [German]O,O-Dimetil-O-(4-nitro-fenil)-monotiofosfato [Italian]O,o-dim ethyl o-p-nitrophenyl thiophosphateO,o-dimethyl o-(p-nitrophenyl) phosphorothioateO,o-dimethyl o-(p-nitrophenyl) thionophosphateO,o-dimethyl o-(p-nitrophenyl) thiophosphateO,o-dimethyl o-p-nitrophenyl phosphorothioateO,o-dimethyl o-p-nitrophenyl thiophosphateO,o-dimethyl-o-(p-nitrophenyl)-thionophosphat [german]O,o-dimethyl-o-p-nitrofenylthiofosfat [czech]OleovofotoxP-nitrophenyldimethylthionophosphateParapest M-50ParatafParathion methylParathion methyl homologParathion-methylParathion-methyl [bsi:iso]Parathion-methyl solutionParathion-metile [italian]ParatoxParatufParton-mPartron mPencap mPenncap MLSPenncap mPenncap-mPhenol, p-nitro-, o-ester with o,o-dimethylphosphorothioatePhosphorothioic acid O,O-dimethyl O-(4-nitrophenyl) esterPhosphorothioic acid, O,O-dimethyl O-(4-nitrophenyl) esterPhosphorothioic acid, o,o-dimethyl o-(p-nitrophenyl) esterQuinophosRCRA waste no. P071RCRA waste number P071Sinafid M-48TekwaisaThiophenitThylpar M-50VofatoxWofatoxWofatox 50 ECWofatox 80WofotoxYphosfolidol-80o,o-Dimethyl o-(4-nitrophenyl) thiophosphate","Methyl parathion is an organophosphate compound insecticide. It is used to kill insects on farm crops, especially cotton. As methyl parathion is toxic to non-target organisms, its use is banned or restricted in many areas. (R1006)",,000298-00-0,4130,,C14228,"",38746,CPD-3721,,,Methyl parathion,,,,,"InChI=1/C8H10NO5PS/c1-12-15(16,13-2)14-8-5-3-7(4-6-8)9(10)11/h3-6H,1-2H3",dimethoxy-(4-nitrophenoxy)-sulfanylidene-$l^{5}-phosphane,http://www.biospider.ca/saved_files/mol/42f8f1f1ba14a168ff0d6b8b034c0607_1237964417.mol,COP(=S)(OC)OC1=CC=C(C=C1)[N+](=O)[O-],COP(=S)(OC)OC1=CC=C(C=C1)[N+](=O)[O-],C8H10NO5PS,263.001730,White powder.,35.5 oC,,,"0.0377 mg/mL at 20 oC [BOWMAN,BT & SANS,WW (1983)]",,,,"Oral
Inhalation
Dermal
(R1006)","Cytochrome P450 3A4 (P08684) 
Cytochrome P450 2C8 (P10632) 
Serum paraoxonase/arylesterase 1 (P27169)
Glutathione S-transferase A1 (P08263)
Glutathione S-transferase theta-1 (P30711)
Serum albumin (P02768)
(R1006, R1011, R1012, R1013)","The active metabolite of methyl parathion, methyl paraoxon, inactivates acetylcholinesterase by phosphorylating the active site of the enzyme, thus inhibiting its activity in the nervous system and at the motor end-plate. As a result, the neurotransmitter acetylcholine accumulates in the nerve synapse or neuromuscular junction, producing overstimulation of cholinergic end organs. The immunotoxicity of methyl parathion and other organophosphates is thought to result from their inhibition of esterases and stabilization of the lysosomal membrane of lymphocytes, thus blocking release of lymphokines. (R1006)","Methyl parathion can be readily absorbed by humans following inhalation, oral, or dermal exposure. It is widely distributed in organs and tissues, then rapidly metabolized in the liver, to polar substances that are quickly excreted in the urine. Oxidative desulfuration by microsomal oxidases transforms methyl parathion into the neurotoxic, active metabolite, methyl paraoxon. Other reactions including oxidation, hydrolysis, dearylation, and dealkylation detoxify methyl parathion. (R1006)","LD50: 417 mg/kg (Oral, Guinea pig) (R373)
LD50: 50 mg/kg (Intravenous, Guinea pig) (R373)
LD50: 300 mg/kg (Dermal, Rabbit) (R263)
LD50: 67 mg/kg (Percutaneous, Rabbit) (R1010)",2.1 mg/kg for an adult human. (R265),"3, not classifiable as to its carcinogenicity to humans. (R264)","Methyl parathion is an insecticide. It is used to kill insects on farm crops, especially cotton. (R1006)","Intermediate Oral: 0.0007 mg/kg/day (R260)
Chronic Oral: 0.0003 mg/kg/day (R260)",Methyl parathion affects the central nervous system. Changes in mental state may last several months after exposure to high levels of methyl parathion has ended. Methyl parathion may also affect the immune system. (R1006),"Exposure to very high levels of methyl parathion may cause death, loss of consciousness, dizziness, confusion, headaches, difficult breathing, chest tightness, wheezing, vomiting, diarrhea, cramps, tremors, blurred vision, and sweating. (R1006)",Parathion poisoning should be treated by administering the antidote atropine. (R1005),P22303
266,T3D0265,2009-03-06 18:58:24 UTC,2009-08-11 03:30:29 UTC,Pentaerythritol tetranitrate,Organic Compound;Explosive;Nitrate,"1,3-Propanediol, 2,2-bis[(nitrooxy)methyl]-, dinitrate1,3-dinitrato-2,2-bis(nitratomethyl)propane1-3 Propanediol,2,2-bis(nitroxy)methyl-,dinitrate(ester)2,2-Bis((nitrooxy)methyl)-1,3-propanediol dinitrate (ester)2,2-Bis(Hydroxymethyl)-1,3-propanediol tetranitrate2,2-Bis[(nitrooxy)methyl]-1,3-propanediol dinitrate (ester)2,2-Bisdihydroxymethyl-1,3-propanediol tetranitrateAlpharma brand of pentaerythritol tetranitrateAngicapAngitetAntoraArcotrateBaritrateC 2 (explosive)CHOTCardiacapDeltrate 20Deltrate-20Dexo brand of pentaerythritol tetranitrateDilcoranDilcoran 80Dilcoran-80DipentrateDuotrateEl petnErinitErynitumExtexHasethrolKaytrateLX 16 (explosive)LentratLowetrateMartrate 45Martrate-45MetranilMikardolMiltrateMixture nameMycardolMyotrate ""10""Myotrate &quot;10&quot;Myotrate 10Neo-corovasNeopentanetetrayl nitrateNexitNexit-starkNexol-eNicochloranNiperytNiperythNirasonNitrinNitrinalNitrineNitrinolNitro-rilettenNitrodexNitrolongNitropentNitropentaNitropenta 7WNitropentaerythriteNitropentaerythritolNitropentonNitrotalansOmnitoxOvadziakP.e.t.n.PENTAERYTHRITOL TETRANITRATE WITH 80% D-LACTOSE MONOHYDRATEPETPETNParke davis brand of pentaerythritol tetranitratePen-tetraPencardPentaPentaerithrityl tetranitratePentaerithrityl tetranitrate (inn)Pentaerithrityli tetranitras [inn-latin]Pentaeritrile tetranitrato [dcit]Pentaerythrite tetranitratePentaerythrite tetranitrate (DRY) [forbidden]Pentaerythrite tetranitrate, with not < 7% water, by massPentaerythritol nitratePentaerythritol tetranPentaerythritol tetranitratePentaerythritol tetranitrate (jan)Pentaerythritol tetranitrate [ban:jan]Pentaerythritol tetranitrate, dilutedPentaerythrityl tetranitratePentaerythritylium tetranitricumPentafilinPentafinPentalogPentanitrinePentanitrolPentanitrolumPentaritPentestan-80Pentetrate unicellesPenthritPenthritePentitratePentral 80PentranPentratePentrinatPentriolPentritePentritolPentritol tempulesPentritol tempules (TN)PentryatePentryate 80PergitralPeridexPeridex-laPeritratePeritylPetn, NFPrevangorQuintrateRavensberg brand of pentaerythritol tetranitrateRythritolSDM No. 23SDM No. 35SubicardTENTanipentTentrate-20TerpateTetranitrate de pentaerithrityle [inn-french]Tetranitrate de pentaerythrityleTetranitrate, pentaerythritolTetranitrato de pentaeritritilo [inn-spanish]TetranitropentaerythriteTetranitropentaerythritolTetrasuleTetrateTranite d-layVanguard brand of pentaerythritol tetranitrateVasitolVaso-80Vaso-80 UnicellesVaso-80 uniceliesVasodiatolVasolatdelt rate-20",,,78-11-5,6518,,"","",25520,"",,,Pentaerythritol tetranitrate,1133,,,,"InChI=1/C5H8N4O12/c10-6(11)18-1-5(2-19-7(12)13,3-20-8(14)15)4-21-9(16)17/h1-4H2","[3-nitrooxy-2,2-bis(nitrooxymethyl)propyl] nitrate",http://www.biospider.ca/saved_files/mol/,C(C(CO[N+](=O)[O-])(CO[N+](=O)[O-])CO[N+](=O)[O-])O[N+](=O)[O-],C(C(CO[N+](=O)[O-])(CO[N+](=O)[O-])CO[N+](=O)[O-])O[N+](=O)[O-],C5H8N4O12,316.013870,,140.5 oC,,,"0.043 mg/mL at 25 oC [RINKENBACK,WH (1965)]",,,,"Oral 
Inhalation 
(S575)",,"Nitrate's toxicity is a result of it's conversion to nitrite once in the body. Nitrite causes the autocatalytic oxidation of oxyhemoglobin to hydrogen peroxide and methemoglobin. This elevation of methemoglobin levels is a condition known as methemoglobinemia, and is characterized by tissue hypoxia, as methemoglobin cannot bind oxygen. (V305, V306, ","Intake of some amount of nitrates and nitrites is a normal part of the nitrogen cycle in humans. In vivo conversion of nitrates to nitrites can occur in the gastrointestional tract under the right conditions, significantly enhancing nitrates' toxic potency. The major metabolic pathway for nitrate is conversion to nitrite, and then to ammonia. Nitrites, nitrates, and their metabolites are excreted in the urine. (S575)",,,"2A, probably carcinogenic to humans. (R264)",,,Nitrate and nitrite poisoning causes methemoglobinemia. Nitrites may cause pregnancy complications and developmental effects. They may also be carcinogenic. (S575),"Nitrate and nitrite poisoning causes methemoglobinemia. Symptoms include cyanosis, cardiac dysrhythmias and circulatory failure, and progressive central nervous system (CNS) effects. CNS effects can range from mild dizziness and lethargy to coma and convulsions. (S575)","Methemoglobinemia can be treated with supplemental oxygen and methylene blue 1% solution administered intravenously slowly over five minutes followed by IV flush with normal saline. Methylene blue restores the iron in hemoglobin to its normal (reduced) oxygen-carrying state. (V306, ",P69905;P68871;P02042;P02100;P69891;P69892;Q6B0K9;P09105;P02008
272,T3D0271,2009-03-06 18:58:25 UTC,2009-08-20 20:38:12 UTC,Styrene,Organic Compound;Aromatic Hydrocarbon;Industrial Precursor/Intermediate,"AnnameneBenzene, ethenyl-Benzene, vinyl-Bulstren K-525-19CarineCinnameneCinnamenolCinnaminolCinnamolDiarex hf 77EthenylbenzeneEthenylbenzene (styrene)Ethylene, phenyl-FEMA No. 3233FEMA Number 3234Monomer, styrenePhenethylenePhenylethenePhenylethylenePhenylethylene, inhibitedPolystyrenePolystyrene high mol. WT.Polystyrene med mol. WT.StiroloStirolo [italian]Stirolo(italian)StyreenStyreen [dutch]Styreen(dutch)StyrenStyren [czech]Styren(czech)Styrene (monomer)Styrene monomerStyrene monomer, inhibitedStyrene monomer, inhibited [UN2055] [Flammable liquid]StyrolStyrol (german)Styrol [german]StyroleStyroleneStyronStyropolStyropol soStyroporViny lbenzolVinyl benzeneVinylbenzenVinylbenzen [czech]Vinylbenzen [dutch]Vinylbenzen(czech)VinylbenzeneVinylbenzene (styrene)Vinylbenzene, inhibitedVinylbenzolvinylbenzene (ACD/Name 4.0)","Styrene is an aromatic hydrocarbon widely used to make plastics and rubber. It is a precursor to polystyrene and may be found in insulation, fiberglass, plastic pipes, automobile parts, shoes, drinking cups and other food containers, and carpet backing. Low levels of styrene also occur naturally in a variety of foods such as fruits, vegetables, nuts, beverages, and meats. Small amounts of styrene can be transferred to food from styrene-based packaging material. (W504)",,100-42-5,7501,,C07083,"",27452,CPD-1075,,,Styrene,,,,http://en.wikipedia.org/wiki/Styrene,"InChI=1/C8H8/c1-2-8-6-4-3-5-7-8/h2-7H,1H2",ethenylbenzene,http://www.biospider.ca/saved_files/mol/b56ad842a1cad8dee303d16ddea9eece_1237965305.mol,C=CC1=CC=CC=C1,C=CC1=CC=CC=C1,C8H8,104.062600,Colorless liquid.,-31 oC,,,"0.31 mg/mL at 25 oC [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral
Inhalation
Dermal
(W505)","Cytochrome P450 2B6 (P20813)
Cytochrome P450 2E1 (P05181)
Cytochrome P450 2F1 (P24903)
(W504)","Styrene 7,8-oxide, a metabolite of styrene, can form DNA adducts by binding to deoxyguanosine. It is also mutagenic and causes increased frequency of sister chromatid exchange, chromosomal aberrations, micronucleated cells, and DNA strand breaks. (W504)","Styrene may be absorbed following ingestion, inhalation, or dermal exposure. It distributes throughout the body in the blood, concentrating in the adipose tissue, kidney, and liver. The primary metabolic pathway is oxidation of the side chain by cytochrome P450 to form styrene 7,8-oxide. Styrene oxide is predominantly metabolized by epoxide hydrolase to form styrene glycol; the styrene glycol is subsequently converted to mandelic acid, phenylglyoxylic acid, and hippuric acid. Styrene 7,8-oxide can also be conjugated with glutathione to ultimately form phenylhydroxylethylmercapturic acids. A minor pathway of styrene metabolism involves the formation of phenylacetaldehyde from styrene 7,8-oxide or cytochrome P450 conversion of styrene to pheylethanol and subsequent metabolism to phenylacetic acid. An alternative minor pathway involves ring oxidation resulting in the production of styrene 3,4-oxide, which is further metabolized to 4-vinylphenol. The metabolites of styrene are excreted mainly in the urine. (R504)","LD50: 316 mg/kg (Oral, Mouse) (R263)
LD50: 898 mg/kg (Intraperitoneal, Rat) (R263)
LC50: 24 g/m3 over 4 hours (Inhalation, Rat) (R263)",,"2B, probably carcinogenic to humans. (R264)","Styrene is used to make plastics and rubber. It is a precursor to polystyrene and may be found in insulation, fiberglass, plastic pipes, automobile parts, shoes, drinking cups and other food containers, and carpet backing. Low levels of styrene also occur naturally in a variety of foods such as fruits, vegetables, nuts, beverages, and meats. Small amounts of styrene can be transferred to food from styrene-based packaging material. (W504)","Acute Inhalation: 2 ppm (R260)
Chronic Inhalation: 0.2 ppm (R260)
Acute Oral: 0.1 mg/kg/day (R260)","Styrene causes nervous system depression and may be carcinogenic. Animals studies have also shown that hearing loss and liver damage may occur. (W504, W505)","Breathing high levels of styrene may cause nervous system effects such as changes in color vision, tiredness, feeling drunk, slowed reaction time, concentration problems, or balance problems. Chest burning, wheezing, and dyspnea may also occur.  Styrene is irritating to the skin, eyes, and respiratory tract. (W504, W505)",Treatment is mainly symptomatic and supportive. Respiratory assistance may be needed. (W505),DNA
274,T3D0273,2009-03-06 18:58:25 UTC,2009-08-16 02:17:15 UTC,"1,2,3,4,6,7,8-Heptachlorodibenzofuran",Organic Compound;Industrial By-product/Pollutant;Aromatic Hydrocarbon;Organochloride;Dibenzofuran,"1,2,3,4,6,7,8-Hepta polychlorinated dibenzofuran1,2,3,4,6,7,8-Heptachlorodibenzo[b,d]furanDibenzofuran, 1,2,3,4,6,7,8-heptachloro-Dibenzofuran, heptachloro-HCDBF CPDHeptachlorodibenzofuran","Chlorinated dibenzofurans (CDFs) are a family of chemical that contain one to eight chlorine atoms attached to the carbon atoms of the parent chemical, dibenzofuran. The CDF family contains 135 individual compounds (known as congeners) with varying harmful health and environmental effects. Of these 135 compounds, those that contain chlorine atoms at the 2,3,7,8-positions of the parent dibenzofuran molecule are especially harmful. Other than for laboratory use of small amounts of CDFs for research and development purposes, these chemicals are not deliberately produced by industry. Most CDFs are produced in very small amounts as unwanted impurities of certain products and processes utilizing chlorinated compounds. Only a few of the 135 CDF compounds have been produced in large enough quantities so that their properties, such as color, smell, taste, and toxicity could be studied. (S290)",,"67562-39-4
",38199,,"","","",1-AMINO-PROPAN-2-OL,,,"1,2,3,4,6,7,8-Heptachlorodibenzofuran",,,,,InChI=1/C12HCl7O/c13-3-1-2-4-6(15)7(16)8(17)10(19)12(4)20-11(2)9(18)5(3)14/h1H,"1,2,3,4,6,7,8-heptachlorodibenzofuran",http://www.biospider.ca/saved_files/mol/,C1=C2C3=C(C(=C(C(=C3Cl)Cl)Cl)Cl)OC2=C(C(=C1Cl)Cl)Cl,C1=C2C3=C(C(=C(C(=C3Cl)Cl)Cl)Cl)OC2=C(C(=C1Cl)Cl)Cl,C12HCl7O,405.784710,Colorless crystals.,233 oC,,,"1.35e-09 mg/mL at 25 oC [FLETCHER,CL & MACKAY,WA (1993)]",,,,"Occupational exposure to dibenzofuran may occur through inhalation and dermal contact, particularly at sites where coal tar, coal tar derivatives, and creosote are produced and used. Consumption of contaminated water and food are the primary sources of exposure for the general population. (S290)",,"Dibenzofurans bind the aryl hydrocarbon receptor, which increases its ability to activate transcription in the XRE promoter region. This alters the expression of a number of genes. (S285)","No information on the metabolism of dibenzofuran in mammalian organisms was found in the available literature. The bacteria Sphingomonas, Brevibacterium, Terrabacter, and Staphylococcus auricularis degrade dibenzofuran to 2,2',3-trihydroxybiphenyl via dibenzofuran 4,4a-dioxygenase. (S290)",,,"3, not classifiable as to its carcinogenicity to humans. (R264)","CDFs are created from production of coal tar and during incineration. They are used as insecticides, in the production of PVC, and in industrial bleaching. (S290)",,"CDFs cause vomiting and diarrhea, anemia, more frequent lung infections, numbness and other effects on the nervous system, and mild changes in the liver. However, there were no permanent liver changes or definite liver damage found in  people who ingested CDFs. (S290)","Skin and eye irritations, especially severe acne, darkened skin color, and swollen eyelids with discharge are the most obvious health effects of the CDF poisoning. (S290)",,P03372;Q92731;P35869
276,T3D0275,2009-03-06 18:58:25 UTC,2009-08-04 21:28:10 UTC,Adamsite,Organic Compound;Arsenic Compound,"10-CHLORO-5,10-DIHYDROPHENARSAZINE10-Chloro-5, 10-dihydrophenarsazine10-Chloro-5,10-dihydroarsacridine10-chloro-5,10-dihydrophenarsazine (ACD/Name 4.0)5-Aza-10-arsenaanthracene chlorideAdamsitAdamsiteCaswell No. 648Chloro diphenylaminearsineChlorophenarsazeneDMDiphenylamine chloroarsineDiphenylamine chloroarsine [UN1698] [Poison]DiphenylaminechlorarsineDiphenylaminechloroarsineDiphenylaminochloroarsineFenarsazinchlorid [czech]Phenarsazine chloridePhenarsazine chloride (acn)Phenarsazine, 10-chloro-Phenarsazine, 10-chloro-5,10-dihydro-Phenarsazine, 10-chloro-5,10-dihydro- ( )Phenazarsine chlorideWLN: T C666 B-AS- IMJ BG","Adamsite is an organoarsenic compound which belongs to the group of chemical warfare agents known as vomiting agents or sneeze gases. Due to its toxicity, it is nowadays considered obsolete. Arsenic is a chemical element that has the symbol As and atomic number 33. It is a poisonous metalloid that has many allotropic forms: yellow (molecular non-metallic) and several black and grey forms (metalloids) are a few that are seen. Three metalloidal forms of arsenic with different crystal structures are found free in nature (the minerals arsenopyrite and the much rarer arsenolamprite and pararsenolamprite), but it is more commonly found as a compound with other elements. (R027, R004)",,578-94-9,11362,,"","","","",,C010283,Adamsite,,,,,"InChI=1/C12H9AsClN/c14-13-9-5-1-3-7-11(9)15-12-8-4-2-6-10(12)13/h1-8,15H",10-chloro-5H-phenarsazinine,http://www.biospider.ca/saved_files/mol/,C1=CC=C2C(=C1)NC3=CC=CC=C3[As]2Cl,C1=CC=C2C(=C1)NC3=CC=CC=C3[As]2Cl,C12H9AsClN,276.963950,Yellow or green crystals.,195 oC,,,"",,,,"Oral 
Inhalation 
Dermal 
(R009)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Arsenite methyltransferase (Q9HBK9) 
(R164)","Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carginogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (R001, R054)","Arsenic is absorbed mainly by inhalation or ingestion, as to a lesser extent, dermal exposure. It is then distributed throughout the body, where it is reduced into arsenite if necessary, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant. (R055)","LD50: 35 mg/kg (Intravenous, Mouse) (R261)",,"1, carcinogenic to humans. (R264)",Adamsite is used mainly as a riot control agent. (R027),"Acute Oral: 0.005 mg/kg/day (R260) 
Chronic Oral: 0.0003 mg/kg/day (R260) 
Chronic Inhalation: 0.01 mg/m3 (R260)","Arsenic poisoning can lead to death from multi-system organ failure, probably from necrotic cell death, not apoptosis. Arsenic is also a known carcinogen, esepcially in skin, liver, bladder and lung cancers. (R001, R055)","Exposure to lower levels of arsenic can cause nausea and vomiting, decreased production of red and white blood cells, abnormal heart rhythm, damage to blood vessels, and a sensation of ","Arsenic poisoning can be treated by chelation therapy, using chelating agents such as dimercaprol, EDTA or DMSA. Charcoal tablets may also be used for less severe cases. In addition, maintaining a diet high in sulfur helps eliminate arsenic from the body. (R055)",P68032;P68133;P62736;P60709;P63261;P63267;P10515;P23025;P03372;P04150;P00390;P00738;P69905;P68871;Q14145;P09874;A6NKZ8 ;Q99867;Q9H853;P08559;P29803;P11177;O00330;Q16881;Q9NNW7;Q86VQ6;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2
277,T3D0276,2009-03-06 18:58:25 UTC,2009-08-26 14:32:33 UTC,Arsenic trisulfide,Inorganic Compound;Arsenic Compound,"Arsenic redArsenic sesquisulfideArsenic sesquisulphideArsenic sulfide (As0.4S0.6)Arsenic sulfide (As2S3)Arsenic sulfide (As2S3), (yellow)Arsenic sulfide (As2S4)Arsenic sulfide [NA1557] [Poison]Arsenic sulfide yellowArsenic sulphideArsenic sulphides, naturalArsenic tersulfideArsenic tersulphideArsenic trisulfideArsenic trisulfide [NA1557] [Poison]Arsenic trisulphideArsenic yellowArsenious sulfideArsenious sulphideArsenous sulfideAuripigmentAuripigmentumC.I. Pigment Yellow 39Diarsenic trisulfideDiarsenic trisulphideKing's goldOrpimentPigment Yellow 39SHIOSekioYellow arsenic sulfide","Arsenic sulfide is a sulfide of arsenic that occurs as the mineral orpiment. In its natural form it is considered non-toxic due to its low solubility, however in its crystalline form it tends to oxidize into arsenic trioxide. In addition, commercial orpiment often contains substantial amounts of arsenic oxides.  Arsenic is a chemical element that has the symbol As and atomic number 33. It is a poisonous metalloid that has many allotropic forms: yellow (molecular non-metallic) and several black and grey forms (metalloids) are a few that are seen. Three metalloidal forms of arsenic with different crystal structures are found free in nature (the minerals arsenopyrite and the much rarer arsenolamprite and pararsenolamprite), but it is more commonly found as a compound with other elements. (R004, R654)",,1303-33-9,5359595,,"","","","",,C045816,Arsenic trisulfide,,,,http://en.wikipedia.org/wiki/arsenic sulfide,InChI=1/2AsH6.3S/h2*1H6;;;/q2*+3;3*-2,arsenic; hydrogen sulfide,http://www.biospider.ca/saved_files/mol/,S.[As],S1[As]2S[As]3S[As]1S[As](S2)S3,AsH2S,108.909320,Yellow or red crystals.,"",,,"",,,,"Oral 
Inhalation 
Dermal 
(R009)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Arsenite methyltransferase (Q9HBK9) 
(R164)","Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carginogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (R001, R054)","Arsenic is absorbed mainly by inhalation or ingestion, as to a lesser extent, dermal exposure. It is then distributed throughout the body, where it is reduced into arsenite if necessary, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant. (R055)","LD50: 185 mg/kg (Oral, Rat) (R655)
LD50: 936 mg/kg (Dermal, Rat) (R655)",Not available.,"1, carcinogenic to humans. (R264)","Arsenic sulfide has been used as pigment, tanning agent, photoresist, and chalcogenide glass. (R654)","Acute Oral: 0.005 mg/kg/day (R260) 
Chronic Oral: 0.0003 mg/kg/day (R260) 
Chronic Inhalation: 0.01 mg/m3 (R260)","Arsenic poisoning can lead to death from multi-system organ failure, probably from necrotic cell death, not apoptosis. Arsenic is also a known carcinogen, esepcially in skin, liver, bladder and lung cancers. (R001, R055)","Exposure to lower levels of arsenic can cause nausea and vomiting, decreased production of red and white blood cells, abnormal heart rhythm, damage to blood vessels, and a sensation of burn (R001).","Arsenic poisoning can be treated by chelation therapy, using chelating agents such as dimercaprol, EDTA or DMSA. Charcoal tablets may also be used for less severe cases. In addition, maintaining a diet high in sulfur helps eliminate arsenic from the body. (R055)",P68032;P68133;P62736;P60709;P63261;P63267;P10515;P23025;P03372;P04150;P00390;P00738;P69905;P68871;P08559;P29803;P11177;Q14145;P09874;A6NKZ8 ;Q99867;Q9H853;O00330;Q16881;Q9NNW7;Q86VQ6;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2
278,T3D0277,2009-03-06 18:58:25 UTC,2009-08-04 21:28:11 UTC,Arsenic disulfide,Inorganic Compound;Arsenic Compound,"Arsenic disulfideArsenic monosulfideArsenic sulfide (As2S2)Arsenic sulfide (As3S3)Arsenic sulfide redArsino, thioxo-Caswell No. 058Red arsenic glassRuby arsenicThioxoarsino","Arsenic disulfide is a sulfide of arsenic that occurs as the mineral realgar. Arsenic is a chemical element that has the symbol As and atomic number 33. It is a poisonous metalloid that has many allotropic forms: yellow (molecular non-metallic) and several black and grey forms (metalloids) are a few that are seen. Three metalloidal forms of arsenic with different crystal structures are found free in nature (the minerals arsenopyrite and the much rarer arsenolamprite and pararsenolamprite), but it is more commonly found as a compound with other elements. (R004)",,1303-32-8,6328537,,"","","","",,,Arsenic disulfide,,,,,InChI=1/AsHS/c1-2/h2H,sulfanylarsenic,http://www.biospider.ca/saved_files/mol/,S[As],S[As],AsHS,107.901490,Red crystals.,"",,,"",,,,"Oral 
Inhalation 
Dermal 
(R009)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Arsenite methyltransferase (Q9HBK9) 
(R164)","Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carginogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (R001, R054)","Arsenic is absorbed mainly by inhalation or ingestion, as to a lesser extent, dermal exposure. It is then distributed throughout the body, where it is reduced into arsenite if necessary, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant. (R055)",Not available.,Not available.,"1, carcinogenic to humans. (R264)","Arsenic disulfide (As), also known as red orpiment and ruby arsenic, is used as a pigment in the manufacture of fireworks and paints (S245).","Acute Oral: 0.005 mg/kg/day (R260) 
Chronic Oral: 0.0003 mg/kg/day (R260) 
Chronic Inhalation: 0.01 mg/m3 (R260)","Arsenic poisoning can lead to death from multi-system organ failure, probably from necrotic cell death, not apoptosis. Arsenic is also a known carcinogen, esepcially in skin, liver, bladder and lung cancers. (R001, R055)","Exposure to lower levels of arsenic can cause nausea and vomiting, decreased production of red and white blood cells, abnormal heart rhythm, damage to blood vessels, and a sensation of burn (R001).","Arsenic poisoning can be treated by chelation therapy, using chelating agents such as dimercaprol, EDTA or DMSA. Charcoal tablets may also be used for less severe cases. In addition, maintaining a diet high in sulfur helps eliminate arsenic from the body. (R055)",P68032;P68133;P62736;P60709;P63261;P63267;P10515;P23025;P03372;P04150;P00390;P00738;P69905;P68871;P08559;P29803;P11177;Q14145;P09874;A6NKZ8 ;Q99867;Q9H853;O00330;Q16881;Q9NNW7;Q86VQ6;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2
279,T3D0278,2009-03-06 18:58:25 UTC,2009-08-25 15:48:47 UTC,Arsenic pentasulfide,Inorganic Compound;Arsenic Compound,Arsenic pentasulfideArsenic sulfideArsenic sulfide (As2S5),"Arsenic pentasulfide is a sulfide of arsenic. Arsenic is a chemical element that has the symbol As and atomic number 33. It is a poisonous metalloid that has many allotropic forms: yellow (molecular non-metallic) and several black and grey forms (metalloids) are a few that are seen. Three metalloidal forms of arsenic with different crystal structures are found free in nature (the minerals arsenopyrite and the much rarer arsenolamprite and pararsenolamprite), but it is more commonly found as a compound with other elements. (R004)",,1303-34-0,6451221,,"","","","",,,Arsenic pentasulfide,,,,,InChI=1/2AsH3.5H2S/h2*1H3;5*1H2,arsenic; hydrogen sulfide,http://www.biospider.ca/saved_files/mol/,S.S.S.S.S.[As].[As],S.S.S.S.S.[As].[As],As2H10S5,319.781800,Yellow-brown glassy solid (S209).,"",,,"",,,,"Oral 
Inhalation 
Dermal 
(R009)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Arsenite methyltransferase (Q9HBK9) 
(R164)","Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carginogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (R001, R054)","Arsenic is absorbed mainly by inhalation or ingestion, as to a lesser extent, dermal exposure. It is then distributed throughout the body, where it is reduced into arsenite if necessary, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant. (R055)",Not available.,Not available.,"1, carcinogenic to humans. (R264)",Arsenic pentasulfide is used as a pigment and as a light filter in thin sheets (S209).,"Acute Oral: 0.005 mg/kg/day (R260) 
Chronic Oral: 0.0003 mg/kg/day (R260) 
Chronic Inhalation: 0.01 mg/m3 (R260)","Arsenic poisoning can lead to death from multi-system organ failure, probably from necrotic cell death, not apoptosis. Arsenic is also a known carcinogen, esepcially in skin, liver, bladder and lung cancers. (R001, R055)","Exposure to lower levels of arsenic can cause nausea and vomiting, decreased production of red and white blood cells, abnormal heart rhythm, damage to blood vessels, and a sensation of burn (R001).","Arsenic poisoning can be treated by chelation therapy, using chelating agents such as dimercaprol, EDTA or DMSA. Charcoal tablets may also be used for less severe cases. In addition, maintaining a diet high in sulfur helps eliminate arsenic from the body. (R055)",P68032;P68133;P62736;P60709;P63261;P63267;P10515;P23025;P03372;P04150;P00390;P00738;P69905;P68871;P08559;P29803;P11177;P68366;Q14145;P09874;A6NKZ8 ;Q99867;Q9H853;O00330;Q16881;Q9NNW7;Q86VQ6;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2
280,T3D0279,2009-03-06 18:58:26 UTC,2009-08-04 21:28:11 UTC,Arsenic trichloride,Inorganic Compound;Arsenic Compound,Arsenic butterArsenic chlorideArsenic chloride (ascl3)Arsenic trichloride [UN1560] [Poison]Arsenic(3+) chlorideArsenic(III) chlorideArsenic(III) trichlorideArsenious chlorideArsenous chlorideArsenous trichlorideArsenous-trichloride-AsCl3Butter of arsenicCaustic arsenic chlorideCaustic oil of arsenicChlorure arsenieuxChlorure arsenieux [french]Chlorure d'arsenicChlorure d'arsenic [french]Fuming liquid arsenicTrichloroarsineTrichlorure d'arsenicTrichlorure d'arsenic [french],"Arsenic trichloride is a chloride of arsenic prepared by the treatment of arsenic(III) oxide with concentrated hydrochloric acid, followed by distillation. It is used in preparation of many chloroderivatives of arsenic that have pharmaceutical and insecticide applications. Arsenic is a chemical element that has the symbol As and atomic number 33. It is a poisonous metalloid that has many allotropic forms: yellow (molecular non-metallic) and several black and grey forms (metalloids) are a few that are seen. Three metalloidal forms of arsenic with different crystal structures are found free in nature (the minerals arsenopyrite and the much rarer arsenolamprite and pararsenolamprite), but it is more commonly found as a compound with other elements. (R004, R656)",,7784-34-1,24570,,"","","","",,C050510,Arsenic trichloride,,,,,InChI=1/AsCl3/c2-1(3)4,trichloroarsane,http://www.biospider.ca/saved_files/mol/,Cl[As](Cl)Cl,Cl[As](Cl)Cl,AsCl3,179.828160,Colourless liquid (R656).,-16 oC,,,"",,,,"Oral 
Inhalation 
Dermal 
(R009)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Arsenite methyltransferase (Q9HBK9) 
(R164)","Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carginogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (R001, R054)","Arsenic is absorbed mainly by inhalation or ingestion, as to a lesser extent, dermal exposure. It is then distributed throughout the body, where it is reduced into arsenite if necessary, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant. (R055)","LD50: 145 mg/kg (Oral, Mouse) (R657)",Not available.,"1, carcinogenic to humans. (R264)","Arsenic trichloride is used in ceramics, organic chemical syntheses, and in the preparation of pharmaceuticals. (R656)","Acute Oral: 0.005 mg/kg/day (R260) 
Chronic Oral: 0.0003 mg/kg/day (R260) 
Chronic Inhalation: 0.01 mg/m3 (R260)","Arsenic poisoning can lead to death from multi-system organ failure, probably from necrotic cell death, not apoptosis. Arsenic is also a known carcinogen, esepcially in skin, liver, bladder and lung cancers. (R001, R055)","Exposure to lower levels of arsenic can cause nausea and vomiting, decreased production of red and white blood cells, abnormal heart rhythm, damage to blood vessels, and a sensation of burn (R001).","Arsenic poisoning can be treated by chelation therapy, using chelating agents such as dimercaprol, EDTA or DMSA. Charcoal tablets may also be used for less severe cases. In addition, maintaining a diet high in sulfur helps eliminate arsenic from the body. (R055)",P68032;P68133;P62736;P60709;P63261;P63267;P10515;P23025;P03372;P04150;P00390;P00738;P69905;P68871;P08559;P29803;P11177;Q14145;P09874;A6NKZ8 ;Q99867;Q9H853;O00330;Q16881;Q9NNW7;Q86VQ6;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2
283,T3D0282,2009-03-06 18:58:26 UTC,2009-08-11 22:05:44 UTC,Arsenous acid,Inorganic Compound;Arsenic Compound,"Arsenenous acid, sodium saltArsenious acid, monosodium saltArsenious acid, sodium saltArsenite de sodium [french]Arsenite, sodiumAtlas ""a""Caswell No. 744Chem pels cChem-Sen 56Kill-allPeniteProdalumnolProdalumnol doubleRat death liquidS7400_SIGMASodanitSodium (meta)arseniteSodium (meta)arsenite solutionSodium arseniteSodium arsenite solutionSodium arsenite, techSodium dioxoarsenateSodium metaarsenite","Arsenous acid is a chemical compound of arsenic. It is the hydrolyzed form of arsenic trioxide and is found in aqueous solutions. Arsenic is a chemical element that has the symbol As and atomic number 33. It is a poisonous metalloid that has many allotropic forms: yellow (molecular non-metallic) and several black and grey forms (metalloids) are a few that are seen. Three metalloidal forms of arsenic with different crystal structures are found free in nature (the minerals arsenopyrite and the much rarer arsenolamprite and pararsenolamprite), but it is more commonly found as a compound with other elements. (R004, R658)",,13464-58-9,443495,,C06697,"",49900,"",,C032793,Arsenous acid,,,,,InChI=1/AsH3O3/c2-1(3)4/h2-4H,arsorous acid,http://www.biospider.ca/saved_files/mol/,[O-][As]=O.[Na+],O[As]=O,AsNaO2,129.901200,White crystals.,"",,,"",,,,"Oral 
Inhalation 
Dermal 
(R009)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Arsenite methyltransferase (Q9HBK9) 
(R164)","Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carginogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (R001, R054)","Arsenic is absorbed mainly by inhalation or ingestion, as to a lesser extent, dermal exposure. It is then distributed throughout the body, where it is reduced into arsenite if necessary, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant. (R055)","LD50: 41 mg/kg (oral, rat) (S246); 12 mg/kg (oral, rabbit) (S246); LD50: 150 mg/kg (dermal, rat) (S246).",Not availble.,"1, carcinogenic to humans. (R264)",,"Acute Oral: 0.005 mg/kg/day (R260) 
Chronic Oral: 0.0003 mg/kg/day (R260) 
Chronic Inhalation: 0.01 mg/m3 (R260)","Arsenic poisoning can lead to death from multi-system organ failure, probably from necrotic cell death, not apoptosis. Arsenic is also a known carcinogen, esepcially in skin, liver, bladder and lung cancers. (R001, R055)","Exposure to lower levels of arsenic can cause nausea and vomiting, decreased production of red and white blood cells, abnormal heart rhythm, damage to blood vessels, and a sensation of ","Arsenic poisoning can be treated by chelation therapy, using chelating agents such as dimercaprol, EDTA or DMSA. Charcoal tablets may also be used for less severe cases. In addition, maintaining a diet high in sulfur helps eliminate arsenic from the body. (R055)",P68032;P68133;P62736;P60709;P63261;P63267;P10515;P23025;P03372;P04150;P00390;P00738;P69905;P68871;P08559;P29803;P11177;P68371;Q14145;P09874;A6NKZ8 ;Q99867;Q9H853;O00330;Q16881;Q9NNW7;Q86VQ6;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2
284,T3D0283,2009-03-06 18:58:26 UTC,2009-08-04 21:28:11 UTC,Arsenenic acid,Inorganic Compound;Arsenic Compound,"AArsenite (AsO33-)ARSENIOUS OXIDE, 99.999%ASTArsenenic acidArsenenous acid, potassium saltArsenic (III) oxideArsenic (III) trioxideArsenic (white)Arsenic acid, (O3-As-H)Arsenic oxideArsenic oxide (3)Arsenic oxide (As2O3)Arsenic sesquioxideArsenic sesquioxide (As2O3)Arsenic trioxideArsenicum albumArsenious acidArsenious oxideArseniteArsenoliteArsenous acidArsenous acid anhydrideArsenous acid ion(3-)Arsenous anhydrideArsenous oxideArsenous oxide anhydrideArsenous trioxideArsodentArsorous acidAs(OH)3ClaudeliteClaudetiteCrude arsenicDiarsenic oxideDiarsenic trioxideDiarsonic trioxideH3AsO3Metaarsenic acidNSC3060 (TRIPOTASSIUM SALT)Potassium arsenitePotassium arsenite, (KAsO2)TASTrihydroxidoarsenicTrioxoarsenate(III)Trioxoarsenic acidWhite arsenic[As(OH)3]arsenite(3-)trihydrogen trioxoarsenate(3-)trioxidoarsenate(3-)trioxoarsenate(3-)","Arsenenic acid is an arsenic compound closely related to arsenous acid. Arsenic is a chemical element that has the symbol As and atomic number 33. It is a poisonous metalloid that has many allotropic forms: yellow (molecular non-metallic) and several black and grey forms (metalloids) are a few that are seen. Three metalloidal forms of arsenic with different crystal structures are found free in nature (the minerals arsenopyrite and the much rarer arsenolamprite and pararsenolamprite), but it is more commonly found as a compound with other elements. (R004)",,10102-53-1,545,,C06697,"",49900,CPD-763,,,Arsenenic acid,,,,,InChI=1/AsO3/c2-1(3)4/q-3,arsenite,http://www.biospider.ca/saved_files/mol/9c7183b48cb0747a5584dc9996c4b3c5_1237966620.mol,[O-][As]([O-])[O-],[O-][As]([O-])[O-],AsO3,122.906340,White crystals.,Boiling Pt : 465 oC,,,"",,,,"Oral 
Inhalation 
Dermal 
(R009)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Arsenite methyltransferase (Q9HBK9) 
(R164)","Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carginogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (R001, R054)","Arsenic is absorbed mainly by inhalation or ingestion, as to a lesser extent, dermal exposure. It is then distributed throughout the body, where it is reduced into arsenite if necessary, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant. (R055)",Not available.,Not available.,"1, carcinogenic to humans. (R264)","It is found free in nature, but it is more commonly found as a compound with other elements. (R004)","Acute Oral: 0.005 mg/kg/day (R260) 
Chronic Oral: 0.0003 mg/kg/day (R260) 
Chronic Inhalation: 0.01 mg/m3 (R260)","Arsenic poisoning can lead to death from multi-system organ failure, probably from necrotic cell death, not apoptosis. Arsenic is also a known carcinogen, esepcially in skin, liver, bladder and lung cancers. (R001, R055)","Exposure to lower levels of arsenic can cause nausea and vomiting, decreased production of red and white blood cells, abnormal heart rhythm, damage to blood vessels, and a sensation of ","Arsenic poisoning can be treated by chelation therapy, using chelating agents such as dimercaprol, EDTA or DMSA. Charcoal tablets may also be used for less severe cases. In addition, maintaining a diet high in sulfur helps eliminate arsenic from the body. (R055)",P68032;P68133;P62736;P60709;P63261;P63267;P10515;P23025;P03372;P04150;P00390;P00738;P69905;P68871;P08559;P29803;P11177;Q14145;P09874;A6NKZ8 ;Q99867;Q9H853;O00330;Q16881;Q9NNW7;Q86VQ6;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2
286,T3D0285,2009-03-06 18:58:26 UTC,2009-08-04 21:28:11 UTC,Ammonium arsenate,Inorganic Compound;Arsenic Compound,"Ammonium acid arsenateAmmonium arsenateAmmonium arsenate [UN1546] [Poison]Arsenic acid, diammonium saltDiammonium arsenateDiammonium hydrogen arsenateDiammonium hydrogenarsenateDiammonium monohydrogen arsenateDibasic ammonium arsenateSecondary ammonium arsenate","Ammonium arsenate is a chemical compound derived from arsenic acid. Arsenic is a chemical element that has the symbol As and atomic number 33. It is a poisonous metalloid that has many allotropic forms: yellow (molecular non-metallic) and several black and grey forms (metalloids) are a few that are seen. Three metalloidal forms of arsenic with different crystal structures are found free in nature (the minerals arsenopyrite and the much rarer arsenolamprite and pararsenolamprite), but it is more commonly found as a compound with other elements. (R004)",,7784-44-3,24574,,"","","","",,,Ammonium arsenate,,,,,"InChI=1/AsH3O4.2H3N/c2-1(3,4)5;;/h(H3,2,3,4,5);2*1H3",diazanium hydrogen arsorate,http://www.biospider.ca/saved_files/mol/,[NH4+].[NH4+].O[As](=O)([O-])[O-],[NH4+].[NH4+].O[As](=O)([O-])[O-],AsH9N2O4,175.977830,White crystals.,"",,,"",,,,"Oral 
Inhalation 
Dermal 
(R009)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Arsenite methyltransferase (Q9HBK9) 
(R164)","Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carginogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (R001, R054)","Arsenic is absorbed mainly by inhalation or ingestion, as to a lesser extent, dermal exposure. It is then distributed throughout the body, where it is reduced into arsenite if necessary, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant. (R055)",Not available.,not available.,"1, carcinogenic to humans. (R264)","It is used as herbicide, insecticide,and rodenticide (S247).","Acute Oral: 0.005 mg/kg/day (R260) 
Chronic Oral: 0.0003 mg/kg/day (R260) 
Chronic Inhalation: 0.01 mg/m3 (R260)","Arsenic poisoning can lead to death from multi-system organ failure, probably from necrotic cell death, not apoptosis. Arsenic is also a known carcinogen, esepcially in skin, liver, bladder and lung cancers. (R001, R055)","Exposure to lower levels of arsenic can cause nausea and vomiting, decreased production of red and white blood cells, abnormal heart rhythm, damage to blood vessels, and a sensation of burn (R001).","Arsenic poisoning can be treated by chelation therapy, using chelating agents such as dimercaprol, EDTA or DMSA. Charcoal tablets may also be used for less severe cases. In addition, maintaining a diet high in sulfur helps eliminate arsenic from the body. (R055)",P68032;P68133;P62736;P60709;P63261;P63267;P10515;P23025;P03372;P04150;P00390;P00738;P69905;P68871;P08559;P29803;P11177;Q14145;P09874;A6NKZ8 ;Q99867;Q9H853;O00330;Q16881;Q9NNW7;Q86VQ6;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2
287,T3D0286,2009-03-06 18:58:26 UTC,2009-08-19 18:48:54 UTC,Copper(II) arsenite,Inorganic Compound;Arsenic Compound;Copper Compound,"Acid copper arseniteAir-flo greenArsenious acid (H3AsO3), copper(2+) salt (1:1)Arsenious acid, copper(II) salt (1:1)Arsonic acid, copper(2+) salt (1:1)Arsonic acid, copper(2+) salt (1:1) (9CI)Caswell No. 233Copper arseniteCopper arsenite [UN1586] [Poison]Copper arsonateCopper orthoarseniteCopper(II) arseniteCupric arseniteCupric greenScheele's mineralScheeles greenSwedish green","Copper(II) arsenite is a chemical compound of arsenic and copper derived from arsenous acid. Copper is a chemical element with the symbol Cu and atomic number 29. Copper is an essential elements in plants and animals as it is required for the normal functioning of more than 30 enzymes. It occurs naturally throughout the environment in rocks, soil, water, and air. Arsenic is a chemical element that has the symbol As and atomic number 33. It is a poisonous metalloid that has many allotropic forms: yellow (molecular non-metallic) and several black and grey forms (metalloids) are a few that are seen. Three metalloidal forms of arsenic with different crystal structures are found free in nature (the minerals arsenopyrite and the much rarer arsenolamprite and pararsenolamprite), but it is more commonly found as a compound with other elements. (R004, R513, R514)",,10290-12-7,25130,,"","","","",,,Copper(II) arsenite,,,,,InChI=1/AsHO3.Cu/c2-1(3)4;/h2H;/q-2;+2,copper hydrogen arsorite,http://www.biospider.ca/saved_files/mol/,O[As]([O-])[O-].[Cu+2],[Cu+2].(O-)[As](O-)O,AsCuHO3,186.843770,Yellow/green powder.,"",,,"",,,,"Oral 
Inhalation 
Dermal 
(R009)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Arsenite methyltransferase (Q9HBK9) 
High affinity copper uptake protein 1 (O15431) 
Probable low affinity copper uptake protein 2 (O15432) Serum albumin (P02768) 
Ceruloplasmin (P00450) 
Copper-transporting ATPase 1 (Q04656) 
Copper-transporting ATPase 2 (P35670) 
Copper transport protein ATOX1 (O00244) 
Copper chaperone for superoxide dismutase (O14618) 
Cytochrome c oxidase copper chaperone (Q14061) 
(R164, R513, R528)","Excess copper is sequestered within hepatocyte lysosomes, where it is complexed with metallothionein. Copper hepatotoxicity is believed to occur when the lysosomes become saturated and copper accumulates in the nucleus, causing nuclear damage. This damage is possibly a result of oxidative damage, including lipid peroxidation. Copper inhibits the sulfhydryl group enzymes such as glucose-6-phosphate 1-dehydrogenase, glutathione reductase, and paraoxonases, which protect the cell from free oxygen radicals. It also influences gene expression and is a co-factor for oxidative enzymes such as cytochrome C oxidase and lysyl oxidase. In addition, the oxidative stress induced by copper is thought to activate acid sphingomyelinase, which lead to the production of ceramide, an apoptotic signal, as well as cause hemolytic anemia. Copper-induced emesis results from stimulation of the vagus nerve. Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carginogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (R001, R054, R513, R523, R525, R526)","Copper is mainly absorbed through the gastrointestinal tract, but it can also be inhalated and absorbed dermally. It passes through the basolateral membrane, possibly via regulatory copper transporters, and is transported to the liver and kidney bound to serum albumin. The liver is the critical organ for copper homoeostasis. In the liver and other tissues, copper is stored bound to metallothionein, amino acids, and in association with copper-dependent enzymes, then partitioned for excretion through the bile or incorporation into intra- and extracellular proteins. The transport of copper to the peripheral tissues is accomplished through the plasma attached to serum albumin, ceruloplasmin or low-molecular-weight complexes. Copper may induce the production of metallothionein and ceruloplasmin. The membrane-bound copper transporting adenosine triphosphatase (Cu-ATPase) transports copper ions into and out of cells. Physiologically normal levels of copper in the body are held constant by alterations in the rate and amount of copper absorption, compartmental distribution, and excretion. Arsenic is absorbed mainly by inhalation or ingestion, as to a lesser extent, dermal exposure. It is then distributed throughout the body, where it is reduced into arsenite if necessary, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant. (R055, R513, R520)",Not availbale.,10 to 20 grams for an adult human (copper salts). (R273),"1, carcinogenic to humans. (R264)","Formerly wiedely used as pigment in wallpaper, calico printing and as wood preservative, but the use for these purposes is now much diminished, partly on account of liberation of toxic gas dimethyl arsine by action of molds (S248).","Acute Oral: 0.01 mg/kg/day (Copper) (R260) 
Intermediate Oral: 0.01 mg/kg/day (Copper) (R260)
Acute Oral: 0.005 mg/kg/day (Arsenic) (R260) 
Chronic Oral: 0.0003 mg/kg/day (Arsenic) (R260) 
Chronic Inhalation: 0.01 mg/m3 (Arsenic) (R260)","People must absorb small amounts of copper every day because copper is essential for good health, however, high levels of copper can be harmful. Very-high doses of copper can cause damage to your liver and kidneys, and can even cause death. Copper may induce allergic responses in sensitive individuals. Arsenic poisoning can lead to death from multi-system organ failure, probably from necrotic cell death, not apoptosis. Arsenic is also a known carcinogen, esepcially in skin, liver, bladder and lung cancers. (R001, R055, R514, R520)","Breathing high levels of copper can cause irritation of the nose and throat. Ingesting high levels of copper can cause nausea, vomiting, diarrhea, headache, dizziness, and respiratory difficulty. Exposure to lower levels of arsenic can cause nausea and vomiting, decreased production of red and white blood cells, abnormal heart rhythm, damage to blood vessels, and a sensation of burn (R001).","Arsenic poisoning can be treated by chelation therapy, using chelating agents such as dimercaprol, EDTA or DMSA. Charcoal tablets may also be used for less severe cases. In addition, maintaining a diet high in sulfur helps eliminate arsenic from the body. (R055)",P68371;Q15166;P37840;P05067;P11413;P00390;P27169;P68032;P68133;P62736;P60709;P63261;P63267;P10515;P23025;P03372;P04150;P00738;P69905;P68871;Q14145;P09874;A6NKZ8 ;Q99867;Q9H853;P08559;P29803;P11177;O00330;Q16881;Q9NNW7;Q86VQ6;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2
288,T3D0287,2009-03-06 18:58:27 UTC,2009-08-04 21:28:12 UTC,Gallium arsenide,Inorganic Compound;Arsenic Compound,GAASGallium arsenide (gaas)Gallium monoarsenideGallium monoarsenide (gaas),"Gallium arsenide is a chemical compound of gallium and arsenic. It is used to make devices such as microwave frequency integrated circuits, infrared light-emitting diodes, laser diodes and solar cells. It is also a semiconductor. Arsenic is a chemical element that has the symbol As and atomic number 33. It is a poisonous metalloid that has many allotropic forms: yellow (molecular non-metallic) and several black and grey forms (metalloids) are a few that are seen. Three metalloidal forms of arsenic with different crystal structures are found free in nature (the minerals arsenopyrite and the much rarer arsenolamprite and pararsenolamprite), but it is more commonly found as a compound with other elements. (R004, R633)",,1303-00-0,14770,,"","","","",,C043055,Gallium arsenide,,,,http://en.wikipedia.org/wiki/gallium arsenide,InChI=1/As.Ga,gallanylidynearsane,http://www.biospider.ca/saved_files/mol/,[Ga]#[As],[Ga]#[As],AsGa,143.847180,Dark grey solid.,1238 °C (1511 K),,,"",,,,"Oral 
Inhalation 
Dermal 
(R009)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Arsenite methyltransferase (Q9HBK9) 
(R164)","Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carginogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (R001, R054)","Arsenic is absorbed mainly by inhalation or ingestion, as to a lesser extent, dermal exposure. It is then distributed throughout the body, where it is reduced into arsenite if necessary, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant. (R055)","LD50: 4700 mg/kg (Intraperitoneal, Mouse) (R263)",Not availble.,"1, carcinogenic to humans. (R264)","Gallium arsenide is used as a semiconductor, as well as in solar cells, x-ray detection diodes, and laser diodes. (R633)","Acute Oral: 0.005 mg/kg/day (R260) 
Chronic Oral: 0.0003 mg/kg/day (R260) 
Chronic Inhalation: 0.01 mg/m3 (R260)","Arsenic poisoning can lead to death from multi-system organ failure, probably from necrotic cell death, not apoptosis. Arsenic is also a known carcinogen, esepcially in skin, liver, bladder and lung cancers. (R001, R055)","Exposure to lower levels of arsenic can cause nausea and vomiting, decreased production of red and white blood cells, abnormal heart rhythm, damage to blood vessels, and a sensation of burn (R001).","Arsenic poisoning can be treated by chelation therapy, using chelating agents such as dimercaprol, EDTA or DMSA. Charcoal tablets may also be used for less severe cases. In addition, maintaining a diet high in sulfur helps eliminate arsenic from the body. (R055)",P68032;P68133;P62736;P60709;P63261;P63267;P10515;P23025;P03372;P04150;P00390;P00738;P69905;P68871;P08559;P29803;P11177;Q14145;P09874;A6NKZ8 ;Q99867;Q9H853;O00330;Q16881;Q9NNW7;Q86VQ6;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2
289,T3D0288,2009-03-06 18:58:27 UTC,2009-08-25 18:00:55 UTC,Copper arsenate,Inorganic Compound;Arsenic Compound;Copper Compound,Copper Arsenate Hydroxide (cu2(aso4)(oh)),"Copper arsenate is a chemical compound of copper and arsenic. It is derived from arsenic acid and used mainly as a pesticide. Copper is a chemical element with the symbol Cu and atomic number 29. Copper is an essential elements in plants and animals as it is required for the normal functioning of more than 30 enzymes. It occurs naturally throughout the environment in rocks, soil, water, and air. Arsenic is a chemical element that has the symbol As and atomic number 33. It is a poisonous metalloid that has many allotropic forms: yellow (molecular non-metallic) and several black and grey forms (metalloids) are a few that are seen. Three metalloidal forms of arsenic with different crystal structures are found free in nature (the minerals arsenopyrite and the much rarer arsenolamprite and pararsenolamprite), but it is more commonly found as a compound with other elements. (R004, R513, R514, R661)",,10103-61-4,3080685,,"","","","",,,Copper arsenate,,,,,"InChI=1/AsH3O4.Cu/c2-1(3,4)5;/h(H3,2,3,4,5);/q;+1/p-1",dicopper arsorate hydroxide,http://www.biospider.ca/saved_files/mol/,"",[OH-].[Cu++].[Cu++].[O-][As]([O-])([O-])=O,AsCu2HO5,281.763200,Blue-green powder.,"",,,"",,,,"Oral 
Inhalation 
Dermal 
(R009)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Arsenite methyltransferase (Q9HBK9) 
High affinity copper uptake protein 1 (O15431) 
Probable low affinity copper uptake protein 2 (O15432) 
Serum albumin (P02768) 
Ceruloplasmin (P00450) 
Copper-transporting ATPase 1 (Q04656) 
Copper-transporting ATPase 2 (P35670) 
Copper transport protein ATOX1 (O00244) 
Copper chaperone for superoxide dismutase (O14618) 
Cytochrome c oxidase copper chaperone (Q14061) 
(R164, R513, R528)","Excess copper is sequestered within hepatocyte lysosomes, where it is complexed with metallothionein. Copper hepatotoxicity is believed to occur when the lysosomes become saturated and copper accumulates in the nucleus, causing nuclear damage. This damage is possibly a result of oxidative damage, including lipid peroxidation. Copper inhibits the sulfhydryl group enzymes such as glucose-6-phosphate 1-dehydrogenase, glutathione reductase, and paraoxonases, which protect the cell from free oxygen radicals. It also influences gene expression and is a co-factor for oxidative enzymes such as cytochrome C oxidase and lysyl oxidase. In addition, the oxidative stress induced by copper is thought to activate acid sphingomyelinase, which lead to the production of ceramide, an apoptotic signal, as well as cause hemolytic anemia. Copper-induced emesis results from stimulation of the vagus nerve. Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carginogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (R001, R054, R513, R523, R525, R526)","Copper is mainly absorbed through the gastrointestinal tract, but it can also be inhalated and absorbed dermally. It passes through the basolateral membrane, possibly via regulatory copper transporters, and is transported to the liver and kidney bound to serum albumin. The liver is the critical organ for copper homoeostasis. In the liver and other tissues, copper is stored bound to metallothionein, amino acids, and in association with copper-dependent enzymes, then partitioned for excretion through the bile or incorporation into intra- and extracellular proteins. The transport of copper to the peripheral tissues is accomplished through the plasma attached to serum albumin, ceruloplasmin or low-molecular-weight complexes. Copper may induce the production of metallothionein and ceruloplasmin. The membrane-bound copper transporting adenosine triphosphatase (Cu-ATPase) transports copper ions into and out of cells. Physiologically normal levels of copper in the body are held constant by alterations in the rate and amount of copper absorption, compartmental distribution, and excretion. Arsenic is absorbed mainly by inhalation or ingestion, as to a lesser extent, dermal exposure. It is then distributed throughout the body, where it is reduced into arsenite if necessary, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant. (R055, R513, R520)","LD50: 2147 mg/kg (oral, rat) (S249).",10 to 20 grams for an adult human (copper salts). (R273),"1, carcinogenic to humans. (R264)","Copper arsenate is used as an insecticide, herbicide, fungicide, and rodenticide. (R661)","Acute Oral: 0.01 mg/kg/day (Copper) (R260) 
Intermediate Oral: 0.01 mg/kg/day (Copper) (R260)
Acute Oral: 0.005 mg/kg/day (Arsenic) (R260) 
Chronic Oral: 0.0003 mg/kg/day (Arsenic) (R260) 
Chronic Inhalation: 0.01 mg/m3 (Arsenic) (R260)","People must absorb small amounts of copper every day because copper is essential for good health, however, high levels of copper can be harmful. Very-high doses of copper can cause damage to your liver and kidneys, and can even cause death. Copper may induce allergic responses in sensitive individuals. Arsenic poisoning can lead to death from multi-system organ failure, probably from necrotic cell death, not apoptosis. Arsenic is also a known carcinogen, esepcially in skin, liver, bladder and lung cancers. (R001, R055, R514, R520)","Breathing high levels of copper can cause irritation of the nose and throat. Ingesting high levels of copper can cause nausea, vomiting, diarrhea, headache, dizziness, and respiratory difficulty. Exposure to lower levels of arsenic can cause nausea and vomiting, decreased production of red and white blood cells, abnormal heart rhythm, damage to blood vessels, and a sensation of burn (R001).","Arsenic poisoning can be treated by chelation therapy, using chelating agents such as dimercaprol, EDTA or DMSA. Charcoal tablets may also be used for less severe cases. In addition, maintaining a diet high in sulfur helps eliminate arsenic from the body. (R055)",P68032;P68133;P62736;P60709;P63261;P63267;P10515;P23025;P03372;P04150;P00390;P00738;P69905;P68871;P08559;P29803;P11177;P37840;P05067;P11413;P27169;Q15166;Q14145;P09874;A6NKZ8 ;Q99867;Q9H853;O00330;Q16881;Q9NNW7;Q86VQ6;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2
290,T3D0289,2009-03-06 18:58:27 UTC,2009-08-25 21:10:37 UTC,Copper arsenate hydroxide,Inorganic Compound;Arsenic Compound;Copper Compound,"","Copper arsenate hydroxide is a variant of copper arsenate found naturally as the mineral olivenite. Copper is a chemical element with the symbol Cu and atomic number 29. Copper is an essential elements in plants and animals as it is required for the normal functioning of more than 30 enzymes. It occurs naturally throughout the environment in rocks, soil, water, and air. Arsenic is a chemical element that has the symbol As and atomic number 33. It is a poisonous metalloid that has many allotropic forms: yellow (molecular non-metallic) and several black and grey forms (metalloids) are a few that are seen. Three metalloidal forms of arsenic with different crystal structures are found free in nature (the minerals arsenopyrite and the much rarer arsenolamprite and pararsenolamprite), but it is more commonly found as a compound with other elements. (R004, R513, R514, R661)",,16102-92-4,"",,"","","","",,,Copper arsenate hydroxide,,,,,"","",http://www.biospider.ca/saved_files/mol/,"",[OH-].[Cu++].[Cu++].[O-][As]([O-])([O-])=O,"","",Dark olive green crystal (S250).,"",,,"",,,,"Oral 
Inhalation 
Dermal 
(R009)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Arsenite methyltransferase (Q9HBK9) 
High affinity copper uptake protein 1 (O15431) 
Probable low affinity copper uptake protein 2 (O15432) 
Serum albumin (P02768) 
Ceruloplasmin (P00450) 
Copper-transporting ATPase 1 (Q04656) 
Copper-transporting ATPase 2 (P35670) 
Copper transport protein ATOX1 (O00244) 
Copper chaperone for superoxide dismutase (O14618) 
Cytochrome c oxidase copper chaperone (Q14061) 
(R164, R513, R528)","Excess copper is sequestered within hepatocyte lysosomes, where it is complexed with metallothionein. Copper hepatotoxicity is believed to occur when the lysosomes become saturated and copper accumulates in the nucleus, causing nuclear damage. This damage is possibly a result of oxidative damage, including lipid peroxidation. Copper inhibits the sulfhydryl group enzymes such as glucose-6-phosphate 1-dehydrogenase, glutathione reductase, and paraoxonases, which protect the cell from free oxygen radicals. It also influences gene expression and is a co-factor for oxidative enzymes such as cytochrome C oxidase and lysyl oxidase. In addition, the oxidative stress induced by copper is thought to activate acid sphingomyelinase, which lead to the production of ceramide, an apoptotic signal, as well as cause hemolytic anemia. Copper-induced emesis results from stimulation of the vagus nerve. Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carginogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (R001, R054, R513, R523, R525, R526)","Copper is mainly absorbed through the gastrointestinal tract, but it can also be inhalated and absorbed dermally. It passes through the basolateral membrane, possibly via regulatory copper transporters, and is transported to the liver and kidney bound to serum albumin. The liver is the critical organ for copper homoeostasis. In the liver and other tissues, copper is stored bound to metallothionein, amino acids, and in association with copper-dependent enzymes, then partitioned for excretion through the bile or incorporation into intra- and extracellular proteins. The transport of copper to the peripheral tissues is accomplished through the plasma attached to serum albumin, ceruloplasmin or low-molecular-weight complexes. Copper may induce the production of metallothionein and ceruloplasmin. The membrane-bound copper transporting adenosine triphosphatase (Cu-ATPase) transports copper ions into and out of cells. Physiologically normal levels of copper in the body are held constant by alterations in the rate and amount of copper absorption, compartmental distribution, and excretion. Arsenic is absorbed mainly by inhalation or ingestion, as to a lesser extent, dermal exposure. It is then distributed throughout the body, where it is reduced into arsenite if necessary, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant. (R055, R513, R520)",Not available.,10 to 20 grams for an adult human (copper salts). (R273),"1, carcinogenic to humans. (R264)","Copper arsenate hydroxide is used as an insecticide, fungicide, and miticide. (R661)","Acute Oral: 0.01 mg/kg/day (Copper) (R260) 
Intermediate Oral: 0.01 mg/kg/day (Copper) (R260)
Acute Oral: 0.005 mg/kg/day (Arsenic) (R260) 
Chronic Oral: 0.0003 mg/kg/day (Arsenic) (R260) 
Chronic Inhalation: 0.01 mg/m3 (Arsenic) (R260)","People must absorb small amounts of copper every day because copper is essential for good health, however, high levels of copper can be harmful. Very-high doses of copper can cause damage to your liver and kidneys, and can even cause death. Copper may induce allergic responses in sensitive individuals. Arsenic poisoning can lead to death from multi-system organ failure, probably from necrotic cell death, not apoptosis. Arsenic is also a known carcinogen, esepcially in skin, liver, bladder and lung cancers. (R001, R055, R514, R520)","Breathing high levels of copper can cause irritation of the nose and throat. Ingesting high levels of copper can cause nausea, vomiting, diarrhea, headache, dizziness, and respiratory difficulty. Exposure to lower levels of arsenic can cause nausea and vomiting, decreased production of red and white blood cells, abnormal heart rhythm, damage to blood vessels, and a sensation of burn (R001).","Arsenic poisoning can be treated by chelation therapy, using chelating agents such as dimercaprol, EDTA or DMSA. Charcoal tablets may also be used for less severe cases. In addition, maintaining a diet high in sulfur helps eliminate arsenic from the body. (R055)",P68032;P68133;P62736;P60709;P63261;P63267;P10515;P23025;P03372;P04150;P00390;P00738;P69905;P68871;P08559;P29803;P11177;P37840;P05067;P11413;P27169;Q15166;Q14145;P09874;A6NKZ8 ;Q99867;Q9H853;O00330;Q16881;Q9NNW7;Q86VQ6;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2
291,T3D0290,2009-03-06 18:58:27 UTC,2009-08-19 18:51:59 UTC,Potassium arsenite,Inorganic Compound;Arsenic Compound,"Arsenenous acid, potassium saltArsenious acid (H3AsO3), potassium saltArsenious acid, potassium saltArsenite de potassium [french]Arsonic acid, potassium saltCaswell No. 682AKaliumarsenit [german]Potassium arsenitePotassium arsenite [UN1678] [Poison]Potassium arsenite, (KAsO2)Potassium arsonatePotassium metaarsenitePotassium metaarsenite, acid","Potassium arsenite is a chemical compound of arsenic and potassium. It is derived from arsenous acid and known mainly for forming the basis of Fowler's solution, a now obsolete medical tonic. Arsenic is a chemical element that has the symbol As and atomic number 33. It is a poisonous metalloid that has many allotropic forms: yellow (molecular non-metallic) and several black and grey forms (metalloids) are a few that are seen. Three metalloidal forms of arsenic with different crystal structures are found free in nature (the minerals arsenopyrite and the much rarer arsenolamprite and pararsenolamprite), but it is more commonly found as a compound with other elements. (R004, R662)",,10124-50-2 ,24967,,"","","","",,,Potassium arsenite,,,,,"InChI=1/AsHO2/c2-1-3/h(H,2,3)",potassium arsorite,http://www.biospider.ca/saved_files/mol/,[O-][As]([O-])[O-].[K+],[K+].[O-][As]([O-])[O-],AsKO3-2,"",White powder.,"",,,"",,,,"Oral 
Inhalation 
Dermal 
(R009)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Arsenite methyltransferase (Q9HBK9) 
(R164)","Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carginogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (R001, R054)","Arsenic is absorbed mainly by inhalation or ingestion, as to a lesser extent, dermal exposure. It is then distributed throughout the body, where it is reduced into arsenite if necessary, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant. (R055)","LD50: 14 mg/kg (Oral, Rat) (R263)
LD50: 150 mg/kg (Dermal, Rat) (R263)",Not available.,"1, carcinogenic to humans. (R264)","Potassium arsenite is known mainly for forming the basis of Fowler's solution, a now obsolete medical tonic. (R662)","Acute Oral: 0.005 mg/kg/day (R260) 
Chronic Oral: 0.0003 mg/kg/day (R260) 
Chronic Inhalation: 0.01 mg/m3 (R260)","Arsenic poisoning can lead to death from multi-system organ failure, probably from necrotic cell death, not apoptosis. Arsenic is also a known carcinogen, esepcially in skin, liver, bladder and lung cancers. (R001, R055)","Exposure to lower levels of arsenic can cause nausea and vomiting, decreased production of red and white blood cells, abnormal heart rhythm, damage to blood vessels, and a sensation of burn (R001).","Arsenic poisoning can be treated by chelation therapy, using chelating agents such as dimercaprol, EDTA or DMSA. Charcoal tablets may also be used for less severe cases. In addition, maintaining a diet high in sulfur helps eliminate arsenic from the body. (R055)",P68032;P68133;P62736;P60709;P63261;P63267;P10515;P23025;P03372;P04150;P00390;P00738;P69905;P68871;P08559;P29803;P11177;Q14145;P09874;A6NKZ8 ;Q99867;Q9H853;O00330;Q16881;Q9NNW7;Q86VQ6;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2
293,T3D0292,2009-03-06 18:58:27 UTC,2009-08-04 21:28:12 UTC,Arsenic pentoxide,Inorganic Compound;Arsenic Compound,Anhydride arsenique [french]Arsenic acid anhydrideArsenic anhydrideArsenic oxideArsenic oxide (As2O5)Arsenic oxide As2O5Arsenic pentaoxideArsenic pentoxideArsenic pentoxide [UN1559] [Poison]Arsenic(5+) oxideArsenic(v) oxideCaswell No. 057Diarsenic pentaoxideDiarsenic pentoxideRCRA waste no. P011RCRA waste number P011,"Arsenic pentoxide is a commerical oxide of arsenic frequently used in the production of other arsenic compounds. It dissolves readily in water to form arsenic acid and decomposes into oxygen and arsenic trioxide when heated. Arsenic pentoxide is used in the manufacturing of arsenates, weed killer, metal adhesives, insecticides, fungicides, wood preservatives, and colored gases, and in printing and dyeing. Arsenic is a chemical element that has the symbol As and atomic number 33. It is a poisonous metalloid that has many allotropic forms: yellow (molecular non-metallic) and several black and grey forms (metalloids) are a few that are seen. Three metalloidal forms of arsenic with different crystal structures are found free in nature (the minerals arsenopyrite and the much rarer arsenolamprite and pararsenolamprite), but it is more commonly found as a compound with other elements. (R004, R663)",,1303-28-2,14771,,"","","","",,C042120,Arsenic pentoxide,10621,,,,InChI=1/As2O5/c3-1(4)7-2(5)6,"",http://www.biospider.ca/saved_files/mol/,O=[As](=O)O[As](=O)=O,O=[As](=O)O[As](=O)=O,As2O5,229.817770,White solid.,"",,,"",,,,"Oral 
Inhalation 
Dermal 
(R009)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Arsenite methyltransferase (Q9HBK9) 
(R164)","Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carginogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (R001, R054)","Arsenic is absorbed mainly by inhalation or ingestion, as to a lesser extent, dermal exposure. It is then distributed throughout the body, where it is reduced into arsenite if necessary, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant. (R055)","LD50: 8 mg/kg (Oral, Rat) (R263)",Not avilable.,"1, carcinogenic to humans. (R264)","Arsenic pentoxide is used in the manufacturing of arsenates, weed killer, metal adhesives, insecticides, fungicides, wood preservatives, and colored gases, and in printing and dyeing. (R663)","Acute Oral: 0.005 mg/kg/day (R260) 
Chronic Oral: 0.0003 mg/kg/day (R260) 
Chronic Inhalation: 0.01 mg/m3 (R260)","Arsenic poisoning can lead to death from multi-system organ failure, probably from necrotic cell death, not apoptosis. Arsenic is also a known carcinogen, esepcially in skin, liver, bladder and lung cancers. (R001, R055)","Exposure to lower levels of arsenic can cause nausea and vomiting, decreased production of red and white blood cells, abnormal heart rhythm, damage to blood vessels, and a sensation of burn (R001).","Arsenic poisoning can be treated by chelation therapy, using chelating agents such as dimercaprol, EDTA or DMSA. Charcoal tablets may also be used for less severe cases. In addition, maintaining a diet high in sulfur helps eliminate arsenic from the body. (R055)",P68032;P68133;P62736;P60709;P63261;P63267;P10515;P23025;P03372;P04150;P00390;P00738;P69905;P68871;P08559;P29803;P11177;Q14145;P09874;A6NKZ8 ;Q99867;Q9H853;O00330;Q16881;Q9NNW7;Q86VQ6;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2
294,T3D0293,2009-03-06 18:58:27 UTC,2009-08-25 19:52:29 UTC,Magnesium arsenate,Inorganic Compound;Arsenic Compound,"Arseniate de magnesium [french]Arsenic acid (H3AsO4), magnesium saltArsenic acid, magnesium saltCaswell No. 529Magnesium arsenateMagnesium arsenate [UN1622] [Poison]Magnesium arsenate phosphorMagnesium o-arsenate","Magnesium arsenate is a chemical compound of magnesium and arsenic. It is derived from arsenic acid. Arsenic is a chemical element that has the symbol As and atomic number 33. It is a poisonous metalloid that has many allotropic forms: yellow (molecular non-metallic) and several black and grey forms (metalloids) are a few that are seen. Three metalloidal forms of arsenic with different crystal structures are found free in nature (the minerals arsenopyrite and the much rarer arsenolamprite and pararsenolamprite), but it is more commonly found as a compound with other elements. (R004)",,10103-50-1,24943,,"","","","",,,Magnesium arsenate,,,,,"InChI=1/2AsH3O4.3Mg/c2*2-1(3,4)5;;;/h2*(H3,2,3,4,5);;;/q;;3*+2/p-6",trimagnesium diarsorate,http://www.biospider.ca/saved_files/mol/,[O-][As](=O)([O-])[O-].[O-][As](=O)([O-])[O-].[Mg+2].[Mg+2].[Mg+2],[O-][As](=O)([O-])[O-].[O-][As](=O)([O-])[O-].[Mg+2].[Mg+2].[Mg+2],As2Mg3O8,349.757630,White powder.,"",,,"",,,,"Oral 
Inhalation 
Dermal 
(R009)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Arsenite methyltransferase (Q9HBK9) 
(R164)","Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carginogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (R001, R054)","Arsenic is absorbed mainly by inhalation or ingestion, as to a lesser extent, dermal exposure. It is then distributed throughout the body, where it is reduced into arsenite if necessary, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant. (R055)","LD50: 315 mg/kg (Acute oral, Mouse) (R263)",Not available.,"1, carcinogenic to humans. (R264)","Magnesium arsenate was first used as an insect stomach poison in the Mexican bean bettle around 1920-1930, but its used is now very limited (S251).","Acute Oral: 0.005 mg/kg/day (R260) 
Chronic Oral: 0.0003 mg/kg/day (R260) 
Chronic Inhalation: 0.01 mg/m3 (R260)","Arsenic poisoning can lead to death from multi-system organ failure, probably from necrotic cell death, not apoptosis. Arsenic is also a known carcinogen, esepcially in skin, liver, bladder and lung cancers. (R001, R055)","Exposure to lower levels of arsenic can cause nausea and vomiting, decreased production of red and white blood cells, abnormal heart rhythm, damage to blood vessels, and a sensation of burn (R001).","Arsenic poisoning can be treated by chelation therapy, using chelating agents such as dimercaprol, EDTA or DMSA. Charcoal tablets may also be used for less severe cases. In addition, maintaining a diet high in sulfur helps eliminate arsenic from the body. (R055)",P68032;P68133;P62736;P60709;P63261;P63267;P10515;P23025;P03372;P04150;P00390;P00738;P69905;P68871;P08559;P29803;P11177;P07451;Q14145;P09874;A6NKZ8 ;Q99867;Q9H853;O00330;Q16881;Q9NNW7;Q86VQ6;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2
295,T3D0294,2009-03-06 18:58:27 UTC,2009-08-25 19:52:30 UTC,Manganese arsenate,Inorganic Compound;Arsenic Compound;Manganese Compound,"Arsenic acid, manganese(2+) salt, hydrate (2:3:6)Manganese Arsenate (mn3(aso4)2) Hexahydrate (6ci)Manganese arsenate","Manganese arsenate is a chemical compound of manganese and aresenic. It is derived from arsenic acid. Arsenic is a chemical element that has the symbol As and atomic number 33. It is a poisonous metalloid that has many allotropic forms: yellow (molecular non-metallic) and several black and grey forms (metalloids) are a few that are seen. Three metalloidal forms of arsenic with different crystal structures are found free in nature (the minerals arsenopyrite and the much rarer arsenolamprite and pararsenolamprite), but it is more commonly found as a compound with other elements. Manganese is a naturally occurring metal with the symbol Mn and the atomic number 25. It does not occur naturally in its pure form, but is found in many types of rocks in combination with other substances such as oxygen, sulfur, or chlorine. Manganese occurs naturally in most foods and small amounts are needed to stay healthy, as manganese ions act as cofactors for a number of enzymes. (R441, R442, R004)",,61136-68-3,3045788,,"","","","",,,Manganese arsenate,,,,,"InChI=1/2AsH3O4.3Mn/c2*2-1(3,4)5;;;/h2*(H3,2,3,4,5);;;/q;;3*+2/p-6",manganese(2+) diarsorate,http://www.biospider.ca/saved_files/mol/,[O-][As](=O)([O-])[O-].[O-][As](=O)([O-])[O-].[Mn+2].[Mn+2].[Mn+2],[O-][As](=O)([O-])[O-].[O-][As](=O)([O-])[O-].[Mn+2].[Mn+2].[Mn+2],As2Mn3O8,442.616660,Not available.,"",,,"",,,,"Oral 
Inhalation 
Dermal 
(R009)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Arsenite methyltransferase (Q9HBK9) 
Alpha-2-macroglobulin (P01023) 
Serum albumin (P02768) 
Serotransferrin (P02787) 
Superoxide dismutase [Mn], mitochondrial (P04179) 
(R441, R164)","Manganese is a cellular toxicant that can impair transport systems, enzyme activities, and receptor functions. It primarily targets the central nervous system, particularily the globus pallidus of the basal ganglia. It is believed that the manganese ion, Mn(II), enhances the autoxidation or turnover of various intracellular catecholamines, leading to increased production of free radicals, reactive oxygen species, and other cytotoxic metabolites, along with a depletion of cellular antioxidant defense mechanisms, leading to oxidative damage and selective destruction of dopaminergic neurons. In addition to dopamine, manganese is thought to perturbations other neurotransmitters, such as GABA and glutamate. In order to produce oxidative damage, manganese must first overwhelm the antioxidant enzyme manganese superoxide dismutase. The neurotoxicity of Mn(II) has also been linked to its ability to substitute for Ca(II) under physiological conditions. It can enter mitochondria via the calcium uniporter and inhibit mitochondrial oxidative phosphorylation. It may also inhibit the efflux of Ca(II), which can result in a loss of mitochondrial membrane integrity. Mn(II) has been shown to inhibit mitochondrial aconitase activity to a significant level, altering amino acid metabolism and cellular iron homeostasis. Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carginogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (R001, R054, R441)","Manganese is absorbed mainly via ingestion, but can also be inhaled. It binds to alpha-2-macroglobulin, albumin, or transferrin in the plasma and is distributed to the brain and all other mammalian tissues, though it tends to accumulate more in the liver, pancreas, and kidney. Manganese is capable of existing in a number of oxidation states and is believed to undergo changes in oxidation state within the body. Manganese oxidation state can influence tissue toxicokinetic behavior, and possibly toxicity. Manganese is excreted primarily in the faeces. Arsenic is absorbed mainly by inhalation or ingestion, as to a lesser extent, dermal exposure. It is then distributed throughout the body, where it is reduced into arsenite if necessary, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant. (R055, R441)",Not available.,Not available.,"1, carcinogenic to humans. (R264)","Manganese arsenates are used as insecticides, fungicides (S253).","Chronic Inhalation: 0.0003 mg/m3 (Manganese) (R260)
Acute Oral: 0.005 mg/kg/day (Arsenic) (R260) 
Chronic Oral: 0.0003 mg/kg/day (Arsenic) (R260) 
Chronic Inhalation: 0.01 mg/m3 (Arsenic) (R260)","Manganese mainly affects the nervous system and may cause behavioral changes and other nervous system effects, which include movements that may become slow and clumsy. This combination of symptoms when sufficiently severe is referred to as manganism. (R441)","The symptoms of manganese toxicity may appear slowly over months and years; they include tremors, difficulty walking, and facial muscle spasms. These symptoms are often preceded by other lesser symptoms, including irritability, aggressiveness, and hallucinations. (R441)","Arsenic poisoning can be treated by chelation therapy, using chelating agents such as dimercaprol, EDTA or DMSA. Charcoal tablets may also be used for less severe cases. In addition, maintaining a diet high in sulfur helps eliminate arsenic from the body. (R055)",P68032;P68133;P62736;P60709;P63261;P63267;P10515;P23025;P03372;P04150;P00390;P00738;P69905;P68871;P08559;P29803;P11177;Q99798;P21399;P48200 ;P04156;Q86SH4;Q14145;P09874;A6NKZ8 ;Q99867;Q9H853;O00330;Q16881;Q9NNW7;Q86VQ6;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2
297,T3D0296,2009-03-06 18:58:28 UTC,2009-08-04 21:28:13 UTC,Lead arsenate,Inorganic Compound;Arsenic Compound;Lead Compound,"Acid lead arsenateAcid lead orthoarsenateArsenate of leadArseniate de plomb [french]Arsenic acid (H3AsO4), lead saltArsenic acid (H3AsO4), lead(2+) salt (1:1)Arsenic acid, lead saltArsenic acid, lead(2+) salt (1:1)Arsenic acid, lead(2+) salt(1:1)ArsinetteCaswell No. 525Dibasic lead arsenateDiplumbic hydrogen arsenateGypsineLead acid arsenateLead arsenateLead arsenate (standard)Lead arsenate, basicLead hydrogen arsenateLead hydrogenarsenateLead(2+) monohydrogen arsenateLead(II) arsenateNat schulteniteOrtho L40 dustPlumbous arsenateSchulteniteStandard lead arsenate","Lead arsenate is a chemical compound of lead and arsenic. It is derived from arsenic acid and originally used as an insecticide against the codling moth and potato beetle. Today its use is officially banned. Arsenic is a chemical element that has the symbol As and atomic number 33. It is a poisonous metalloid that has many allotropic forms: yellow (molecular non-metallic) and several black and grey forms (metalloids) are a few that are seen. Three metalloidal forms of arsenic with different crystal structures are found free in nature (the minerals arsenopyrite and the much rarer arsenolamprite and pararsenolamprite), but it is more commonly found as a compound with other elements. (R004, R664)",,7784-40-9,24572,,"","","","",,,Lead arsenate,,,,,"InChI=1/AsH3O4.Pb/c2-1(3,4)5;/h(H3,2,3,4,5);/q;+2/p-2",hydrogen arsorate; lead(2+),http://www.biospider.ca/saved_files/mol/,O[As](=O)([O-])[O-].[Pb+2],O[As](=O)([O-])[O-].[Pb+2],AsHO4Pb,347.885720,White crystals.,"",,,"",,,,"Oral 
Inhalation 
Dermal 
(R009)","Delta-aminolevulinic acid dehydratase (P13716) 
Serum albumin (P02768) Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Arsenite methyltransferase (Q9HBK9) 
(R164, R266)","Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carginogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. Lead mimics other biologically important metals, such as zinc, calcium, and iron, competing as cofactors for many of their respective enzymatic reactions. For example, lead has been shown to competitively inhibit calcium's binding of calmodulin, interferring with neurotransmitter release. It exhibits similar competitive inhibition at the NMDA receptor and protein kinase C, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Lead also affects the nervous system by impairing regulation of dopamine synthesis and blocking evoked release of acetylcholine. However, it's main mechanism of action occurs by inhibiting delta-aminolevulinic acid dehydratase, an enzyme vital in the biosynthesis of heme, which is a necesssary cofactor of hemoglobin. (R001, R008, R054, R061, R063, R266)","Lead and arsenic are absorbed following inhalation, oral, and dermal exposure. Arsenic is then distributed throughout the body, where it is reduced into arsenite if necessary, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant.  Lead is distributed mainly to the bones and red blood cells. In the blood lead may be found bound to serum albumin or the metal-binding protein metallothionein. Organic lead is metabolized by cytochrome P-450 enzymes, whereas inorganic lead forms complexes with delta-aminolevulinic acid dehydratase. Lead is excreted mainly in the urine and faeces. (R266, R055)","LD50: 175 mg/kg (Oral, Rat) (R009)
LD50: 128 mg/kg (Intraperitoneal, Mouse) (R263)",Not available.,"1, carcinogenic to humans. (R264)",Lead arsenate is used as an insecticide. (R664),"Acute Oral: 0.005 mg/kg/day (Arsenic) (R260) 
Chronic Oral: 0.0003 mg/kg/day (Arsenic) (R260) 
Chronic Inhalation: 0.01 mg/m3 (Arsenic) (R260)
Chronic Inhalation: 0.05 mg/m3 (Lead) (R260)","Arsenic poisoning can lead to death from multi-system organ failure, probably from necrotic cell death, not apoptosis. Arsenic is also a known carcinogen, esepcially in skin, liver, bladder and lung cancers. Lead is a neurotoxin and has been known to cause brain damage and reduced cognitive capacity, especially in children. Lead exposure can result in nephropathy, as well as blood disorders such as high blood pressure and anemia. Lead also exhibits reproductive toxicity and can results in miscarriages and reduced sperm production. (R001, R055, R056)","Exposure to lower levels of arsenic can cause nausea and vomiting, decreased production of red and white blood cells, abnormal heart rhythm, damage to blood vessels, and a sensation of burn (R001).","Both arsenic and poisoning can be treated by chelation therapy, using chelating agents such as dimercaprol, EDTA or DMSA. Charcoal tablets may also be used for less severe cases. In addition, maintaining a diet high in sulfur helps eliminate arsenic from the body. (R055)",P68032;P68133;P62736;P60709;P63261;P63267;P10515;P23025;P03372;P04150;P00390;P00738;P69905;P68871;P08559;P29803;P11177;P07108;P62158;P13716;P22830;Q8TCU5;O60391;Q12879;Q13224;Q14957;O15399;Q05586;P17252;P05771;Q05655;Q02156;P24723;P05129;P41743;Q04759;Q05513;P54710;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P62328;Q14145;P09874;A6NKZ8 ;Q99867;Q9H853;O00330;Q16881;Q9NNW7;Q86VQ6;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2
298,T3D0297,2009-03-06 18:58:28 UTC,2009-08-25 18:01:04 UTC,Potassium arsenate,Inorganic Compound;Arsenic Compound,"Arsenic acid (H3AsO4), monopotassium saltArsenic acid, monopotassium saltMacquer's saltMonopotassium arsenateMonopotassium dihydrogen arsenatePotassium acid arsenatePotassium arsenatePotassium arsenate [UN1677] [Poison]Potassium arsenate, monobasicPotassium dihydrogen arsenatePotassium dihydrogen arsenate (KH2AsO4)Potassium dihydrogenarsenatePotassium hydrogen arsenatePotassium hydrogen arsenate (KH2AsO4)Potassium orthoarsenate, monobasic","Potassium arsenate is a chemical compound of potassium and arsenic. It is derived from arsenic acid. Arsenic is a chemical element that has the symbol As and atomic number 33. It is a poisonous metalloid that has many allotropic forms: yellow (molecular non-metallic) and several black and grey forms (metalloids) are a few that are seen. Three metalloidal forms of arsenic with different crystal structures are found free in nature (the minerals arsenopyrite and the much rarer arsenolamprite and pararsenolamprite), but it is more commonly found as a compound with other elements. (R004)",,7784-41-0,516881,,"","","","",,,Potassium arsenate,,,,,"InChI=1/AsH3O4.K/c2-1(3,4)5;/h(H3,2,3,4,5);/q;+1/p-1",potassium dihydrogen arsorate,http://www.biospider.ca/saved_files/mol/,O[As](=O)(O)[O-].[K+],O[As](O)(=O)O[K],AsH2KO4,179.880610,Colorless crystals.,"",,,"",,,,"Oral 
Inhalation 
Dermal 
(R009)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Arsenite methyltransferase (Q9HBK9) 
(R164)","Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carginogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (R001, R054)","Arsenic is absorbed mainly by inhalation or ingestion, as to a lesser extent, dermal exposure. It is then distributed throughout the body, where it is reduced into arsenite if necessary, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant. (R055)","LD50: 14 mg/kg (oral, Rat) (R665)",Not available.,"1, carcinogenic to humans. (R264)","Potassium arsenate used as an insecticide, analytical reagent, and in hide preservation and textile printing (S254).","Acute Oral: 0.005 mg/kg/day (R260) 
Chronic Oral: 0.0003 mg/kg/day (R260) 
Chronic Inhalation: 0.01 mg/m3 (R260)","Arsenic poisoning can lead to death from multi-system organ failure, probably from necrotic cell death, not apoptosis. Arsenic is also a known carcinogen, esepcially in skin, liver, bladder and lung cancers. (R001, R055)","Exposure to lower levels of arsenic can cause nausea and vomiting, decreased production of red and white blood cells, abnormal heart rhythm, damage to blood vessels, and a sensation of burn (R001).","Arsenic poisoning can be treated by chelation therapy, using chelating agents such as dimercaprol, EDTA or DMSA. Charcoal tablets may also be used for less severe cases. In addition, maintaining a diet high in sulfur helps eliminate arsenic from the body. (R055)",P68032;P68133;P62736;P60709;P63261;P63267;P10515;P23025;P03372;P04150;P00390;P00738;P69905;P68871;P08559;P29803;P11177;Q14145;P09874;A6NKZ8 ;Q99867;Q9H853;O00330;Q16881;Q9NNW7;Q86VQ6;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2
299,T3D0298,2009-03-06 18:58:28 UTC,2009-08-25 18:01:08 UTC,Sodium arsenate,Inorganic Compound;Arsenic Compound,"Arsenate, sodiumArsenic acid (H3AsO4), monosodium saltArsenic acid, monosodium saltMonosodium arsenateSodium arsenateSodium arsenate (NaH2AsO4)Sodium dihydrogen arsenateSodium dihydrogen orthoarsenate","Sodium arsenate is a chemical compound of sodium and arsenic. It is derived from arsenic acid. Arsenic is a chemical element that has the symbol As and atomic number 33. It is a poisonous metalloid that has many allotropic forms: yellow (molecular non-metallic) and several black and grey forms (metalloids) are a few that are seen. Three metalloidal forms of arsenic with different crystal structures are found free in nature (the minerals arsenopyrite and the much rarer arsenolamprite and pararsenolamprite), but it is more commonly found as a compound with other elements. (R004)",,7631-89-2,23677060,,"","","","",,C009277,Sodium arsenate,,,,,"InChI=1/AsH3O4.Na/c2-1(3,4)5;/h(H3,2,3,4,5);/q;+1",sodium dihydrogen arsorate,http://www.biospider.ca/saved_files/mol/,O[As](=O)(O)[O-].[Na+],O[As](O)(=O)O[Na],AsH2NaO4,163.906680,Colorless solid.,86.3 oC,,,"267 mg/mL at 17 oC [SHIU,WY et al. (1990)]",,,,"Oral 
Inhalation 
Dermal 
(R009)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Arsenite methyltransferase (Q9HBK9) 
(R164)","Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carginogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (R001, R054)","Arsenic is absorbed mainly by inhalation or ingestion, as to a lesser extent, dermal exposure. It is then distributed throughout the body, where it is reduced into arsenite if necessary, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant. (R055)","LD50: 41 mg/kg (oral, rat) ; LD50: 1-20 mg/kg  (oral, mouse) (S255).",Not available.,"1, carcinogenic to humans. (R264)","Sodium arsenate was formerly used in the treatment of chronic skin diseases, in parasitic diseases of the blood, and in some forms of anaemia (S256).","Acute Oral: 0.005 mg/kg/day (R260) 
Chronic Oral: 0.0003 mg/kg/day (R260) 
Chronic Inhalation: 0.01 mg/m3 (R260)","Arsenic poisoning can lead to death from multi-system organ failure, probably from necrotic cell death, not apoptosis. Arsenic is also a known carcinogen, esepcially in skin, liver, bladder and lung cancers. (R001, R055)","Exposure to lower levels of arsenic can cause nausea and vomiting, decreased production of red and white blood cells, abnormal heart rhythm, damage to blood vessels, and a sensation of burn (R001).","Arsenic poisoning can be treated by chelation therapy, using chelating agents such as dimercaprol, EDTA or DMSA. Charcoal tablets may also be used for less severe cases. In addition, maintaining a diet high in sulfur helps eliminate arsenic from the body. (R055)",P68032;P68133;P62736;P60709;P63261;P63267;P10515;P23025;P03372;P04150;P00390;P00738;P69905;P68871;P08559;P29803;P11177;Q14145;P09874;A6NKZ8 ;Q99867;Q9H853;O00330;Q16881;Q9NNW7;Q86VQ6;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2
300,T3D0299,2009-03-06 18:58:28 UTC,2009-08-25 18:01:13 UTC,Zinc arsenate,Inorganic Compound;Arsenic Compound;Zinc Compound,"Arsenic acid, zinc saltZinc arsenateZinc arsenate, basic","Zinc arsenate is a chemical compound of zinc and arsenic derived from arsenic acid. Zinc is a metallic element with the atomic number 30. It is found in nature most often as the mineral sphalerite. Though excess zinc in harmful, in smaller amounts it is an essential element for life, as it is a cofactor for over 300 enzymes and is found in just as many transcription factors. Arsenic is a chemical element that has the symbol As and atomic number 33. It is a poisonous metalloid that has many allotropic forms: yellow (molecular non-metallic) and several black and grey forms (metalloids) are a few that are seen. Three metalloidal forms of arsenic with different crystal structures are found free in nature (the minerals arsenopyrite and the much rarer arsenolamprite and pararsenolamprite), but it is more commonly found as a compound with (R112, R113)",,13464-44-3,6451222,,"","","","",,,Zinc arsenate,,,,,"InChI=1/2AsH3O4.3Zn/c2*2-1(3,4)5;;;/h2*(H3,2,3,4,5);;;/q;;3*+2/p-6",trizinc diarsorate,http://www.biospider.ca/saved_files/mol/,"",[Zn++].[Zn++].[Zn++].[O-][As]([O-])([O-])=O.[O-][As]([O-])([O-])=O,As2O8Zn3,469.589950,Deep green color (S258).,"","","","","","","","Oral 
Inhalation 
Dermal 
(R009)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Arsenite methyltransferase (Q9HBK9) 
Cysteine-rich protein 1 (P50238) 
Cysteine-rich protein 2 (P52943) 
Cysteine-rich protein 3 (Q6Q6R5) 
Serum albumin (P02768) 
(R113, R128, R164)","Anaemia results from the excessive absorption of zinc suppressing copper and iron absorption, most likely through competitive binding of intestinal mucosal cells. Unbalanced levels of copper and zinc binding to Cu,Zn-superoxide dismutase has been linked to amyotrophic lateral sclerosis (ALS). Stomach acid dissolves metallic zinc to give corrosive zinc chloride, which can cause damage to the stomach lining. Metal fume fever is thought to be an immune response to inhaled zinc. Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carginogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (R001, R054, R112, R113, R128)","Zinc can enter the body through the lungs, skin, and gastrointestinal tract. Intestinal absorption of zinc is controlled by zinc carrier protein CRIP. Zinc also binds to metallothioneins, which help prevent absorption of excess zinc. Zinc is widely distributed and found in all tissues and tissues fluids, concentrating in the liver, gastrointestinal tract, kidney, skin, lung, brain, heart, and pancreas. In the bloodstream zinc is found bound to carbonic anhydrase in erythrocytes, as well as bound to albumin, _2-macroglobulin, and amino acids in the the plasma. Albumin and amino acid bound zinc can diffuse across tissue membranes. Zinc is excreted in the urine and faeces. Arsenic is absorbed mainly by inhalation or ingestion, as to a lesser extent, dermal exposure. It is then distributed throughout the body, where it is reduced into arsenite if necessary, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant. (R055, R113)",Not available.,Not available.,"1, carcinogenic to humans. (R264)",Zinc arsenate is used as an insecticide and to preserve timber from decay (S257). ,"Intermediate Oral: 0.3 mg/kg/day (Zinc) (R260) 
Chronic Oral: 0.3 mg/kg/day (Zinc) (R260)
Acute Oral: 0.005 mg/kg/day (Arsenic) (R260) 
Chronic Oral: 0.0003 mg/kg/day (Arsenic) (R260) 
Chronic Inhalation: 0.01 mg/m3 (Arsenic) (R260)","Chronic exposure to zinc causes anemia, atazia, lethargy, and decreases the level of good cholesterol in the body. It is also believed to cause pancreatic and reproductive damage. Arsenic poisoning can lead to death from multi-system organ failure, probably from necrotic cell death, not apoptosis. Arsenic is also a known carcinogen, esepcially in skin, liver, bladder and lung cancers. (R001, R055, R113)","Ingestion of large doses of zinc causes stomach cramps, nausea, and vomiting. Acute inhalation of large amounts of zinc causes metal fume fever, which is characterized by chills, fever, headache, weakness, dryness of the nose and throat, chest pain, and coughing. Dermal contact with zinc results in skin irritation. Exposure to lower levels of arsenic can cause nausea and vomiting, decreased production of red and white blood cells, abnormal heart rhythm, damage to blood vessels, and a sensation of burn (R001).","Zinc poisoning is treated symptomatically, often by administering fluids such as water or milk, or with gastric lavage. Arsenic poisoning can be treated by chelation therapy, using chelating agents such as dimercaprol, EDTA or DMSA. Charcoal tablets may also be used for less severe cases. In addition, maintaining a diet high in sulfur helps eliminate arsenic from the body. (R055, R113)",P68032;P68133;P62736;P60709;P63261;P63267;P10515;P23025;P03372;P04150;P00390;P00738;P69905;P68871;P08559;P29803;P11177;P00441;Q14145;P09874;A6NKZ8 ;Q99867;Q9H853;O00330;Q16881;Q9NNW7;Q86VQ6;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2
301,T3D0300,2009-03-06 18:58:28 UTC,2009-08-04 21:28:14 UTC,Arsanilic acid,Organic Compound;Arsenic Compound;Organometallic;Aromatic Hydrocarbon,"(4-aminophenyl)arsonic acid(p-aminophenyl)arsonic acid4-Aminophenylarsonsaeure4-aminobenzenearsonic acid4-aminophenylarsonic acid (ACD/Name 4.0)4-arsanilic acidA9258_ALDRICHA9258_SIGMAAS-101 (VAN)ASRAcide arsanilique [inn-french]Acide p-arsanilique [french]Acido arsanilico [inn-spanish]Acidum arsanilicum [inn-latin]Aminophenylarsine acidAntoxylic acidArsanilic Acid-100Arsanilic acidArsanilic acid (usp/inn)Arsanilic acid [usan:ban:inn]Arsanilic acid [usan:inn:ban]ArsanilsaeureArsonic acid, (4-aminophenyl)-Atoxylic acidBenzenearsonic acid, p-amino-C6H8AsNO3Kyselina arsanilova [czech]O-aminobenzenearsonic acidO-arsanilic acidP-aminobenzenearsonic acidP-aminophenylarsine acidP-aminophenylarsonic acidP-anilinearsonic acidP-arsanilic acidPro-Gen 227 PremixPro-genProgen 90R-sonicWLN: ZR d-as-qqo","Arsanilic acid is an organoarsenic compound derived from orthoarsenic acid. It was once used as a human drug, but is now only found in veterinary medicine, where its use is controversial (R668).",,98-50-0,7389,,"","",49477,"",,,Arsanilic acid,,,,,"InChI=1/C6H8AsNO3/c8-6-3-1-5(2-4-6)7(9,10)11/h1-4H,8H2,(H2,9,10,11)",(4-aminophenyl)arsonic acid,http://www.biospider.ca/saved_files/mol/,C1=CC(=CC=C1N)[As](=O)(O)O,C1=CC(=CC=C1N)[As](=O)(O)O,C6H8AsNO3,216.972010,White solid.,232 oC,,,"",,,,"Oral
Inhalation
Dermal",No data.,"After absorption, arsenic may cause multi-organ failure by inhibiting sulfhydryl-containing enzymes (R624).",Not available.,"LD50: 248 mg/kg (Acute intraperitoneal, Mouse)
LD50: 100 mg/kg (Acute intravenous, Mouse)",Not available.,"1, carcinogenic to humans. (R264)",Arsanilic acid is used to treate dysentery in swine.,"Acute Oral: 0.005 mg/kg/da
Chronic Oral: 0.0003 mg/kg/day
Chronic Inhalation: 0.01 mg/m3","Hypovolemia from capillary leakage (third-spacing of fluids) is a common, serious, early effect. Muscle cramps, facial edema, bronchitis, dyspnea, chest pain, dehydration, intense thirst, and fluid-electrolyte disturbances are also common following significant exposures. A garlic-like odor of the breath and feces may also occur. After absorption, arsenic may cause multi-organ failure by inhibiting sulfhydryl-containing enzymes. Encephalopathy, with headache, lethargy, mental confusion, hallucinations, emotional lability, memory loss and delirium may occur; seizures, stupor, convulsions, coma, and death may follow within 24 hours of a severe acute exposure. Dysrhythmias (particularly QTc prolongation and torsade de pointes), cardiomyopathy, ARDS, hepatitis, rhabdomyolysis, hemolysis, and renal failure may develop over several days. The sequence of chronic poisoning involves hyperpigmentation, and eczematoid and allergic dermatitis. muscle fasciculations; gross tremors; ataxia; incoordination; and mental confusion. Muscular weakness, limb tenderness and difficulty walking may follow. The final phase consists of peripheral sensory neuropathy of the hands and feet. That may be associated with a motor neuropathy as well (R624).


","Initial signs and symptoms of arsenic ingestion include burning lips, throat constriction and dysphagia, followed by excruciating abdominal pain, hemorrhagic gastritis, gastroenteritis, severe nausea, projectile voting, profuse ""rice water-like"" diarrhea, with hypovolemia that may result in hypotension and an irregular pulse.  The sequence of chronic poisoning involves weakness, anorexia, hepatomegaly, jaundice, and gastrointestinal complaints, followed by conjunctivitis, irritation of the throat and respiratory tract. ther effects of chronic exposure include conjunctivitis with irritation and lacrimation; hair, skin and nail changes; hyperkeratosis of feet and hands; and melanosis, with pigment spots in corneal and conjunctival epithelium. Peripheral nervous system symptoms may include numbness, burning, and tingling of the hands and feet; pain; paresthesias; tenderness (R624).


",Aggressive decontamination with gastric lavage is recommended if the patient has consumed a potentially life-threatening dose and if the patient is not vomiting (R624). ,P09923
302,T3D0301,2009-03-06 18:58:28 UTC,2009-08-04 21:28:14 UTC,Arsenobetaine,Organic Compound;Arsenic Compound;Organometallic,"(carboxymethyl)trimethylarsonium hydroxide inner salt2-(Trimethylarsonio)acetateArsenobetaineArsenobetaine monohydrateArsenobetaine solutionArsenobetaine standard solutionArsonium, (carboxymethyl)trimethyl-, hydroxide, inner saltBCR626_FLUKA","Arsenobetaine is a organoarsenic compound that is the main source of arsenic found in fish. It is the arsenic analogue of trimethylglycine, commonly known as betaine. Arsenic is a chemical element that has the symbol As and atomic number 33. It is a poisonous metalloid that has many allotropic forms: yellow (molecular non-metallic) and several black and grey forms (metalloids) are a few that are seen. Three metalloidal forms of arsenic with different crystal structures are found free in nature (the minerals arsenopyrite and the much rarer arsenolamprite and pararsenolamprite), but it is more commonly found as a compound with other elements. (R004, R669)",,64436-13-1,47364,,"","","","",,C038992,Arsenobetaine,,,,,"InChI=1/C5H11AsO2/c1-6(2,3)4-5(7)8/h4H2,1-3H3",2-trimethylarsoniumylacetate,http://www.biospider.ca/saved_files/mol/,C[As+](C)(C)CC(=O)[O-],C[As+](C)(C)CC(=O)[O-],C5H11AsO2,177.997500,No data.,"",,,"",,,,"Oral 
Inhalation 
Dermal 
(R009)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Arsenite methyltransferase (Q9HBK9) 
(R164)","Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carginogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (R001, R054)","Arsenic is absorbed mainly by inhalation or ingestion, as to a lesser extent, dermal exposure. It is then distributed throughout the body, where it is reduced into arsenite if necessary, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant. (R055)","LD50:  >4260 mg/kg (oral, mice) (S260).",Not available.,"1, carcinogenic to humans. (R264)",Arsenobetaine is found in marine biological systems. (R669),"Acute Oral: 0.005 mg/kg/day (R260) 
Chronic Oral: 0.0003 mg/kg/day (R260) 
Chronic Inhalation: 0.01 mg/m3 (R260)","Arsenic poisoning can lead to death from multi-system organ failure, probably from necrotic cell death, not apoptosis. Arsenic is also a known carcinogen, esepcially in skin, liver, bladder and lung cancers. (R001, R055)","Exposure to lower levels of arsenic can cause nausea and vomiting, decreased production of red and white blood cells, abnormal heart rhythm, damage to blood vessels, and a sensation of burn (R001).","Arsenic poisoning can be treated by chelation therapy, using chelating agents such as dimercaprol, EDTA or DMSA. Charcoal tablets may also be used for less severe cases. In addition, maintaining a diet high in sulfur helps eliminate arsenic from the body. (R055)",P68032;P68133;P62736;P60709;P63261;P63267;P10515;P23025;P03372;P04150;P00390;P00738;P69905;P68871;P08559;P29803;P11177;Q14145;P09874;A6NKZ8 ;Q99867;Q9H853;O00330;Q16881;Q9NNW7;Q86VQ6;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2
303,T3D0302,2009-03-06 18:58:29 UTC,2009-08-04 21:28:14 UTC,Arsenocholine,Organic Compound;Arsenic Compound;Organometallic,"(2-Hydroxyethyl)trimethylarsoniumArsenocholineArsonium, (2-hydroxyethyl)trimethyl-","Arsenocholine is a organoarsenic compound and the arsenic analogue of choline. Arsenic is a chemical element that has the symbol As and atomic number 33. It is a poisonous metalloid that has many allotropic forms: yellow (molecular non-metallic) and several black and grey forms (metalloids) are a few that are seen. Three metalloidal forms of arsenic with different crystal structures are found free in nature (the minerals arsenopyrite and the much rarer arsenolamprite and pararsenolamprite), but it is more commonly found as a compound with other elements. (R004)",,39895-81-3,104820,,"","","","",,C039920,Arsenocholine,,,,,"InChI=1/C5H14AsO/c1-6(2,3)4-5-7/h7H,4-5H2,1-3H3/q+1",2-hydroxyethyl(trimethyl)arsanium,http://www.biospider.ca/saved_files/mol/,C[As+](C)(C)CCO,C[As+](C)(C)CCO,C5H14AsO+,"",No data.,"",,,"",,,,"Oral 
Inhalation 
Dermal 
(R009)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Arsenite methyltransferase (Q9HBK9) 
(R164)","Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carginogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (R001, R054)","Arsenic is absorbed mainly by inhalation or ingestion, as to a lesser extent, dermal exposure. It is then distributed throughout the body, where it is reduced into arsenite if necessary, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant. (R055)","LD50: 6.5 g/kg (oral, rodent) (S261).",No data.,"1, carcinogenic to humans. (R264)",No data.,"Acute Oral: 0.005 mg/kg/day (R260) 
Chronic Oral: 0.0003 mg/kg/day (R260) 
Chronic Inhalation: 0.01 mg/m3 (R260)","Arsenic poisoning can lead to death from multi-system organ failure, probably from necrotic cell death, not apoptosis. Arsenic is also a known carcinogen, esepcially in skin, liver, bladder and lung cancers. (R001, R055)","Exposure to lower levels of arsenic can cause nausea and vomiting, decreased production of red and white blood cells, abnormal heart rhythm, damage to blood vessels, and a sensation of burn (R001).","Arsenic poisoning can be treated by chelation therapy, using chelating agents such as dimercaprol, EDTA or DMSA. Charcoal tablets may also be used for less severe cases. In addition, maintaining a diet high in sulfur helps eliminate arsenic from the body. (R055)",P68032;P68133;P62736;P60709;P63261;P63267;P10515;P23025;P03372;P04150;P00390;P00738;P69905;P68871;P08559;P29803;P11177;Q14145;P09874;A6NKZ8 ;Q99867;Q9H853;O00330;Q16881;Q9NNW7;Q86VQ6;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2
304,T3D0303,2009-03-06 18:58:29 UTC,2009-08-04 21:28:14 UTC,Methylarsine,Organic Compound;Arsenic Compound;Organometallic,"Arsine, methyl-CH3AsH2Monomethylarsine","Methylarsine is an organic derivative of arsine. Arsenic is a chemical element that has the symbol As and atomic number 33. It is a poisonous metalloid that has many allotropic forms: yellow (molecular non-metallic) and several black and grey forms (metalloids) are a few that are seen. Three metalloidal forms of arsenic with different crystal structures are found free in nature (the minerals arsenopyrite and the much rarer arsenolamprite and pararsenolamprite), but it is more commonly found as a compound with other elements. (R004, R670)",,593-52-2,79054,,"","","","",,,Methylarsine,,,,,"InChI=1/CH5As/c1-2/h2H2,1H3",methylarsane,http://www.biospider.ca/saved_files/mol/,C[AsH2],C[AsH2],CH5As,91.960720,No data.,-143 oC,,,"0.085 mg/mL at 20 oC [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral 
Inhalation 
Dermal 
(R009)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Arsenite methyltransferase (Q9HBK9) 
(R164)","Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carginogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (R001, R054)","Arsenic is absorbed mainly by inhalation or ingestion, as to a lesser extent, dermal exposure. It is then distributed throughout the body, where it is reduced into arsenite if necessary, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant. (R055)",No data.,No data.,"1, carcinogenic to humans. (R264)",Methylarsine is found in marine biological systems. (R670),"Acute Oral: 0.005 mg/kg/day (R260) 
Chronic Oral: 0.0003 mg/kg/day (R260) 
Chronic Inhalation: 0.01 mg/m3 (R260)","Arsenic poisoning can lead to death from multi-system organ failure, probably from necrotic cell death, not apoptosis. Arsenic is also a known carcinogen, esepcially in skin, liver, bladder and lung cancers. (R001, R055)","Exposure to lower levels of arsenic can cause nausea and vomiting, decreased production of red and white blood cells, abnormal heart rhythm, damage to blood vessels, and a sensation of burn (R001).","Arsenic poisoning can be treated by chelation therapy, using chelating agents such as dimercaprol, EDTA or DMSA. Charcoal tablets may also be used for less severe cases. In addition, maintaining a diet high in sulfur helps eliminate arsenic from the body. (R055)",P68032;P68133;P62736;P60709;P63261;P63267;P10515;P23025;P03372;P04150;P00390;P00738;P69905;P68871;P08559;P29803;P11177;Q14145;P09874;A6NKZ8 ;Q99867;Q9H853;O00330;Q16881;Q9NNW7;Q86VQ6;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2
305,T3D0304,2009-03-06 18:58:29 UTC,2009-08-04 21:28:14 UTC,Dimethylarsine,Organic Compound;Arsenic Compound;Organometallic,"(CH3)2AsHArsine, dimethyl-","Dimethylarsine is an organic derivative of arsine. Arsenic is a chemical element that has the symbol As and atomic number 33. It is a poisonous metalloid that has many allotropic forms: yellow (molecular non-metallic) and several black and grey forms (metalloids) are a few that are seen. Three metalloidal forms of arsenic with different crystal structures are found free in nature (the minerals arsenopyrite and the much rarer arsenolamprite and pararsenolamprite), but it is more commonly found as a compound with other elements. (R004, R670)",,593-57-7,79055,,"","","","",,C062856,Dimethylarsine,,,,,"InChI=1/C2H7As/c1-3-2/h3H,1-2H3",dimethylarsane,http://www.biospider.ca/saved_files/mol/,C[AsH]C,C[AsH]C,C2H7As,105.976370,No data.,-136.1 oC,,,"",,,,"Oral 
Inhalation 
Dermal 
(R009)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Arsenite methyltransferase (Q9HBK9) 
(R164)","Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carginogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (R001, R054)","Arsenic is absorbed mainly by inhalation or ingestion, as to a lesser extent, dermal exposure. It is then distributed throughout the body, where it is reduced into arsenite if necessary, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant. (R055)",No data.,No data.,"1, carcinogenic to humans. (R264)",Dimethylarsine is found in marine biological systems. (R670),"Acute Oral: 0.005 mg/kg/day (R260) 
Chronic Oral: 0.0003 mg/kg/day (R260) 
Chronic Inhalation: 0.01 mg/m3 (R260)","Arsenic poisoning can lead to death from multi-system organ failure, probably from necrotic cell death, not apoptosis. Arsenic is also a known carcinogen, esepcially in skin, liver, bladder and lung cancers. (R001, R055)","Exposure to lower levels of arsenic can cause nausea and vomiting, decreased production of red and white blood cells, abnormal heart rhythm, damage to blood vessels, and a sensation of burn (R001).","Arsenic poisoning can be treated by chelation therapy, using chelating agents such as dimercaprol, EDTA or DMSA. Charcoal tablets may also be used for less severe cases. In addition, maintaining a diet high in sulfur helps eliminate arsenic from the body. (R055)",P68032;P68133;P62736;P60709;P63261;P63267;P10515;P23025;P03372;P04150;P00390;P00738;P69905;P68871;P08559;P29803;P11177;Q14145;P09874;A6NKZ8 ;Q99867;Q9H853;O00330;Q16881;Q9NNW7;Q86VQ6;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2
306,T3D0305,2009-03-06 18:58:29 UTC,2009-08-04 21:28:14 UTC,Trimethylarsine,Organic Compound;Arsenic Compound;Organometallic,(CH3)3AsAsMe3TrimethylarsaneTrimethylarsenicTrimethylarsine,"Trimethylarsine is an organic derivative of arsine, as well as the byproduct of microbial action on naturally occuring inorganic forms of arsenic. It is often used in the production of other organoarsenic compounds. Arsenic is a chemical element that has the symbol As and atomic number 33. It is a poisonous metalloid that has many allotropic forms: yellow (molecular non-metallic) and several black and grey forms (metalloids) are a few that are seen. Three metalloidal forms of arsenic with different crystal structures are found free in nature (the minerals arsenopyrite and the much rarer arsenolamprite and pararsenolamprite), but it is more commonly found as a compound with other elements. (R004, R670)",,593-88-4,68978,,"","",27130,CPD-7058,,C009572,Trimethylarsine,,,,,InChI=1/C3H9As/c1-4(2)3/h1-3H3,trimethylarsane,http://www.biospider.ca/saved_files/mol/,C[As](C)C,C[As](C)C,C3H9As,119.992020,Colorless liquid.,-87.3 oC,,,"",,,,"Oral 
Inhalation 
Dermal 
(R009)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Arsenite methyltransferase (Q9HBK9) 
(R164)","Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carginogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (R001, R054)","Arsenic is absorbed mainly by inhalation or ingestion, as to a lesser extent, dermal exposure. It is then distributed throughout the body, where it is reduced into arsenite if necessary, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant. (R055)","LD50: 7870mg/kg (oral, mouse); LC50: 20500ppm/4hr (inhalation, mouse) (S262).",No data.,"1, carcinogenic to humans. (R264)","Trimethylarsine is used in the microelectronics industry, the production of other organoarsenic compounds, and as a ligand in coordination chemistry. (R670)","Acute Oral: 0.005 mg/kg/day (R260) 
Chronic Oral: 0.0003 mg/kg/day (R260) 
Chronic Inhalation: 0.01 mg/m3 (R260)","Arsenic poisoning can lead to death from multi-system organ failure, probably from necrotic cell death, not apoptosis. Arsenic is also a known carcinogen, esepcially in skin, liver, bladder and lung cancers. (R001, R055)","Exposure to lower levels of arsenic can cause nausea and vomiting, decreased production of red and white blood cells, abnormal heart rhythm, damage to blood vessels, and a sensation of burn (R001).","Arsenic poisoning can be treated by chelation therapy, using chelating agents such as dimercaprol, EDTA or DMSA. Charcoal tablets may also be used for less severe cases. In addition, maintaining a diet high in sulfur helps eliminate arsenic from the body. (R055)",P68032;P68133;P62736;P60709;P63261;P63267;P10515;P23025;P03372;P04150;P00390;P00738;P69905;P68871;P08559;P29803;P11177;Q14145;P09874;A6NKZ8 ;Q99867;Q9H853;O00330;Q16881;Q9NNW7;Q86VQ6;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2
308,T3D0307,2009-03-06 18:58:29 UTC,2009-08-04 21:28:15 UTC,Methylarsonic acid,Organic Compound;Arsenic Compound;Organometallic,"Arsonic acid, methyl-Dsma (jmaf)Kyselina methylarsonovaKyselina methylarsonova [czech]MAAMeAsO(OH)2Methanearsonic acidMethylarsenic acidMethylarsinic acidMethylarsonateMethylarsonic acidMethylarsonic acid [iso]Monomethylarsinic acidMonomethylarsonateMonomethylarsonic acid","Methylarsonic acid is an organoarsenic compound formed from the methylation of inorganic arsenic by living organisms. Arsenic is a chemical element that has the symbol As and atomic number 33. It is a poisonous metalloid that has many allotropic forms: yellow (molecular non-metallic) and several black and grey forms (metalloids) are a few that are seen. Three metalloidal forms of arsenic with different crystal structures are found free in nature (the minerals arsenopyrite and the much rarer arsenolamprite and pararsenolamprite), but it is more commonly found as a compound with other elements. (R004, R671)",,124-58-3,8948,,C07294,"",29852,METHYLARSONATE,,C020300,Methylarsonic acid,,,,,"InChI=1/CH5AsO3/c1-2(3,4)5/h1H3,(H2,3,4,5)",methylarsonic acid,http://www.biospider.ca/saved_files/mol/f9cd84053e27d194d63073a2181df29f_1237968921.mol,C[As](=O)(O)O,C[As](=O)(O)O,CH5AsO3,139.945470,White solid.,160.5 oC,,,"256 mg/mL at 20 oC [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral 
Inhalation 
Dermal 
(R009)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Arsenite methyltransferase (Q9HBK9) 
(R164)","Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carginogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (R001, R054)","Arsenic is absorbed mainly by inhalation or ingestion, as to a lesser extent, dermal exposure. It is then distributed throughout the body, where it is reduced into arsenite if necessary, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant. (R055)","LD50: 961 mg/kg (Oral, Rat) (R263)
LD50: 794 mg/kg (Subcutaneous, Mouse) (R263)",No data.,"1, carcinogenic to humans. (R264)",Methylarsonic acid is used as an herbicide and pesticide. (R671),"Acute Oral: 0.005 mg/kg/day (R260) 
Chronic Oral: 0.0003 mg/kg/day (R260) 
Chronic Inhalation: 0.01 mg/m3 (R260)","Arsenic poisoning can lead to death from multi-system organ failure, probably from necrotic cell death, not apoptosis. Arsenic is also a known carcinogen, esepcially in skin, liver, bladder and lung cancers. (R001, R055)","Exposure to lower levels of arsenic can cause nausea and vomiting, decreased production of red and white blood cells, abnormal heart rhythm, damage to blood vessels, and a sensation of burn (R001).","Arsenic poisoning can be treated by chelation therapy, using chelating agents such as dimercaprol, EDTA or DMSA. Charcoal tablets may also be used for less severe cases. In addition, maintaining a diet high in sulfur helps eliminate arsenic from the body. (R055)",P68032;P68133;P62736;P60709;P63261;P63267;P10515;P23025;P03372;P04150;P00390;P00738;P69905;P68871;P08559;P29803;P11177;Q14145;P09874;A6NKZ8 ;Q99867;Q9H853;O00330;Q16881;Q9NNW7;Q86VQ6;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2
309,T3D0308,2009-03-06 18:58:29 UTC,2009-08-04 21:28:15 UTC,"Methylarsonic acid, disodium salt",Organic Compound;Arsenic Compound;Organometallic,"Ansar 184Ansar dsma liquidArrhenalArsinylArsonic acid, methyl-Arsonic acid, methyl-, disodium saltArsynalCacodyl newChipco crab kleenCloutCrab-3-rad 100Crab-e-radCralo-e-radDSMADal-e-rad 100Di-tacDiarsenDimetDisodium methanearsenateDisodium methanearsonateDisodium methylarsenateDisodium methylarsonateDisodium monomethylarsonateDisomarDisomearDma (van)Dsma (jmaf)Jon-trolKyselina methylarsonova [czech]Maa sodium saltMeAsO(OH)2Methanearsonic acidMethanearsonic acid, disodium saltMetharMetharsanMetharsinatMethylarsenic acidMethylarsinic acidMethylarsonateMethylarsonic acidMethylarsonic acid [iso]Monomethylarsinic acidMonomethylarsonateMonomethylarsonic acidNamateNeo-asycodileSodarSodium methanearsonateSodium metharsonateSodium methylarsonateSomarStenosineTonarsanTonarsinWeed broomWeed-e-radWeed-hoemethylarsonic acid (ACD/Name 4.0)","Methylarsonic acid, disodium salt is an organoarsenic compound formed from the methylation of inorganic arsenic by living organisms. Arsenic is a chemical element that has the symbol As and atomic number 33. It is a poisonous metalloid that has many allotropic forms: yellow (molecular non-metallic) and several black and grey forms (metalloids) are a few that are seen. Three metalloidal forms of arsenic with different crystal structures are found free in nature (the minerals arsenopyrite and the much rarer arsenolamprite and pararsenolamprite), but it is more commonly found as a compound with other elements. (R004, R671)",,144-21-8 ,8948,,C07294,"",16005,METHYLARSONATE,,,"Methylarsonic acid, disodium salt",9576,,,,"InChI=1/CH5AsO3.2Na/c1-2(3,4)5;;/h1H3,(H2,3,4,5);;/q;2*+1/p-2",methylarsonic acid,http://www.biospider.ca/saved_files/mol/,C[As](=O)(O)O,C[As](=O)(O)O,CH5AsO3,139.945470,White solid.,132-139 oC,,,"432 mg/mL at 25 oC [SHIU,WY et al. (1990)]",,,,"Oral 
Inhalation 
Dermal 
(R009)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Arsenite methyltransferase (Q9HBK9) 
(R164)","Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carginogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (R001, R054)","Arsenic is absorbed mainly by inhalation or ingestion, as to a lesser extent, dermal exposure. It is then distributed throughout the body, where it is reduced into arsenite if necessary, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant. (R055)",No data.,No data.,"1, carcinogenic to humans. (R264)","Methylarsonic acid, disodium salt is used as an herbicide and pesticide. (R671)","Acute Oral: 0.005 mg/kg/day (R260) 
Chronic Oral: 0.0003 mg/kg/day (R260) 
Chronic Inhalation: 0.01 mg/m3 (R260)","Arsenic poisoning can lead to death from multi-system organ failure, probably from necrotic cell death, not apoptosis. Arsenic is also a known carcinogen, esepcially in skin, liver, bladder and lung cancers. (R001, R055)","Exposure to lower levels of arsenic can cause nausea and vomiting, decreased production of red and white blood cells, abnormal heart rhythm, damage to blood vessels, and a sensation of burn (R001).","Arsenic poisoning can be treated by chelation therapy, using chelating agents such as dimercaprol, EDTA or DMSA. Charcoal tablets may also be used for less severe cases. In addition, maintaining a diet high in sulfur helps eliminate arsenic from the body. (R055)",P68032;P68133;P62736;P60709;P63261;P63267;P10515;P23025;P03372;P04150;P00390;P00738;P69905;P68871;P08559;P29803;P11177;Q14145;P09874;A6NKZ8 ;Q99867;Q9H853;O00330;Q16881;Q9NNW7;Q86VQ6;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2
310,T3D0309,2009-03-06 18:58:29 UTC,2009-08-25 18:01:17 UTC,"Methylarsonic acid, monosodium salt",Organic Compound;Arsenic Compound;Organometallic,"Ansar 170Ansar 170LAnsar 529Ansar 529 HCAnsar 6.6Arsonic acid, methyl-, monosodium saltAsazolBuenoBueno 6Caswell No. 582DaconateDaconate 6Dal-E-Rad 120Dal-e-radDrexarGepironHerb-allHerban mMSMAMergeMerge 823MesamateMesamate concentrateMesamate h.cMesamate h.c.Mesamate-400Mesamate-600Methanearsonic acid, monosodium saltMethylarsenic acid, sodium saltMethylarsonat monosodny [czech]Methylarsonic acid, sodium saltMonateMonexMonobanMonomethylarsonic acid sodium saltMonosodium acid methanearsonateMonosodium acid metharsonateMonosodium methane arsenateMonosodium methanearsenateMonosodium methanearsonateMonosodium methanearsonic acidMonosodium methylarsonatePhybanPhyban h.cPhyban h.c.Silvisar 550Sodium acid methanearsonateSodium hydrogen methylarsonateSodium methanearsonateSodium methylarsonateSuper arsonateTarget msmaTrans-vertWeed-hoe-108","Methylarsonic acid, monosodium salt is an organoarsenic compound formed from the methylation of inorganic arsenic by living organisms. AArsenic is a chemical element that has the symbol As and atomic number 33. It is a poisonous metalloid that has many allotropic forms: yellow (molecular non-metallic) and several black and grey forms (metalloids) are a few that are seen. Three metalloidal forms of arsenic with different crystal structures are found free in nature (the minerals arsenopyrite and the much rarer arsenolamprite and pararsenolamprite), but it is more commonly found as a compound with other elements. (R004, R671)",,2163-80-6,23664719,,"","","","",,,"Methylarsonic acid, monosodium salt",7396,,,,"InChI=1/CH5AsO3.2Na/c1-2(3,4)5;;/h1H3,(H2,3,4,5);;/q;2*+1/p-2",sodium hydroxy(methyl)arsinate,http://www.biospider.ca/saved_files/mol/,C[As](=O)(O)[O-].[Na+],C[As](O)(=O)O[Na],CH4AsNaO3,161.927410,White solid.,"",,,"580 mg/mL at 20 oC [TOMLIN,C (1997)]",,,,"Oral 
Inhalation 
Dermal 
(R009)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Arsenite methyltransferase (Q9HBK9) 
(R164)","Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carginogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (R001, R054)","Arsenic is absorbed mainly by inhalation or ingestion, as to a lesser extent, dermal exposure. It is then distributed throughout the body, where it is reduced into arsenite if necessary, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant. (R055)",No data.,No data.,"1, carcinogenic to humans. (R264)","Methylarsonic acid, monosodium salt is used as an herbicide and pesticide. (R671)","Acute Oral: 0.005 mg/kg/day (R260) 
Chronic Oral: 0.0003 mg/kg/day (R260) 
Chronic Inhalation: 0.01 mg/m3 (R260)","Arsenic poisoning can lead to death from multi-system organ failure, probably from necrotic cell death, not apoptosis. Arsenic is also a known carcinogen, esepcially in skin, liver, bladder and lung cancers. (R001, R055)","Exposure to lower levels of arsenic can cause nausea and vomiting, decreased production of red and white blood cells, abnormal heart rhythm, damage to blood vessels, and a sensation of burn (R001).","Arsenic poisoning can be treated by chelation therapy, using chelating agents such as dimercaprol, EDTA or DMSA. Charcoal tablets may also be used for less severe cases. In addition, maintaining a diet high in sulfur helps eliminate arsenic from the body. (R055)",P68032;P68133;P62736;P60709;P63261;P63267;P10515;P23025;P03372;P04150;P00390;P00738;P69905;P68871;P08559;P29803;P11177;Q14145;P09874;A6NKZ8 ;Q99867;Q9H853;O00330;Q16881;Q9NNW7;Q86VQ6;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2
311,T3D0310,2009-03-06 18:58:30 UTC,2009-08-04 21:28:16 UTC,Benzenearsonic acid,Organic Compound;Arsenic Compound;Organometallic;Aromatic Hydrocarbon,"Arsonic acid, phenyl-Benzenearsonic acidKyselina benzenarsonova [czech]Monophenylarsonic acidPhAsO(OH)2Phenylarsonic acidWLN: q-as-qo & rphenylarsonic acid (ACD/Name 4.0)","Benzenearsonic acid is an organoarsenic compound. Arsenic is a chemical element that has the symbol As and atomic number 33. It is a poisonous metalloid that has many allotropic forms: yellow (molecular non-metallic) and several black and grey forms (metalloids) are a few that are seen. Three metalloidal forms of arsenic with different crystal structures are found free in nature (the minerals arsenopyrite and the much rarer arsenolamprite and pararsenolamprite), but it is more commonly found as a compound with other elements.  (R004)",,98-05-5,7365,,"","",29851,"",,C020979,Benzenearsonic acid,,,,,"InChI=1/C6H7AsO3/c8-7(9,10)6-4-2-1-3-5-6/h1-5H,(H2,8,9,10)",phenylarsonic acid,http://www.biospider.ca/saved_files/mol/,C1=CC=C(C=C1)[As](=O)(O)O,C1=CC=C(C=C1)[As](=O)(O)O,C6H7AsO3,201.961120,Colorless crystals.,158 oC,,,"",,,,"Oral 
Inhalation 
Dermal 
(R009)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Arsenite methyltransferase (Q9HBK9) 
(R164)","Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carginogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (R001, R054)","Arsenic is absorbed mainly by inhalation or ingestion, as to a lesser extent, dermal exposure. It is then distributed throughout the body, where it is reduced into arsenite if necessary, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant. (R055)","LD50: 270 ug/kg (Oral, Mouse) (R263)
lD50: 16 mg/kg (Intravenous, Rabbit) (R263)",No data.,"2B, possibly carcinogenic to humans. (R264)",Not available.,"Acute Oral: 0.005 mg/kg/day (R260) 
Chronic Oral: 0.0003 mg/kg/day (R260) 
Chronic Inhalation: 0.01 mg/m3 (R260)","Arsenic poisoning can lead to death from multi-system organ failure, probably from necrotic cell death, not apoptosis. Arsenic is also a known carcinogen, esepcially in skin, liver, bladder and lung cancers. (R001, R055)","Exposure to lower levels of arsenic can cause nausea and vomiting, decreased production of red and white blood cells, abnormal heart rhythm, damage to blood vessels, and a sensation of burn (R001).","Arsenic poisoning can be treated by chelation therapy, using chelating agents such as dimercaprol, EDTA or DMSA. Charcoal tablets may also be used for less severe cases. In addition, maintaining a diet high in sulfur helps eliminate arsenic from the body. (R055)",P68032;P68133;P62736;P60709;P63261;P63267;P10515;P23025;P03372;P04150;P00390;P00738;P69905;P68871;Q14145;P09874;A6NKZ8 ;Q99867;Q9H853;P08559;P29803;P11177;O00330;Q16881;Q9NNW7;Q86VQ6;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2
312,T3D0311,2009-03-06 18:58:30 UTC,2009-08-11 21:57:38 UTC,3-Nitro-4-hydroxy-phenyl-arsonic acid,Organic Compound;Arsenic Compound;Organometallic;Aromatic Hydrocarbon,"(4-hydroxy-3-nitrophenyl)arsonic acid2-Nitro-1-hydroxybenzene-4-arsonic acid2-Nitrophenol-4-arsonic acid3-Nitro3-Nitro-103-Nitro-203-Nitro-4-hydroxybenzenearsonic acid3-Nitro-4-hydroxyphenylarsonic acid3-Nitro-503-Nitro-803N4hpa4-Hydroxy-3-nitrobenzenearsonic acid4-Hydroxy-3-nitrobenzolarsonsaeure4-Hydroxy-3-nitrophenylarsonic acid4-hydroxy-3-nitrophenyl arsonic acidAklomix-3Arsonic acid, (4-hydroxy-3-nitrophenyl)-Benzenearsonic acid, 4-hydroxy-3-nitro-C6H6AsNO6Kyselina 4-hydroxy-3-nitrofenylarsonova [Czech]Nitro acid 100 per centNitrophenolarsonic acidNitrophenoloarsonic acidRen o-salRen-o-salRistatRoxarsonRoxarson [inn-spanish]RoxarsoneRoxarsone (usp/inn)Roxarsone [usan:ban:inn]Roxarsone [usan:inn:ban]Roxarsone(usan)RoxarsonumRoxarsonum [inn-latin]WLN: WNR bq e-as-qqo",3-nitro-4-hydroxy-phenyl-arsonic acid is a derivative of phenylarsonic acid used as food additive for poultry due to its growth promoting abilities.,,121-19-7,5104,,"","",35817,"",,D012406,3-Nitro-4-hydroxy-phenyl-arsonic acid,,,,,"InChI=1/C6H6AsNO6/c9-6-2-1-4(7(10,11)12)3-5(6)8(13)14/h1-3,9H,(H2,10,11,12)",(4-hydroxy-3-nitrophenyl)arsonic acid,http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C=C1[As](=O)(O)O)[N+](=O)[O-])O,C1=CC(=C(C=C1[As](=O)(O)O)[N+](=O)[O-])O,C6H6AsNO6,262.941110,Pale yellow solid.,"",,,"",,,,"Oral 
Inhalation 
Dermal 
(R009)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Arsenite methyltransferase (Q9HBK9) 
(R164)","Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carcinogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (R001, R054)","Arsenic is absorbed mainly by inhalation or ingestion, as to a lesser extent, dermal exposure. It is then distributed throughout the body, where it is reduced into arsenite if necessary, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant. (R055)","LD50: 81 mg/kg (Acute oral, Rat)",No data.,"1, carcinogenic to humans. (R264)",3-nitro-4-hydroxy-phenyl-arsonic acid is found in poultry feed.,"Acute Oral: 0.005 mg/kg/day (R260)
Chronic Oral: 0.0003 mg/kg/day (R260)
Chronic Inhalation: 0.01 mg/m3 (R260)","Hypovolemia from capillary leakage (third-spacing of fluids) is a common, serious, early effect. Muscle cramps, facial edema, bronchitis, dyspnea, chest pain, dehydration, intense thirst, and fluid-electrolyte disturbances are also common following significant exposures. A garlic-like odor of the breath and feces may also occur. After absorption, arsenic may cause multi-organ failure by inhibiting sulfhydryl-containing enzymes. Encephalopathy, with headache, lethargy, mental confusion, hallucinations, emotional lability, memory loss and delirium may occur; seizures, stupor, convulsions, coma, and death may follow within 24 hours of a severe acute exposure. Dysrhythmias (particularly QTc prolongation and torsade de pointes), cardiomyopathy, ARDS, hepatitis, rhabdomyolysis, hemolysis, and renal failure may develop over several days. The sequence of chronic poisoning involves hyperpigmentation, and eczematoid and allergic dermatitis. muscle fasciculations; gross tremors; ataxia; incoordination; and mental confusion. Muscular weakness, limb tenderness and difficulty walking may follow. The final phase consists of peripheral sensory neuropathy of the hands and feet. That may be associated with a motor neuropathy as well (R624). ","Initial signs and symptoms of arsenic ingestion include burning lips, throat constriction and dysphagia, followed by excruciating abdominal pain, hemorrhagic gastritis, gastroenteritis, severe nausea, projectile voting, profuse ""rice water-like"" diarrhea, with hypovolemia that may result in hypotension and an irregular pulse. The sequence of chronic poisoning involves weakness, anorexia, hepatomegaly, jaundice, and gastrointestinal complaints, followed by conjunctivitis, irritation of the throat and respiratory tract. ther effects of chronic exposure include conjunctivitis with irritation and lacrimation; hair, skin and nail changes; hyperkeratosis of feet and hands; and melanosis, with pigment spots in corneal and conjunctival epithelium. Peripheral nervous system symptoms may include numbness, burning, and tingling of the hands and feet; pain; paresthesias; tenderness (R624). ","Arsenic poisoning can be treated by chelation therapy, using chelating agents such as dimercaprol, EDTA or DMSA. Charcoal tablets may also be used for less severe cases. In addition, maintaining a diet high in sulfur helps eliminate arsenic from the body. (R055)",P68032;P68133;P62736;P60709;P63261;P63267;P10515;P23025;P03372;P04150;P00390;P00738;P69905;P68871;Q14145;P09874;A6NKZ8 ;Q99867;Q9H853;P08559;P29803;P11177;O00330;Q16881;Q9NNW7;Q86VQ6;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2
313,T3D0312,2009-03-06 18:58:30 UTC,2009-08-11 21:57:43 UTC,"4,4-Arsenobis(2-aminophenol) dihydrochloride",Organic Compound;Arsenic Compound;Organometallic;Aromatic Hydrocarbon,"3,3'-Diamino-4, 4'-dihydroxyarsenobenzene dihydrochloride3,3'-Diamino-4,4'-dihydroxyarsenobenzene dihydrochloride4,4'-(1,2-Diarsenediyl)bis(2-aminophenol) dihydrochloride6,6'-Dihydroxy-3,3'-diarsene-1,2-diyldianilinium dichlorideArsabenzosolArsaminolArsenobenzolArsenobenzol dihydrochlorideArsenphenolamine hydrochlorideArsfenamin [czech]ArsphenamineDiarsenolEhrlich 606EparsenolKharsivanNovarsolPhenarsenaminePhenol, 4,4'-arsenobis(2-amino-Phenol, 4,4'-arsenobis(2-amino-, dihydrochloridePhenol, {4,4'-arsenobis[2-amino-,} dihydrochlorideSalavarsanSalvarsanSanluolSix hundred sixSodium arsenobenzolTanvarsan","4,4-arsenobis(2-aminophenol) dihydrochloride is an arsenical drug believed to be the first modern chemotherapeutic agent. It was used to treat syphilis and trypanosomiasis.",,139-93-5,8774,,C11744,"",9016,"",,D001153,"4,4-Arsenobis(2-aminophenol) dihydrochloride",,,,,"InChI=1/C12H12As2N2O2.2ClH/c15-9-5-7(1-3-11(9)17)13-14-8-2-4-12(18)10(16)6-8;;/h1-6,17-18H,15-16H2;2*1H",2-amino-4-(3-amino-4-hydroxyphenyl)arsanylidenearsanylphenol dihydrochloride,http://www.biospider.ca/saved_files/mol/0eb297d869f1c72507ac6f7dda8eb964_1237969495.mol,C1=CC(=C(C=C1[As]=[As]C2=CC(=C(C=C2)O)N)N)O.Cl.Cl,C1=CC(=C(C=C1[As]=[As]C2=CC(=C(C=C2)O)N)N)O.Cl.Cl,C12H14As2Cl2N2O2,437.886430,No data.,190 oC,,,"",,,,"Oral 
Inhalation 
Dermal 
(R009)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Arsenite methyltransferase (Q9HBK9) 
(R164)","Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carcinogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (R001, R054)","Arsenic is absorbed mainly by inhalation or ingestion, as to a lesser extent, dermal exposure. It is then distributed throughout the body, where it is reduced into arsenite if necessary, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant. (R055)",No data.,No data.,"1, carcinogenic to humans. (R264)","4,4-arsenobis(2-aminophenol) dihydrochloride was used to treat syphilis and trypanosomiasis.","Acute Oral: 0.005 mg/kg/day (R260)
Chronic Oral: 0.0003 mg/kg/day (R260)
Chronic Inhalation: 0.01 mg/m3 (R260)","Hypovolemia from capillary leakage (third-spacing of fluids) is a common, serious, early effect. Muscle cramps, facial edema, bronchitis, dyspnea, chest pain, dehydration, intense thirst, and fluid-electrolyte disturbances are also common following significant exposures. A garlic-like odor of the breath and feces may also occur. After absorption, arsenic may cause multi-organ failure by inhibiting sulfhydryl-containing enzymes. Encephalopathy, with headache, lethargy, mental confusion, hallucinations, emotional lability, memory loss and delirium may occur; seizures, stupor, convulsions, coma, and death may follow within 24 hours of a severe acute exposure. Dysrhythmias (particularly QTc prolongation and torsade de pointes), cardiomyopathy, ARDS, hepatitis, rhabdomyolysis, hemolysis, and renal failure may develop over several days. The sequence of chronic poisoning involves hyperpigmentation, and eczematoid and allergic dermatitis. muscle fasciculations; gross tremors; ataxia; incoordination; and mental confusion. Muscular weakness, limb tenderness and difficulty walking may follow. The final phase consists of peripheral sensory neuropathy of the hands and feet. That may be associated with a motor neuropathy as well (R624). ","Initial signs and symptoms of arsenic ingestion include burning lips, throat constriction and dysphagia, followed by excruciating abdominal pain, hemorrhagic gastritis, gastroenteritis, severe nausea, projectile voting, profuse ""rice water-like"" diarrhea, with hypovolemia that may result in hypotension and an irregular pulse. The sequence of chronic poisoning involves weakness, anorexia, hepatomegaly, jaundice, and gastrointestinal complaints, followed by conjunctivitis, irritation of the throat and respiratory tract. ther effects of chronic exposure include conjunctivitis with irritation and lacrimation; hair, skin and nail changes; hyperkeratosis of feet and hands; and melanosis, with pigment spots in corneal and conjunctival epithelium. Peripheral nervous system symptoms may include numbness, burning, and tingling of the hands and feet; pain; paresthesias; tenderness (R624). ",Aggressive decontamination with gastric lavage is recommended if the patient has consumed a potentially life-threatening dose and if the patient is not vomiting (R624). ,P68032;P68133;P62736;P60709;P63261;P63267;P10515;P23025;P03372;P04150;P00390;P00738;P69905;P68871;Q14145;P09874;A6NKZ8 ;Q99867;Q9H853;P08559;P29803;P11177;O00330;Q16881;Q9NNW7;Q86VQ6;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2
314,T3D0313,2009-03-06 18:58:30 UTC,2009-08-11 21:57:47 UTC,[4-(Aminocarbonyl-amino)phenyl] arsonic acid,Organic Compound;Arsenic Compound;Organometallic;Aromatic Hydrocarbon,"(4-((Aminocarbonyl)amino)phenyl)arsonic acid4-((aminocarbonyl)amino)phenylarsonic acid (ACD/Name 4.0)4-Carbamylaminophenylarsonic acid4-Ureido-1-phenylarsonic acid4-Ureidobenzenearsonic acid4-Ureidobenzolarsonsaeure4-Ureidophenylarsonic acidAmabevanAmebanAmebarseneAmebarsoneAmibiarsonAminarsonAminarsoneAminarsonumAminoarsonArsambideArsanilic acid, n-carbamoyl-Arsonic acid, (4-((aminocarbonyl)amino)phenyl)-Arsonic acid, [4-[(aminocarbonyl)amino]phenyl]-Arsonic acid, {[4-[(aminocarbonyl)amino]phenyl]-}Benzenearsonic acid, p-ureido-C7H9AsN2O4Carb-o-sepCarbamidophenyl-p-arsonic acidCarbaminophenyl-p-arsonic acidCarbarsonCarbarson [inn-spanish]CarbarsoneCarbarsone [inn]Carbarsonum [inn-latin]CarbarzoneCarbasoneFenarsoneHistocarbHistocarb (van)Histocarb-sol.Histocarb-solubleKutanKyselina n-karbamylarsanilova [czech]LeucarsoneN-carbamoylarsanilic acidN-carbamyl arsanilic acidP-arsonophenylureaP-carbamidobenzenearsonic acidP-carbamidophenylarsonic acidP-carbamino phenyl arsonic acidP-ureidobenzenearsonic acidPentarsonePhenarsoneWLN: ZVMR d-as-qqo[4-[(AMINOCARBONYL)AMINO]PHENYL]ARSONIC ACID{4-[(aminocarbonyl)amino]phenyl}arsonic acid",[4-(aminocarbonyl-amino)phenyl] arsonic acid is an arsenic-based antiprotozoal drug which has been used in the treatment of infections.,,121-59-5,8480,,"","","","",,C033007,[4-(Aminocarbonyl-amino)phenyl] arsonic acid,,,,,"InChI=1/C7H9AsN2O4/c9-7(11)10-6-3-1-5(2-4-6)8(12,13)14/h1-4H,(H3,9,10,11)(H2,12,13,14)",[4-(carbamoylamino)phenyl]arsonic acid,http://www.biospider.ca/saved_files/mol/,C1=CC(=CC=C1NC(=O)N)[As](=O)(O)O,C1=CC(=CC=C1NC(=O)N)[As](=O)(O)O,C7H9AsN2O4,259.977830,No data.,174 oC,,,"",,,,"Oral 
Inhalation 
Dermal 
(R009)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Arsenite methyltransferase (Q9HBK9) 
(R164)","Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carcinogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (R001, R054)","Arsenic is absorbed mainly by inhalation or ingestion, as to a lesser extent, dermal exposure. It is then distributed throughout the body, where it is reduced into arsenite if necessary, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant. (R055)",,,"1, carcinogenic to humans. (R264)",[4-(aminocarbonyl-amino)phenyl] arsonic acid was used as a drug to treat infections. It is now found in poultry feed and used to treat some avian diseases.,"Acute Oral: 0.005 mg/kg/day (R260)
Chronic Oral: 0.0003 mg/kg/day (R260)
Chronic Inhalation: 0.01 mg/m3 (R260)","Hypovolemia from capillary leakage (third-spacing of fluids) is a common, serious, early effect. Muscle cramps, facial edema, bronchitis, dyspnea, chest pain, dehydration, intense thirst, and fluid-electrolyte disturbances are also common following significant exposures. A garlic-like odor of the breath and feces may also occur. After absorption, arsenic may cause multi-organ failure by inhibiting sulfhydryl-containing enzymes. Encephalopathy, with headache, lethargy, mental confusion, hallucinations, emotional lability, memory loss and delirium may occur; seizures, stupor, convulsions, coma, and death may follow within 24 hours of a severe acute exposure. Dysrhythmias (particularly QTc prolongation and torsade de pointes), cardiomyopathy, ARDS, hepatitis, rhabdomyolysis, hemolysis, and renal failure may develop over several days. The sequence of chronic poisoning involves hyperpigmentation, and eczematoid and allergic dermatitis. muscle fasciculations; gross tremors; ataxia; incoordination; and mental confusion. Muscular weakness, limb tenderness and difficulty walking may follow. The final phase consists of peripheral sensory neuropathy of the hands and feet. That may be associated with a motor neuropathy as well (R624). ","Initial signs and symptoms of arsenic ingestion include burning lips, throat constriction and dysphagia, followed by excruciating abdominal pain, hemorrhagic gastritis, gastroenteritis, severe nausea, projectile voting, profuse ""rice water-like"" diarrhea, with hypovolemia that may result in hypotension and an irregular pulse. The sequence of chronic poisoning involves weakness, anorexia, hepatomegaly, jaundice, and gastrointestinal complaints, followed by conjunctivitis, irritation of the throat and respiratory tract. ther effects of chronic exposure include conjunctivitis with irritation and lacrimation; hair, skin and nail changes; hyperkeratosis of feet and hands; and melanosis, with pigment spots in corneal and conjunctival epithelium. Peripheral nervous system symptoms may include numbness, burning, and tingling of the hands and feet; pain; paresthesias; tenderness (R624). ",Aggressive decontamination with gastric lavage is recommended if the patient has consumed a potentially life-threatening dose and if the patient is not vomiting (R624). ,P68032;P68133;P62736;P60709;P63261;P63267;P10515;P23025;P03372;P04150;P00390;P00738;P69905;P68871;Q14145;P09874;A6NKZ8 ;Q99867;Q9H853;P08559;P29803;P11177;O00330;Q16881;Q9NNW7;Q86VQ6;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2
315,T3D0314,2009-03-06 18:58:30 UTC,2009-08-19 19:04:43 UTC,[4-[(2-Amino-2-oxoethyl)amino]phenyl] arsonic acid,Organic Compound;Arsenic Compound;Organometallic;Aromatic Hydrocarbon,"Arsanilic acid, n-(carbamoylmethyl)-, monosodium saltC8H10AsN2NaO4GlyphenarsineMonosodium n-(carbamoylmethyl)arsanilateMonosodium n-phenylglycinamide-p-arsonateN-(carbamoylmethyl)arsanilic acid sodium saltN-(carbamoylmethyl)arsanilic acid, monosodium saltN-phenyl glycineamide-p-arsonic acid sodium saltNovatoxylSodium 4-(carbamoylmethylamino)benzenearsonateSodium 4-arsonophenylglycinamideSodium 4-arsonophenylglycineamideSodium N-phenylglycylamide-4-arsonateTriparsamida [inn-spanish]TriparsamideTriparsamide [dcit]TryparsamidTryparsamideTryparsamide [inn]Tryparsamidum [inn-latin]TryparsoneTryponarsylTrypothane",[4-[(2-amino-2-oxoethyl)amino]phenyl] arsonic acid is a synthetic arsenical drug used to treat trypanosomiasis (African sleeping sickness).,,554-72-3,23665572,,"","","","",,C073345,[4-[(2-Amino-2-oxoethyl)amino]phenyl] arsonic acid,,,,,"InChI=1/C8H11AsN2O4.Na/c10-8(12)5-11-7-3-1-6(2-4-7)9(13,14)15;/h1-4,11H,5H2,(H2,10,12)(H2,13,14,15);/q;+1/p-1",sodium [4-[(2-amino-2-oxoethyl)amino]phenyl]-hydroxyarsinate,http://www.biospider.ca/saved_files/mol/,C1=CC(=CC=C1NCC(=O)N)[As](=O)(O)[O-].[Na+],[Na+].NC(=O)CNc1ccc(cc1)[As](O)([O-])=O,C8H10AsN2NaO4,295.975420,White powder.,"",,,"",,,,"Oral 
Inhalation 
Dermal 
(R009)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Arsenite methyltransferase (Q9HBK9) 
(R164)","Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carcinogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (R001, R054)","Arsenic is absorbed mainly by inhalation or ingestion, as to a lesser extent, dermal exposure. It is then distributed throughout the body, where it is reduced into arsenite if necessary, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant. (R055)",No data.,No data.,"1, carcinogenic to humans. (R264)",[4-[(2-amino-2-oxoethyl)amino]phenyl] arsonic acid is a drug used to treat trypanosomiasis.,"Acute Oral: 0.005 mg/kg/day (R260)
Chronic Oral: 0.0003 mg/kg/day (R260)
Chronic Inhalation: 0.01 mg/m3 (R260)","Hypovolemia from capillary leakage (third-spacing of fluids) is a common, serious, early effect. Muscle cramps, facial edema, bronchitis, dyspnea, chest pain, dehydration, intense thirst, and fluid-electrolyte disturbances are also common following significant exposures. A garlic-like odor of the breath and feces may also occur. After absorption, arsenic may cause multi-organ failure by inhibiting sulfhydryl-containing enzymes. Encephalopathy, with headache, lethargy, mental confusion, hallucinations, emotional lability, memory loss and delirium may occur; seizures, stupor, convulsions, coma, and death may follow within 24 hours of a severe acute exposure. Dysrhythmias (particularly QTc prolongation and torsade de pointes), cardiomyopathy, ARDS, hepatitis, rhabdomyolysis, hemolysis, and renal failure may develop over several days. The sequence of chronic poisoning involves hyperpigmentation, and eczematoid and allergic dermatitis. muscle fasciculations; gross tremors; ataxia; incoordination; and mental confusion. Muscular weakness, limb tenderness and difficulty walking may follow. The final phase consists of peripheral sensory neuropathy of the hands and feet. That may be associated with a motor neuropathy as well (R624). ","Initial signs and symptoms of arsenic ingestion include burning lips, throat constriction and dysphagia, followed by excruciating abdominal pain, hemorrhagic gastritis, gastroenteritis, severe nausea, projectile voting, profuse ""rice water-like"" diarrhea, with hypovolemia that may result in hypotension and an irregular pulse. The sequence of chronic poisoning involves weakness, anorexia, hepatomegaly, jaundice, and gastrointestinal complaints, followed by conjunctivitis, irritation of the throat and respiratory tract. ther effects of chronic exposure include conjunctivitis with irritation and lacrimation; hair, skin and nail changes; hyperkeratosis of feet and hands; and melanosis, with pigment spots in corneal and conjunctival epithelium. Peripheral nervous system symptoms may include numbness, burning, and tingling of the hands and feet; pain; paresthesias; tenderness (R624). ",Aggressive decontamination with gastric lavage is recommended if the patient has consumed a potentially life-threatening dose and if the patient is not vomiting (R624). ,P68032;P68133;P62736;P60709;P63261;P63267;P10515;P23025;P03372;P04150;P00390;P00738;P69905;P68871;Q14145;P09874;A6NKZ8 ;Q99867;Q9H853;P08559;P29803;P11177;O00330;Q16881;Q9NNW7;Q86VQ6;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2
316,T3D0315,2009-03-06 18:58:30 UTC,2009-08-11 21:57:53 UTC,(4-Nitrophenyl)arsonic acid,Organic Compound;Arsenic Compound;Organometallic;Aromatic Hydrocarbon,"(4-NITROPHENYL)ARSONIC ACID(p-nitrophenyl)arsonic acid4-(Hydroxy(oxido)amino)phenylarsonic acid4-(hydroxy(oxido)amino)phenylarsonic acid (ACD/Name 4.0)4-Nitrobenzenearsonic acid4-Nitrophenylarsonic acidArsonic acid, (4-nitrophenyl)-Arsonic acid, 4-nitrophenylBenzenearsonic acid, p-nitro-C6H6AsNO5Hep-a-statHistostatHistostat 50Histostat-50NitarsonNitarson [inn-spanish]NitarsoneNitarsone (usan/inn)Nitarsone [usan:inn]Nitarsone(usan)Nitarsonum [inn-latin]P-nitrobenzenearsonic acidP-nitrophenylarsonic acidWLN: WNR d-as-qqo",(4-nitrophenyl)arsonic acid is a derivative of phenylarsonic acid used as food additive in animal feed due to its growth promoting properties.,,98-72-6,66826,,"","","","",,C015389,(4-Nitrophenyl)arsonic acid,,,,,"InChI=1/C6H6AsNO5/c9-7(10,11)5-1-3-6(4-2-5)8(12)13/h1-4H,(H2,9,10,11)",(4-nitrophenyl)arsonic acid,http://www.biospider.ca/saved_files/mol/,C1=CC(=CC=C1[N+](=O)[O-])[As](=O)(O)O,C1=CC(=CC=C1[N+](=O)[O-])[As](=O)(O)O,C6H6AsNO5,246.946190,No data.,>310 oC,,,"",,,,"Oral 
Inhalation 
Dermal 
(R009)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Arsenite methyltransferase (Q9HBK9) 
(R164)","Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carcinogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (R001, R054)","Arsenic is absorbed mainly by inhalation or ingestion, as to a lesser extent, dermal exposure. It is then distributed throughout the body, where it is reduced into arsenite if necessary, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant. (R055)",No data.,No data.,"1, carcinogenic to humans. (R264)","(4-nitrophenyl)arsonic acid is found in animal feed.
","Acute Oral: 0.005 mg/kg/day (R260)
Chronic Oral: 0.0003 mg/kg/day (R260)
Chronic Inhalation: 0.01 mg/m3 (R260)","Hypovolemia from capillary leakage (third-spacing of fluids) is a common, serious, early effect. Muscle cramps, facial edema, bronchitis, dyspnea, chest pain, dehydration, intense thirst, and fluid-electrolyte disturbances are also common following significant exposures. A garlic-like odor of the breath and feces may also occur. After absorption, arsenic may cause multi-organ failure by inhibiting sulfhydryl-containing enzymes. Encephalopathy, with headache, lethargy, mental confusion, hallucinations, emotional lability, memory loss and delirium may occur; seizures, stupor, convulsions, coma, and death may follow within 24 hours of a severe acute exposure. Dysrhythmias (particularly QTc prolongation and torsade de pointes), cardiomyopathy, ARDS, hepatitis, rhabdomyolysis, hemolysis, and renal failure may develop over several days. The sequence of chronic poisoning involves hyperpigmentation, and eczematoid and allergic dermatitis. muscle fasciculations; gross tremors; ataxia; incoordination; and mental confusion. Muscular weakness, limb tenderness and difficulty walking may follow. The final phase consists of peripheral sensory neuropathy of the hands and feet. That may be associated with a motor neuropathy as well (R624). ","Initial signs and symptoms of arsenic ingestion include burning lips, throat constriction and dysphagia, followed by excruciating abdominal pain, hemorrhagic gastritis, gastroenteritis, severe nausea, projectile voting, profuse ""rice water-like"" diarrhea, with hypovolemia that may result in hypotension and an irregular pulse. The sequence of chronic poisoning involves weakness, anorexia, hepatomegaly, jaundice, and gastrointestinal complaints, followed by conjunctivitis, irritation of the throat and respiratory tract. ther effects of chronic exposure include conjunctivitis with irritation and lacrimation; hair, skin and nail changes; hyperkeratosis of feet and hands; and melanosis, with pigment spots in corneal and conjunctival epithelium. Peripheral nervous system symptoms may include numbness, burning, and tingling of the hands and feet; pain; paresthesias; tenderness (R624). ",Aggressive decontamination with gastric lavage is recommended if the patient has consumed a potentially life-threatening dose and if the patient is not vomiting (R624). ,P68032;P68133;P62736;P60709;P63261;P63267;P10515;P23025;P03372;P04150;P00390;P00738;P69905;P68871;Q14145;P09874;A6NKZ8 ;Q99867;Q9H853;P08559;P29803;P11177;O00330;Q16881;Q9NNW7;Q86VQ6;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2
317,T3D0316,2009-03-06 18:58:30 UTC,2009-08-25 18:01:21 UTC,Sodium arsanilate,Organic Compound;Arsenic Compound;Organometallic,"(4-Aminophenyl)arsonic acid sodium tetrahydrate(4-aminophenyl)arsonic acid sodium saltAnhydrous sodium arsanilateArsaminArsanilic acid sodium saltArsanilic acid sodium salt tetrahydrateArsanilic acid, monosodium saltArsanilic acid, monosodium salt, tetrahydrateArsinosolvinArsonic acid, (4-aminophenyl)-, monosodium saltArsonic acid, (4-aminophenyl)-, monosodium salt (9CI)AtoxylC6H7AsNNaO3NuarsolPiglet pro-gen vPro-gen sodiumProtoxylSoaminSodium aminarsonateSodium aminophenol arsonateSodium aminophenylarsonateSodium anilarsonateSodium aniline-arsonateSodium arsanilateSodium arsanilate [UN2473] [Poison]Sodium arsanilate tetrahydrateSodium arsenilateSodium arsonilateSodium p-aminobenzenearsonateSodium p-aminophenylarsonateSodium p-aminophenylarsonate tetrahydrateSodium p-arsanilateSodium-analine arsonateSonateTrypoxylmonosodium (4-aminophenyl)arsonatesodium hydrogen (4-aminophenyl)arsonatesodium hydrogen 4-aminophenylarsonate",Sodium arsanilate is an arsenic compound used mainly in veterinary medicine as an anthelmintic. it is also used as a growth promoter in animal feed.,,127-85-5,23670523,,"","",36049,"",,,Sodium arsanilate,,,,,"InChI=1/C6H8AsNO3.Na/c8-6-3-1-5(2-4-6)7(9,10)11;/h1-4H,8H2,(H2,9,10,11);/q;+1/p-1",sodium (4-aminophenyl)-hydroxyarsinate,http://www.biospider.ca/saved_files/mol/,C1=CC(=CC=C1N)[As](=O)(O)[O-].[Na+],Nc1ccc(cc1)[As](O)(=O)O[Na],C6H7AsNNaO3,238.953960,White solid.,"",,,167 mg/mL [MERCK INDEX (1996)],,,,"Oral 
Inhalation 
Dermal 
(R009)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Arsenite methyltransferase (Q9HBK9) 
(R164)","Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carcinogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (R001, R054)","Arsenic is absorbed mainly by inhalation or ingestion, as to a lesser extent, dermal exposure. It is then distributed throughout the body, where it is reduced into arsenite if necessary, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant. (R055)","LD50: 75 mg/kg (Acute subcutaneous, Rat)
LD50: 335 mg/kg (Acute intravenous, Rat)",No data.,"1, carcinogenic to humans. (R264)","Sodium arsanilate is found in animal feed, and is also used in veterinary medicine, mainly to treat swine dysentry.","Acute Oral: 0.005 mg/kg/day (R260)
Chronic Oral: 0.0003 mg/kg/day (R260)
Chronic Inhalation: 0.01 mg/m3 (R260)","Hypovolemia from capillary leakage (third-spacing of fluids) is a common, serious, early effect. Muscle cramps, facial edema, bronchitis, dyspnea, chest pain, dehydration, intense thirst, and fluid-electrolyte disturbances are also common following significant exposures. A garlic-like odor of the breath and feces may also occur. After absorption, arsenic may cause multi-organ failure by inhibiting sulfhydryl-containing enzymes. Encephalopathy, with headache, lethargy, mental confusion, hallucinations, emotional lability, memory loss and delirium may occur; seizures, stupor, convulsions, coma, and death may follow within 24 hours of a severe acute exposure. Dysrhythmias (particularly QTc prolongation and torsade de pointes), cardiomyopathy, ARDS, hepatitis, rhabdomyolysis, hemolysis, and renal failure may develop over several days. The sequence of chronic poisoning involves hyperpigmentation, and eczematoid and allergic dermatitis. muscle fasciculations; gross tremors; ataxia; incoordination; and mental confusion. Muscular weakness, limb tenderness and difficulty walking may follow. The final phase consists of peripheral sensory neuropathy of the hands and feet. That may be associated with a motor neuropathy as well (R624). ","Initial signs and symptoms of arsenic ingestion include burning lips, throat constriction and dysphagia, followed by excruciating abdominal pain, hemorrhagic gastritis, gastroenteritis, severe nausea, projectile voting, profuse ""rice water-like"" diarrhea, with hypovolemia that may result in hypotension and an irregular pulse. The sequence of chronic poisoning involves weakness, anorexia, hepatomegaly, jaundice, and gastrointestinal complaints, followed by conjunctivitis, irritation of the throat and respiratory tract. ther effects of chronic exposure include conjunctivitis with irritation and lacrimation; hair, skin and nail changes; hyperkeratosis of feet and hands; and melanosis, with pigment spots in corneal and conjunctival epithelium. Peripheral nervous system symptoms may include numbness, burning, and tingling of the hands and feet; pain; paresthesias; tenderness (R624). ",Aggressive decontamination with gastric lavage is recommended if the patient has consumed a potentially life-threatening dose and if the patient is not vomiting. Administer charcoal as a slurry (R624). ,P68032;P68133;P62736;P60709;P63261;P63267;P10515;P23025;P03372;P04150;P00390;P00738;P69905;P68871;Q14145;P09874;A6NKZ8 ;Q99867;Q9H853;P08559;P29803;P11177;O00330;Q16881;Q9NNW7;Q86VQ6;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2
318,T3D0317,2009-03-06 18:58:31 UTC,2009-08-25 18:01:26 UTC,Sodium dimethylarsinate,Organic Compound;Arsenic Compound;Organometallic,"AlkarsodylAnsar 160Ansar 560ArsecodileArsicodileArsine oxide, hydroxydimethyl-, sodium saltArsinic acid, dimethyl-, sodium saltArsycodileCacodylate de sodiumCacodylate de sodium(french)Cacodylic acid, sodium saltDimethylarsinic acid, sodium saltHydroxydimethylarsine oxide sodium saltPhytar 560Rad-e-cate 25Sodium cacodylateSodium dimethylarsinateSodium salt of cacodylic acidWLN: Q-AS-O & 1 & 1 &-NA-dimethylarsinic acid (ACD/Name 4.0)",Sodium dimethylarsinate is an arsenic compound used as a drug in veterinary medicine to treat anaemia and eczema.,,124-65-2,23615615,,"","","","",,,Sodium dimethylarsinate,9481,,,,"InChI=1/C2H7AsO2.Na/c1-3(2,4)5;/h1-2H3,(H,4,5);/q;+1/p-1",sodium dimethylarsinic acid,http://www.biospider.ca/saved_files/mol/,C[As](=O)(C)O.[Na+],C[As](C)(=O)O[Na],C2H7AsNaO2+,"",Colorless or light yellow solid.,200 oC,,,"2000 mg/mL at 25 oC [TOMLIN,C (1997)]",,,,"Oral 
Inhalation 
Dermal 
(R009)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Arsenite methyltransferase (Q9HBK9) 
(R164)","Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carcinogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (R001, R054)","Arsenic is absorbed mainly by inhalation or ingestion, as to a lesser extent, dermal exposure. It is then distributed throughout the body, where it is reduced into arsenite if necessary, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant. (R055)","LD50: 2600 mg/kg (Acute oral, Rat)",No data.,"1, carcinogenic to humans. (R264)","Sodium dimethylarsinate is used as a drug in veterinary medicine to treat anaemia and eczema, and is also an herbicide.","Acute Oral: 0.005 mg/kg/day (R260)
Chronic Oral: 0.0003 mg/kg/day (R260)
Chronic Inhalation: 0.01 mg/m3 (R260)","Hypovolemia from capillary leakage (third-spacing of fluids) is a common, serious, early effect. Muscle cramps, facial edema, bronchitis, dyspnea, chest pain, dehydration, intense thirst, and fluid-electrolyte disturbances are also common following significant exposures. A garlic-like odor of the breath and feces may also occur. After absorption, arsenic may cause multi-organ failure by inhibiting sulfhydryl-containing enzymes. Encephalopathy, with headache, lethargy, mental confusion, hallucinations, emotional lability, memory loss and delirium may occur; seizures, stupor, convulsions, coma, and death may follow within 24 hours of a severe acute exposure. Dysrhythmias (particularly QTc prolongation and torsade de pointes), cardiomyopathy, ARDS, hepatitis, rhabdomyolysis, hemolysis, and renal failure may develop over several days. The sequence of chronic poisoning involves hyperpigmentation, and eczematoid and allergic dermatitis. muscle fasciculations; gross tremors; ataxia; incoordination; and mental confusion. Muscular weakness, limb tenderness and difficulty walking may follow. The final phase consists of peripheral sensory neuropathy of the hands and feet. That may be associated with a motor neuropathy as well (R624). ","Initial signs and symptoms of arsenic ingestion include burning lips, throat constriction and dysphagia, followed by excruciating abdominal pain, hemorrhagic gastritis, gastroenteritis, severe nausea, projectile voting, profuse ""rice water-like"" diarrhea, with hypovolemia that may result in hypotension and an irregular pulse. The sequence of chronic poisoning involves weakness, anorexia, hepatomegaly, jaundice, and gastrointestinal complaints, followed by conjunctivitis, irritation of the throat and respiratory tract. ther effects of chronic exposure include conjunctivitis with irritation and lacrimation; hair, skin and nail changes; hyperkeratosis of feet and hands; and melanosis, with pigment spots in corneal and conjunctival epithelium. Peripheral nervous system symptoms may include numbness, burning, and tingling of the hands and feet; pain; paresthesias; tenderness (R624). ",Aggressive decontamination with gastric lavage is recommended if the patient has consumed a potentially life-threatening dose and if the patient is not vomiting. Administer charcoal as a slurry (R624).,P68032;P68133;P62736;P60709;P63261;P63267;P10515;P23025;P03372;P04150;P00390;P00738;P69905;P68871;Q14145;P09874;A6NKZ8 ;Q99867;Q9H853;P08559;P29803;P11177;O00330;Q16881;Q9NNW7;Q86VQ6;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2
319,T3D0318,2009-03-06 18:58:31 UTC,2009-08-04 21:28:17 UTC,Trimethylarsine oxide,Organic Compound;Arsenic Compound;Organometallic,(CH3)3As=OTrimethylarsane oxideTrimethylarsine oxide,"Trimethylarsine oxide is an organic derivative of arsenic. Arsenic is a chemical element that has the symbol As and atomic number 33. It is a poisonous metalloid that has many allotropic forms: yellow (molecular non-metallic) and several black and grey forms (metalloids) are a few that are seen. Three metalloidal forms of arsenic with different crystal structures are found free in nature (the minerals arsenopyrite and the much rarer arsenolamprite and pararsenolamprite), but it is more commonly found as a compound with other elements. (R004)",,4964-14-1,104930,,"","",27131,CPD-7058,,C052920,Trimethylarsine oxide,,,,,"InChI=1/C3H9AsO/c1-4(2,3)5/h1-3H3",dimethylarsorylmethane,http://www.biospider.ca/saved_files/mol/,C[As](=O)(C)C,C[As](=O)(C)C,C3H9AsO,135.986940,No data.,"",,,"",,,,"Oral 
Inhalation 
Dermal 
(R009)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Arsenite methyltransferase (Q9HBK9) 
(R164)","Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carginogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (R001, R054)","Arsenic is absorbed mainly by inhalation or ingestion, as to a lesser extent, dermal exposure. It is then distributed throughout the body, where it is reduced into arsenite if necessary, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant. (R055)","LD50: 10.6 g/kg (oral, mice) (S265).",No data.,"1, carcinogenic to humans. (R264)",No data.,"Acute Oral: 0.005 mg/kg/day (R260) 
Chronic Oral: 0.0003 mg/kg/day (R260) 
Chronic Inhalation: 0.01 mg/m3 (R260)","Arsenic poisoning can lead to death from multi-system organ failure, probably from necrotic cell death, not apoptosis. Arsenic is also a known carcinogen, esepcially in skin, liver, bladder and lung cancers. (R001, R055)","Exposure to lower levels of arsenic can cause nausea and vomiting, decreased production of red and white blood cells, abnormal heart rhythm, damage to blood vessels, and a sensation of burn (R001).","Arsenic poisoning can be treated by chelation therapy, using chelating agents such as dimercaprol, EDTA or DMSA. Charcoal tablets may also be used for less severe cases. In addition, maintaining a diet high in sulfur helps eliminate arsenic from the body. (R055)",P68032;P68133;P62736;P60709;P63261;P63267;P10515;P23025;P03372;P04150;P00390;P00738;P69905;P68871;P08559;P29803;P11177;Q14145;P09874;A6NKZ8 ;Q99867;Q9H853;O00330;Q16881;Q9NNW7;Q86VQ6;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2
320,T3D0319,2009-03-06 18:58:31 UTC,2009-08-25 18:01:30 UTC,Lead acetate,Organic Compound;Lead Compound;Organometallic,"Acetate de plomb [french]Acetate de plomb(french)Acetic acid lead(2+) saltAcetic acid, lead saltAcetic acid, lead(2 +) saltAcetic acid, lead(2+) saltAcetic acid, lead(2+) salt ( )Bleiacetat [german]Caswell No. 523ADibasic lead acetateLEAD ACETATE (SEE ALSO LEAD ACETATE 301-04-2)Lead acetateLead acetate (Pb(Ac)2)Lead acetate (Pb(O2C2H3)2)Lead acetate (Pb(OAc)2)Lead acetate (acn)Lead acetate (anhydrous)Lead acetate [UN1616] [Poison]Lead acetate, hydrateLead di(acetate)Lead diacetateLead dibasic acetateLead(2+) acetateLead(II) acetateLead(II)salt acetic acidNeutral lead acetateNormal lead acetatePb(CH3COO)2Plumbous acetateRCRA waste no. U144RCRA waste number U144Salt of saturnSugar of leadUnichem pbaacetic acid (ACD/Name 4.0)lead(2+) diacetate","Lead acetate is a chemical compound made by treating lead(II) oxide with acetic acid. Due to its sweet taste, it was used as a sweetner before its toxicity was recognized. Today it can be found in low concentrations in some hair dyes. Lead is a heavy metal and stable element with the symbol Pb and the atomic number 82, existing in metallic, organic, and inorganic forms. It is mainly found in nature as the mineral galena (PbS), cerussite (PbCO3) or anglesite (PbSO4), usually in ore with zinc, silver, or copper. (R056, R690)",,301-04-2,9317,,C00033,"276100
601705",31767,ACET,,C008261,Lead acetate,,,,,"InChI=1/C2H4O2/c1-2(3)4/h1H3,(H,3,4)",lead(2+) diacetate,http://www.biospider.ca/saved_files/mol/,CC(=O)[O-].CC(=O)[O-].[Pb+2],CC(=O)O[Pb]OCC=O,C4H6O4Pb,326.003240,White solid.,327.4 oC,,,1.6 mg/mL [MERCK INDEX (1989)],,,,"Oral 
Inhalation 
Dermal 
(R266)","Delta-aminolevulinic acid dehydratase (P13716) 
Serum albumin (P02768) 
Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
(R266)","Lead mimics other biologically important metals, such as zinc, calcium, and iron, competing as cofactors for many of their respective enzymatic reactions. For example, lead has been shown to competitively inhibit calcium's binding of calmodulin, interferring with neurotransmitter release. It exhibits similar competitive inhibition at the NMDA receptor and protein kinase C, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Lead also affects the nervous system by impairing regulation of dopamine synthesis and blocking evoked release of acetylcholine. However, it's main mechanism of action occurs by inhibiting delta-aminolevulinic acid dehydratase, an enzyme vital in the biosynthesis of heme, which is a necesssary cofactor of hemoglobin. (R008, R061, R063, R266)","Lead is absorbed following inhalation, oral, and dermal exposure. It is then distributed mainly to the bones and red blood cells. In the blood lead may be found bound to serum albumin or the metal-binding protein metallothionein. Organic lead is metabolized by cytochrome P-450 enzymes, whereas inorganic lead forms complexes with delta-aminolevulinic acid dehydratase. Lead is excreted mainly in the urine and faeces. (R266)","LD50: 150 mg (Intraperitoneal, Rat) (R263)
LD50: 104 mg/kg (Intravenous, Rat) (R263)",10 to 30 grams for and adult human (lead salts). (R273),"2B, possibly carcinogenic to humans. (R264)","Lead acetate is used as a reagent to make other lead compounds and as a fixative for some dyes. It is also found in paints and varnishes, as well as in low concentrations in hair dyes. (R690)",Chronic Inhalation: 0.05 mg/m3 (R260),"Lead is a neurotoxin and has been known to cause brain damage and reduced cognitive capacity, especially in children. Lead exposure can result in nephropathy, as well as blood disorders such as high blood pressure and anemia. Lead also exhibits reproductive toxicity and can results in miscarriages and reduced sperm production. (R056)","Symptions of chronic lead poisoning include reduced cognitive abilities, nausea, abdominal pain, irritability, insomnia, metal taste in the mouth, excess lethargy or hyperactivity, chest pain, headache and, in extreme cases, seizures, comas, and death. There are also associated gastrointestinal problems, such as constipation, diarrhea, vomiting, poor appetite, weight loss, which are common in acute poisoning. (R007, R056)","Lead poisoning is usually treated with chelation therapy using DMSA, EDTA, or dimercaprol. (R056)",P07108;P62158;P13716;P22830;Q8TCU5;O60391;Q12879;Q13224;Q14957;O15399;Q05586;P17252;P05771;Q05655;Q02156;P24723;P05129;P41743;Q04759;Q05513;P54710;P05023;P50993;P13637;Q13733;P05026;P14415;P54709;P62328
321,T3D0320,2009-03-06 18:58:31 UTC,2009-08-25 18:01:34 UTC,Lead arsenite,Inorganic Compound;Arsenic Compound;Lead Compound,Lead arseniteLead(II) arsenite,"Lead arsenite is a chemical compound of lead and arsenic. Lead is a heavy metal and stable element with the symbol Pb and the atomic number 82, existing in metallic, organic, and inorganic forms. It is mainly found in nature as the mineral galena (PbS), cerussite (PbCO3) or anglesite (PbSO4), usually in ore with zinc, silver, or copper. Arsenic is a chemical element that has the symbol As and atomic number 33. It is a poisonous metalloid that has many allotropic forms: yellow (molecular non-metallic) and several black and grey forms (metalloids) are a few that are seen. Three metalloidal forms of arsenic with different crystal structures are found free in nature (the minerals arsenopyrite and the much rarer arsenolamprite and pararsenolamprite), but it is more commonly found as a compound with other elements. (R056, R004)",,10031-13-7,197119,,"","","","",,,Lead arsenite,,,,,"InChI=1/2AsHO2.Pb/c2*2-1-3;/h2*(H,2,3);/q;;+2/p-2","",http://www.biospider.ca/saved_files/mol/,[O-][As]=O.[O-][As]=O.[Pb+2],O=[As]O[Pb]O[As]=O,As2O4Pb,421.799490,White powder.,"",,,"",,,,"Oral 
Inhalation 
Dermal 
(R266)","Delta-aminolevulinic acid dehydratase (P13716) 
Serum albumin (P02768) Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Arsenite methyltransferase (Q9HBK9) 
(R164, R266)","Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carginogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. Lead mimics other biologically important metals, such as zinc, calcium, and iron, competing as cofactors for many of their respective enzymatic reactions. For example, lead has been shown to competitively inhibit calcium's binding of calmodulin, interferring with neurotransmitter release. It exhibits similar competitive inhibition at the NMDA receptor and protein kinase C, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Lead also affects the nervous system by impairing regulation of dopamine synthesis and blocking evoked release of acetylcholine. However, it's main mechanism of action occurs by inhibiting delta-aminolevulinic acid dehydratase, an enzyme vital in the biosynthesis of heme, which is a necesssary cofactor of hemoglobin. (R001, R008, R054, R061, R063, R266)","Lead and arsenic are absorbed following inhalation, oral, and dermal exposure. Arsenic is then distributed throughout the body, where it is reduced into arsenite if necessary, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant.  Lead is distributed mainly to the bones and red blood cells. In the blood lead may be found bound to serum albumin or the metal-binding protein metallothionein. Organic lead is metabolized by cytochrome P-450 enzymes, whereas inorganic lead forms complexes with delta-aminolevulinic acid dehydratase. Lead is excreted mainly in the urine and faeces. (R266, R055)",No data.,10 to 30 grams for and adult human (lead salts). (R273),"1, carcinogenic to humans. (R264)",Used as an insecticide (S266).,"Acute Oral: 0.005 mg/kg/day (Arsenic) (R260) 
Chronic Oral: 0.0003 mg/kg/day (Arsenic) (R260) 
Chronic Inhalation: 0.01 mg/m3 (Arsenic) (R260)
Chronic Inhalation: 0.05 mg/m3 (Lead) (R260)","Arsenic poisoning can lead to death from multi-system organ failure, probably from necrotic cell death, not apoptosis. Arsenic is also a known carcinogen, esepcially in skin, liver, bladder and lung cancers. Lead is a neurotoxin and has been known to cause brain damage and reduced cognitive capacity, especially in children. Lead exposure can result in nephropathy, as well as blood disorders such as high blood pressure and anemia. Lead also exhibits reproductive toxicity and can results in miscarriages and reduced sperm production. (R001, R055, R056)","Exposure to lower levels of arsenic can cause nausea and vomiting, decreased production of red and white blood cells, abnormal heart rhythm, damage to blood vessels, and a sensation of burn (R001).","Both arsenic and poisoning can be treated by chelation therapy, using chelating agents such as dimercaprol, EDTA or DMSA. Charcoal tablets may also be used for less severe cases. In addition, maintaining a diet high in sulfur helps eliminate arsenic from the body. (R055, R056)",P07108;P62158;P13716;P22830;Q12879;Q13224;Q14957;P17252;P05771;Q05655;Q02156;P24723;P05129;P41743;Q04759;Q05513;P54710;P05023;P50993;P13637;P05026;P14415;P54709;P62328;P68032;P68133;P62736;P60709;P63261;P63267;P10515;P23025;P03372;P04150;P00390;P00738;P69905;P68871;Q14145;P09874;A6NKZ8 ;Q99867;Q9H853;P08559;P29803;P11177;O00330;Q16881;Q9NNW7;Q86VQ6;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2;Q8TCU5;O60391;O15399;Q05586;Q13733
322,T3D0321,2009-03-06 18:58:31 UTC,2009-08-04 21:28:17 UTC,Lead azide,Inorganic Compound;Lead Compound,Lead azideLead azide (DRY) [forbidden]Lead azide (P6N6)Lead azide (Pb(N3)2)Lead diazideLead(2+) azide,"Lead azide is an explosive chemical compound of lead used mainly in detonators. Lead is a heavy metal and stable element with the symbol Pb and the atomic number 82, existing in metallic, organic, and inorganic forms. It is mainly found in nature as the mineral galena (PbS), cerussite (PbCO3) or anglesite (PbSO4), usually in ore with zinc, silver, or copper. (R056, R693)",,13424-46-9,61600,,"","","","",,C037372,Lead azide,,,,,InChI=1/2N3.Pb/c2*1-3-2;/q2*-1;+2,diazidolead,http://www.biospider.ca/saved_files/mol/,[N-]=[N+]=N[Pb]N=[N+]=[N-],[N-]=[N+]=N[Pb]N=[N+]=[N-],N6Pb,291.995080,White powder.,"",,,"",,,,"Oral 
Inhalation 
Dermal 
(R266)","Delta-aminolevulinic acid dehydratase (P13716) 
Serum albumin (P02768) 
Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
(R266)","Lead mimics other biologically important metals, such as zinc, calcium, and iron, competing as cofactors for many of their respective enzymatic reactions. For example, lead has been shown to competitively inhibit calcium's binding of calmodulin, interferring with neurotransmitter release. It exhibits similar competitive inhibition at the NMDA receptor and protein kinase C, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Lead also affects the nervous system by impairing regulation of dopamine synthesis and blocking evoked release of acetylcholine. However, it's main mechanism of action occurs by inhibiting delta-aminolevulinic acid dehydratase, an enzyme vital in the biosynthesis of heme, which is a necesssary cofactor of hemoglobin. (R008, R061, R063, R266)","Lead is absorbed following inhalation, oral, and dermal exposure. It is then distributed mainly to the bones and red blood cells. In the blood lead may be found bound to serum albumin or the metal-binding protein metallothionein. Organic lead is metabolized by cytochrome P-450 enzymes, whereas inorganic lead forms complexes with delta-aminolevulinic acid dehydratase. Lead is excreted mainly in the urine and faeces. (R266)",No data.,10 to 30 grams for and adult human (lead salts). (R273),"2B, possibly carcinogenic to humans. (R264)",Lead azide is used in detonators. (R693),Chronic Inhalation: 0.05 mg/m3 (R260),"Lead is a neurotoxin and has been known to cause brain damage and reduced cognitive capacity, especially in children. Lead exposure can result in nephropathy, as well as blood disorders such as high blood pressure and anemia. Lead also exhibits reproductive toxicity and can results in miscarriages and reduced sperm production. (R056)","Symptions of chronic lead poisoning include reduced cognitive abilities, nausea, abdominal pain, irritability, insomnia, metal taste in the mouth, excess lethargy or hyperactivity, chest pain, headache and, in extreme cases, seizures, comas, and death. There are also associated gastrointestinal problems, such as constipation, diarrhea, vomiting, poor appetite, weight loss, which are common in acute poisoning. (R007, R056)","Lead poisoning is usually treated with chelation therapy using DMSA, EDTA, or dimercaprol. (R056)",P07108;P62158;P13716;P22830;Q12879;Q13224;Q14957;P17252;P05771;Q05655;Q02156;P24723;P05129;P41743;Q04759;Q05513;P54710;P05023;P50993;P13637;P05026;P14415;P54709;P62328;Q8TCU5;O60391;O15399;Q05586;Q13733
323,T3D0322,2009-03-06 18:58:31 UTC,2009-08-04 21:28:18 UTC,Lead bromide,Inorganic Compound;Lead Compound;Bromide Compound,"Lead (II) bromide, anhydrousLead bromideLead bromide (PbBr2)Lead(2+) bromideLead(II) bromidePbBr2","Lead bromide is a bromide of lead. Lead is a heavy metal and stable element with the symbol Pb and the atomic number 82, existing in metallic, organic, and inorganic forms. It is mainly found in nature as the mineral galena (PbS), cerussite (PbCO3) or anglesite (PbSO4), usually in ore with zinc, silver, or copper. Bromine is a halogen element with the symbol Br and atomic number 35. Diatomic bromine does not occur naturally, but bromine salts can be found in crustal rock. (R987, R056)",,10031-22-8,24831,,"","","","",,C032721,Lead bromide,,,,http://en.wikipedia.org/wiki/Lead dibromide,InChI=1/2BrH.Pb/h2*1H;/q;;+2/p-2,dibromolead,http://www.biospider.ca/saved_files/mol/,Br[Pb]Br,Br[Pb]Br,Br2Pb,365.813310,White crystals.,367 °C,,,"",,,,"Oral 
Inhalation 
Dermal 
(R266)","Delta-aminolevulinic acid dehydratase (P13716) 
Serum albumin (P02768) 
Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
(R266)","Lead mimics other biologically important metals, such as zinc, calcium, and iron, competing as cofactors for many of their respective enzymatic reactions. For example, lead has been shown to competitively inhibit calcium's binding of calmodulin, interferring with neurotransmitter release. It exhibits similar competitive inhibition at the NMDA receptor and protein kinase C, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Lead also affects the nervous system by impairing regulation of dopamine synthesis and blocking evoked release of acetylcholine. However, it's main mechanism of action occurs by inhibiting delta-aminolevulinic acid dehydratase, an enzyme vital in the biosynthesis of heme, which is a necesssary cofactor of hemoglobin. Bromine is a powerful oxidizing agent and is able to release oxygen free radicals from the water in mucous membranes. These free radicals are also potent oxidizers and produce tissue damage. In additon, the formation of hydrobromic and bromic acids will result in secondary irritation. The bromide ion is also known to affect the central nervous system, causing bromism. This is believed to be a result of bromide ions substituting for chloride ions in the in actions of neurotransmitters and transport systems, thus affecting numerous synaptic processes. (R989, R990, R991, R008, R061, R063, R266)","Lead is absorbed following inhalation, oral, and dermal exposure. It is then distributed mainly to the bones and red blood cells. In the blood lead may be found bound to serum albumin or the metal-binding protein metallothionein. Organic lead is metabolized by cytochrome P-450 enzymes, whereas inorganic lead forms complexes with delta-aminolevulinic acid dehydratase. Lead is excreted mainly in the urine and faeces. Bromine is mainly absorbed via inhalation, but may also enter the body through dermal contact. Bromine salts can be ingested. Due to its reactivity, bromine quickly forms bromide and may be deposited in the tissues, displacing other halogens. (R989, R266)",Not availalble.,10 to 30 grams for and adult human (lead salts). (R273),"2B, possibly carcinogenic to humans. (R264)",No data.,Chronic Inhalation: 0.05 mg/m3 (Lead) (R260),"Lead is a neurotoxin and has been known to cause brain damage and reduced cognitive capacity, especially in children. Lead exposure can result in nephropathy, as well as blood disorders such as high blood pressure and anemia. Lead also exhibits reproductive toxicity and can results in miscarriages and reduced sperm production. Bromine vapour causes irritation and direct damage to the mucous membranes. Elemental bromine also burns the skin. The bromide ion is a central nervous system depressant and chronic exposure produces neuronal effects. This is called bromism and can result in central reactions reaching from somnolence to coma, cachexia, exicosis, loss of reflexes or pathologic reflexes, clonic seizures, tremor, ataxia, loss of neural sensitivity, paresis, papillar edema of the eyes, abnormal speech, cerebral edema, delirium, aggressiveness, and psychoses. (R987, R989, R990, R056)","Symptions of chronic lead poisoning include reduced cognitive abilities, nausea, abdominal pain, irritability, insomnia, metal taste in the mouth, excess lethargy or hyperactivity, chest pain, headache and, in extreme cases, seizures, comas, and death. There are also associated gastrointestinal problems, such as constipation, diarrhea, vomiting, poor appetite, weight loss, which are common in acute poisoning. Bromine vapour causes irritation and direct damage to the mucous membranes. Symptoms include lacrimation, rhinorrhoea, eye irritation with mucous secretions from the oropharyngeal and upper airways, coughing, dyspnoea, choking, wheezing, epistaxis, and headache. The bromide ion is a central nervous system depressant producing ataxia, slurred speech, tremor, nausea, vomiting, lethargy, dizziness, visual disturbances, unsteadiness, headaches, impaired memory and concentration, disorientation and hallucinations. This is called bromism. (R989, R990, R007, R056)","Lead poisoning is usually treated with chelation therapy using DMSA, EDTA, or dimercaprol. Bromine should be washed with water from any areas of dermal or ocular contact. If inhaled, treatment is mainly symptomatic and may include maintaining an adequate airway, administering oxygen, antibronchospasm therapy, and/or antibiotics. (R989, R056)",P07108;P62158;P13716;P22830;Q12879;Q13224;Q14957;P17252;P05771;Q05655;Q02156;P24723;P05129;P41743;Q04759;Q05513;P54710;P05023;P50993;P13637;P05026;P14415;P54709;P62328;Q8TCU5;O60391;O15399;Q05586;Q13733
324,T3D0323,2009-03-06 18:58:31 UTC,2009-08-19 19:10:15 UTC,Lead carbonate,Inorganic Compound;Lead Compound,"Carbonic acid, lead saltCarbonic acid, lead(2+) saltCarbonic acid, lead(2+) salt (1:1)CerusseteCerussiteDibasic lead carbonateLead carbonateLead carbonate (PbCO3)Lead(2+) carbonatePlumbous carbonate","Lead carbonate is a chemical compound prepared industrially from lead(II) acetate and carbon dioxide. It also occurs naturally as the mineral cerussite. Lead is a heavy metal and stable element with the symbol Pb and the atomic number 82, existing in metallic, organic, and inorganic forms. It is mainly found in nature as the mineral galena (PbS), cerussite (PbCO3) or anglesite (PbSO4), usually in ore with zinc, silver, or copper. (R056, R694)",,598-63-0,11727,,"","","","",,C043262,Lead carbonate,,,,,"InChI=1/CH2O3.Pb/c2-1(3)4;/h(H2,2,3,4);/q;+2/p-2",lead(2+) carbonate,http://www.biospider.ca/saved_files/mol/,C(=O)([O-])[O-].[Pb+2],[Pb++].[O-]C([O-])=O,CO3Pb,267.961380,Colorless crystals.,"",,,"0.0011 mg/mL at 20 oC [ULLMANN'S ENCYCL; Online, J1583]",,,,"Oral 
Inhalation 
Dermal 
(R266)","Delta-aminolevulinic acid dehydratase (P13716) 
Serum albumin (P02768) 
Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
(R266)","Lead mimics other biologically important metals, such as zinc, calcium, and iron, competing as cofactors for many of their respective enzymatic reactions. For example, lead has been shown to competitively inhibit calcium's binding of calmodulin, interferring with neurotransmitter release. It exhibits similar competitive inhibition at the NMDA receptor and protein kinase C, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Lead also affects the nervous system by impairing regulation of dopamine synthesis and blocking evoked release of acetylcholine. However, it's main mechanism of action occurs by inhibiting delta-aminolevulinic acid dehydratase, an enzyme vital in the biosynthesis of heme, which is a necesssary cofactor of hemoglobin. (R008, R061, R063, R266)","Lead is absorbed following inhalation, oral, and dermal exposure. It is then distributed mainly to the bones and red blood cells. In the blood lead may be found bound to serum albumin or the metal-binding protein metallothionein. Organic lead is metabolized by cytochrome P-450 enzymes, whereas inorganic lead forms complexes with delta-aminolevulinic acid dehydratase. Lead is excreted mainly in the urine and faeces. (R266)",No data.,10 to 30 grams for and adult human (lead salts). (R273),"2B, possibly carcinogenic to humans. (R264)","Catalyst for the polymerization of formaldehyde to high molecular weight crystalline poly(oxymethylene) products; in PVC friction liners for pulleys or drive cables of hoisting engines; to improve bonding of polychloroprene to metals in wire-reinforced hoses, 10-25 parts of lead caronate are used in the elastomer; component of high pressure lubricating greases; component of high pressure lubricating greases; catalysts in the curing of moldable thermosetting silicone resins; in coating on vinyl chloride polymers to improve dielectric properties; component of corrosion-resistant, dispersion-strengthened grids in lead-acid storage batteries; as a photoconductor for electrophotography, in coatings on heat-sensitive sheets for thermographic copying; component of a lubricant-stabilizer for PVC; component in the manuacture of thermistors; component in slip-preventing waxes for steel cables to provide higher wear resistence (S267).",Chronic Inhalation: 0.05 mg/m3 (R260),"Lead is a neurotoxin and has been known to cause brain damage and reduced cognitive capacity, especially in children. Lead exposure can result in nephropathy, as well as blood disorders such as high blood pressure and anemia. Lead also exhibits reproductive toxicity and can results in miscarriages and reduced sperm production. (R056)","Symptions of chronic lead poisoning include reduced cognitive abilities, nausea, abdominal pain, irritability, insomnia, metal taste in the mouth, excess lethargy or hyperactivity, chest pain, headache and, in extreme cases, seizures, comas, and death. There are also associated gastrointestinal problems, such as constipation, diarrhea, vomiting, poor appetite, weight loss, which are common in acute poisoning. (R007, R056)","Lead poisoning is usually treated with chelation therapy using DMSA, EDTA, or dimercaprol. (R056)",P07108;P62158;P13716;P22830;Q12879;Q13224;Q14957;P17252;P05771;Q05655;Q02156;P24723;P05129;P41743;Q04759;Q05513;P54710;P05023;P50993;P13637;P05026;P14415;P54709;P62328;Q8TCU5;O60391;O15399;Q05586;Q13733
325,T3D0324,2009-03-06 18:58:31 UTC,2009-08-04 21:28:18 UTC,Lead chloride,Inorganic Compound;Lead Compound,"Lead (II) chlorideLead chlorideLead chloride (PbCl2)Lead(2+) chlorideLead(II) chlorideLecloPbCl2Plumbous chloridedichloro-l2-plumbanelead chloride, (35)lead, 1-(37)chlorine-labeledlead chloride, (35)lead-labeledlead chloride, (37)lead-labeled","Lead chloride is a chloride of lead that occurs naturally as the mineral cotunnite. It is used in the synthesis of other lead compounds. Lead is a heavy metal and stable element with the symbol Pb and the atomic number 82, existing in metallic, organic, and inorganic forms. It is mainly found in nature as the mineral galena (PbS), cerussite (PbCO3) or anglesite (PbSO4), usually in ore with zinc, silver, or copper. (R056, R695)",,7758-95-4,24459,,"","","","",,C029891,Lead chloride,12174,,,,InChI=1/2ClH.Pb/h2*1H;/q;;+2/p-2,dichlorolead,http://www.biospider.ca/saved_files/mol/,Cl[Pb]Cl,Cl[Pb]Cl,Cl2Pb,277.914340,White solid.,501 oC,,,"",,,,"Oral 
Inhalation 
Dermal 
(R266)","Delta-aminolevulinic acid dehydratase (P13716) 
Serum albumin (P02768) 
Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
(R266)","Lead mimics other biologically important metals, such as zinc, calcium, and iron, competing as cofactors for many of their respective enzymatic reactions. For example, lead has been shown to competitively inhibit calcium's binding of calmodulin, interferring with neurotransmitter release. It exhibits similar competitive inhibition at the NMDA receptor and protein kinase C, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Lead also affects the nervous system by impairing regulation of dopamine synthesis and blocking evoked release of acetylcholine. However, it's main mechanism of action occurs by inhibiting delta-aminolevulinic acid dehydratase, an enzyme vital in the biosynthesis of heme, which is a necesssary cofactor of hemoglobin. (R008, R061, R063, R266)","Lead is absorbed following inhalation, oral, and dermal exposure. It is then distributed mainly to the bones and red blood cells. In the blood lead may be found bound to serum albumin or the metal-binding protein metallothionein. Organic lead is metabolized by cytochrome P-450 enzymes, whereas inorganic lead forms complexes with delta-aminolevulinic acid dehydratase. Lead is excreted mainly in the urine and faeces. (R266)","LD50: 27 mg/kg (oral, rat) (S268).",10 to 30 grams for and adult human (lead salts). (R273),"2B, possibly carcinogenic to humans. (R264)",Lead chloride is used in the synthesis of other lead compounds. It is also used in the production of certain types of glass and in white pigments. (R695),Chronic Inhalation: 0.05 mg/m3 (R260),"Lead is a neurotoxin and has been known to cause brain damage and reduced cognitive capacity, especially in children. Lead exposure can result in nephropathy, as well as blood disorders such as high blood pressure and anemia. Lead also exhibits reproductive toxicity and can results in miscarriages and reduced sperm production. (R056)","Symptions of chronic lead poisoning include reduced cognitive abilities, nausea, abdominal pain, irritability, insomnia, metal taste in the mouth, excess lethargy or hyperactivity, chest pain, headache and, in extreme cases, seizures, comas, and death. There are also associated gastrointestinal problems, such as constipation, diarrhea, vomiting, poor appetite, weight loss, which are common in acute poisoning. (R007, R056)","Lead poisoning is usually treated with chelation therapy using DMSA, EDTA, or dimercaprol. (R056)",P07108;P62158;P13716;P22830;Q12879;Q13224;Q14957;P17252;P05771;Q05655;Q02156;P24723;P05129;P41743;Q04759;Q05513;P54710;P05023;P50993;P13637;P05026;P14415;P54709;P62328;Q8TCU5;O60391;O15399;Q05586;Q13733
326,T3D0325,2009-03-06 18:58:32 UTC,2009-08-19 19:11:53 UTC,Lead chromate,Inorganic Compound;Lead Compound;Chromium Compound,"Basic lead chromateChromate de plomb [french]Chrome orangeChrome yellowChromic acid (H2CrO4), lead(2+) salt (1:1)Chromic acid, lead saltChromic acid, lead salt, basicChromic acid, lead(2+) salt (1:1)Chromium lead oxideLead chromateLead chromate (PbCrO4)Lead chromate [chromium and chromium compounds]Lead chromate oxideLead chromate yellowLead chromate(vi)PhoenicochroitePlumbous chromatelead chromate, Pb(2+) (1:1)","Lead chromate is a chemical compound of lead and chromium commonly found in paints under the name ""chrome yellow"". It is made by reacting a lead(II) salt with a chromate or dichromate salt in solution. Lead is a heavy metal and stable element with the symbol Pb and the atomic number 82, existing in metallic, organic, and inorganic forms. It is mainly found in nature as the mineral galena (PbS), cerussite (PbCO3) or anglesite (PbSO4), usually in ore with zinc, silver, or copper. Hexavalent chromium refers to chemical compounds that contain the element chromium in the +6 oxidation state. Chromium(VI) is more toxic than other oxidation states of the chromium atom because of its greater ability to enter cells and higher redox potential. (R042, R056, R120)",,7758-97-6,24460,,"","","","",,,Lead chromate,12175,,,,InChI=1/Cr.4O.Pb/q;;;2*-1;+2,dioxido(dioxo)chromium; lead(2+),http://www.biospider.ca/saved_files/mol/,[O-][Cr](=O)(=O)[O-].[Pb+2],[Pb++].[O-][Cr]([O-])(=O)=O,CrO4Pb,323.896810,Orange/yellow solid.,"","","","","","","","Oral 
Inhalation 
Dermal 
(R266)","Delta-aminolevulinic acid dehydratase (P13716) 
Serum albumin (P02768) 
Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Sulfate transporter (P50443) 
Sulfate anion transporter 1 (Q9H2B4)
(R041, R266)","Lead mimics other biologically important metals, such as zinc, calcium, and iron, competing as cofactors for many of their respective enzymatic reactions. For example, lead has been shown to competitively inhibit calcium's binding of calmodulin, interferring with neurotransmitter release. It exhibits similar competitive inhibition at the NMDA receptor and protein kinase C, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Lead also affects the nervous system by impairing regulation of dopamine synthesis and blocking evoked release of acetylcholine. However, its main mechanism of action occurs by inhibiting delta-aminolevulinic acid dehydratase, an enzyme vital in the biosynthesis of heme, which is a necesssary cofactor of hemoglobin. Hexavalent chromium's carcinogenic effects are caused by its metabolites, pentavalent and trivalent chromium. The DNA damage may be caused by hydroxyl radicals produced during reoxidation of pentavalent chromium by hydrogen peroxide molecules present in the cell. Trivalent chromium may also form complexes with peptides, proteins, and DNA, resulting in DNA-protein crosslinks, DNA strand breaks, DNA-DNA interstrand crosslinks, chromium-DNA adducts, chromosomal aberrations and alterations in cellular signaling pathways. It has been shown to induce carcinogenesis by overstimulating cellular regulatory pathways and increasing peroxide levels by activating certain mitogen-activated protein kinases. It can also cause transcriptional repression by cross-linking histone deacetylase 1-DNA methyltransferase 1 complexes to CYP1A1 promoter chromatin, inhibiting histone modification. Chromium may increase its own toxicity by modifying metal regulatory transcription factor 1, causing the inhibition of zinc-induced metallothionein transcription. (R041, R042, R075, R076, R077, R008, R061, R063, R266)","Lead and chromium are absorbed following inhalation, oral, and dermal exposure. It is then distributed mainly to the bones and red blood cells. In the blood lead may be found bound to serum albumin or the metal-binding protein metallothionein. Organic lead is metabolized by cytochrome P-450 enzymes, whereas inorganic lead forms complexes with delta-aminolevulinic acid dehydratase. Lead is excreted mainly in the urine and faeces. Chromium distributes to nearly all tissues, with the highest concentrations found in kidney and liver. Bone is also a major storage site and may contribute to long-term retention. Hexavalent chromium's similarity to sulfate and chromate allow it to be transported into cells via sulfate transport mechanisms. Inside the cell, hexavalent chromium is reduced first to pentavalent chromium, then to trivalent chromium by many substances including ascorbate, glutathione, and nicotinamide adenine dinucleotide. Chromium is almost entirely excreted with the urine. (R041, R042, R266)","LD50: >12 g/kg (Oral, Mouse) (R263)
LD50: 400 mg/kg (Intraperitoneal, Guinea pig) (R838)",1 to 3 grams for an adult human (hexavalent chromium). (R331),"1, carcinogenic to humans. (R264)","Lead chromate is used in pigments, as well as in some pyrotechnic compositions. (R120)","Chronic Inhalation: 0.05 mg/m3 (Lead) (R260)
Intermediate Oral: 0.005 mg/kg/day (Hexavalent chromium) (R260) 
Chronic Oral: 0.001 mg/kg/day (Hexavalent chromium) (R260)","Lead is a neurotoxin and has been known to cause brain damage and reduced cognitive capacity, especially in children. Lead exposure can result in nephropathy, as well as blood disorders such as high blood pressure and anemia. Lead also exhibits reproductive toxicity and can results in miscarriages and reduced sperm production. Hexavalent chromium is a known carcinogen. Chronic inhalation especially has been linked to lung cancer. Hexavalent chromium has also been know to cause reproductive and developmental defects. (R041, R056)","Symptions of chronic lead poisoning include reduced cognitive abilities, nausea, abdominal pain, irritability, insomnia, metal taste in the mouth, excess lethargy or hyperactivity, chest pain, headache and, in extreme cases, seizures, comas, and death. There are also associated gastrointestinal problems, such as constipation, diarrhea, vomiting, poor appetite, weight loss, which are common in acute poisoning. Breathing hexavalent chromium can cause irritation to the lining of the nose, nose ulcers, runny nose, and breathing problems, such as asthma, cough, shortness of breath, or wheezing. Ingestion of hexavalent chromium causes irritation and ulcers in the stomach and small intestine, as well as anemia. Skin contact can cause skin ulcers. (R042, R007, R056)","Lead poisoning is usually treated with chelation therapy using DMSA, EDTA, or dimercaprol. There is no know antidote for chromium poisoning. Exposure is usually handled with symptomatic treatment. (R042, R056)",P07108;P62158;P13716;P22830;Q12879;Q13224;Q14957;P17252;P05771;Q05655;Q02156;P24723;P05129;P41743;Q04759;Q05513;P54710;P05023;P50993;P13637;P05026;P14415;P54709;P62328;DNA;Q13547;Q14872;P28482;P27361;Q8TCU5;O60391;O15399;Q05586;Q13733
327,T3D0326,2009-03-06 18:58:32 UTC,2009-08-25 18:01:39 UTC,Lead fluoroborate,Inorganic Compound;Lead Compound;Fluoride Compound,"","Lead fluoroborate is a chemical compound of lead. Lead is a heavy metal and stable element with the symbol Pb and the atomic number 82, existing in metallic, organic, and inorganic forms. It is mainly found in nature as the mineral galena (PbS), cerussite (PbCO3) or anglesite (PbSO4), usually in ore with zinc, silver, or copper. (R056)",,13814-96-5,21225560,,"","","","",,,Lead fluoroborate,,,,,"InChI=1/2BF4.Pb/c2*2-1(3,4)5;/q2*-1;+2",lead ditetrafluoroborate,http://www.biospider.ca/saved_files/mol/,"",F[B](F)(F)(F)[Pb][B](F)(F)(F)F,B2F8Pb-2,"",Colorless crystals.,"",,,"",,,,"Oral 
Inhalation 
Dermal 
(R266)","Delta-aminolevulinic acid dehydratase (P13716) 
Serum albumin (P02768) 
Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
(R266)","Lead mimics other biologically important metals, such as zinc, calcium, and iron, competing as cofactors for many of their respective enzymatic reactions. For example, lead has been shown to competitively inhibit calcium's binding of calmodulin, interferring with neurotransmitter release. It exhibits similar competitive inhibition at the NMDA receptor and protein kinase C, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Lead also affects the nervous system by impairing regulation of dopamine synthesis and blocking evoked release of acetylcholine. However, it's main mechanism of action occurs by inhibiting delta-aminolevulinic acid dehydratase, an enzyme vital in the biosynthesis of heme, which is a necesssary cofactor of hemoglobin. (R008, R061, R063, R266)","Lead is absorbed following inhalation, oral, and dermal exposure. It is then distributed mainly to the bones and red blood cells. In the blood lead may be found bound to serum albumin or the metal-binding protein metallothionein. Organic lead is metabolized by cytochrome P-450 enzymes, whereas inorganic lead forms complexes with delta-aminolevulinic acid dehydratase. Lead is excreted mainly in the urine and faeces. (R266)",,10 to 30 grams for and adult human (lead salts). (R273),"2B, possibly carcinogenic to humans. (R264)",Lead fluoroborate is used for electroplating where speed and quality are important. Sound insulators are made as lead-plastic laminates by plating lead from a fluoroborate bath (S267).,Chronic Inhalation: 0.05 mg/m3 (R260),"Lead is a neurotoxin and has been known to cause brain damage and reduced cognitive capacity, especially in children. Lead exposure can result in nephropathy, as well as blood disorders such as high blood pressure and anemia. Lead also exhibits reproductive toxicity and can results in miscarriages and reduced sperm production. (R056)","Symptions of chronic lead poisoning include reduced cognitive abilities, nausea, abdominal pain, irritability, insomnia, metal taste in the mouth, excess lethargy or hyperactivity, chest pain, headache and, in extreme cases, seizures, comas, and death. There are also associated gastrointestinal problems, such as constipation, diarrhea, vomiting, poor appetite, weight loss, which are common in acute poisoning. (R007, R056)","Lead poisoning is usually treated with chelation therapy using DMSA, EDTA, or dimercaprol. (R056)",P07108;P62158;P13716;P22830;Q12879;Q13224;Q14957;P17252;P05771;Q05655;Q02156;P24723;P05129;P41743;Q04759;Q05513;P54710;P05023;P50993;P13637;P05026;P14415;P54709;P62328;Q8TCU5;O60391;O15399;Q05586;Q13733
328,T3D0327,2009-03-06 18:58:32 UTC,2009-08-04 21:28:18 UTC,Lead iodide,Inorganic Compound;Lead Compound,Blei(II)-iodidLead iodideLead iodide (PbI2)Lead(II) iodidePbI2Plumbous iodidePlumbum jodatum,"Lead iodide is a iodide of lead that varies in color from yellow to red, depending of the temperature. It is formed by mixing by mixing lead(II) nitrate and potassium iodide. It is used as a detector material for high energy photons including x-rays and gamma rays. Lead is a heavy metal and stable element with the symbol Pb and the atomic number 82, existing in metallic, organic, and inorganic forms. It is mainly found in nature as the mineral galena (PbS), cerussite (PbCO3) or anglesite (PbSO4), usually in ore with zinc, silver, or copper. (R054, R696)",,10101-63-0,24931,,"","","","",,,Lead iodide,,,,http://en.wikipedia.org/wiki/Lead diiodide,InChI=1/2HI.Pb/h2*1H;/q;;+2/p-2,diiodolead,http://www.biospider.ca/saved_files/mol/,I[Pb]I,I[Pb]I,I2Pb,461.785570,Bright yellow crystals.,403 °C,,,"",,,,"Oral 
Inhalation 
Dermal 
(R266)","Delta-aminolevulinic acid dehydratase (P13716) 
Serum albumin (P02768) 
Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
(R266)","Lead mimics other biologically important metals, such as zinc, calcium, and iron, competing as cofactors for many of their respective enzymatic reactions. For example, lead has been shown to competitively inhibit calcium's binding of calmodulin, interferring with neurotransmitter release. It exhibits similar competitive inhibition at the NMDA receptor and protein kinase C, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Lead also affects the nervous system by impairing regulation of dopamine synthesis and blocking evoked release of acetylcholine. However, it's main mechanism of action occurs by inhibiting delta-aminolevulinic acid dehydratase, an enzyme vital in the biosynthesis of heme, which is a necesssary cofactor of hemoglobin. (R008, R061, R063, R266)","Lead is absorbed following inhalation, oral, and dermal exposure. It is then distributed mainly to the bones and red blood cells. In the blood lead may be found bound to serum albumin or the metal-binding protein metallothionein. Organic lead is metabolized by cytochrome P-450 enzymes, whereas inorganic lead forms complexes with delta-aminolevulinic acid dehydratase. Lead is excreted mainly in the urine and faeces. (R266)",No data.,10 to 30 grams for and adult human (lead salts). (R273),"2B, possibly carcinogenic to humans. (R264)",Lead iodide is used in the detection of x-rays and gamma rays. (R696),Chronic Inhalation: 0.05 mg/m3 (R260),"Lead is a neurotoxin and has been known to cause brain damage and reduced cognitive capacity, especially in children. Lead exposure can result in nephropathy, as well as blood disorders such as high blood pressure and anemia. Lead also exhibits reproductive toxicity and can results in miscarriages and reduced sperm production. (R056)","Symptions of chronic lead poisoning include reduced cognitive abilities, nausea, abdominal pain, irritability, insomnia, metal taste in the mouth, excess lethargy or hyperactivity, chest pain, headache and, in extreme cases, seizures, comas, and death. There are also associated gastrointestinal problems, such as constipation, diarrhea, vomiting, poor appetite, weight loss, which are common in acute poisoning. (R007, R056)","Lead poisoning is usually treated with chelation therapy using DMSA, EDTA, or dimercaprol. (R056)",P07108;P62158;P13716;P22830;Q12879;Q13224;Q14957;P17252;P05771;Q05655;Q02156;P24723;P05129;P41743;Q04759;Q05513;P54710;P05023;P50993;P13637;P05026;P14415;P54709;P62328;Q8TCU5;O60391;O15399;Q05586;Q13733
329,T3D0328,2009-03-06 18:58:32 UTC,2009-08-04 21:28:19 UTC,Lead molybdenum chromate,Inorganic Compound;Lead Compound;Chromium Compound,"Chromic acid lead salt with lead molybdateChromic acid, lead and molybdenum saltChromium lead molybdenum oxideLead chromate molybdateLead molybdate chromateLead molybdenum chromateLead-molybdenum chromateMolybdenum-lead chromate","Lead molybdenum chromate is a chemical compound of lead, molybedunum, and chromium. Lead is a heavy metal and stable element with the symbol Pb and the atomic number 82, existing in metallic, organic, and inorganic forms. It is mainly found in nature as the mineral galena (PbS), cerussite (PbCO3) or anglesite (PbSO4), usually in ore with zinc, silver, or copper. Hexavalent chromium refers to chemical compounds that contain the element chromium in the +6 oxidation state. Chromium(VI) is more toxic than other oxidation states of the chromium atom because of its greater ability to enter cells and higher redox potential. (R042, R056)",,12709-98-7,166736,,"","","","",,,Lead molybdenum chromate,,,,,InChI=1/2Cr.2Mo.11O.2Pb/q2*+3;;;11*-2;2*+2,chromium(3+); lead(2+); molybdenum; oxygen(2-),http://www.biospider.ca/saved_files/mol/,[O-2].[O-2].[O-2].[O-2].[O-2].[O-2].[O-2].[O-2].[O-2].[O-2].[O-2].[Cr+3].[Cr+3].[Mo].[Mo].[Pb+2].[Pb+2],[O-2].[O-2].[O-2].[O-2].[O-2].[O-2].[O-2].[O-2].[O-2].[O-2].[O-2].[Cr+3].[Cr+3].[Mo].[Mo].[Pb+2].[Pb+2],Cr2Mo2O11Pb2-12,"",No data.,"",,,"",,,,"Oral 
Inhalation 
Dermal 
(R266)","Delta-aminolevulinic acid dehydratase (P13716) 
Serum albumin (P02768) 
Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Sulfate transporter (P50443) 
Sulfate anion transporter 1 (Q9H2B4)
(R041, R266)","Lead mimics other biologically important metals, such as zinc, calcium, and iron, competing as cofactors for many of their respective enzymatic reactions. For example, lead has been shown to competitively inhibit calcium's binding of calmodulin, interferring with neurotransmitter release. It exhibits similar competitive inhibition at the NMDA receptor and protein kinase C, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Lead also affects the nervous system by impairing regulation of dopamine synthesis and blocking evoked release of acetylcholine. However, it's main mechanism of action occurs by inhibiting delta-aminolevulinic acid dehydratase, an enzyme vital in the biosynthesis of heme, which is a necesssary cofactor of hemoglobin. Hexavalent chromium's carcinogenic effects are caused by its metabolites, pentavalent and trivalent chromium. The DNA damage may be caused by hydroxyl radicals produced during reoxidation of pentavalent chromium by hydrogen peroxide molecules present in the cell. Trivalent chromium may also form complexes with peptides, proteins, and DNA, resulting in DNA-protein crosslinks, DNA strand breaks, DNA-DNA interstrand crosslinks, chromium-DNA adducts, chromosomal aberrations and alterations in cellular signaling pathways. It has been shown to induce carcinogenesis by overstimulating cellular regulatory pathways and increasing peroxide levels by activating certain mitogen-activated protein kinases. It can also cause transcriptional repression by cross-linking histone deacetylase 1-DNA methyltransferase 1 complexes to CYP1A1 promoter chromatin, inhibiting histone modification. Chromium may increase its own toxicity by modifying metal regulatory transcription factor 1, causing the inhibition of zinc-induced metallothionein transcription. (R041, R042, R075, R076, R077, R008, R061, R063, R266)","Lead and chromium are absorbed following inhalation, oral, and dermal exposure. It is then distributed mainly to the bones and red blood cells. In the blood lead may be found bound to serum albumin or the metal-binding protein metallothionein. Organic lead is metabolized by cytochrome P-450 enzymes, whereas inorganic lead forms complexes with delta-aminolevulinic acid dehydratase. Lead is excreted mainly in the urine and faeces. Chromium distributes to nearly all tissues, with the highest concentrations found in kidney and liver. Bone is also a major storage site and may contribute to long-term retention. Hexavalent chromium's similarity to sulfate and chromate allow it to be transported into cells via sulfate transport mechanisms. Inside the cell, hexavalent chromium is reduced first to pentavalent chromium, then to trivalent chromium by many substances including ascorbate, glutathione, and nicotinamide adenine dinucleotide. Chromium is almost entirely excreted with the urine. (R041, R042, R266)",No data.,1 to 3 grams for an adult human (hexavalent chromium). (R331),"1, carcinogenic to humans. (R264)",No data.,"Chronic Inhalation: 0.05 mg/m3 (Lead) (R260)
Intermediate Oral: 0.005 mg/kg/day (Hexavalent chromium) (R260) 
Chronic Oral: 0.001 mg/kg/day (Hexavalent chromium) (R260)","Lead is a neurotoxin and has been known to cause brain damage and reduced cognitive capacity, especially in children. Lead exposure can result in nephropathy, as well as blood disorders such as high blood pressure and anemia. Lead also exhibits reproductive toxicity and can results in miscarriages and reduced sperm production. Hexavalent chromium is a known carcinogen. Chronic inhalation especially has been linked to lung cancer. Hexavalent chromium has also been know to cause reproductive and developmental defects. (R041, R056)","Symptions of chronic lead poisoning include reduced cognitive abilities, nausea, abdominal pain, irritability, insomnia, metal taste in the mouth, excess lethargy or hyperactivity, chest pain, headache and, in extreme cases, seizures, comas, and death. There are also associated gastrointestinal problems, such as constipation, diarrhea, vomiting, poor appetite, weight loss, which are common in acute poisoning. Breathing hexavalent chromium can cause irritation to the lining of the nose, nose ulcers, runny nose, and breathing problems, such as asthma, cough, shortness of breath, or wheezing. Ingestion of hexavalent chromium causes irritation and ulcers in the stomach and small intestine, as well as anemia. Skin contact can cause skin ulcers. (R042, R007, R056)","Lead poisoning is usually treated with chelation therapy using DMSA, EDTA, or dimercaprol. There is no know antidote for chromium poisoning. Exposure is usually handled with symptomatic treatment. (R042, R056)",P07108;P62158;P13716;P22830;Q12879;Q13224;Q14957;P17252;P05771;Q05655;Q02156;P24723;P05129;P41743;Q04759;Q05513;P54710;P05023;P50993;P13637;P05026;P14415;P54709;P62328;DNA;Q13547;Q14872;P28482;P27361;Q8TCU5;O60391;O15399;Q05586;Q13733
330,T3D0329,2009-03-06 18:58:32 UTC,2009-08-25 18:01:43 UTC,Lead nitrate,Inorganic Compound;Lead Compound;Nitrate,"Lead dinitrateLead nitrateLead nitrate (Pb(NO3)2)Lead nitrate [UN1469] [Oxidizer]Lead(2+) nitrateLead(II) nitrate (1:2)Nitrate de plomb [french]Nitric acid, lead(2+) saltPlumbous nitratelead (2+) nitratelead nitrate, 210Pb(2+)-labeled","Lead nitrate is a nitrate of lead produced synthetically by dissolving metallic lead or lead(II) oxide in nitric acid. It is an oxidizing agent and is used to make other lead compounds. It is also used as a heat stabiliser in nylon and polyesters, as a coating for photothermographic paper, and in rodenticides. Lead is a heavy metal and stable element with the symbol Pb and the atomic number 82, existing in metallic, organic, and inorganic forms. It is mainly found in nature as the mineral galena (PbS), cerussite (PbCO3) or anglesite (PbSO4), usually in ore with zinc, silver, or copper. Nitrite is a toxic compound known to cause methemoglobinemia. (S575,  R056, R697)",,10099-74-8,24924,,C15234,"",37187,"",,,Lead nitrate,,,,http://en.wikipedia.org/wiki/lead(II) nitrate,InChI=1/2NO3.Pb/c2*2-1(3)4;/q2*-1;+2,lead(2+) dinitrate,http://www.biospider.ca/saved_files/mol/7549ef1da7646da4d088794c278adf38_1237971121.mol,[N+](=O)([O-])[O-].[N+](=O)([O-])[O-].[Pb+2],[O-][N+](=O)O[Pb]O[N+]([O-])=O,N2O6Pb,331.952270,Colorless or white solid.,290 °C decomp.,,,"",,,,"Oral 
Inhalation 
Dermal 
(R266)","Delta-aminolevulinic acid dehydratase (P13716) 
Serum albumin (P02768) 
Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
(R266)","Lead mimics other biologically important metals, such as zinc, calcium, and iron, competing as cofactors for many of their respective enzymatic reactions. For example, lead has been shown to competitively inhibit calcium's binding of calmodulin, interferring with neurotransmitter release. It exhibits similar competitive inhibition at the NMDA receptor and protein kinase C, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Lead also affects the nervous system by impairing regulation of dopamine synthesis and blocking evoked release of acetylcholine. However, it's main mechanism of action occurs by inhibiting delta-aminolevulinic acid dehydratase, an enzyme vital in the biosynthesis of heme, which is a necesssary cofactor of hemoglobin. Nitrate's toxicity is a result of it's conversion to nitrite once in the body. Nitrite causes the autocatalytic oxidation of oxyhemoglobin to hydrogen peroxide and methemoglobin. This elevation of methemoglobin levels is a condition known as methemoglobinemia, and is characterized by tissue hypoxia, as methemoglobin cannot bind oxygen. (V305, V306, R008, R061, R063, R266)","Lead is absorbed following inhalation, oral, and dermal exposure. It is then distributed mainly to the bones and red blood cells. In the blood lead may be found bound to serum albumin or the metal-binding protein metallothionein. Organic lead is metabolized by cytochrome P-450 enzymes, whereas inorganic lead forms complexes with delta-aminolevulinic acid dehydratase. Lead is excreted mainly in the urine and faeces. Intake of some amount of nitrates and nitrites is a normal part of the nitrogen cycle in humans. In vivo conversion of nitrates to nitrites can occur in the gastrointestional tract under the right conditions, significantly enhancing nitrates' toxic potency. The major metabolic pathway for nitrate is conversion to nitrite, and then to ammonia. Nitrites, nitrates, and their metabolites are excreted in the urine. (S575, R266)","LD50: 93 mg/kg (Intravenous, Rat) (R263)
LD50: 74 mg/kg (Intraperitoneal, Mouse) (R263)",10 to 30 grams for and adult human (lead salts). (R273),"2A, probably carcinogenic to humans. (R264)","Lead nitrate is used as a heat stabiliser in nylon and polyesters, as a coating for photothermographic paper, in rodenticides, and in gold cyanidation. (R697)",Chronic Inhalation: 0.05 mg/m3 (R260),"Lead is a neurotoxin and has been known to cause brain damage and reduced cognitive capacity, especially in children. Lead exposure can result in nephropathy, as well as blood disorders such as high blood pressure and anemia. Lead also exhibits reproductive toxicity and can results in miscarriages and reduced sperm production. Nitrate and nitrite poisoning causes methemoglobinemia. Nitrites may cause pregnancy complications and developmental effects. They may also be carcinogenic. (S575, R056)","Symptions of chronic lead poisoning include reduced cognitive abilities, nausea, abdominal pain, irritability, insomnia, metal taste in the mouth, excess lethargy or hyperactivity, chest pain, headache and, in extreme cases, seizures, comas, and death. There are also associated gastrointestinal problems, such as constipation, diarrhea, vomiting, poor appetite, weight loss, which are common in acute poisoning. Nitrate and nitrite poisoning causes methemoglobinemia. Symptoms include cyanosis, cardiac dysrhythmias and circulatory failure, and progressive central nervous system (CNS) effects. CNS effects can range from mild dizziness and lethargy to coma and convulsions. (S575, R007, R056)","Lead poisoning is usually treated with chelation therapy using DMSA, EDTA, or dimercaprol. Methemoglobinemia can be treated with supplemental oxygen and methylene blue 1% solution administered intravenously slowly over five minutes followed by IV flush with normal saline. Methylene blue restores the iron in hemoglobin to its normal (reduced) oxygen-carrying state. (V306, R056)",P07108;P62158;P13716;P22830;Q12879;Q13224;Q14957;P17252;P05771;Q05655;Q02156;P24723;P05129;P41743;Q04759;Q05513;P54710;P05023;P50993;P13637;P05026;P14415;P54709;P62328;Q8TCU5;O60391;O15399;Q05586;Q13733;P69905;P68871;P02042;P02100;P69891;P69892;Q6B0K9;P09105;P02008
331,T3D0330,2009-03-06 18:58:32 UTC,2009-08-04 21:28:19 UTC,Lead oxide,Inorganic Compound;Lead Compound,"BleimonoxidBleioxydC.I. Pigment Red 105C.I. Pigment Yellow 46CI Pigment Red 105CI Pigment Yellow 46Gold satinobreHeuconin 5Lead monooxideLead orthoplumbateLead oxideLead oxide (3:4)Lead oxide (Pb3O4)Lead oxide (pbo)Lead oxide (van)Lead oxide redLead oxide yellowLead oxide, (pbo)Lead oxide, pboLead protoxideLead tetraoxideLead tetroxideLead(2+) oxideLead(II) oxideLead(II)oxideLithargeLitharge Yellow L-28Litharge pureMassicotMassicotiteMennigeMineral orangeMineral redMiniumMinium Non-Setting RL 95Minium redOrange leadParis redPigment Red 105Plumbi monoxidumPlumboplumbic oxidePlumbous oxidePlumbum oxydatumRed Lead Oxide (Pb3O4)Red leadRed lead oxideSandixSaturn redTrilead tetraoxideTrilead tetroxideWLN: PB oYellow lead ocher","Lead oxide is an oxide of lead that occurs in both a red and yellow form. It occurs naturally as the minerals litharge (red form) and massicot (yellow form).  Lead oxide is found in paints and is used extensively in the manufacturing of lead glasses, ceramic glazes, and batteries. Lead is a heavy metal and stable element with the symbol Pb and the atomic number 82, existing in metallic, organic, and inorganic forms. It is mainly found in nature as the mineral galena (PbS), cerussite (PbCO3) or anglesite (PbSO4), usually in ore with zinc, silver, or copper. (R056, R699)",,1317-36-8,14827,,C17379,"","","",,C047365,Lead oxide,6112,,,http://en.wikipedia.org/wiki/Lead monoxide,InChI=1/O.Pb,oxolead,http://www.biospider.ca/saved_files/mol/,O=[Pb],O=[Pb],OPb,223.971550,Reddish-yellow solid.,888 °C,,,"",,,,"Oral 
Inhalation 
Dermal 
(R266)","Delta-aminolevulinic acid dehydratase (P13716) 
Serum albumin (P02768) 
Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
(R266)","Lead mimics other biologically important metals, such as zinc, calcium, and iron, competing as cofactors for many of their respective enzymatic reactions. For example, lead has been shown to competitively inhibit calcium's binding of calmodulin, interferring with neurotransmitter release. It exhibits similar competitive inhibition at the NMDA receptor and protein kinase C, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Lead also affects the nervous system by impairing regulation of dopamine synthesis and blocking evoked release of acetylcholine. However, it's main mechanism of action occurs by inhibiting delta-aminolevulinic acid dehydratase, an enzyme vital in the biosynthesis of heme, which is a necesssary cofactor of hemoglobin. (R008, R061, R063, R266)","Lead is absorbed following inhalation, oral, and dermal exposure. It is then distributed mainly to the bones and red blood cells. In the blood lead may be found bound to serum albumin or the metal-binding protein metallothionein. Organic lead is metabolized by cytochrome P-450 enzymes, whereas inorganic lead forms complexes with delta-aminolevulinic acid dehydratase. Lead is excreted mainly in the urine and faeces. (R266)","LD50: 40 mg/100 g (Intraperitoneal, Rat) (R700)",10 to 30 grams for and adult human (lead salts). (R273),"2B, possibly carcinogenic to humans. (R264)","Lead oxide is found in paints and is used extensively in the manufacturing of lead glasses, ceramic glazes, and batteries. It is also used in the vulcanization of rubber, in cathode ray tube glass, and in organic synthesis. (R699)",Chronic Inhalation: 0.05 mg/m3 (R260),"Lead is a neurotoxin and has been known to cause brain damage and reduced cognitive capacity, especially in children. Lead exposure can result in nephropathy, as well as blood disorders such as high blood pressure and anemia. Lead also exhibits reproductive toxicity and can results in miscarriages and reduced sperm production. (R056)","Symptions of chronic lead poisoning include reduced cognitive abilities, nausea, abdominal pain, irritability, insomnia, metal taste in the mouth, excess lethargy or hyperactivity, chest pain, headache and, in extreme cases, seizures, comas, and death. There are also associated gastrointestinal problems, such as constipation, diarrhea, vomiting, poor appetite, weight loss, which are common in acute poisoning. (R007, R056)","Lead poisoning is usually treated with chelation therapy using DMSA, EDTA, or dimercaprol. (R056)",P07108;P62158;P13716;P22830;Q12879;Q13224;Q14957;P17252;P05771;Q05655;Q02156;P24723;P05129;P41743;Q04759;Q05513;P54710;P05023;P50993;P13637;P05026;P14415;P54709;P62328;Q8TCU5;O60391;O15399;Q05586;Q13733
332,T3D0331,2009-03-06 18:58:32 UTC,2009-08-04 21:28:19 UTC,Lead dioxide,Inorganic Compound;Lead Compound,Bioxyde de plombBioxyde de plomb [french]Lead (su)peroxideLead brownLead dioxide [UN1872] [Oxidizer]Lead oxideLead oxide (PbO2)Lead oxide brownLead peroxideLead peroxide (PbO2)Lead superoxideLead(IV) oxideLeproPbO2Peroxyde de plombPeroxyde de plomb [french],"Lead dioxide is an oxide of lead that occurs naturally as the mineral plattnerite. It is an amphoteric substance used often as the cathode of lead-acid batteries. Lead is a heavy metal and stable element with the symbol Pb and the atomic number 82, existing in metallic, organic, and inorganic forms. It is mainly found in nature as the mineral galena (PbS), cerussite (PbCO3) or anglesite (PbSO4), usually in ore with zinc, silver, or copper. (R056, R701)",,1309-60-0,14793,,"","","","",,,Lead dioxide,,,,http://en.wikipedia.org/wiki/Lead dioxide,InChI=1/2O.Pb,dioxolead,http://www.biospider.ca/saved_files/mol/,O=[Pb]=O,O=[Pb]=O,O2Pb,239.966460,Black powder,290 ºC decomp.,,,"",,,,"Oral 
Inhalation 
Dermal 
(R266)","Delta-aminolevulinic acid dehydratase (P13716) 
Serum albumin (P02768) 
Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
(R266)","Lead mimics other biologically important metals, such as zinc, calcium, and iron, competing as cofactors for many of their respective enzymatic reactions. For example, lead has been shown to competitively inhibit calcium's binding of calmodulin, interferring with neurotransmitter release. It exhibits similar competitive inhibition at the NMDA receptor and protein kinase C, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Lead also affects the nervous system by impairing regulation of dopamine synthesis and blocking evoked release of acetylcholine. However, it's main mechanism of action occurs by inhibiting delta-aminolevulinic acid dehydratase, an enzyme vital in the biosynthesis of heme, which is a necesssary cofactor of hemoglobin. (R008, R061, R063, R266)","Lead is absorbed following inhalation, oral, and dermal exposure. It is then distributed mainly to the bones and red blood cells. In the blood lead may be found bound to serum albumin or the metal-binding protein metallothionein. Organic lead is metabolized by cytochrome P-450 enzymes, whereas inorganic lead forms complexes with delta-aminolevulinic acid dehydratase. Lead is excreted mainly in the urine and faeces. (R266)","LD50: 220 mg/kg (Intraperitoneal, Guinea pig) (R263)",10 to 30 grams for and adult human (lead salts). (R273),"2B, possibly carcinogenic to humans. (R264)",Lead dioxide is found in lead-acid batteries. (R701),Chronic Inhalation: 0.05 mg/m3 (R260),"Lead is a neurotoxin and has been known to cause brain damage and reduced cognitive capacity, especially in children. Lead exposure can result in nephropathy, as well as blood disorders such as high blood pressure and anemia. Lead also exhibits reproductive toxicity and can results in miscarriages and reduced sperm production. (R056)","Symptions of chronic lead poisoning include reduced cognitive abilities, nausea, abdominal pain, irritability, insomnia, metal taste in the mouth, excess lethargy or hyperactivity, chest pain, headache and, in extreme cases, seizures, comas, and death. There are also associated gastrointestinal problems, such as constipation, diarrhea, vomiting, poor appetite, weight loss, which are common in acute poisoning. (R007, R056)","Lead poisoning is usually treated with chelation therapy using DMSA, EDTA, or dimercaprol. (R056)",P07108;P62158;P13716;P22830;Q12879;Q13224;Q14957;P17252;P05771;Q05655;Q02156;P24723;P05129;P41743;Q04759;Q05513;P54710;P05023;P50993;P13637;P05026;P14415;P54709;P62328;Q8TCU5;O60391;O15399;Q05586;Q13733
333,T3D0332,2009-03-06 18:58:33 UTC,2009-08-04 21:28:19 UTC,Lead tetroxide,Inorganic Compound;Lead Compound,"BleimonoxidBleioxydC.I. Pigment Yellow 46C.I. Pigment red 105CI Pigment Red 105CI Pigment Yellow 46Gold satinobreHeuconin 5Lead monooxideLead monoxideLead orthoplumbateLead oxideLead oxide (3:4)Lead oxide (Pb3O4)Lead oxide (pbo)Lead oxide (van)Lead oxide redLead oxide yellowLead oxide, (pbo)Lead oxide, pboLead protoxideLead tetraoxideLead tetroxideLead(2+) oxideLead(II) oxideLead(II)oxideLead(II,III) oxideLithargeLitharge Yellow L-28Litharge pureMassicotMassicotiteMennigeMineral orangeMineral redMiniumMinium Non-Setting RL 95Minium non setting rl-95Minium redMinium tegoOrange leadParis redPigment Red 105Plumbi monoxidumPlumboplumbic oxidePlumbous oxidePlumbum oxydatumRed Lead Oxide (Pb3O4)Red leadRed lead oxideRed lead oxide, minium, paris red, satum redSandixSaturn redTrilead tetraoxideTrilead tetroxideWLN: PB oYellow lead ocher","Lead tetroxide is an oxide of lead the occurs naturally as the mineral minium. It is most often used in the production of batteries, pigments and lead glass. Lead is a heavy metal and stable element with the symbol Pb and the atomic number 82, existing in metallic, organic, and inorganic forms. It is mainly found in nature as the mineral galena (PbS), cerussite (PbCO3) or anglesite (PbSO4), usually in ore with zinc, silver, or copper. (R056, R702)",,1314-41-6,14827,,"","","",CPD-527,,C028356,Lead tetroxide,,,,,InChI=1/4O.3Pb,oxolead,http://www.biospider.ca/saved_files/mol/,O=[Pb],O=[Pb],OPb,223.971550,Red or orange crystals.,"",,,"",,,,"Oral 
Inhalation 
Dermal 
(R266)","Delta-aminolevulinic acid dehydratase (P13716) 
Serum albumin (P02768) 
Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
(R266)","Lead mimics other biologically important metals, such as zinc, calcium, and iron, competing as cofactors for many of their respective enzymatic reactions. For example, lead has been shown to competitively inhibit calcium's binding of calmodulin, interferring with neurotransmitter release. It exhibits similar competitive inhibition at the NMDA receptor and protein kinase C, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Lead also affects the nervous system by impairing regulation of dopamine synthesis and blocking evoked release of acetylcholine. However, it's main mechanism of action occurs by inhibiting delta-aminolevulinic acid dehydratase, an enzyme vital in the biosynthesis of heme, which is a necesssary cofactor of hemoglobin. (R008, R061, R063, R266)","Lead is absorbed following inhalation, oral, and dermal exposure. It is then distributed mainly to the bones and red blood cells. In the blood lead may be found bound to serum albumin or the metal-binding protein metallothionein. Organic lead is metabolized by cytochrome P-450 enzymes, whereas inorganic lead forms complexes with delta-aminolevulinic acid dehydratase. Lead is excreted mainly in the urine and faeces. (R266)","LD50: 630mg/kg (Intraperitoneal, Rat) (R263)",10 to 30 grams for and adult human (lead salts). (R273),"2B, possibly carcinogenic to humans. (R264)","Lead tetroxide is used the production of batteries, pigments, and lead glass. (R702)",Chronic Inhalation: 0.05 mg/m3 (R260),"Lead is a neurotoxin and has been known to cause brain damage and reduced cognitive capacity, especially in children. Lead exposure can result in nephropathy, as well as blood disorders such as high blood pressure and anemia. Lead also exhibits reproductive toxicity and can results in miscarriages and reduced sperm production. (R056)","Symptions of chronic lead poisoning include reduced cognitive abilities, nausea, abdominal pain, irritability, insomnia, metal taste in the mouth, excess lethargy or hyperactivity, chest pain, headache and, in extreme cases, seizures, comas, and death. There are also associated gastrointestinal problems, such as constipation, diarrhea, vomiting, poor appetite, weight loss, which are common in acute poisoning. (R007, R056)","Lead poisoning is usually treated with chelation therapy using DMSA, EDTA, or dimercaprol. (R056)",P07108;P62158;P13716;P22830;Q12879;Q13224;Q14957;P17252;P05771;Q05655;Q02156;P24723;P05129;P41743;Q04759;Q05513;P54710;P05023;P50993;P13637;P05026;P14415;P54709;P62328;Q8TCU5;O60391;O15399;Q05586;Q13733
334,T3D0333,2009-03-06 18:58:33 UTC,2009-08-26 20:29:23 UTC,Lead phosphate,Inorganic Compound;Lead Compound,"Phosphoric acid, lead saltPlumbum phosphoricum","Lead phosphate is a phosphate of lead used as a stabilizer in plastics. Lead is a heavy metal and stable element with the symbol Pb and the atomic number 82, existing in metallic, organic, and inorganic forms. It is mainly found in nature as the mineral galena (PbS), cerussite (PbCO3) or anglesite (PbSO4), usually in ore with zinc, silver, or copper. (R056, R270)",,7446-27-7,167506,,"","","","",,,Lead phosphate,,,,,"InChI=1/2H3O4P.3Pb/c2*1-5(2,3)4;;;/h2*(H3,1,2,3,4);;;/q;;3*+2/p-6",lead(2+) diphosphate,http://www.biospider.ca/saved_files/mol/,[O-]P(=O)([O-])[O-].[O-]P(=O)([O-])[O-].[Pb+2].[Pb+2],[Pb++].[Pb++].[Pb++].[O-]P([O-])([O-])=O.[O-]P([O-])([O-])=O,O8P2Pb3,811.542722,White solid.,1014 oC,,,"",,,,"Oral 
Inhalation 
Dermal 
(R266)","Delta-aminolevulinic acid dehydratase (P13716) 
Serum albumin (P02768) 
Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
(R266)","Lead mimics other biologically important metals, such as zinc, calcium, and iron, competing as cofactors for many of their respective enzymatic reactions. For example, lead has been shown to competitively inhibit calcium's binding of calmodulin, interferring with neurotransmitter release. It exhibits similar competitive inhibition at the NMDA receptor and protein kinase C, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Lead also affects the nervous system by impairing regulation of dopamine synthesis and blocking evoked release of acetylcholine. However, it's main mechanism of action occurs by inhibiting delta-aminolevulinic acid dehydratase, an enzyme vital in the biosynthesis of heme, which is a necesssary cofactor of hemoglobin. (R008, R061, R063, R266)","Lead is absorbed following inhalation, oral, and dermal exposure. It is then distributed mainly to the bones and red blood cells. In the blood lead may be found bound to serum albumin or the metal-binding protein metallothionein. Organic lead is metabolized by cytochrome P-450 enzymes, whereas inorganic lead forms complexes with delta-aminolevulinic acid dehydratase. Lead is excreted mainly in the urine and faeces. (R266)",No data.,10 to 30 grams for and adult human (lead salts). (R273),"2B, possibly carcinogenic to humans. (R264)",Lead phophate is used as a stabilizer in plastics. (R270),Chronic Inhalation: 0.05 mg/m3 (R260),"Lead is a neurotoxin and has been known to cause brain damage and reduced cognitive capacity, especially in children. Lead exposure can result in nephropathy, as well as blood disorders such as high blood pressure and anemia. Lead also exhibits reproductive toxicity and can results in miscarriages and reduced sperm production. (R056)","Symptions of chronic lead poisoning include reduced cognitive abilities, nausea, abdominal pain, irritability, insomnia, metal taste in the mouth, excess lethargy or hyperactivity, chest pain, headache and, in extreme cases, seizures, comas, and death. There are also associated gastrointestinal problems, such as constipation, diarrhea, vomiting, poor appetite, weight loss, which are common in acute poisoning. (R007, R056)","Lead poisoning is usually treated with chelation therapy using DMSA, EDTA, or dimercaprol. (R056)",P07108;P62158;P13716;P22830;Q12879;Q13224;Q14957;P17252;P05771;Q05655;Q02156;P24723;P05129;P41743;Q04759;Q05513;P54710;P05023;P50993;P13637;P05026;P14415;P54709;P62328;Q8TCU5;O60391;O15399;Q05586;Q13733
335,T3D0334,2009-03-06 18:58:33 UTC,2009-08-18 00:00:22 UTC,Lead styphnate,Inorganic Compound;Lead Compound,"1,3-Benzenediol, 2,4,6-trinitro-, lead(2+) salt (1:1)Lead 2,4,6-trinitro-m-phenylene dioxideLead styphnateLead styphnate (DRY) [forbidden]Lead trinitroresorcinate","Lead styphnate is an explosive chemical compound of lead used as a detonator. It exists in two forms of crystals and varies in color from yellow to brown. Lead is a heavy metal and stable element with the symbol Pb and the atomic number 82, existing in metallic, organic, and inorganic forms. It is mainly found in nature as the mineral galena (PbS), cerussite (PbCO3) or anglesite (PbSO4), usually in ore with zinc, silver, or copper. (R056, R703)",,15245-44-0,61789,,"","","","",,,Lead styphnate,12775,,,,"InChI=1/C6H3N3O8.Pb/c10-5-2(7(12)13)1-3(8(14)15)6(11)4(5)9(16)17;/h1,10-11H;/q;+2/p-2","lead(2+); 2,4,6-trinitrobenzene-1,3-diolate",http://www.biospider.ca/saved_files/mol/,C1=C(C(=C(C(=C1[N+](=O)[O-])[O-])[N+](=O)[O-])[O-])[N+](=O)[O-].[Pb+2],C1=C(C(=C(C(=C1[N+](=O)[O-])[O-])[N+](=O)[O-])[O-])[N+](=O)[O-].[Pb+2],C6HN3O8Pb,450.953000,Orange/yellow solid.,"",,,"",,,,"Oral 
Inhalation 
Dermal 
(R266)","Delta-aminolevulinic acid dehydratase (P13716) 
Serum albumin (P02768) 
Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
(R266)","Lead mimics other biologically important metals, such as zinc, calcium, and iron, competing as cofactors for many of their respective enzymatic reactions. For example, lead has been shown to competitively inhibit calcium's binding of calmodulin, interferring with neurotransmitter release. It exhibits similar competitive inhibition at the NMDA receptor and protein kinase C, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Lead also affects the nervous system by impairing regulation of dopamine synthesis and blocking evoked release of acetylcholine. However, it's main mechanism of action occurs by inhibiting delta-aminolevulinic acid dehydratase, an enzyme vital in the biosynthesis of heme, which is a necesssary cofactor of hemoglobin. (R008, R061, R063, R266)","Lead is absorbed following inhalation, oral, and dermal exposure. It is then distributed mainly to the bones and red blood cells. In the blood lead may be found bound to serum albumin or the metal-binding protein metallothionein. Organic lead is metabolized by cytochrome P-450 enzymes, whereas inorganic lead forms complexes with delta-aminolevulinic acid dehydratase. Lead is excreted mainly in the urine and faeces. (R266)",No data.,10 to 30 grams for and adult human (lead salts). (R273),"2B, possibly carcinogenic to humans. (R264)",Lead styphnate is used as a detonator. (R703),Chronic Inhalation: 0.05 mg/m3 (R260),"Lead is a neurotoxin and has been known to cause brain damage and reduced cognitive capacity, especially in children. Lead exposure can result in nephropathy, as well as blood disorders such as high blood pressure and anemia. Lead also exhibits reproductive toxicity and can results in miscarriages and reduced sperm production. (R056)","Symptions of chronic lead poisoning include reduced cognitive abilities, nausea, abdominal pain, irritability, insomnia, metal taste in the mouth, excess lethargy or hyperactivity, chest pain, headache and, in extreme cases, seizures, comas, and death. There are also associated gastrointestinal problems, such as constipation, diarrhea, vomiting, poor appetite, weight loss, which are common in acute poisoning. (R007, R056)","Lead poisoning is usually treated with chelation therapy using DMSA, EDTA, or dimercaprol. (R056)",P07108;P62158;P13716;P22830;Q12879;Q13224;Q14957;P17252;P05771;Q05655;Q02156;P24723;P05129;P41743;Q04759;Q05513;P54710;P05023;P50993;P13637;P05026;P14415;P54709;P62328;Q8TCU5;O60391;O15399;Q05586;Q13733
336,T3D0335,2009-03-06 18:58:33 UTC,2009-08-04 21:28:20 UTC,Lead sulfate,Inorganic Compound;Lead Compound,"AnglisliteBleisulfatBleisulfat [german]C.I. Pigment white 3CI pigment white 3Fast whiteFreemans white leadHaro chem PTS-eLead bottomsLead drossLead monosulfateLead sulfate with >3% free acid [UN1794] [Corrosive]Lead sulfate, tetrabasicLead sulphateLead(+2) sulfateLead(II) sulfateLead(ii) sulfate (1:1)Milk whiteMulhouse whiteNatural anglesitePigment White 3Sulfate de plombSulfate de plomb [french]Sulfuric acid, lead saltSulfuric acid, lead salt, tetrabasicSulfuric acid, lead(2+) saltSulfuric acid, lead(2+) salt (1:1)Sulphuric acid, lead saltTS 100 (sulfate)Tetrabasic lead sulfateTribasic lead sulfate","Lead sulfate is a sulfate of lead that occurs naturally as the mineral anglesite. It is used most often in lead-acid batteries. Lead is a heavy metal and stable element with the symbol Pb and the atomic number 82, existing in metallic, organic, and inorganic forms. It is mainly found in nature as the mineral galena (PbS), cerussite (PbCO3) or anglesite (PbSO4), usually in ore with zinc, silver, or copper. (R056, R704)",,7446-14-2,24008,,"","","",CPD-530,,C032722,Lead sulfate,,,,,"InChI=1/H2O4S.Pb/c1-5(2,3)4;/h(H2,1,2,3,4);/q;+2/p-2",lead(2+) sulfate,http://www.biospider.ca/saved_files/mol/,[O-]S(=O)(=O)[O-].[Pb+2],[O-]S(=O)(=O)[O-].[Pb+2],O4PbS,303.928360,White solid.,1170 oC,,,"0.032 mg/mL at 15 oC [MITCHELL,S (1926)]",,,,"Oral 
Inhalation 
Dermal 
(R266)","Delta-aminolevulinic acid dehydratase (P13716) 
Serum albumin (P02768) 
Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
(R266)","Lead mimics other biologically important metals, such as zinc, calcium, and iron, competing as cofactors for many of their respective enzymatic reactions. For example, lead has been shown to competitively inhibit calcium's binding of calmodulin, interferring with neurotransmitter release. It exhibits similar competitive inhibition at the NMDA receptor and protein kinase C, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Lead also affects the nervous system by impairing regulation of dopamine synthesis and blocking evoked release of acetylcholine. However, it's main mechanism of action occurs by inhibiting delta-aminolevulinic acid dehydratase, an enzyme vital in the biosynthesis of heme, which is a necesssary cofactor of hemoglobin. (R008, R061, R063, R266)","Lead is absorbed following inhalation, oral, and dermal exposure. It is then distributed mainly to the bones and red blood cells. In the blood lead may be found bound to serum albumin or the metal-binding protein metallothionein. Organic lead is metabolized by cytochrome P-450 enzymes, whereas inorganic lead forms complexes with delta-aminolevulinic acid dehydratase. Lead is excreted mainly in the urine and faeces. (R266)","LD50: 300 mg/kg (Intraperitoneal, Guinea pig) (R618)",10 to 30 grams for and adult human (lead salts). (R273),"2B, possibly carcinogenic to humans. (R264)",Lead sulphate is found in lead-acid batteries. (R704),Chronic Inhalation: 0.05 mg/m3 (R260),"Lead is a neurotoxin and has been known to cause brain damage and reduced cognitive capacity, especially in children. Lead exposure can result in nephropathy, as well as blood disorders such as high blood pressure and anemia. Lead also exhibits reproductive toxicity and can results in miscarriages and reduced sperm production. (R056)","Symptions of chronic lead poisoning include reduced cognitive abilities, nausea, abdominal pain, irritability, insomnia, metal taste in the mouth, excess lethargy or hyperactivity, chest pain, headache and, in extreme cases, seizures, comas, and death. There are also associated gastrointestinal problems, such as constipation, diarrhea, vomiting, poor appetite, weight loss, which are common in acute poisoning. (R007, R056)","Lead poisoning is usually treated with chelation therapy using DMSA, EDTA, or dimercaprol. (R056)",P07108;P62158;P13716;P22830;Q12879;Q13224;Q14957;P17252;P05771;Q05655;Q02156;P24723;P05129;P41743;Q04759;Q05513;P54710;P05023;P50993;P13637;P05026;P14415;P54709;P62328;Q8TCU5;O60391;O15399;Q05586;Q13733
337,T3D0336,2009-03-06 18:58:33 UTC,2009-08-04 21:28:20 UTC,Lead sulfide,Inorganic Compound;Lead Compound,GalenaGalena (PBS)Lead (II) sulfideLead sulfideLead sulfide (PBS)Lead sulphideLead(2)sulfideLead(2+) sulfideLead(II) sulfideNatural galenaNatural lead sulfideP 128 (sulfide)P 37 (filter)PBSPlumbous sulfide,"Lead sulfide is a sulfide of lead that occurs naturally as the mineral galena. It is used as a semiconductor and infrared detector. Lead is a heavy metal and stable element with the symbol Pb and the atomic number 82, existing in metallic, organic, and inorganic forms. It is mainly found in nature as the mineral galena (PbS), cerussite (PbCO3) or anglesite (PbSO4), usually in ore with zinc, silver, or copper. (R056, R705)",,1314-87-0,14819,,"","","",CPD-527,,C018391,Lead sulfide,,,,,InChI=1/Pb.S,sulfanylidenelead,http://www.biospider.ca/saved_files/mol/,S=[Pb],S=[Pb],PbS,239.948710,"Black, blue,  or silvery crystals.","",,,"",,,,"Oral 
Inhalation 
Dermal 
(R266)","Delta-aminolevulinic acid dehydratase (P13716) 
Serum albumin (P02768) 
Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
(R266)","Lead mimics other biologically important metals, such as zinc, calcium, and iron, competing as cofactors for many of their respective enzymatic reactions. For example, lead has been shown to competitively inhibit calcium's binding of calmodulin, interferring with neurotransmitter release. It exhibits similar competitive inhibition at the NMDA receptor and protein kinase C, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Lead also affects the nervous system by impairing regulation of dopamine synthesis and blocking evoked release of acetylcholine. However, it's main mechanism of action occurs by inhibiting delta-aminolevulinic acid dehydratase, an enzyme vital in the biosynthesis of heme, which is a necesssary cofactor of hemoglobin. (R008, R061, R063, R266)","Lead is absorbed following inhalation, oral, and dermal exposure. It is then distributed mainly to the bones and red blood cells. In the blood lead may be found bound to serum albumin or the metal-binding protein metallothionein. Organic lead is metabolized by cytochrome P-450 enzymes, whereas inorganic lead forms complexes with delta-aminolevulinic acid dehydratase. Lead is excreted mainly in the urine and faeces. (R266)","LD50: 1600 mg/kg (Intraperitoneal, Rat) (R706)",10 to 30 grams for and adult human (lead salts). (R273),"2B, possibly carcinogenic to humans. (R264)","Lead sulfide is used as a semiconductor, infrared detector, and can be found in batteries and ceramic paints. (R705)",Chronic Inhalation: 0.05 mg/m3 (R260),"Lead is a neurotoxin and has been known to cause brain damage and reduced cognitive capacity, especially in children. Lead exposure can result in nephropathy, as well as blood disorders such as high blood pressure and anemia. Lead also exhibits reproductive toxicity and can results in miscarriages and reduced sperm production. (R056)","Symptions of chronic lead poisoning include reduced cognitive abilities, nausea, abdominal pain, irritability, insomnia, metal taste in the mouth, excess lethargy or hyperactivity, chest pain, headache and, in extreme cases, seizures, comas, and death. There are also associated gastrointestinal problems, such as constipation, diarrhea, vomiting, poor appetite, weight loss, which are common in acute poisoning. (R007, R056)","Lead poisoning is usually treated with chelation therapy using DMSA, EDTA, or dimercaprol. (R056)",P07108;P62158;P13716;P22830;Q12879;Q13224;Q14957;P17252;P05771;Q05655;Q02156;P24723;P05129;P41743;Q04759;Q05513;P54710;P05023;P50993;P13637;P05026;P14415;P54709;P62328;Q8TCU5;O60391;O15399;Q05586;Q13733
338,T3D0337,2009-03-06 18:58:33 UTC,2009-08-04 21:28:20 UTC,Tetramethyl lead,Inorganic Compound;Lead Compound,"(CH3)4PbBleitetramethylLead tetramethylPbMe4Piombo tetra-metilePiombo tetra-metile [italian]Plumbane, tetramethyl-TMLTetramethyl leadTetramethylleadTetramethylolovoTetramethylolovo [czech]Tetramethylplumbane","Tetramethyl lead is an organolead compound used primarily as an antiknock additive for gasolines. Lead is a heavy metal and stable element with the symbol Pb and the atomic number 82, existing in metallic, organic, and inorganic forms. It is mainly found in nature as the mineral galena (PbS), cerussite (PbCO3) or anglesite (PbSO4), usually in ore with zinc, silver, or copper. (R056, R353)",,75-74-1,6394,,"","",30183,CPD0-1640,,C014849,Tetramethyl lead,,,,,InChI=1/4CH3.Pb/h4*1H3;,tetramethylplumbane,http://www.biospider.ca/saved_files/mol/,C[Pb](C)(C)C,C[Pb](C)(C)C,C4H12Pb,268.070540,Colorless liquid.,-27.5 oC,,,"0.015 mg/mL at 25 oC [WANG,Y et al. (1996)]",,,,"Oral 
Inhalation 
Dermal 
(R266)","Delta-aminolevulinic acid dehydratase (P13716) 
Serum albumin (P02768) 
Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
(R266)","Lead mimics other biologically important metals, such as zinc, calcium, and iron, competing as cofactors for many of their respective enzymatic reactions. For example, lead has been shown to competitively inhibit calcium's binding of calmodulin, interferring with neurotransmitter release. It exhibits similar competitive inhibition at the NMDA receptor and protein kinase C, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Lead also affects the nervous system by impairing regulation of dopamine synthesis and blocking evoked release of acetylcholine. However, it's main mechanism of action occurs by inhibiting delta-aminolevulinic acid dehydratase, an enzyme vital in the biosynthesis of heme, which is a necesssary cofactor of hemoglobin. (R008, R061, R063, R266)","Lead is absorbed following inhalation, oral, and dermal exposure. It is then distributed mainly to the bones and red blood cells. In the blood lead may be found bound to serum albumin or the metal-binding protein metallothionein. Organic lead is metabolized by cytochrome P-450 enzymes, whereas inorganic lead forms complexes with delta-aminolevulinic acid dehydratase. Lead is excreted mainly in the urine and faeces. (R266)","LD50: 109 mg/kg (Oral, Guinea pig) (R707)
LD50: 90 mg/kg (Intraperitoneal, Rabbit) (R707)
LD50: 88 mg/kg (Intravenous, Rat) (R707)
LC50: 8500 mg/m3 (Inhalation, Mouse) (R707)",No data.,"2B, possibly carcinogenic to humans. (R264)",Tetramethyl lead is used primarily as an antiknock additive for gasolines. (R353),Chronic Inhalation: 0.05 mg/m3 (R260),"Lead is a neurotoxin and has been known to cause brain damage and reduced cognitive capacity, especially in children. Lead exposure can result in nephropathy, as well as blood disorders such as high blood pressure and anemia. Lead also exhibits reproductive toxicity and can results in miscarriages and reduced sperm production. (R056)","Symptions of chronic lead poisoning include reduced cognitive abilities, nausea, abdominal pain, irritability, insomnia, metal taste in the mouth, excess lethargy or hyperactivity, chest pain, headache and, in extreme cases, seizures, comas, and death. There are also associated gastrointestinal problems, such as constipation, diarrhea, vomiting, poor appetite, weight loss, which are common in acute poisoning. (R007, R056)","Lead poisoning is usually treated with chelation therapy using DMSA, EDTA, or dimercaprol. (R056)",P07108;P62158;P13716;P22830;Q12879;Q13224;Q14957;P17252;P05771;Q05655;Q02156;P24723;P05129;P41743;Q04759;Q05513;P54710;P05023;P50993;P13637;P05026;P14415;P54709;P62328;Q8TCU5;O60391;O15399;Q05586;Q13733
339,T3D0338,2009-03-06 18:58:33 UTC,2009-08-04 21:28:20 UTC,Tetraethyl lead,Inorganic Compound;Lead Compound,"BleitetraethylCzteroetylek olowiuCzteroetylek olowiu (polish)Czteroetylek olowiu [polish]Lead tetraethideLead tetraethylLead, tetraethyl-PbEt4Piombo tetra-etilePiombo tetra-etile [italian]Plumbane, tetraethyl-RCRA waste no. P110Rcra waste number P110TELTel-TML, reactedTetra(methylethyl)leadTetraethyl leadTetraethyl lead, liquidTetraethyl lead, liquid (dot)Tetraethyl lead, liquid [NA1649] [Poison]Tetraethyllead solutionTetraethyllead, liquidTetraethylolovoTetraethylolovo [czech]TetraethylplumbaneTetraethylplumbium[PbEt4]tetraethylplumbane (ACD/Name 4.0)","Tetraethyl lead is an organolead compound produced by reacting ethyl chloride with a sodium-lead alloy. It was originally used as an antiknock additive in gasoline, but is now found only in some aircraft fuels. Lead is a heavy metal and stable element with the symbol Pb and the atomic number 82, existing in metallic, organic, and inorganic forms. It is mainly found in nature as the mineral galena (PbS), cerussite (PbCO3) or anglesite (PbSO4), usually in ore with zinc, silver, or copper. (R056, R708)",,78-00-2,6511,,"","",30182,"",,D013756,Tetraethyl lead,3306,,,,"InChI=1/4C2H5.Pb/c4*1-2;/h4*1H2,2H3;",tetraethylplumbane,http://www.biospider.ca/saved_files/mol/,CC[Pb](CC)(CC)CC,CC[Pb](CC)(CC)CC,C8H20Pb,324.133140,"Colorless, oily liquid.",-136 oC,,,"0.00029 mg/mL at 26 oC [FELDHAKE,CJ & STEVENS,CD (1963)]",,,,"Oral 
Inhalation 
Dermal 
(R266)","Delta-aminolevulinic acid dehydratase (P13716) 
Serum albumin (P02768) 
Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
(R266)","Lead mimics other biologically important metals, such as zinc, calcium, and iron, competing as cofactors for many of their respective enzymatic reactions. For example, lead has been shown to competitively inhibit calcium's binding of calmodulin, interferring with neurotransmitter release. It exhibits similar competitive inhibition at the NMDA receptor and protein kinase C, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Lead also affects the nervous system by impairing regulation of dopamine synthesis and blocking evoked release of acetylcholine. However, it's main mechanism of action occurs by inhibiting delta-aminolevulinic acid dehydratase, an enzyme vital in the biosynthesis of heme, which is a necesssary cofactor of hemoglobin. (R008, R061, R063, R266)","Lead is absorbed following inhalation, oral, and dermal exposure. It is then distributed mainly to the bones and red blood cells. In the blood lead may be found bound to serum albumin or the metal-binding protein metallothionein. Organic lead is metabolized by cytochrome P-450 enzymes, whereas inorganic lead forms complexes with delta-aminolevulinic acid dehydratase. Lead is excreted mainly in the urine and faeces. (R266)","LD50: 12.3 mg/kg (Oral, Rat) (R263)
LD50: 14.4 mg/kg (Intravenous, Rat) (R263)
LD50: 15 mg/kg (Intraperitoneal, Rat) (R263)
LD50: 13 mg/kg (Subcutaneous, Mouse) (R710)
LC50: 850 mg/m3 over 1 hour (Inhalation, Rat) (R263)",1 gram for an adult human. (R273),"2B, possibly carcinogenic to humans. (R264)","Tetraethyl lead was originally used as an antiknock additive in gasoline, but is now found only in some aircraft fuels. (R708)",Chronic Inhalation: 0.05 mg/m3 (R260),"Lead is a neurotoxin and has been known to cause brain damage and reduced cognitive capacity, especially in children. Lead exposure can result in nephropathy, as well as blood disorders such as high blood pressure and anemia. Lead also exhibits reproductive toxicity and can results in miscarriages and reduced sperm production. (R056)","Symptions of chronic lead poisoning include reduced cognitive abilities, nausea, abdominal pain, irritability, insomnia, metal taste in the mouth, excess lethargy or hyperactivity, chest pain, headache and, in extreme cases, seizures, comas, and death. There are also associated gastrointestinal problems, such as constipation, diarrhea, vomiting, poor appetite, weight loss, which are common in acute poisoning. (R007, R056)","Lead poisoning is usually treated with chelation therapy using DMSA, EDTA, or dimercaprol. (R056)",P07108;P62158;P13716;P22830;Q12879;Q13224;Q14957;P17252;P05771;Q05655;Q02156;P24723;P05129;P41743;Q04759;Q05513;P54710;P05023;P50993;P13637;P05026;P14415;P54709;P62328;Q8TCU5;O60391;O15399;Q05586;Q13733
341,T3D0340,2009-03-06 18:58:34 UTC,2009-08-05 21:38:42 UTC,Mercury(II) fulminate,Inorganic Compound;Mercury Compound,"Bis[(oxidoazanylidyne)methyl]mercuryFulminate of mercuryFulminic acid, mercury(II) saltHg(CNO)2KnallquecksilberMercury difulminateMercury fulminateMercury(II) fulminateO-n#c-HG-c#n-oQuecksilber(II)-fulminatfulminic acid, mercury(2+) salt","Mercury(II) fulminate is a chemical compound of mercury. It is a primary explosive and highly sensitive to friction and shock, thus mainly used as a trigger for other explosives in percussion caps and blasting caps. Mercury is a heavy, silvery d-block metal and one of six elements that are liquid at or near room temperature and pressure. It is a naturally occuring substance, and combines with other elements such as chlorine, sulfur, or oxygen to form inorganic mercury compounds (salts). Mercury also combines with carbon to make organic mercury compounds. (R005, R721)",,628-86-4,11022444,,"","",39152,"",,C070787,Mercury(II) fulminate,,,,,InChI=1/2CNO.Hg/c2*1-2-3;,dioxycyanomercury,http://www.biospider.ca/saved_files/mol/,C(#[N+][O-])[Hg]C#[N+][O-],C(#[N+][O-])[Hg]C#[N+][O-],C2HgN2O2,285.966600,Grey crystals.,"","","","0.1 mg/mL at 15 oC [KIRK-OTHMER; 1st ed, v6:11 (1951)]","","","","Oral 
Inhalation 
Dermal 
(R022)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Catalase (P04040) 
Hemoglobin subunit alpha (P69905) 
Hemoglobin subunit beta (P68871) 
Hemoglobin subunit gamma-1 (P69891) 
Hemoglobin subunit gamma-2 (P69892) 
Hemoglobin subunit delta (P02042) 
Hemoglobin subunit epsilon (P02100) 
Hemoglobin subunit theta-1 (P09105) 
Hemoglobin subunit zeta (P02008) 
Hemoglobin subunit mu (Q6B0K9) 
(R022, R164) ","High-affinity binding of the divalent mercuric ion to thiol or sulfhydryl groups of proteins is believed to be the major mechanism for the activity of mercury. Through alterations in intracellular thiol status, mercury can promote oxidative stress, lipid peroxidation, mitochondrial dysfunction, and changes in heme metabolism. Mercury is known to bind to microsomal and mitochondrial enzymes, resulting in cell injury and death. For example, mercury is known to inhibit aquaporins, halting water flow across the cell membrane. It also inhibits the protein LCK, which causes decreased T-cell signalling and immune system depression. Mercury is also believed to inhibit neuronal excitability by acting on the postsynaptic neuronal membrane. It also affects the nervous system by inhibiting protein kinase C and alkaline phosphatase, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Mercury also produces an autoimmune response, likely by modification of major histocompatibility complex (MHC) class II molecules, self peptides, T-cell receptors, or cell-surface adhesion molecules. (R022, R025, R066, R067)","Mercury is absorbed mainly via ingestion and inhalation, then distributed throughout the body via the bloodstream, where a portion binds to sulfhydryl groups on haemoglobin. Mercury can undergo oxidation to mercuric mercury, which takes place via the catalase-hydrogen peroxide pathway. The mercury atom is able to diffuse down the cleft in the catalase enzyme to reach the active site where the heme ring is located. Oxidation most likely occurs in all tissue, as the catalase hydrogen peroxide pathway is ubiquitous. Following oxidation, mercury tends to accumulate in the kidneys. Mercury is excreted mainly by exhalation and in the faeces. (R021, R022)",No data.,1 gram for an adult human (average for inorganic mercurials). (R273),"3, not classifiable as to its carcinogenicity to humans. (R264)",Mercury(II) fulminate is used as a trigger for other explosives in percussion caps and blasting caps. (R721),Chronic Inhalation: 0.0002 mg/m3 (R260),"Mercury mainly affects the nervous system. Exposure to high levels of metallic, inorganic, or organic mercury can permanently damage the brain, kidneys, and developing fetus. Effects on brain functioning may result in irritability, shyness, tremors, changes in vision or hearing, and memory problems. Acrodynia, a type of mercury poisoning in children, is characterized by pain and pink discoloration of the hands and feet. Mercury poisoning can also cause Hunter-Russell syndrome and Minamata disease. (R022)","Common symptoms include peripheral neuropathy (presenting as paresthesia or itching, burning or pain), skin discoloration (pink cheeks, fingertips and toes), edema (swelling), and desquamation (dead skin peels off in layers). (R020)","Mercury poisoning is treated by immediate decontamination and chelation therapy using DMSA, DMPS, DPCN, or dimercaprol. (R023)",P06239;P05186;P29972;Q96PS8;Q8NBQ7;Q8IXF9;A6NM10;P41181;Q92482;P55087;P55064;Q13520;O14520;O94778;O43315;P30301;P17252;P05771;Q05655;Q02156;P24723;P05129;P41743;Q04759;Q05513;A6NKZ8 ;Q99867;Q9H853;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2;Q9UJT1;Q9UJT0;P23258;Q9NRH3
342,T3D0341,2009-03-06 18:58:34 UTC,2009-08-05 21:38:42 UTC,Mercury(II) sulfide,Inorganic Compound;Mercury Compound,"AlmadenBeta-mercuric sulfideC.I. Pigment Red 106Chinese vermilionCinnabarCinnabar (HGS)CinnabariteEthiops mineralHydrargyrum sulfuratum rubrumMercuric sulfideMercuric sulfide redMercuric sulfide, blackMercuric sulfide, redMercuric sulphideMercurius 6aMercury monosulfideMercury ores, cinnabarMercury sulfideMercury sulfide (HGS)Mercury sulphideMercury sulphide, naturalMercury(2+) sulfideMercury(II) sulfide redMonomercury sulfideOrange vermilionParagitePigment Red 106Pure english (quicksilver) vermilionQuecksilber(II)-sulfid, rotesRed cinnabarRed mercury sulphideRotes quecksilbersulfidScarlet vermilionVermilionVermilion (HGS)","Mercury(II) sulfide is a sulfide of mercury that occurs naturally as the minerals red cinnabar and black metacinnabar. It is a semiconductor and used as a red pigment, vermillion. Mercury is a heavy, silvery d-block metal and one of six elements that are liquid at or near room temperature and pressure. It is a naturally occuring substance, and combines with other elements such as chlorine, sulfur, or oxygen to form inorganic mercury compounds (salts). Mercury also combines with carbon to make organic mercury compounds. (R005, R722)",,1344-48-5,62402,,"","","","",,,Mercury(II) sulfide,,,,http://en.wikipedia.org/wiki/mercury(II) sulfide,InChI=1/Hg.S,sulfanylidenemercury,http://www.biospider.ca/saved_files/mol/,S=[Hg],S=[Hg],HgS,233.942700,Black or red crystals.,580 °C decomp.,"","","","","","","Oral 
Inhalation 
Dermal 
(R022)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Catalase (P04040) 
Hemoglobin subunit alpha (P69905) 
Hemoglobin subunit beta (P68871) 
Hemoglobin subunit gamma-1 (P69891) 
Hemoglobin subunit gamma-2 (P69892) 
Hemoglobin subunit delta (P02042) 
Hemoglobin subunit epsilon (P02100) 
Hemoglobin subunit theta-1 (P09105) 
Hemoglobin subunit zeta (P02008) 
Hemoglobin subunit mu (Q6B0K9) 
(R022, R164) ","High-affinity binding of the divalent mercuric ion to thiol or sulfhydryl groups of proteins is believed to be the major mechanism for the activity of mercury. Through alterations in intracellular thiol status, mercury can promote oxidative stress, lipid peroxidation, mitochondrial dysfunction, and changes in heme metabolism. Mercury is known to bind to microsomal and mitochondrial enzymes, resulting in cell injury and death. For example, mercury is known to inhibit aquaporins, halting water flow across the cell membrane. It also inhibits the protein LCK, which causes decreased T-cell signalling and immune system depression. Mercury is also believed to inhibit neuronal excitability by acting on the postsynaptic neuronal membrane. It also affects the nervous system by inhibiting protein kinase C and alkaline phosphatase, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Mercury also produces an autoimmune response, likely by modification of major histocompatibility complex (MHC) class II molecules, self peptides, T-cell receptors, or cell-surface adhesion molecules. (R022, R025, R066, R067)","Mercury is absorbed mainly via ingestion and inhalation, then distributed throughout the body via the bloodstream, where a portion binds to sulfhydryl groups on haemoglobin. Mercury can undergo oxidation to mercuric mercury, which takes place via the catalase-hydrogen peroxide pathway. The mercury atom is able to diffuse down the cleft in the catalase enzyme to reach the active site where the heme ring is located. Oxidation most likely occurs in all tissue, as the catalase hydrogen peroxide pathway is ubiquitous. Following oxidation, mercury tends to accumulate in the kidneys. Mercury is excreted mainly by exhalation and in the faeces. (R021, R022)",No data.,1 gram for an adult human (average for inorganic mercurials). (R273),"3, not classifiable as to its carcinogenicity to humans. (R264)","Mercury(II) sulfide is used as a semiconductor and as a red pigment, vermillion. (R722)",Chronic Inhalation: 0.0002 mg/m3 (R260),"Mercury mainly affects the nervous system. Exposure to high levels of metallic, inorganic, or organic mercury can permanently damage the brain, kidneys, and developing fetus. Effects on brain functioning may result in irritability, shyness, tremors, changes in vision or hearing, and memory problems. Acrodynia, a type of mercury poisoning in children, is characterized by pain and pink discoloration of the hands and feet. Mercury poisoning can also cause Hunter-Russell syndrome and Minamata disease. (R022)","Common symptoms include peripheral neuropathy (presenting as paresthesia or itching, burning or pain), skin discoloration (pink cheeks, fingertips and toes), edema (swelling), and desquamation (dead skin peels off in layers). (R020)","Mercury poisoning is treated by immediate decontamination and chelation therapy using DMSA, DMPS, DPCN, or dimercaprol. (R023)",P06239;P05186;P29972;P55087;P55064;O14520;O94778;O43315;P30301;P17252;P05771;Q05655;Q02156;P24723;P05129;P41743;Q04759;Q05513;Q9UJT1;Q9UJT0;Q96PS8;Q8NBQ7;Q8IXF9;A6NM10;P41181;Q92482;Q13520;A6NKZ8 ;Q99867;Q9H853;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2;P23258;Q9NRH3
343,T3D0342,2009-03-06 18:58:34 UTC,2009-08-05 21:38:42 UTC,Mercury(II) oxide,Inorganic Compound;Mercury Compound,"Caswell No. 544AGelbes quecksilberoxydHGOHydrargyrum oxid flavHydrargyrum oxydatum rubrumKankerexMercuric oxideMercuric oxide (hgo)Mercuric oxide (red)Mercuric oxide [iso]Mercuric oxide [mercury and mercury compounds]Mercuric oxide redMercuric oxide yellowMercuric oxide, redMercuric oxide, red and yellowMercuric oxide, yellowMercuric oxide,redMercury monoxideMercury oxideMercury oxide (hgo)Mercury oxide [UN1641] [Poison]Mercury(2+) oxideMercury(II) oxide redMercury(II) oxide yellowMercury(II)oxide,yellowNatural montroyditeOxide mercurique jauneOxido amarillo de mercurioOxyde de mercure [french]Oxyde mercurique [iso-french]Red mercuric oxideRed oxide of mercuryRed precipitateSantarSantar mYellow mercuric oxideYellow oxide of mercuryYellow precipitate","Mercury(II) oxide is an oxide of mercury that occurs naturally as the mineral montroydite. It is often used in the production of mercury and as a material for cathodes for mercury batteries. Mercury is a heavy, silvery d-block metal and one of six elements that are liquid at or near room temperature and pressure. It is a naturally occuring substance, and combines with other elements such as chlorine, sulfur, or oxygen to form inorganic mercury compounds (salts). Mercury also combines with carbon to make organic mercury compounds. (R005, R723)",,21908-53-2,30856,,"","","","",,C019468,Mercury(II) oxide,,,,,InChI=1/Hg.O,oxomercury,http://www.biospider.ca/saved_files/mol/,O=[Hg],O=[Hg],HgO,217.965540,Red or yellow solid.,"","","","","","","","Oral 
Inhalation 
Dermal 
(R022)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Catalase (P04040) 
Hemoglobin subunit alpha (P69905) 
Hemoglobin subunit beta (P68871) 
Hemoglobin subunit gamma-1 (P69891) 
Hemoglobin subunit gamma-2 (P69892) 
Hemoglobin subunit delta (P02042) 
Hemoglobin subunit epsilon (P02100) 
Hemoglobin subunit theta-1 (P09105) 
Hemoglobin subunit zeta (P02008) 
Hemoglobin subunit mu (Q6B0K9) 
(R022, R164) ","High-affinity binding of the divalent mercuric ion to thiol or sulfhydryl groups of proteins is believed to be the major mechanism for the activity of mercury. Through alterations in intracellular thiol status, mercury can promote oxidative stress, lipid peroxidation, mitochondrial dysfunction, and changes in heme metabolism. Mercury is known to bind to microsomal and mitochondrial enzymes, resulting in cell injury and death. For example, mercury is known to inhibit aquaporins, halting water flow across the cell membrane. It also inhibits the protein LCK, which causes decreased T-cell signalling and immune system depression. Mercury is also believed to inhibit neuronal excitability by acting on the postsynaptic neuronal membrane. It also affects the nervous system by inhibiting protein kinase C and alkaline phosphatase, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Mercury also produces an autoimmune response, likely by modification of major histocompatibility complex (MHC) class II molecules, self peptides, T-cell receptors, or cell-surface adhesion molecules. (R022, R025, R066, R067)","Mercury is absorbed mainly via ingestion and inhalation, then distributed throughout the body via the bloodstream, where a portion binds to sulfhydryl groups on haemoglobin. Mercury can undergo oxidation to mercuric mercury, which takes place via the catalase-hydrogen peroxide pathway. The mercury atom is able to diffuse down the cleft in the catalase enzyme to reach the active site where the heme ring is located. Oxidation most likely occurs in all tissue, as the catalase hydrogen peroxide pathway is ubiquitous. Following oxidation, mercury tends to accumulate in the kidneys. Mercury is excreted mainly by exhalation and in the faeces. (R021, R022)","LD50: 18 mg/kg (Oral, Rat) (R724)",1 gram for an adult human (average for inorganic mercurials). (R273),"3, not classifiable as to its carcinogenicity to humans. (R264)",Mercury(II) oxide is used in the production of mercury and as a material for cathodes for mercury batteries. (R723),Chronic Inhalation: 0.0002 mg/m3 (R260),"Mercury mainly affects the nervous system. Exposure to high levels of metallic, inorganic, or organic mercury can permanently damage the brain, kidneys, and developing fetus. Effects on brain functioning may result in irritability, shyness, tremors, changes in vision or hearing, and memory problems. Acrodynia, a type of mercury poisoning in children, is characterized by pain and pink discoloration of the hands and feet. Mercury poisoning can also cause Hunter-Russell syndrome and Minamata disease. (R022)","Common symptoms include peripheral neuropathy (presenting as paresthesia or itching, burning or pain), skin discoloration (pink cheeks, fingertips and toes), edema (swelling), and desquamation (dead skin peels off in layers). (R020)","Mercury poisoning is treated by immediate decontamination and chelation therapy using DMSA, DMPS, DPCN, or dimercaprol. (R023)",P06239;P05186;P29972;P55087;P55064;O14520;O94778;O43315;P30301;P17252;P05771;Q05655;Q02156;P24723;P05129;P41743;Q04759;Q05513;Q9UJT1;Q9UJT0;Q96PS8;Q8NBQ7;Q8IXF9;A6NM10;P41181;Q92482;Q13520;A6NKZ8 ;Q99867;Q9H853;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2;P23258;Q9NRH3
344,T3D0343,2009-03-06 18:58:34 UTC,2009-08-05 21:38:42 UTC,Mercury(I) chloride,Inorganic Compound;Mercury Compound,(dimercury) dichlorideCalogreenCalomelCalotabChlorure mercureuxChlorure mercureux [french]ClhghgclCyclosanDimercury dichlorideHg2-Cl2Hg2Cl2Hydrochloric acid mercury salt (1:1)KalomelMercurius Dulcis 3ch-30ch Gran and GlobMercurous chloride (Hg2Cl2)Mercury chlorideMercury chloride (Hg2Cl2)Mercury monochlorideMercury protochlorideMercury subchlorideMercury(I) chlorideMild mercury chlorideQuecksilber(I)-chloriddimercury(2+) chloride,"Mercury(I) chloride is a chloride of mercury that occurs naturally as the mineral calomel. It is used primarily for reference electrodes in electrochemistry. Mercury is a heavy, silvery d-block metal and one of six elements that are liquid at or near room temperature and pressure. It is a naturally occuring substance, and combines with other elements such as chlorine, sulfur, or oxygen to form inorganic mercury compounds (salts). Mercury also combines with carbon to make organic mercury compounds. (R005, R725)",,10112-91-1,24956,,"","",33050,"",,C015728,Mercury(I) chloride,,,,http://en.wikipedia.org/wiki/Mercurous chloride,InChI=1/2ClH.2Hg/h2*1H;;/q;;2*+1/p-2,chloromercury,http://www.biospider.ca/saved_files/mol/,Cl[Hg].Cl[Hg],Cl[Hg].Cl[Hg],Cl2Hg2,473.878960,White crystals.,525 °C (triple point),"","","0.002 mg/mL at 18 oC [SHIU,WY et al. (1990)]","","","","Oral 
Inhalation 
Dermal 
(R022)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Catalase (P04040) 
Hemoglobin subunit alpha (P69905) 
Hemoglobin subunit beta (P68871) 
Hemoglobin subunit gamma-1 (P69891) 
Hemoglobin subunit gamma-2 (P69892) 
Hemoglobin subunit delta (P02042) 
Hemoglobin subunit epsilon (P02100) 
Hemoglobin subunit theta-1 (P09105) 
Hemoglobin subunit zeta (P02008) 
Hemoglobin subunit mu (Q6B0K9) 
(R022, R164) ","High-affinity binding of the divalent mercuric ion to thiol or sulfhydryl groups of proteins is believed to be the major mechanism for the activity of mercury. Through alterations in intracellular thiol status, mercury can promote oxidative stress, lipid peroxidation, mitochondrial dysfunction, and changes in heme metabolism. Mercury is known to bind to microsomal and mitochondrial enzymes, resulting in cell injury and death. For example, mercury is known to inhibit aquaporins, halting water flow across the cell membrane. It also inhibits the protein LCK, which causes decreased T-cell signalling and immune system depression. Mercury is also believed to inhibit neuronal excitability by acting on the postsynaptic neuronal membrane. It also affects the nervous system by inhibiting protein kinase C and alkaline phosphatase, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Mercury also produces an autoimmune response, likely by modification of major histocompatibility complex (MHC) class II molecules, self peptides, T-cell receptors, or cell-surface adhesion molecules. (R022, R025, R066, R067)","Mercury is absorbed mainly via ingestion and inhalation, then distributed throughout the body via the bloodstream, where a portion binds to sulfhydryl groups on haemoglobin. Mercury can undergo oxidation to mercuric mercury, which takes place via the catalase-hydrogen peroxide pathway. The mercury atom is able to diffuse down the cleft in the catalase enzyme to reach the active site where the heme ring is located. Oxidation most likely occurs in all tissue, as the catalase hydrogen peroxide pathway is ubiquitous. Following oxidation, mercury tends to accumulate in the kidneys. Mercury is excreted mainly by exhalation and in the faeces. (R021, R022)","LD50: 210 mg/kg (Oral, Rat) (R726)",1 gram for an adult human (average for inorganic mercurials). (R273),"3, not classifiable as to its carcinogenicity to humans. (R264)",Mercury(I) chloride is used primarily for reference electrodes in electrochemistry. (R725),Chronic Inhalation: 0.0002 mg/m3 (R260),"Mercury mainly affects the nervous system. Exposure to high levels of metallic, inorganic, or organic mercury can permanently damage the brain, kidneys, and developing fetus. Effects on brain functioning may result in irritability, shyness, tremors, changes in vision or hearing, and memory problems. Acrodynia, a type of mercury poisoning in children, is characterized by pain and pink discoloration of the hands and feet. Mercury poisoning can also cause Hunter-Russell syndrome and Minamata disease. (R022)","Common symptoms include peripheral neuropathy (presenting as paresthesia or itching, burning or pain), skin discoloration (pink cheeks, fingertips and toes), edema (swelling), and desquamation (dead skin peels off in layers). (R020)","Mercury poisoning is treated by immediate decontamination and chelation therapy using DMSA, DMPS, DPCN, or dimercaprol. (R023)",P06239;P05186;P29972;P55087;P55064;O14520;O94778;O43315;P30301;P17252;P05771;Q05655;Q02156;P24723;P05129;P41743;Q04759;Q05513;P68366;Q9UJT1;Q9UJT0;Q96PS8;Q8NBQ7;Q8IXF9;A6NM10;P41181;Q92482;Q13520;A6NKZ8 ;Q99867;Q9H853;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2;P23258;Q9NRH3
345,T3D0344,2009-03-06 18:58:34 UTC,2009-08-04 21:28:21 UTC,Phenylmercuric acetate,Organic Compound;Mercury Compound;Organometallic;Aromatic Hydrocarbon,"(acetato)phenylmercury(acetato-kappao)(phenyl)mercury(acetato-o)phenylmercury(aceto)phenylmercury(acetoxymercuri)benzene(acetoxymercurio)-benzeneAcetate de phenylmercure [iso-french]Acetate phenylmercuriqueAcetate phenylmercurique (french)Acetate phenylmercurique [french]Acetato(phenyl)mercuryAcetic acid, phenylmercury derivAcetic acid, phenylmercury deriv.Acetic acid, phenylmercury(II) saltAcetoxyphenylmercuryAdvacide PMA 18AgrosanAgrosan dAgrosan gn 5AlgimycinAlgimycin 200AnticonAntimucin WBRAntimucin WDRBenzene, (acetoxymercuri)-Benzene, (acetoxymercurio)-BufenBufen 30C.I. Pigment Green 2Caswell No. 656CekusilCelmerCeresanCeresan universalCeresolContra cremeCosan pmaDyanacideFMAFemmaFenylmercuriacetatFenylmercuriacetat (czech)Fenylmercuriacetat [czech]Fenylmerkuriacetat [czech]Fungicide rFungitoxFungitox orGallotoxHexasanHexasan (fungicide)Hexasan, fungicideHong nienHostaquickHostaquikIntercide 60Intercide PMA 18KwiksanLeytosanLiquipheneLorophynMeracenMercronMercuriphenyl acetateMercuronMercury phenyl acetateMercury(II) acetate, phenyl-Mercury, (acetato)phenyl-Mercury, (acetato-kappao)phenyl-Mercury, (acetato-o)phenyl-Mercury, acetoxyphenyl-Mergal A 25Mergal A25MersoliteMersolite 8Mersolite dMetasol 30NeantinaNildew AC 30NorformsNuodex PMA 18NylmerateOctan fenylrtutnatyOctan fenylrtutnaty (czech)Octan fenylrtutnaty [czech]PHIXPMAPMACPMALPMASPamisanPanomaticParasanParasan (bactericide)PhenmadPhenomercuric acetatePhenyl mercuric acetatePhenylmercuriacetatePhenylmercuric acetatePhenylmercuric acetate (NF)Phenylmercuric acetate [UN1674] [Poison]Phenylmercuric acetate [usan]Phenylmercury acetatePhenylmercury acetate [bsi:iso]Phenylmercury acetate [mercury and mercury compounds]Phenylmercury deriv.Phenylmercury(II) acetatePhenylmercury(II)acetatePhenylquecksilberacetatPhenylquecksilberacetat (german)Phenylquecksilberacetat [german]PhenylquecksilberacetatePma (fungicide)PmacetatePrograminPurasan-sc-10Puraturf 10QuicksanQuicksan 20RCRA waste no. P092RCRA waste number P092RiogenRuberonSamtolSanitized SPGSanitolSanmicronScutlSeed dressing rSeedtoxSetreteShimmer-exShimmerexSpor-kilSpruce sealTAGTag (van)Tag HL 331Tag HL-331Tag fungicideTrigosanTroysan 30Troysan PMA 30UnisanVerdasanVerdasan (van)VolparWLN: 1VO-HG-RZaprawa nasienna rZiarnik","Phenylmercuric acetate is an organomercuric compound. It is used as a fungicide. Mercury is a heavy, silvery d-block metal and one of six elements that are liquid at or near room temperature and pressure. It is a naturally occuring substance, and combines with other elements such as chlorine, sulfur, or oxygen to form inorganic mercury compounds (salts). Mercury also combines with carbon to make organic mercury compounds. (R005, R486)",,62-38-4,16682730,,C11151,"",27684,"",,D010662,Phenylmercuric acetate,1175,,,,"InChI=1/C6H5.C2H4O2.Hg/c1-2-4-6-5-3-1;1-2(3)4;/h1-5H;1H3,(H,3,4);/q;;+1/p-1",acetyloxy(phenyl)mercury,http://www.biospider.ca/saved_files/mol/d01de9fd9067a36f90a39dd38c922a58_1237972566.mol,CC(=O)O[Hg]C1=CC=CC=C1,CC(=O)O[Hg]C1=CC=CC=C1,C8H8HgO2,338.023060,White crystals.,153 oC,"","","4.37 mg/mL at 15 oC [TOMLIN,C (1994)]","","","","Oral 
Inhalation 
Dermal 
(R022)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Catalase (P04040) 
Hemoglobin subunit alpha (P69905) 
Hemoglobin subunit beta (P68871) 
Hemoglobin subunit gamma-1 (P69891) 
Hemoglobin subunit gamma-2 (P69892) 
Hemoglobin subunit delta (P02042) 
Hemoglobin subunit epsilon (P02100) 
Hemoglobin subunit theta-1 (P09105) 
Hemoglobin subunit zeta (P02008) 
Hemoglobin subunit mu (Q6B0K9) 
(R022, R164) ","High-affinity binding of the divalent mercuric ion to thiol or sulfhydryl groups of proteins is believed to be the major mechanism for the activity of mercury. Through alterations in intracellular thiol status, mercury can promote oxidative stress, lipid peroxidation, mitochondrial dysfunction, and changes in heme metabolism. Mercury is known to bind to microsomal and mitochondrial enzymes, resulting in cell injury and death. For example, mercury is known to inhibit aquaporins, halting water flow across the cell membrane. It also inhibits the protein LCK, which causes decreased T-cell signalling and immune system depression. Mercury is also believed to inhibit neuronal excitability by acting on the postsynaptic neuronal membrane. It also affects the nervous system by inhibiting protein kinase C and alkaline phosphatase, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Organic mercury exerts developmental effects by binding to tubulin, preventing microtubule assembly and causing mitotic inhibition. Mercury also produces an autoimmune response, likely by modification of major histocompatibility complex (MHC) class II molecules, self peptides, T-cell receptors, or cell-surface adhesion molecules. (R022, R025, R066, R067)","Organic mercury is absorbed mainly by the gastrointestinal tract, then distributed throughout the body via the bloodstream. Organic mercury complexes with free cysteine and the cysteine and sulfhydryl groups on proteins such as haemoglobin. These complexes are able to mimic methionine and thus be transported throughout the body, including through the blood-brain barrier and placenta. Organic mercury is metabolized into inorganic mercury, which is eventually excreted in the urine and faeces. (R033)","LD50: 22 mg/kg (Oral, Rat) (R603)",100 mg for an adult human (average for organic mercurials). (R273),"2B, possibly carcinogenic to humans. (R264)","Phenylmercuric acetate is used mainly as a fungicide, herbicide, slimicide, and bacteriocide. (R486)",Chronic Inhalation: 0.0002 mg/m3 (R260),"Mercury mainly affects the nervous system. Exposure to high levels of metallic, inorganic, or organic mercury can permanently damage the brain, kidneys, and developing fetus. Effects on brain functioning may result in irritability, shyness, tremors, changes in vision or hearing, and memory problems. Acrodynia, a type of mercury poisoning in children, is characterized by pain and pink discoloration of the hands and feet. Mercury poisoning can also cause Hunter-Russell syndrome and Minamata disease. (R022)","Common symptoms include peripheral neuropathy (presenting as paresthesia or itching, burning or pain), skin discoloration (pink cheeks, fingertips and toes), edema (swelling), and desquamation (dead skin peels off in layers). (R020)","Mercury poisoning is treated by immediate decontamination and chelation therapy using DMSA, DMPS, DPCN, or dimercaprol. (R023)",P06239;P05186;P29972;P55087;P55064;O14520;O94778;O43315;P30301;P17252;P05771;Q05655;Q02156;P24723;P05129;P41743;Q04759;Q05513;Q9UJT1;Q9UJT0;Q96PS8;Q8NBQ7;Q8IXF9;A6NM10;P41181;Q92482;Q13520;A6NKZ8 ;Q99867;Q9H853;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2;P23258;Q9NRH3
346,T3D0345,2009-03-06 18:58:34 UTC,2009-08-05 21:38:43 UTC,Mercury selenide,Inorganic Compound;Mercury Compound;Selenium Compound,Mercuric selenide,"Mercury selenide is a chemical compound of mercury and selenium that occurs naturally as the mineral tiemannite. It is used as an ohmic contact to wide-gap II-VI semconductors. Mercury is a heavy, silvery d-block metal and one of six elements that are liquid at or near room temperature and pressure. It is a naturally occuring substance, and combines with other elements such as chlorine, sulfur, or oxygen to form inorganic mercury compounds (salts). Mercury also combines with carbon to make organic mercury compounds. Selenium is a nonmetal element with the atomic number 34 and the chemical symbol Se. Selenium rarely occurs in its elemental state in nature and is usually found in sulfide ores such as pyrite, partially replacing the sulfur in the ore matrix. It may also be found in silver, copper, lead, and nickel minerals. Though selenium salts are toxic in large amounts, trace amounts of the element are necessary for cellular function in most animals, forming the active center of the enzymes glutathione peroxidase, thioredoxin reductase, and three known deiodinase enzymes. (R976, R005, R727)",,20601-83-6,9838575,,"","","","",,C032901,Mercury selenide,,,,http://en.wikipedia.org/wiki/mercury selenide,InChI=1/Hg.Se,mercury(2+); selenium(2-),http://www.biospider.ca/saved_files/mol/,[Se-2].[Hg+2],[Se-2].[Hg+2],HgSe,281.887150,Grey/black solid.,1270 K,"","","","","","","Oral 
Inhalation 
Dermal 
(R022)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Catalase (P04040) 
Hemoglobin subunit alpha (P69905) 
Hemoglobin subunit beta (P68871) 
Hemoglobin subunit gamma-1 (P69891) 
Hemoglobin subunit gamma-2 (P69892) 
Hemoglobin subunit delta (P02042) 
Hemoglobin subunit epsilon (P02100) 
Hemoglobin subunit theta-1 (P09105) 
Hemoglobin subunit zeta (P02008) 
Hemoglobin subunit mu (Q6B0K9) 
(R022, R164) ","High-affinity binding of the divalent mercuric ion to thiol or sulfhydryl groups of proteins is believed to be the major mechanism for the activity of mercury. Through alterations in intracellular thiol status, mercury can promote oxidative stress, lipid peroxidation, mitochondrial dysfunction, and changes in heme metabolism. Mercury is known to bind to microsomal and mitochondrial enzymes, resulting in cell injury and death. For example, mercury is known to inhibit aquaporins, halting water flow across the cell membrane. It also inhibits the protein LCK, which causes decreased T-cell signalling and immune system depression. Mercury is also believed to inhibit neuronal excitability by acting on the postsynaptic neuronal membrane. It also affects the nervous system by inhibiting protein kinase C and alkaline phosphatase, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Mercury also produces an autoimmune response, likely by modification of major histocompatibility complex (MHC) class II molecules, self peptides, T-cell receptors, or cell-surface adhesion molecules. Selenium readily substitutes for sulfur in biomolecules and in many biochemical reactions, especially when the concentration of selenium is high and the concentration of sulfur is low. Inactivation of the sulfhydryl enzymes necessary for oxidative reactions in cellular respiration, through effects on mitochondrial and microsomal electron transport, might contribute to acute selenium toxicity. Selenomethionine (a common organic selenium compound) also appears to randomly substitute for methionine in protein synthesis. This substitution may affect the structure and functionability of the protein, for example, by altering disulfide bridges. Inorganic forms of selenium appear to react with tissue thiols by redox catalysis, resulting in formation of reactive oxygen species and causing damage by oxidative stress. (R975, R022, R025, R066, R067)","Mercury is absorbed mainly via ingestion and inhalation, then distributed throughout the body via the bloodstream, where a portion binds to sulfhydryl groups on haemoglobin. Mercury can undergo oxidation to mercuric mercury, which takes place via the catalase-hydrogen peroxide pathway. The mercury atom is able to diffuse down the cleft in the catalase enzyme to reach the active site where the heme ring is located. Oxidation most likely occurs in all tissue, as the catalase hydrogen peroxide pathway is ubiquitous. Following oxidation, mercury tends to accumulate in the kidneys. Mercury is excreted mainly by exhalation and in the faeces. Selenium may be absorbed through inhalation and ingestion, while some selenium compounds may also be absorbed dermally. Once in the body, selenium is distributed mainly to the liver and kidney. Selenium is an essential micronutrient and is a component of glutathione peroxidase, iodothyronine 5'-deiodinases, and thioredoxin reductase. Organic selenium is first metabolized into inorganic selenium. Inorganic selenium is reduced stepwise to the intermediate hydrogen selenide, which is either incorporated into selenoproteins after being transformed to selenophosphate and selenocysteinyl tRNA or excreted into the urine after being transformed into methylated metabolites of selenide. Elemental selenium is also methylated before excretion. Selenium is primarily eliminated in the urine and feces, but certain selenium compounds may also be exhaled. (R975, R021, R022)",No data.,1 gram for an adult human (average for inorganic mercurials). (R273),"3, not classifiable as to its carcinogenicity to humans. (R264)",Mercury selenide is used as an ohmic contact to wide-gap II-VI semconductors. It is also a byproduct of steel processing. (R727),"Chronic Inhalation: 0.0002 mg/m3 (Mercury) (R260)
Chronic Oral: 0.005 mg/kg/day (Selenium) (R260)","Mercury mainly affects the nervous system. Exposure to high levels of metallic, inorganic, or organic mercury can permanently damage the brain, kidneys, and developing fetus. Effects on brain functioning may result in irritability, shyness, tremors, changes in vision or hearing, and memory problems. Acrodynia, a type of mercury poisoning in children, is characterized by pain and pink discoloration of the hands and feet. Mercury poisoning can also cause Hunter-Russell syndrome and Minamata disease. Chronic oral exposure to high concentrations of selenium compounds can produce a disease called selenosis. The major signs of selenosis are hair loss, nail brittleness, and neurological abnormalities (such as numbness and other odd sensations in the extremities). Animal studies have shown that selenium may also affect sperm production and the female reproductive cycle. (R975, R022)","Common symptoms include peripheral neuropathy (presenting as paresthesia or itching, burning or pain), skin discoloration (pink cheeks, fingertips and toes), edema (swelling), and desquamation (dead skin peels off in layers). Short-term oral exposure to high concentrations of selenium may cause nausea, vomiting, and diarrhea. Brief exposures to high levels of elemental selenium or selenium dioxide in air can result in respiratory tract irritation, bronchitis, difficulty breathing, and stomach pains. Longer-term exposure to either of these air-borne forms can cause respiratory irritation, bronchial spasms, and coughing. (R975, R020)","Mercury poisoning is treated by immediate decontamination and chelation therapy using DMSA, DMPS, DPCN, or dimercaprol. (R023)",P06239;P05186;P29972;P55087;P55064;O14520;O94778;O43315;P30301;P17252;P05771;Q05655;Q02156;P24723;P05129;P41743;Q04759;Q05513;P68371;Q9UJT1;Q9UJT0;Q96PS8;Q8NBQ7;Q8IXF9;A6NM10;P41181;Q92482;Q13520;A6NKZ8 ;Q99867;Q9H853;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2;P23258;Q9NRH3
347,T3D0346,2009-03-06 18:58:35 UTC,2009-08-05 21:38:43 UTC,Mercury telluride,Inorganic Compound;Mercury Compound,Mercurous tellurideMercury tellurideMercury telluride (hgte),"Mercury telluride is a chemical compound of mercury and tellurium that occurs naturally as the mineral coloradoite. It is found in semiconductors. Mercury is a heavy, silvery d-block metal and one of six elements that are liquid at or near room temperature and pressure. It is a naturally occuring substance, and combines with other elements such as chlorine, sulfur, or oxygen to form inorganic mercury compounds (salts). Mercury also combines with carbon to make organic mercury compounds. (R005, R728)",,12068-90-5,82914,,"","","","",,,Mercury telluride,,,,http://en.wikipedia.org/wiki/mercury(II) telluride,InChI=1/Hg.Te,tellanylidenemercury,http://www.biospider.ca/saved_files/mol/,[Te]=[Hg],[Te]=[Hg],HgTe,331.876850,Black crystals.,943 K,"","","","","","","Oral 
Inhalation 
Dermal 
(R022)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Catalase (P04040) 
Hemoglobin subunit alpha (P69905) 
Hemoglobin subunit beta (P68871) 
Hemoglobin subunit gamma-1 (P69891) 
Hemoglobin subunit gamma-2 (P69892) 
Hemoglobin subunit delta (P02042) 
Hemoglobin subunit epsilon (P02100) 
Hemoglobin subunit theta-1 (P09105) 
Hemoglobin subunit zeta (P02008) 
Hemoglobin subunit mu (Q6B0K9) 
(R022, R164) ","High-affinity binding of the divalent mercuric ion to thiol or sulfhydryl groups of proteins is believed to be the major mechanism for the activity of mercury. Through alterations in intracellular thiol status, mercury can promote oxidative stress, lipid peroxidation, mitochondrial dysfunction, and changes in heme metabolism. Mercury is known to bind to microsomal and mitochondrial enzymes, resulting in cell injury and death. For example, mercury is known to inhibit aquaporins, halting water flow across the cell membrane. It also inhibits the protein LCK, which causes decreased T-cell signalling and immune system depression. Mercury is also believed to inhibit neuronal excitability by acting on the postsynaptic neuronal membrane. It also affects the nervous system by inhibiting protein kinase C and alkaline phosphatase, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Mercury also produces an autoimmune response, likely by modification of major histocompatibility complex (MHC) class II molecules, self peptides, T-cell receptors, or cell-surface adhesion molecules. (R022, R025, R066, R067)","Mercury is absorbed mainly via ingestion and inhalation, then distributed throughout the body via the bloodstream, where a portion binds to sulfhydryl groups on haemoglobin. Mercury can undergo oxidation to mercuric mercury, which takes place via the catalase-hydrogen peroxide pathway. The mercury atom is able to diffuse down the cleft in the catalase enzyme to reach the active site where the heme ring is located. Oxidation most likely occurs in all tissue, as the catalase hydrogen peroxide pathway is ubiquitous. Following oxidation, mercury tends to accumulate in the kidneys. Mercury is excreted mainly by exhalation and in the faeces. (R021, R022)",No data.,1 gram for an adult human (average for inorganic mercurials). (R273),"3, not classifiable as to its carcinogenicity to humans. (R264)",Mercury telluride is used as a semiconductor. (R728),Chronic Inhalation: 0.0002 mg/m3 (R260),"Mercury mainly affects the nervous system. Exposure to high levels of metallic, inorganic, or organic mercury can permanently damage the brain, kidneys, and developing fetus. Effects on brain functioning may result in irritability, shyness, tremors, changes in vision or hearing, and memory problems. Acrodynia, a type of mercury poisoning in children, is characterized by pain and pink discoloration of the hands and feet. Mercury poisoning can also cause Hunter-Russell syndrome and Minamata disease. (R022)","Common symptoms include peripheral neuropathy (presenting as paresthesia or itching, burning or pain), skin discoloration (pink cheeks, fingertips and toes), edema (swelling), and desquamation (dead skin peels off in layers). (R020)","Mercury poisoning is treated by immediate decontamination and chelation therapy using DMSA, DMPS, DPCN, or dimercaprol. (R023)",P06239;P05186;P29972;P55087;P55064;O14520;O94778;O43315;P30301;P17252;P05771;Q05655;Q02156;P24723;P05129;P41743;Q04759;Q05513;Q9UJT1;Q9UJT0;Q96PS8;Q8NBQ7;Q8IXF9;A6NM10;P41181;Q92482;Q13520;A6NKZ8 ;Q99867;Q9H853;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2;P23258;Q9NRH3
348,T3D0347,2009-03-06 18:58:35 UTC,2009-08-05 21:38:43 UTC,Mercury cadmium telluride,Inorganic Compound;Mercury Compound;Cadmium Compound,"Cadmium mercury tellurideCadmium mercury telluride ((CD,hg)te)Mercury cadmium telluride","Mercury cadmium telluride is an alloy of mercury telluride and cadmium telluride. It is an important semiconductor and also used in infrared detection. Mercury is a heavy, silvery d-block metal and one of six elements that are liquid at or near room temperature and pressure. It is a naturally occuring substance, and combines with other elements such as chlorine, sulfur, or oxygen to form inorganic mercury compounds (salts). Mercury also combines with carbon to make organic mercury compounds. (R005, R729)",,29870-72-2,94407,,"","","","",,C104191,Mercury cadmium telluride,,,,,InChI=1/Cd.Hg.Te,"",http://www.biospider.ca/saved_files/mol/,[Cd]=[Te]=[Hg],[Cd]=[Te]=[Hg],CdHgTe,445.780210,Black crystals.,"","","","","","","","Oral 
Inhalation 
Dermal 
(R022)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Catalase (P04040) 
Hemoglobin subunit alpha (P69905) 
Hemoglobin subunit beta (P68871) 
Hemoglobin subunit gamma-1 (P69891) 
Hemoglobin subunit gamma-2 (P69892) 
Hemoglobin subunit delta (P02042) 
Hemoglobin subunit epsilon (P02100) 
Hemoglobin subunit theta-1 (P09105) 
Hemoglobin subunit zeta (P02008) 
Hemoglobin subunit mu (Q6B0K9)
Serum albumin (P02768) 
(R019, R022, R164) ","High-affinity binding of the divalent mercuric ion to thiol or sulfhydryl groups of proteins is believed to be the major mechanism for the activity of mercury. Through alterations in intracellular thiol status, mercury can promote oxidative stress, lipid peroxidation, mitochondrial dysfunction, and changes in heme metabolism. Mercury is known to bind to microsomal and mitochondrial enzymes, resulting in cell injury and death. For example, mercury is known to inhibit aquaporins, halting water flow across the cell membrane. It also inhibits the protein LCK, which causes decreased T-cell signalling and immune system depression. Mercury is also believed to inhibit neuronal excitability by acting on the postsynaptic neuronal membrane. It also affects the nervous system by inhibiting protein kinase C and alkaline phosphatase, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Mercury also produces an autoimmune response, likely by modification of major histocompatibility complex (MHC) class II molecules, self peptides, T-cell receptors, or cell-surface adhesion molecules. Cadmium initially binds to metallothionein and is transported to the kidney. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Accumulation of cadmium in the kidney results in increased excretion of vital low and high weight molecular proteins. Cadmium is a high affinity zinc analog and can interfere in its biological processes. It also binds to and activates the estrogen receptor, likely stimulating the growth of certain types of cancer cells and causing other estrogenic effects, such as reproductive dysfunction. Cadmium causes cell apoptosis by activating mitogen-activated protein kinases. (R022, R025, R026, R058, R059, R066, R067, R069)","Cadmium and mercury may be absorbed from oral, inhalation, and dermal routes.  Mercury is distributed throughout the body via the bloodstream, where a portion binds to sulfhydryl groups on haemoglobin. Mercury can undergo oxidation to mercuric mercury, which takes place via the catalase-hydrogen peroxide pathway. The mercury atom is able to diffuse down the cleft in the catalase enzyme to reach the active site where the heme ring is located. Oxidation most likely occurs in all tissue, as the catalase hydrogen peroxide pathway is ubiquitous. Following oxidation, mercury tends to accumulate in the kidneys. Mercury is excreted mainly by exhalation and in the faeces. Cadmium initially binds to metallothionein and albumin and is transported mainly to the kidney and liver. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Cadmium is not known to undergo any direct metabolic conversion and is excreted unchanged, mainly in the urine. (R019, R021, R022)",No data.,1 gram for an adult human (average for inorganic mercurials). (R273),"3, not classifiable as to its carcinogenicity to humans. (R264)",Mercury cadmium telluride is an important semiconductor and also used in infrared detection. (R729),"Chronic Inhalation: 0.0002 mg/m3 (Mercury) (R260) 
Acute Inhalation: 0.00003 mg/m3 (Cadmium) (R260) 
Chronic Inhalation: 0.00001 mg/m3 (Cadmium) (R260) 
Intermediate Oral: 0.0005 mg/kg/day (Cadmium) (R260) 
Chronic Oral: 0.0001 mg/kg/day (Cadmium) (R260)","Mercury mainly affects the nervous system. Exposure to high levels of metallic, inorganic, or organic mercury can permanently damage the brain, kidneys, and developing fetus. Effects on brain functioning may result in irritability, shyness, tremors, changes in vision or hearing, and memory problems. Acrodynia, a type of mercury poisoning in children, is characterized by pain and pink discoloration of the hands and feet. Mercury poisoning can also cause Hunter-Russell syndrome and Minamata disease. Chronic exposure to cadmium fumes can cause chemical pneumonitis, pulmonary edema, and lung diseases such as bronchitis and emphysema. Cadmium also accumulates in the kidneys, causing permanent damage. Loss of bone density also occurs. (R019, R022)","Common symptoms of mercury poisoning include peripheral neuropathy (presenting as paresthesia or itching, burning or pain), skin discoloration (pink cheeks, fingertips and toes), edema (swelling), and desquamation (dead skin peels off in layers). Acute inhalation of cadmium fumes results in metal fume fever, which is characterized by chills, fever, headache, weakness, dryness of the nose and throat, chest pain, and coughing. Ingestion of cadmium causes vomiting and diarrhea. (R019, R020)","Mercury poisoning is treated by immediate decontamination and chelation therapy using DMSA, DMPS, DPCN, or dimercaprol. Cadmium poisoning is treated by removal from exposure and supportive care. If ingested, induced vomiting or gastric lavage may be performed. (R023, R272)",P06239;P05186;P29972;P55087;P55064;O14520;O94778;O43315;P30301;P17252;P05771;Q05655;Q02156;P24723;P05129;P41743;Q04759;Q05513;Q9UJT1;Q9UJT0;Q9UQF2;Q13387;Q9UPT6;O60271;P03372;Q92731;P28482;P53779;Q15759;P53778;O15264;Q16539;Q8TD08;P27361;P31152;Q16659;Q13164;P45983;P45984;Q96PS8;Q8NBQ7;Q8IXF9;A6NM10;P41181;Q92482;Q13520;A6NKZ8 ;Q99867;Q9H853;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2;P23258;Q9NRH3
349,T3D0348,2009-03-06 18:58:35 UTC,2009-08-25 18:01:48 UTC,Mercury(II) acetate,Organic Compound;Mercury Compound;Organometallic,"Acetic acid, mercuridi-Acetic acid, mercury(2+) saltBis(acetyloxy)mercuryCaswell No. 543ADiacetoxymercuryMercuriacetateMercuric acetateMercuric acetate [mercury and mercury compounds]Mercuric diacetateMercury acetateMercury acetate (Hg(CH3CO2)2)Mercury acetate (Hg(O2C2H3)2)Mercury acetate [UN1629] [Poison]Mercury di(acetate)Mercury diacetateMercury(2+) acetateMercury(II) acetateMercuryl acetate","Mercury(II) acetate is chemical compound of mercury used mainly in the synthesis of organomercury compounds. Mercury is a heavy, silvery d-block metal and one of six elements that are liquid at or near room temperature and pressure. It is a naturally occuring substance, and combines with other elements such as chlorine, sulfur, or oxygen to form inorganic mercury compounds (salts). Mercury also combines with carbon to make organic mercury compounds. (R005, R730)",,1600-27-7,15337,,C00033,"276100
601705",33211,ACET,,C029823,Mercury(II) acetate,,,,,"InChI=1/C2H4O2/c1-2(3)4/h1H3,(H,3,4)",mercury(2+) diacetate,http://www.biospider.ca/saved_files/mol/,CC(=O)[O-].CC(=O)[O-].[Hg+2],CC(=O)O[Hg]OC(C)=O,C4H6HgO4,319.997230,White crystals.,178-180 oC,"","","250 mg/mL at 10 oC [ROSENBLATT,DH et al. (1975)]","","","","Oral 
Inhalation 
Dermal 
(R022)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Catalase (P04040) 
Hemoglobin subunit alpha (P69905) 
Hemoglobin subunit beta (P68871) 
Hemoglobin subunit gamma-1 (P69891) 
Hemoglobin subunit gamma-2 (P69892) 
Hemoglobin subunit delta (P02042) 
Hemoglobin subunit epsilon (P02100) 
Hemoglobin subunit theta-1 (P09105) 
Hemoglobin subunit zeta (P02008) 
Hemoglobin subunit mu (Q6B0K9) 
(R022, R164) ","High-affinity binding of the divalent mercuric ion to thiol or sulfhydryl groups of proteins is believed to be the major mechanism for the activity of mercury. Through alterations in intracellular thiol status, mercury can promote oxidative stress, lipid peroxidation, mitochondrial dysfunction, and changes in heme metabolism. Mercury is known to bind to microsomal and mitochondrial enzymes, resulting in cell injury and death. For example, mercury is known to inhibit aquaporins, halting water flow across the cell membrane. It also inhibits the protein LCK, which causes decreased T-cell signalling and immune system depression. Mercury is also believed to inhibit neuronal excitability by acting on the postsynaptic neuronal membrane. It also affects the nervous system by inhibiting protein kinase C and alkaline phosphatase, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Mercury also produces an autoimmune response, likely by modification of major histocompatibility complex (MHC) class II molecules, self peptides, T-cell receptors, or cell-surface adhesion molecules. (R022, R025, R066, R067)","Mercury is absorbed mainly via ingestion and inhalation, then distributed throughout the body via the bloodstream, where a portion binds to sulfhydryl groups on haemoglobin. Mercury can undergo oxidation to mercuric mercury, which takes place via the catalase-hydrogen peroxide pathway. The mercury atom is able to diffuse down the cleft in the catalase enzyme to reach the active site where the heme ring is located. Oxidation most likely occurs in all tissue, as the catalase hydrogen peroxide pathway is ubiquitous. Following oxidation, mercury tends to accumulate in the kidneys. Mercury is excreted mainly by exhalation and in the faeces. (R021, R022)","LD50: 41 mg/kg (Oral, Rat) (R731)
LD50: 570 mg/kg (Dermal, Rat) (R731)
LD50: 6.5 mg (Intraperitoneal, Mouse) (R731)
LD50: 4.4 mg (Intravenous, Mouse ) (R731)",1 gram for an adult human (average for inorganic mercurials). (R273),"3, not classifiable as to its carcinogenicity to humans. (R264)",Mercury(II) acetate is used mainly in the synthesis of organomercury compounds. (R730),Chronic Inhalation: 0.0002 mg/m3 (R260),"Mercury mainly affects the nervous system. Exposure to high levels of metallic, inorganic, or organic mercury can permanently damage the brain, kidneys, and developing fetus. Effects on brain functioning may result in irritability, shyness, tremors, changes in vision or hearing, and memory problems. Acrodynia, a type of mercury poisoning in children, is characterized by pain and pink discoloration of the hands and feet. Mercury poisoning can also cause Hunter-Russell syndrome and Minamata disease. (R022)","Common symptoms include peripheral neuropathy (presenting as paresthesia or itching, burning or pain), skin discoloration (pink cheeks, fingertips and toes), edema (swelling), and desquamation (dead skin peels off in layers). (R020)","Mercury poisoning is treated by immediate decontamination and chelation therapy using DMSA, DMPS, DPCN, or dimercaprol. (R023)",P06239;P05186;P29972;P55087;P55064;O14520;O94778;O43315;P30301;P17252;P05771;Q05655;Q02156;P24723;P05129;P41743;Q04759;Q05513;P68371;Q9UJT1;Q9UJT0;Q96PS8;Q8NBQ7;Q8IXF9;A6NM10;P41181;Q92482;Q13520;A6NKZ8 ;Q99867;Q9H853;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2;P23258;Q9NRH3
350,T3D0349,2009-03-06 18:58:35 UTC,2009-08-25 18:01:52 UTC,Mercury(I) acetate,Organic Compound;Mercury Compound;Organometallic,"Acetic acid, mercury (1+) saltDimercury di(acetate)Mercurous acetateMercury acetateMercury acetate (hgoac)Mercury monoacetate","Mercury(I) acetate is a chemical compound of mercury. Mercury is a heavy, silvery d-block metal and one of six elements that are liquid at or near room temperature and pressure. It is a naturally occuring substance, and combines with other elements such as chlorine, sulfur, or oxygen to form inorganic mercury compounds (salts). Mercury also combines with carbon to make organic mercury compounds. (R005)",,631-60-7,61181,,"","",33210,"",,,Mercury(I) acetate,,,,,"InChI=1/C2H4O2.Hg/c1-2(3)4;/h1H3,(H,3,4);/q;+1/p-1",mercury(1+) acetate,http://www.biospider.ca/saved_files/mol/,CC(=O)[O-].[Hg+],CC(=O)O[Hg],C2H3HgO2,260.983930,No data.,"","","","","","","","Oral 
Inhalation 
Dermal 
(R022)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Catalase (P04040) 
Hemoglobin subunit alpha (P69905) 
Hemoglobin subunit beta (P68871) 
Hemoglobin subunit gamma-1 (P69891) 
Hemoglobin subunit gamma-2 (P69892) 
Hemoglobin subunit delta (P02042) 
Hemoglobin subunit epsilon (P02100) 
Hemoglobin subunit theta-1 (P09105) 
Hemoglobin subunit zeta (P02008) 
Hemoglobin subunit mu (Q6B0K9) 
(R022, R164) ","High-affinity binding of the divalent mercuric ion to thiol or sulfhydryl groups of proteins is believed to be the major mechanism for the activity of mercury. Through alterations in intracellular thiol status, mercury can promote oxidative stress, lipid peroxidation, mitochondrial dysfunction, and changes in heme metabolism. Mercury is known to bind to microsomal and mitochondrial enzymes, resulting in cell injury and death. For example, mercury is known to inhibit aquaporins, halting water flow across the cell membrane. It also inhibits the protein LCK, which causes decreased T-cell signalling and immune system depression. Mercury is also believed to inhibit neuronal excitability by acting on the postsynaptic neuronal membrane. It also affects the nervous system by inhibiting protein kinase C and alkaline phosphatase, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Mercury also produces an autoimmune response, likely by modification of major histocompatibility complex (MHC) class II molecules, self peptides, T-cell receptors, or cell-surface adhesion molecules. (R022, R025, R066, R067)","Mercury is absorbed mainly via ingestion and inhalation, then distributed throughout the body via the bloodstream, where a portion binds to sulfhydryl groups on haemoglobin. Mercury can undergo oxidation to mercuric mercury, which takes place via the catalase-hydrogen peroxide pathway. The mercury atom is able to diffuse down the cleft in the catalase enzyme to reach the active site where the heme ring is located. Oxidation most likely occurs in all tissue, as the catalase hydrogen peroxide pathway is ubiquitous. Following oxidation, mercury tends to accumulate in the kidneys. Mercury is excreted mainly by exhalation and in the faeces. (R021, R022)","LD50: 23900 ug/kg (oral, mouse) (S270); LD50: 40900 ug/kg (oral, rat) (S270); LD50: 570 mg/kg (dermal, rat) (S270).",1 gram for an adult human (average for inorganic mercurials). (R273),"3, not classifiable as to its carcinogenicity to humans. (R264)",No data.,Chronic Inhalation: 0.0002 mg/m3 (R260),"Mercury mainly affects the nervous system. Exposure to high levels of metallic, inorganic, or organic mercury can permanently damage the brain, kidneys, and developing fetus. Effects on brain functioning may result in irritability, shyness, tremors, changes in vision or hearing, and memory problems. Acrodynia, a type of mercury poisoning in children, is characterized by pain and pink discoloration of the hands and feet. Mercury poisoning can also cause Hunter-Russell syndrome and Minamata disease. (R022)","Common symptoms include peripheral neuropathy (presenting as paresthesia or itching, burning or pain), skin discoloration (pink cheeks, fingertips and toes), edema (swelling), and desquamation (dead skin peels off in layers). (R020)","Mercury poisoning is treated by immediate decontamination and chelation therapy using DMSA, DMPS, DPCN, or dimercaprol. (R023)",P06239;P05186;P29972;P55087;P55064;O14520;O94778;O43315;P30301;P17252;P05771;Q05655;Q02156;P24723;P05129;P41743;Q04759;Q05513;Q9UJT1;Q9UJT0;Q96PS8;Q8NBQ7;Q8IXF9;A6NM10;P41181;Q92482;Q13520;A6NKZ8 ;Q99867;Q9H853;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2;P23258;Q9NRH3
351,T3D0350,2009-03-06 18:58:35 UTC,2009-08-05 21:38:43 UTC,Mercury(II) iodide,Inorganic Compound;Mercury Compound,"Alpha-mercury(II) iodideDIIodomercuryHGIHgI2Hydrargyrum bijodatumHydrargyrum bijodatum [german]Hydrargyrum diodatumMercuric iodideMercuric iodide redMercuric iodide, redMercuric iodide,redMercurius bijodatusMercury (II) iodideMercury biniodideMercury iodideMercury iodide (HgI2)Mercury(II) iodideMercury(II) iodide redRed mercuric iodidemercury(2+) iodide","Mercury(II) iodide is an iodide of mercury that occurs naturally as the mineral coccinite. It is a semiconductor and also used in x-ray and gamma ray detection, as well as veterinary medicine. Mercury is a heavy, silvery d-block metal and one of six elements that are liquid at or near room temperature and pressure. It is a naturally occuring substance, and combines with other elements such as chlorine, sulfur, or oxygen to form inorganic mercury compounds (salts). Mercury also combines with carbon to make organic mercury compounds. (R005, R735)",,7774-29-0,24485,,"","",49659,"",,C025718,Mercury(II) iodide,,,,,InChI=1/Hg.2HI/h;2*1H/q+2;;/p-2,diiodomercury,http://www.biospider.ca/saved_files/mol/,I[Hg]I,I[Hg]I,HgI2,455.779560,Red/orange crystals.,"","","","","","","","Oral 
Inhalation 
Dermal 
(R022)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Catalase (P04040) 
Hemoglobin subunit alpha (P69905) 
Hemoglobin subunit beta (P68871) 
Hemoglobin subunit gamma-1 (P69891) 
Hemoglobin subunit gamma-2 (P69892) 
Hemoglobin subunit delta (P02042) 
Hemoglobin subunit epsilon (P02100) 
Hemoglobin subunit theta-1 (P09105) 
Hemoglobin subunit zeta (P02008) 
Hemoglobin subunit mu (Q6B0K9) 
(R022, R164) ","High-affinity binding of the divalent mercuric ion to thiol or sulfhydryl groups of proteins is believed to be the major mechanism for the activity of mercury. Through alterations in intracellular thiol status, mercury can promote oxidative stress, lipid peroxidation, mitochondrial dysfunction, and changes in heme metabolism. Mercury is known to bind to microsomal and mitochondrial enzymes, resulting in cell injury and death. For example, mercury is known to inhibit aquaporins, halting water flow across the cell membrane. It also inhibits the protein LCK, which causes decreased T-cell signalling and immune system depression. Mercury is also believed to inhibit neuronal excitability by acting on the postsynaptic neuronal membrane. It also affects the nervous system by inhibiting protein kinase C and alkaline phosphatase, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Mercury also produces an autoimmune response, likely by modification of major histocompatibility complex (MHC) class II molecules, self peptides, T-cell receptors, or cell-surface adhesion molecules. (R022, R025, R066, R067)","Mercury is absorbed mainly via ingestion and inhalation, then distributed throughout the body via the bloodstream, where a portion binds to sulfhydryl groups on haemoglobin. Mercury can undergo oxidation to mercuric mercury, which takes place via the catalase-hydrogen peroxide pathway. The mercury atom is able to diffuse down the cleft in the catalase enzyme to reach the active site where the heme ring is located. Oxidation most likely occurs in all tissue, as the catalase hydrogen peroxide pathway is ubiquitous. Following oxidation, mercury tends to accumulate in the kidneys. Mercury is excreted mainly by exhalation and in the faeces. (R021, R022)","LD50: 18 mg/kg (Oral, Rat) (R736)
LD50: 4.2 mg/kg (Intraperitoneal, Rat) (R736)",1 gram for an adult human (average for inorganic mercurials). (R273),"3, not classifiable as to its carcinogenicity to humans. (R264)","Mercury(II) iodide is aa semiconductor and also used in x-ray and gamma ray detection, as well as veterinary medicine. (R735)",Chronic Inhalation: 0.0002 mg/m3 (R260),"Mercury mainly affects the nervous system. Exposure to high levels of metallic, inorganic, or organic mercury can permanently damage the brain, kidneys, and developing fetus. Effects on brain functioning may result in irritability, shyness, tremors, changes in vision or hearing, and memory problems. Acrodynia, a type of mercury poisoning in children, is characterized by pain and pink discoloration of the hands and feet. Mercury poisoning can also cause Hunter-Russell syndrome and Minamata disease. (R022)","Common symptoms include peripheral neuropathy (presenting as paresthesia or itching, burning or pain), skin discoloration (pink cheeks, fingertips and toes), edema (swelling), and desquamation (dead skin peels off in layers). (R020)","Mercury poisoning is treated by immediate decontamination and chelation therapy using DMSA, DMPS, DPCN, or dimercaprol. (R023)",P06239;P05186;P29972;P55087;P55064;O14520;O94778;O43315;P30301;P17252;P05771;Q05655;Q02156;P24723;P05129;P41743;Q04759;Q05513;Q9UJT1;Q9UJT0;Q96PS8;Q8NBQ7;Q8IXF9;A6NM10;P41181;Q92482;Q13520;A6NKZ8 ;Q99867;Q9H853;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2;P23258;Q9NRH3
352,T3D0351,2009-03-06 18:58:35 UTC,2009-08-05 21:38:44 UTC,Mercury(I) iodide,Inorganic Compound;Mercury Compound,"Dimercury dIIodideMercurous iodideMercurous iodide yellowMercury iodide (Hg2I2)Mercury iodide, solutionMercury protoiodideMercury(I) iodideYellow mercury iodide","Mercury(I) iodide is an iodide of mercury. Mercury is a heavy, silvery d-block metal and one of six elements that are liquid at or near room temperature and pressure. It is a naturally occuring substance, and combines with other elements such as chlorine, sulfur, or oxygen to form inorganic mercury compounds (salts). Mercury also combines with carbon to make organic mercury compounds. (R005)",,15385-57-6,27243,,"","","","",,,Mercury(I) iodide,,,,http://en.wikipedia.org/wiki/Mercury iodide,InChI=1/2Hg.2HI/h;;2*1H/q2*+1;;/p-2,iodomercury,http://www.biospider.ca/saved_files/mol/,I[Hg].I[Hg],I[Hg].I[Hg],Hg2I2,657.750190,Yellow powder.,259 °C,"","","","","","","Oral 
Inhalation 
Dermal 
(R022)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Catalase (P04040) 
Hemoglobin subunit alpha (P69905) 
Hemoglobin subunit beta (P68871) 
Hemoglobin subunit gamma-1 (P69891) 
Hemoglobin subunit gamma-2 (P69892) 
Hemoglobin subunit delta (P02042) 
Hemoglobin subunit epsilon (P02100) 
Hemoglobin subunit theta-1 (P09105) 
Hemoglobin subunit zeta (P02008) 
Hemoglobin subunit mu (Q6B0K9) 
(R022, R164) ","High-affinity binding of the divalent mercuric ion to thiol or sulfhydryl groups of proteins is believed to be the major mechanism for the activity of mercury. Through alterations in intracellular thiol status, mercury can promote oxidative stress, lipid peroxidation, mitochondrial dysfunction, and changes in heme metabolism. Mercury is known to bind to microsomal and mitochondrial enzymes, resulting in cell injury and death. For example, mercury is known to inhibit aquaporins, halting water flow across the cell membrane. It also inhibits the protein LCK, which causes decreased T-cell signalling and immune system depression. Mercury is also believed to inhibit neuronal excitability by acting on the postsynaptic neuronal membrane. It also affects the nervous system by inhibiting protein kinase C and alkaline phosphatase, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Mercury also produces an autoimmune response, likely by modification of major histocompatibility complex (MHC) class II molecules, self peptides, T-cell receptors, or cell-surface adhesion molecules. (R022, R025, R066, R067)","Mercury is absorbed mainly via ingestion and inhalation, then distributed throughout the body via the bloodstream, where a portion binds to sulfhydryl groups on haemoglobin. Mercury can undergo oxidation to mercuric mercury, which takes place via the catalase-hydrogen peroxide pathway. The mercury atom is able to diffuse down the cleft in the catalase enzyme to reach the active site where the heme ring is located. Oxidation most likely occurs in all tissue, as the catalase hydrogen peroxide pathway is ubiquitous. Following oxidation, mercury tends to accumulate in the kidneys. Mercury is excreted mainly by exhalation and in the faeces. (R021, R022)",No data.,1 gram for an adult human (average for inorganic mercurials). (R273),"3, not classifiable as to its carcinogenicity to humans. (R264)",No data.,Chronic Inhalation: 0.0002 mg/m3 (R260),"Mercury mainly affects the nervous system. Exposure to high levels of metallic, inorganic, or organic mercury can permanently damage the brain, kidneys, and developing fetus. Effects on brain functioning may result in irritability, shyness, tremors, changes in vision or hearing, and memory problems. Acrodynia, a type of mercury poisoning in children, is characterized by pain and pink discoloration of the hands and feet. Mercury poisoning can also cause Hunter-Russell syndrome and Minamata disease. (R022)","Common symptoms include peripheral neuropathy (presenting as paresthesia or itching, burning or pain), skin discoloration (pink cheeks, fingertips and toes), edema (swelling), and desquamation (dead skin peels off in layers). (R020)","Mercury poisoning is treated by immediate decontamination and chelation therapy using DMSA, DMPS, DPCN, or dimercaprol. (R023)",P06239;P05186;P29972;P55087;P55064;O14520;O94778;O43315;P30301;P17252;P05771;Q05655;Q02156;P24723;P05129;P41743;Q04759;Q05513;Q13520;Q9UJT1;Q9UJT0;Q96PS8;Q8NBQ7;Q8IXF9;A6NM10;P41181;Q92482;A6NKZ8 ;Q99867;Q9H853;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2;P23258;Q9NRH3
353,T3D0352,2009-03-06 18:58:35 UTC,2009-08-27 14:35:33 UTC,Mercury(I) bromide,Inorganic Compound;Mercury Compound;Bromide Compound,Hg2Br2Mercurous bromideMercury bromide (HGBR)Mercury bromide (Hg2Br2)Mercury monobromideMercury(I) bromide (1:1),"Mercury(I) bromide is a bromide of mercury that occurs naturally as the mineral kuzminite. It is formed by the oxidation of elemental mercury with elemental bromine or by adding sodium bromide to a solution of mercury(I) nitrate. Mercury is a heavy, silvery d-block metal and one of six elements that are liquid at or near room temperature and pressure. It is a naturally occuring substance, and combines with other elements such as chlorine, sulfur, or oxygen to form inorganic mercury compounds (salts). Mercury also combines with carbon to make organic mercury compounds. Bromine is a halogen element with the symbol Br and atomic number 35. Diatomic bromine does not occur naturally, but bromine salts can be found in crustal rock. (R987, R005, R732)",,15385-58-7,24829,,"","",49639,"",,,Mercury(I) bromide,,,,http://en.wikipedia.org/wiki/Mercury bromide,InChI=1/2BrH.2Hg/h2*1H;;/q;;2*+1/p-2,bromomercury,http://www.biospider.ca/saved_files/mol/,Br[Hg].Br[Hg],Br[Hg].Br[Hg],Br2Hg2,561.777930,White crystals.,"","","","","","","","Oral 
Inhalation 
Dermal 
(R022)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Catalase (P04040) 
Hemoglobin subunit alpha (P69905) 
Hemoglobin subunit beta (P68871) 
Hemoglobin subunit gamma-1 (P69891) 
Hemoglobin subunit gamma-2 (P69892) 
Hemoglobin subunit delta (P02042) 
Hemoglobin subunit epsilon (P02100) 
Hemoglobin subunit theta-1 (P09105) 
Hemoglobin subunit zeta (P02008) 
Hemoglobin subunit mu (Q6B0K9) 
(R022, R164) ","High-affinity binding of the divalent mercuric ion to thiol or sulfhydryl groups of proteins is believed to be the major mechanism for the activity of mercury. Through alterations in intracellular thiol status, mercury can promote oxidative stress, lipid peroxidation, mitochondrial dysfunction, and changes in heme metabolism. Mercury is known to bind to microsomal and mitochondrial enzymes, resulting in cell injury and death. For example, mercury is known to inhibit aquaporins, halting water flow across the cell membrane. It also inhibits the protein LCK, which causes decreased T-cell signalling and immune system depression. Mercury is also believed to inhibit neuronal excitability by acting on the postsynaptic neuronal membrane. It also affects the nervous system by inhibiting protein kinase C and alkaline phosphatase, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Mercury also produces an autoimmune response, likely by modification of major histocompatibility complex (MHC) class II molecules, self peptides, T-cell receptors, or cell-surface adhesion molecules. Bromine is a powerful oxidizing agent and is able to release oxygen free radicals from the water in mucous membranes. These free radicals are also potent oxidizers and produce tissue damage. In additon, the formation of hydrobromic and bromic acids will result in secondary irritation. The bromide ion is also known to affect the central nervous system, causing bromism. This is believed to be a result of bromide ions substituting for chloride ions in the in actions of neurotransmitters and transport systems, thus affecting numerous synaptic processes. (R989, R990, R991, R022, R025, R066, R067)","Mercury is absorbed mainly via ingestion and inhalation, then distributed throughout the body via the bloodstream, where a portion binds to sulfhydryl groups on haemoglobin. Mercury can undergo oxidation to mercuric mercury, which takes place via the catalase-hydrogen peroxide pathway. The mercury atom is able to diffuse down the cleft in the catalase enzyme to reach the active site where the heme ring is located. Oxidation most likely occurs in all tissue, as the catalase hydrogen peroxide pathway is ubiquitous. Following oxidation, mercury tends to accumulate in the kidneys. Mercury is excreted mainly by exhalation and in the faeces. Bromine is mainly absorbed via inhalation, but may also enter the body through dermal contact. Bromine salts can be ingested. Due to its reactivity, bromine quickly forms bromide and may be deposited in the tissues, displacing other halogens. (R989, R021, R022)",No data.,1 gram for an adult human (average for inorganic mercurials). (R273),"3, not classifiable as to its carcinogenicity to humans. (R264)",Mercury(I) bromide is used in acousto-optical devices. (R732),Chronic Inhalation: 0.0002 mg/m3 Mercury(R260),"Mercury mainly affects the nervous system. Exposure to high levels of metallic, inorganic, or organic mercury can permanently damage the brain, kidneys, and developing fetus. Effects on brain functioning may result in irritability, shyness, tremors, changes in vision or hearing, and memory problems. Acrodynia, a type of mercury poisoning in children, is characterized by pain and pink discoloration of the hands and feet. Mercury poisoning can also cause Hunter-Russell syndrome and Minamata disease. Bromine vapour causes irritation and direct damage to the mucous membranes. Elemental bromine also burns the skin. The bromide ion is a central nervous system depressant and chronic exposure produces neuronal effects. This is called bromism and can result in central reactions reaching from somnolence to coma, cachexia, exicosis, loss of reflexes or pathologic reflexes, clonic seizures, tremor, ataxia, loss of neural sensitivity, paresis, papillar edema of the eyes, abnormal speech, cerebral edema, delirium, aggressiveness, and psychoses. (R987, R989, R990, R022)","Common symptoms include peripheral neuropathy (presenting as paresthesia or itching, burning or pain), skin discoloration (pink cheeks, fingertips and toes), edema (swelling), and desquamation (dead skin peels off in layers). Bromine vapour causes irritation and direct damage to the mucous membranes. Symptoms include lacrimation, rhinorrhoea, eye irritation with mucous secretions from the oropharyngeal and upper airways, coughing, dyspnoea, choking, wheezing, epistaxis, and headache. The bromide ion is a central nervous system depressant producing ataxia, slurred speech, tremor, nausea, vomiting, lethargy, dizziness, visual disturbances, unsteadiness, headaches, impaired memory and concentration, disorientation and hallucinations. This is called bromism. (R989, R990, R020)","Mercury poisoning is treated by immediate decontamination and chelation therapy using DMSA, DMPS, DPCN, or dimercaprol. Bromine should be washed with water from any areas of dermal or ocular contact. If inhaled, treatment is mainly symptomatic and may include maintaining an adequate airway, administering oxygen, antibronchospasm therapy, and/or antibiotics. (R989, R023)",P06239;P05186;P29972;P55087;P55064;O14520;O94778;O43315;P30301;P17252;P05771;Q05655;Q02156;P24723;P05129;P41743;Q04759;Q05513;Q9UJT1;Q9UJT0;Q96PS8;Q8NBQ7;Q8IXF9;A6NM10;P41181;Q92482;Q13520;A6NKZ8 ;Q99867;Q9H853;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2;P23258;Q9NRH3
354,T3D0353,2009-03-06 18:58:36 UTC,2009-08-05 21:38:44 UTC,Mercury(II) bromide,Inorganic Compound;Mercury Compound;Bromide Compound,DibromomercuryHgBr2Mercuric bromideMercuric dibromideMercury bromideMercury bromide (HgBr2)Mercury(2)bromideMercury(II) bromideMercury(ii) bromide (1:2)mercury(2+) bromide,"Mercury(II) bromide is a bromide of mercury used mainly as a laboratory reagent. Mercury is a heavy, silvery d-block metal and one of six elements that are liquid at or near room temperature and pressure. It is a naturally occuring substance, and combines with other elements such as chlorine, sulfur, or oxygen to form inorganic mercury compounds (salts). Mercury also combines with carbon to make organic mercury compounds. Bromine is a halogen element with the symbol Br and atomic number 35. Diatomic bromine does not occur naturally, but bromine salts can be found in crustal rock. (R987, R005, R737)",,7789-47-1,24612,,"","",49639,"",,C042720,Mercury(II) bromide,,,,,InChI=1/2BrH.Hg/h2*1H;/q;;+2/p-2,dibromomercury,http://www.biospider.ca/saved_files/mol/,Br[Hg]Br,Br[Hg]Br,Br2Hg,359.807300,White crystals.,"","","","","","","","Oral 
Inhalation 
Dermal 
(R022)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Catalase (P04040) 
Hemoglobin subunit alpha (P69905) 
Hemoglobin subunit beta (P68871) 
Hemoglobin subunit gamma-1 (P69891) 
Hemoglobin subunit gamma-2 (P69892) 
Hemoglobin subunit delta (P02042) 
Hemoglobin subunit epsilon (P02100) 
Hemoglobin subunit theta-1 (P09105) 
Hemoglobin subunit zeta (P02008) 
Hemoglobin subunit mu (Q6B0K9) 
(R022, R164) ","High-affinity binding of the divalent mercuric ion to thiol or sulfhydryl groups of proteins is believed to be the major mechanism for the activity of mercury. Through alterations in intracellular thiol status, mercury can promote oxidative stress, lipid peroxidation, mitochondrial dysfunction, and changes in heme metabolism. Mercury is known to bind to microsomal and mitochondrial enzymes, resulting in cell injury and death. For example, mercury is known to inhibit aquaporins, halting water flow across the cell membrane. It also inhibits the protein LCK, which causes decreased T-cell signalling and immune system depression. Mercury is also believed to inhibit neuronal excitability by acting on the postsynaptic neuronal membrane. It also affects the nervous system by inhibiting protein kinase C and alkaline phosphatase, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Mercury also produces an autoimmune response, likely by modification of major histocompatibility complex (MHC) class II molecules, self peptides, T-cell receptors, or cell-surface adhesion molecules. Bromine is a powerful oxidizing agent and is able to release oxygen free radicals from the water in mucous membranes. These free radicals are also potent oxidizers and produce tissue damage. In additon, the formation of hydrobromic and bromic acids will result in secondary irritation. The bromide ion is also known to affect the central nervous system, causing bromism. This is believed to be a result of bromide ions substituting for chloride ions in the in actions of neurotransmitters and transport systems, thus affecting numerous synaptic processes. (R989, R990, R991, R022, R025, R066, R067)","Mercury is absorbed mainly via ingestion and inhalation, then distributed throughout the body via the bloodstream, where a portion binds to sulfhydryl groups on haemoglobin. Mercury can undergo oxidation to mercuric mercury, which takes place via the catalase-hydrogen peroxide pathway. The mercury atom is able to diffuse down the cleft in the catalase enzyme to reach the active site where the heme ring is located. Oxidation most likely occurs in all tissue, as the catalase hydrogen peroxide pathway is ubiquitous. Following oxidation, mercury tends to accumulate in the kidneys. Mercury is excreted mainly by exhalation and in the faeces. Bromine is mainly absorbed via inhalation, but may also enter the body through dermal contact. Bromine salts can be ingested. Due to its reactivity, bromine quickly forms bromide and may be deposited in the tissues, displacing other halogens. (R989, R021, R022)","LD50: 35 mg/kg (Oral, mouse) (S271); LD50: 40 mg/kg (Oral, rat) (S271); LD50: 100 mg/kg (Skin, rat) (S271).",1 gram for an adult human (average for inorganic mercurials). (R273),"3, not classifiable as to its carcinogenicity to humans. (R264)",Mercury(II) bromide is used mainly as a laboratory reagent. (R737),Chronic Inhalation: 0.0002 mg/m3 Mercury(R260),"Mercury mainly affects the nervous system. Exposure to high levels of metallic, inorganic, or organic mercury can permanently damage the brain, kidneys, and developing fetus. Effects on brain functioning may result in irritability, shyness, tremors, changes in vision or hearing, and memory problems. Acrodynia, a type of mercury poisoning in children, is characterized by pain and pink discoloration of the hands and feet. Mercury poisoning can also cause Hunter-Russell syndrome and Minamata disease. Bromine vapour causes irritation and direct damage to the mucous membranes. Elemental bromine also burns the skin. The bromide ion is a central nervous system depressant and chronic exposure produces neuronal effects. This is called bromism and can result in central reactions reaching from somnolence to coma, cachexia, exicosis, loss of reflexes or pathologic reflexes, clonic seizures, tremor, ataxia, loss of neural sensitivity, paresis, papillar edema of the eyes, abnormal speech, cerebral edema, delirium, aggressiveness, and psychoses. (R987, R989, R990, R022)","Common symptoms include peripheral neuropathy (presenting as paresthesia or itching, burning or pain), skin discoloration (pink cheeks, fingertips and toes), edema (swelling), and desquamation (dead skin peels off in layers). (R020)","Mercury poisoning is treated by immediate decontamination and chelation therapy using DMSA, DMPS, DPCN, or dimercaprol. Bromine should be washed with water from any areas of dermal or ocular contact. If inhaled, treatment is mainly symptomatic and may include maintaining an adequate airway, administering oxygen, antibronchospasm therapy, and/or antibiotics. (R989, R023)",P06239;P05186;P29972;P55087;P55064;O14520;O94778;O43315;P30301;P17252;P05771;Q05655;Q02156;P24723;P05129;P41743;Q04759;Q05513;Q9UJT1;Q9UJT0;Q96PS8;Q8NBQ7;Q8IXF9;A6NM10;P41181;Q92482;Q13520;A6NKZ8 ;Q99867;Q9H853;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2;P23258;Q9NRH3
355,T3D0354,2009-03-06 18:58:36 UTC,2009-08-25 18:01:56 UTC,Mercury(II) nitrate,Inorganic Compound;Mercury Compound;Nitrate,"Mercury nitrateNitric acid, mercury salt (van)","Mercury(II) nitrate is a nitrate of mercury previously used to treat fur and make felt. Today it is used mainly in the synthesis of other mercuric compounds. Mercury is a heavy, silvery d-block metal and one of six elements that are liquid at or near room temperature and pressure. It is a naturally occuring substance, and combines with other elements such as chlorine, sulfur, or oxygen to form inorganic mercury compounds (salts). Mercury also combines with carbon to make organic mercury compounds. Nitrite is a toxic compound known to cause methemoglobinemia. (S575,  R005, R738)",,10045-94-0,115042,,"","","","",,,Mercury(II) nitrate,,,,http://en.wikipedia.org/wiki/Mercury(II)_nitrate,InChI=1/Hg.2NO3/c;2*2-1(3)4/q+2;2*-1,mercury; nitric acid,http://www.biospider.ca/saved_files/mol/,[N+](=O)(O)[O-].[Hg],O[N+](=O)O[Hg+],HHgNO3,264.966270,Colorless or white crystals.,"","","","","","","","Oral 
Inhalation 
Dermal 
(R022)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Catalase (P04040) 
Hemoglobin subunit alpha (P69905) 
Hemoglobin subunit beta (P68871) 
Hemoglobin subunit gamma-1 (P69891) 
Hemoglobin subunit gamma-2 (P69892) 
Hemoglobin subunit delta (P02042) 
Hemoglobin subunit epsilon (P02100) 
Hemoglobin subunit theta-1 (P09105) 
Hemoglobin subunit zeta (P02008) 
Hemoglobin subunit mu (Q6B0K9) 
(R022, R164) ","High-affinity binding of the divalent mercuric ion to thiol or sulfhydryl groups of proteins is believed to be the major mechanism for the activity of mercury. Through alterations in intracellular thiol status, mercury can promote oxidative stress, lipid peroxidation, mitochondrial dysfunction, and changes in heme metabolism. Mercury is known to bind to microsomal and mitochondrial enzymes, resulting in cell injury and death. For example, mercury is known to inhibit aquaporins, halting water flow across the cell membrane. It also inhibits the protein LCK, which causes decreased T-cell signalling and immune system depression. Mercury is also believed to inhibit neuronal excitability by acting on the postsynaptic neuronal membrane. It also affects the nervous system by inhibiting protein kinase C and alkaline phosphatase, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Mercury also produces an autoimmune response, likely by modification of major histocompatibility complex (MHC) class II molecules, self peptides, T-cell receptors, or cell-surface adhesion molecules. Nitrate's toxicity is a result of it's conversion to nitrite once in the body. Nitrite causes the autocatalytic oxidation of oxyhemoglobin to hydrogen peroxide and methemoglobin. This elevation of methemoglobin levels is a condition known as methemoglobinemia, and is characterized by tissue hypoxia, as methemoglobin cannot bind oxygen. (V305, V306, R022, R025, R066, R067)","Mercury is absorbed mainly via ingestion and inhalation, then distributed throughout the body via the bloodstream, where a portion binds to sulfhydryl groups on haemoglobin. Mercury can undergo oxidation to mercuric mercury, which takes place via the catalase-hydrogen peroxide pathway. The mercury atom is able to diffuse down the cleft in the catalase enzyme to reach the active site where the heme ring is located. Oxidation most likely occurs in all tissue, as the catalase hydrogen peroxide pathway is ubiquitous. Following oxidation, mercury tends to accumulate in the kidneys. Mercury is excreted mainly by exhalation and in the faeces. Intake of some amount of nitrates and nitrites is a normal part of the nitrogen cycle in humans. In vivo conversion of nitrates to nitrites can occur in the gastrointestional tract under the right conditions, significantly enhancing nitrates' toxic potency. The major metabolic pathway for nitrate is conversion to nitrite, and then to ammonia. Nitrites, nitrates, and their metabolites are excreted in the urine. (S575, R021, R022)","LD50: 26 mg/kg (Oral, Rat) (R740)
LD50: 75 mg/kg (Dermal, Rat) (R740)
LD50: 7 mg/kg (Intraperitoneal, Mouse) (R740)",1 gram for an adult human (average for inorganic mercurials). (R273),"2A, probably carcinogenic to humans. (R264)",Mercury(II) nitrate is used mainly in the synthesis of other mercuric compounds. (R738),Chronic Inhalation: 0.0002 mg/m3 (R260),"Mercury mainly affects the nervous system. Exposure to high levels of metallic, inorganic, or organic mercury can permanently damage the brain, kidneys, and developing fetus. Effects on brain functioning may result in irritability, shyness, tremors, changes in vision or hearing, and memory problems. Acrodynia, a type of mercury poisoning in children, is characterized by pain and pink discoloration of the hands and feet. Mercury poisoning can also cause Hunter-Russell syndrome and Minamata disease. Nitrate and nitrite poisoning causes methemoglobinemia. Nitrites may cause pregnancy complications and developmental effects. They may also be carcinogenic. (S575, R022)","Common symptoms include peripheral neuropathy (presenting as paresthesia or itching, burning or pain), skin discoloration (pink cheeks, fingertips and toes), edema (swelling), and desquamation (dead skin peels off in layers). Nitrate and nitrite poisoning causes methemoglobinemia. Symptoms include cyanosis, cardiac dysrhythmias and circulatory failure, and progressive central nervous system (CNS) effects. CNS effects can range from mild dizziness and lethargy to coma and convulsions. (S575, R020)","Mercury poisoning is treated by immediate decontamination and chelation therapy using DMSA, DMPS, DPCN, or dimercaprol. Methemoglobinemia can be treated with supplemental oxygen and methylene blue 1% solution administered intravenously slowly over five minutes followed by IV flush with normal saline. Methylene blue restores the iron in hemoglobin to its normal (reduced) oxygen-carrying state. (V306, R023)",P06239;P05186;P29972;P55087;P55064;O14520;O94778;O43315;P30301;P17252;P05771;Q05655;Q02156;P24723;P05129;P41743;Q04759;Q05513;Q9UJT1;Q9UJT0;Q96PS8;Q8NBQ7;Q8IXF9;A6NM10;P41181;Q92482;Q13520;A6NKZ8 ;Q99867;Q9H853;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2;P23258;Q9NRH3;P69905;P68871;P02042;P02100;P69891;P69892;Q6B0K9;P09105;P02008
356,T3D0355,2009-03-06 18:58:36 UTC,2009-08-25 18:02:01 UTC,Mercury(I) nitrate,Inorganic Compound;Mercury Compound;Nitrate,"Mercury nitrateNitric acid, mercury salt (van)","Mercury(I) nitrate is a chemical compound of mercury used mainly in the synthesis of other mercuric compounds. Mercury is a heavy, silvery d-block metal and one of six elements that are liquid at or near room temperature and pressure. It is a naturally occuring substance, and combines with other elements such as chlorine, sulfur, or oxygen to form inorganic mercury compounds (salts). Mercury also combines with carbon to make organic mercury compounds. Nitrite is a toxic compound known to cause methemoglobinemia. (S575,  R005, R270)",,10415-75-5,115042,,"","","","",,,Mercury(I) nitrate,,,,http://en.wikipedia.org/wiki/Mercury(I)_nitrate,InChI=1/Hg.NO3/c;2-1(3)4/q+1;-1,mercury; nitric acid,http://www.biospider.ca/saved_files/mol/,[N+](=O)(O)[O-].[Hg],O[N+](=O)O[Hg],HHgNO3,264.966270,White crystals.,"","","","","","","","Oral 
Inhalation 
Dermal 
(R022)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Catalase (P04040) 
Hemoglobin subunit alpha (P69905) 
Hemoglobin subunit beta (P68871) 
Hemoglobin subunit gamma-1 (P69891) 
Hemoglobin subunit gamma-2 (P69892) 
Hemoglobin subunit delta (P02042) 
Hemoglobin subunit epsilon (P02100) 
Hemoglobin subunit theta-1 (P09105) 
Hemoglobin subunit zeta (P02008) 
Hemoglobin subunit mu (Q6B0K9) 
(R022, R164) ","High-affinity binding of the divalent mercuric ion to thiol or sulfhydryl groups of proteins is believed to be the major mechanism for the activity of mercury. Through alterations in intracellular thiol status, mercury can promote oxidative stress, lipid peroxidation, mitochondrial dysfunction, and changes in heme metabolism. Mercury is known to bind to microsomal and mitochondrial enzymes, resulting in cell injury and death. For example, mercury is known to inhibit aquaporins, halting water flow across the cell membrane. It also inhibits the protein LCK, which causes decreased T-cell signalling and immune system depression. Mercury is also believed to inhibit neuronal excitability by acting on the postsynaptic neuronal membrane. It also affects the nervous system by inhibiting protein kinase C and alkaline phosphatase, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Mercury also produces an autoimmune response, likely by modification of major histocompatibility complex (MHC) class II molecules, self peptides, T-cell receptors, or cell-surface adhesion molecules. Nitrate's toxicity is a result of it's conversion to nitrite once in the body. Nitrite causes the autocatalytic oxidation of oxyhemoglobin to hydrogen peroxide and methemoglobin. This elevation of methemoglobin levels is a condition known as methemoglobinemia, and is characterized by tissue hypoxia, as methemoglobin cannot bind oxygen. (V305, V306, R022, R025, R066, R067)","Mercury is absorbed mainly via ingestion and inhalation, then distributed throughout the body via the bloodstream, where a portion binds to sulfhydryl groups on haemoglobin. Mercury can undergo oxidation to mercuric mercury, which takes place via the catalase-hydrogen peroxide pathway. The mercury atom is able to diffuse down the cleft in the catalase enzyme to reach the active site where the heme ring is located. Oxidation most likely occurs in all tissue, as the catalase hydrogen peroxide pathway is ubiquitous. Following oxidation, mercury tends to accumulate in the kidneys. Mercury is excreted mainly by exhalation and in the faeces. Intake of some amount of nitrates and nitrites is a normal part of the nitrogen cycle in humans. In vivo conversion of nitrates to nitrites can occur in the gastrointestional tract under the right conditions, significantly enhancing nitrates' toxic potency. The major metabolic pathway for nitrate is conversion to nitrite, and then to ammonia. Nitrites, nitrates, and their metabolites are excreted in the urine. (S575, R021, R022)","LD50: 170 mg/kg (Oral, Mouse) (R741)
LD50: 5 mg/kg (Intraperitoneal, Mouse) (R741)",1 gram for an adult human (average for inorganic mercurials). (R273),"2A, probably carcinogenic to humans. (R264)",Mercury(I) nitrate is used mainly in the synthesis of other mercuric compounds. (R270),Chronic Inhalation: 0.0002 mg/m3 (R260),"Mercury mainly affects the nervous system. Exposure to high levels of metallic, inorganic, or organic mercury can permanently damage the brain, kidneys, and developing fetus. Effects on brain functioning may result in irritability, shyness, tremors, changes in vision or hearing, and memory problems. Acrodynia, a type of mercury poisoning in children, is characterized by pain and pink discoloration of the hands and feet. Mercury poisoning can also cause Hunter-Russell syndrome and Minamata disease. Nitrate and nitrite poisoning causes methemoglobinemia. Nitrites may cause pregnancy complications and developmental effects. They may also be carcinogenic. (S575, R022)","Common symptoms include peripheral neuropathy (presenting as paresthesia or itching, burning or pain), skin discoloration (pink cheeks, fingertips and toes), edema (swelling), and desquamation (dead skin peels off in layers). Nitrate and nitrite poisoning causes methemoglobinemia. Symptoms include cyanosis, cardiac dysrhythmias and circulatory failure, and progressive central nervous system (CNS) effects. CNS effects can range from mild dizziness and lethargy to coma and convulsions. (S575, R020)","Mercury poisoning is treated by immediate decontamination and chelation therapy using DMSA, DMPS, DPCN, or dimercaprol. Methemoglobinemia can be treated with supplemental oxygen and methylene blue 1% solution administered intravenously slowly over five minutes followed by IV flush with normal saline. Methylene blue restores the iron in hemoglobin to its normal (reduced) oxygen-carrying state. (V306, R023)",P06239;P05186;P29972;P55087;P55064;O14520;O94778;O43315;P30301;P17252;P05771;Q05655;Q02156;P24723;P05129;P41743;Q04759;Q05513;Q9UJT1;Q9UJT0;Q96PS8;Q8NBQ7;Q8IXF9;A6NM10;P41181;Q92482;Q13520;A6NKZ8 ;Q99867;Q9H853;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2;P23258;Q9NRH3;P69905;P68871;P02042;P02100;P69891;P69892;Q6B0K9;P09105;P02008
357,T3D0356,2009-03-06 18:58:36 UTC,2009-08-25 19:52:52 UTC,Mercury(II) thiocyanate,Inorganic Compound;Mercury Compound;Cyanide Compound,Mercury dipotassium tetrathiocyanatePotassium mercuric thiocyanate,"Mercury(II) thiocyanate is a chemical compound of mercury made by reacting a mercury(II) salt with a thiocyanate salt. It has previously been used in pyrotechnics. Mercury is a heavy, silvery d-block metal and one of six elements that are liquid at or near room temperature and pressure. It is a naturally occuring substance, and combines with other elements such as chlorine, sulfur, or oxygen to form inorganic mercury compounds (salts). Mercury also combines with carbon to make organic mercury compounds. (R005, R742)",,592-85-8,167003,,"","","","",,,Mercury(II) thiocyanate,,,,,InChI=1/2CHNS.Hg/c2*2-1-3;/h2*3H;/q;;+2/p-2,dipotassium mercury(2+) tetrathiocyanate,http://www.biospider.ca/saved_files/mol/,C(#N)[S-].C(#N)[S-].C(#N)[S-].C(#N)[S-].[K+].[K+].[Hg+2],C(#N)[S-].C(#N)[S-].C(#N)[S-].C(#N)[S-].[K+].[K+].[Hg+2],C4HgK2N4S4,511.798620,White powder.,decomposes at 165°C,"","",0.69 mg/mL at 25 oC [MERCK INDEX (1996)],"","","","Oral 
Inhalation 
Dermal 
(R022)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Catalase (P04040) 
Hemoglobin subunit alpha (P69905) 
Hemoglobin subunit beta (P68871) 
Hemoglobin subunit gamma-1 (P69891) 
Hemoglobin subunit gamma-2 (P69892) 
Hemoglobin subunit delta (P02042) 
Hemoglobin subunit epsilon (P02100) 
Hemoglobin subunit theta-1 (P09105) 
Hemoglobin subunit zeta (P02008) 
Hemoglobin subunit mu (Q6B0K9)
Thiosulfate sulfurtransferase (Q16762) 
3-mercaptopyruvate sulfurtransferase (P25325)  
(R022, R164, R172)","High-affinity binding of the divalent mercuric ion to thiol or sulfhydryl groups of proteins is believed to be the major mechanism for the activity of mercury. Through alterations in intracellular thiol status, mercury can promote oxidative stress, lipid peroxidation, mitochondrial dysfunction, and changes in heme metabolism. Mercury is known to bind to microsomal and mitochondrial enzymes, resulting in cell injury and death. For example, mercury is known to inhibit aquaporins, halting water flow across the cell membrane. It also inhibits the protein LCK, which causes decreased T-cell signalling and immune system depression. Mercury is also believed to inhibit neuronal excitability by acting on the postsynaptic neuronal membrane. It also affects the nervous system by inhibiting protein kinase C and alkaline phosphatase, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Mercury also produces an autoimmune response, likely by modification of major histocompatibility complex (MHC) class II molecules, self peptides, T-cell receptors, or cell-surface adhesion molecules. Cyanide is an inhibitor of cytochrome c oxidase in the fourth complex of the electron transport chain (found in the membrane of the mitochondria of eukaryotic cells). It complexes with the ferric iron atom in this enzyme. The binding of cyanide to this cytochrome prevents transport of electrons from cytochrome c oxidase to oxygen. As a result, the electron transport chain is disrupted and the cell can no longer aerobically produce ATP for energy. Tissues that mainly depend on aerobic respiration, such as the central nervous system and the heart, are particularly affected. Cyanide is also known produce some of its toxic effects by binding to catalase, glutathione peroxidase, methemoglobin, hydroxocobalamin, phosphatase, tyrosinase, ascorbic acid oxidase, xanthine oxidase, succinic dehydrogenase, and Cu/Zn superoxide dismutase. Cyanide binds to the ferric ion of methemoglobin to form inactive cyanmethemoglobin. (R022, R025, R066, R067, R173)","Mercury is absorbed mainly via ingestion and inhalation, then distributed throughout the body via the bloodstream, where a portion binds to sulfhydryl groups on haemoglobin. Mercury can undergo oxidation to mercuric mercury, which takes place via the catalase-hydrogen peroxide pathway. The mercury atom is able to diffuse down the cleft in the catalase enzyme to reach the active site where the heme ring is located. Oxidation most likely occurs in all tissue, as the catalase hydrogen peroxide pathway is ubiquitous. Following oxidation, mercury tends to accumulate in the kidneys. Mercury is excreted mainly by exhalation and in the faeces. Cyanide is rapidly alsorbed through oral, inhalation, and dermal routes and distributed throughout the body. Cyanide is mainly metabolized into thiocyanate by either rhodanese or 3-mercaptopyruvate sulfur transferase. Cyanide metabolites are excreted in the urine. (R021, R022, R172)","LD50: 46 mg/kg (Oral, Rat) (R742)
LD50: 685 mg/kg (Dermal, Rat) (R742)
LD50: 3.5 mg/kg (Intraperitoneal, Mouse) (R742)",200 to 300 milligrams for an adult human (cyanide salts). (R906),"3, not classifiable as to its carcinogenicity to humans. (R264)",Mercury(II) thiocyanate has previously been used in pyrotechnics. (R742),Chronic Inhalation: 0.0002 mg/m3 (Mercury) (R260),"Mercury mainly affects the nervous system. Exposure to high levels of metallic, inorganic, or organic mercury can permanently damage the brain, kidneys, and developing fetus. Effects on brain functioning may result in irritability, shyness, tremors, changes in vision or hearing, and memory problems. Acrodynia, a type of mercury poisoning in children, is characterized by pain and pink discoloration of the hands and feet. Mercury poisoning can also cause Hunter-Russell syndrome and Minamata disease. Exposure to high levels of cyanide for a short time harms the brain and heart and can even cause coma, seizures, apnea, cardiac arrest and death. Chronic inhalation of cyanide causes breathing difficulties, chest pain, vomiting, blood changes, headaches, and enlargement of the thyroid gland. Skin contact with cyanide salts can irritate and produce sores. (R022, R172, R173)","Common symptoms include peripheral neuropathy (presenting as paresthesia or itching, burning or pain), skin discoloration (pink cheeks, fingertips and toes), edema (swelling), and desquamation (dead skin peels off in layers). Cyanide poisoning is identified by rapid, deep breathing and shortness of breath, general weakness, giddiness, headaches, vertigo, confusion, convulsions/seizures and eventually loss of consciousness. (R020, R172, R173)","Mercury poisoning is treated by immediate decontamination and chelation therapy using DMSA, DMPS, DPCN, or dimercaprol. Antidotes to cyanide poisoning include hydroxocobalamin and sodium nitrite, which release the cyanide from the cytochrome system, and rhodanase, which is an enzyme occurring naturally in mammals that combines serum cyanide with thiosulfate, producing comparatively harmless thiocyanate. Oxygen therapy can also be administered. (R023, R173)",P04040;P06239;P05186;P29972;P55087;P55064;O14520;O94778;O43315;P30301;P17252;P05771;Q05655;Q02156;P24723;P05129;P41743;Q04759;Q05513;Q9UJT1;Q9UJT0;P10696;P24310;P14406;P00395;P00403;P00414;P13073;Q96KJ9;P20674;P10606;P12074;Q02221;P14854;Q6YFQ2;P09669;O60397;P24311;Q8TF08;P15954;P10176;Q7Z4L0;O75715;P08294;P07203;P18283;P22352;P59796;Q96SL4;P00390;P36969;Q8TED1 ;Q99643;O14521;P31040;P21912;P00441;P14679;Q96PS8;Q8NBQ7;Q8IXF9;A6NM10;P41181;Q92482;Q13520;A6NKZ8 ;Q99867;Q9H853;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2;P23258;Q9NRH3
358,T3D0357,2009-03-06 18:58:36 UTC,2009-08-25 19:52:52 UTC,Mercury(II) sulfate,Inorganic Compound;Mercury Compound,"Mercuric bisulphateMercuric sulfateMercuric sulphateMercurous bisulphateMercury bisulfateMercury bisulphatesMercury disulfateMercury persulfateMercury sulfate (HgSO4)Mercury sulphateMercury(II) sulfateMercury(II) sulfate (1:1)Mercury(II) sulfate-sulfuric acid solutionSulfate mercurique [french]Sulfuric acid, mercury(2+) salt (1:1)","Mercury(II) sulfate is a sulfate of mercury used mainly as a catalyst in the production of acetaldehyde. Mercury is a heavy, silvery d-block metal and one of six elements that are liquid at or near room temperature and pressure. It is a naturally occuring substance, and combines with other elements such as chlorine, sulfur, or oxygen to form inorganic mercury compounds (salts). Mercury also combines with carbon to make organic mercury compounds. (R005, R744)",,7783-35-9,24544,,"","","","",,C028430,Mercury(II) sulfate,,,,,"InChI=1/Hg.H2O4S/c;1-5(2,3)4/h;(H2,1,2,3,4)/q+2;/p-2",mercury(2+) sulfate,http://www.biospider.ca/saved_files/mol/,[O-]S(=O)(=O)[O-].[Hg+2],[O-]S(=O)(=O)[O-].[Hg+2],HgO4S,297.922350,White crystals.,"","","","","","","","Oral 
Inhalation 
Dermal 
(R022)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Catalase (P04040) 
Hemoglobin subunit alpha (P69905) 
Hemoglobin subunit beta (P68871) 
Hemoglobin subunit gamma-1 (P69891) 
Hemoglobin subunit gamma-2 (P69892) 
Hemoglobin subunit delta (P02042) 
Hemoglobin subunit epsilon (P02100) 
Hemoglobin subunit theta-1 (P09105) 
Hemoglobin subunit zeta (P02008) 
Hemoglobin subunit mu (Q6B0K9) 
(R022, R164) ","High-affinity binding of the divalent mercuric ion to thiol or sulfhydryl groups of proteins is believed to be the major mechanism for the activity of mercury. Through alterations in intracellular thiol status, mercury can promote oxidative stress, lipid peroxidation, mitochondrial dysfunction, and changes in heme metabolism. Mercury is known to bind to microsomal and mitochondrial enzymes, resulting in cell injury and death. For example, mercury is known to inhibit aquaporins, halting water flow across the cell membrane. It also inhibits the protein LCK, which causes decreased T-cell signalling and immune system depression. Mercury is also believed to inhibit neuronal excitability by acting on the postsynaptic neuronal membrane. It also affects the nervous system by inhibiting protein kinase C and alkaline phosphatase, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Mercury also produces an autoimmune response, likely by modification of major histocompatibility complex (MHC) class II molecules, self peptides, T-cell receptors, or cell-surface adhesion molecules. (R022, R025, R066, R067)","Mercury is absorbed mainly via ingestion and inhalation, then distributed throughout the body via the bloodstream, where a portion binds to sulfhydryl groups on haemoglobin. Mercury can undergo oxidation to mercuric mercury, which takes place via the catalase-hydrogen peroxide pathway. The mercury atom is able to diffuse down the cleft in the catalase enzyme to reach the active site where the heme ring is located. Oxidation most likely occurs in all tissue, as the catalase hydrogen peroxide pathway is ubiquitous. Following oxidation, mercury tends to accumulate in the kidneys. Mercury is excreted mainly by exhalation and in the faeces. (R021, R022)","LD50: 57 mg/kg (Oral, Rat) (R263)
LD50: 6300 ug/kg (Intraperitoneal, Mouse) (R743)",1 gram for an adult human (average for inorganic mercurials). (R273),"3, not classifiable as to its carcinogenicity to humans. (R264)",Mercury(II) sulfate is used mainly as a catalyst in the production of acetaldehyde. (R744),Chronic Inhalation: 0.0002 mg/m3 (R260),"Mercury mainly affects the nervous system. Exposure to high levels of metallic, inorganic, or organic mercury can permanently damage the brain, kidneys, and developing fetus. Effects on brain functioning may result in irritability, shyness, tremors, changes in vision or hearing, and memory problems. Acrodynia, a type of mercury poisoning in children, is characterized by pain and pink discoloration of the hands and feet. Mercury poisoning can also cause Hunter-Russell syndrome and Minamata disease. (R022)","Common symptoms include peripheral neuropathy (presenting as paresthesia or itching, burning or pain), skin discoloration (pink cheeks, fingertips and toes), edema (swelling), and desquamation (dead skin peels off in layers). (R020)","Mercury poisoning is treated by immediate decontamination and chelation therapy using DMSA, DMPS, DPCN, or dimercaprol. (R023)",P06239;P05186;P29972;P55087;P55064;O14520;O94778;O43315;P30301;P17252;P05771;Q05655;Q02156;P24723;P05129;P41743;Q04759;Q05513;Q9UJT1;Q9UJT0;Q96PS8;Q8NBQ7;Q8IXF9;A6NM10;P41181;Q92482;Q13520;A6NKZ8 ;Q99867;Q9H853;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2;P23258;Q9NRH3
359,T3D0358,2009-03-06 18:58:36 UTC,2009-08-25 19:52:52 UTC,Mercury(I) sulfate,Inorganic Compound;Mercury Compound,"Mercuric bisulphateMercuric sulfateMercuric sulphateMercurous bisulphateMercury bisulfateMercury bisulphatesMercury disulfateMercury persulfateMercury sulfate (HgSO4)Mercury sulphateMercury(II) sulfate (1:1)Mercury(II) sulfate-sulfuric acid solutionSulfate mercurique [french]Sulfuric acid, mercury(2+) salt (1:1)","Mercury(I) sulfate is a sulfate  of mercury used in the production of batteries. Mercury is a heavy, silvery d-block metal and one of six elements that are liquid at or near room temperature and pressure. It is a naturally occuring substance, and combines with other elements such as chlorine, sulfur, or oxygen to form inorganic mercury compounds (salts). Mercury also combines with carbon to make organic mercury compounds. (R005, R270)",,7783-36-0,24544,,"","","","",,,Mercury(I) sulfate,,,,,"InChI=1/Hg.H2O4S/c;1-5(2,3)4/h;(H2,1,2,3,4)/q+2;/p-2",mercury(2+) sulfate,http://www.biospider.ca/saved_files/mol/,[O-]S(=O)(=O)[O-].[Hg+2],[O-]S(=O)(=O)[O-].[Hg+2],HgO4S,297.922350,White crystals.,"","","","","","","","Oral 
Inhalation 
Dermal 
(R022)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Catalase (P04040) 
Hemoglobin subunit alpha (P69905) 
Hemoglobin subunit beta (P68871) 
Hemoglobin subunit gamma-1 (P69891) 
Hemoglobin subunit gamma-2 (P69892) 
Hemoglobin subunit delta (P02042) 
Hemoglobin subunit epsilon (P02100) 
Hemoglobin subunit theta-1 (P09105) 
Hemoglobin subunit zeta (P02008) 
Hemoglobin subunit mu (Q6B0K9) 
(R022, R164) ","High-affinity binding of the divalent mercuric ion to thiol or sulfhydryl groups of proteins is believed to be the major mechanism for the activity of mercury. Through alterations in intracellular thiol status, mercury can promote oxidative stress, lipid peroxidation, mitochondrial dysfunction, and changes in heme metabolism. Mercury is known to bind to microsomal and mitochondrial enzymes, resulting in cell injury and death. For example, mercury is known to inhibit aquaporins, halting water flow across the cell membrane. It also inhibits the protein LCK, which causes decreased T-cell signalling and immune system depression. Mercury is also believed to inhibit neuronal excitability by acting on the postsynaptic neuronal membrane. It also affects the nervous system by inhibiting protein kinase C and alkaline phosphatase, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Mercury also produces an autoimmune response, likely by modification of major histocompatibility complex (MHC) class II molecules, self peptides, T-cell receptors, or cell-surface adhesion molecules. (R022, R025, R066, R067)","Mercury is absorbed mainly via ingestion and inhalation, then distributed throughout the body via the bloodstream, where a portion binds to sulfhydryl groups on haemoglobin. Mercury can undergo oxidation to mercuric mercury, which takes place via the catalase-hydrogen peroxide pathway. The mercury atom is able to diffuse down the cleft in the catalase enzyme to reach the active site where the heme ring is located. Oxidation most likely occurs in all tissue, as the catalase hydrogen peroxide pathway is ubiquitous. Following oxidation, mercury tends to accumulate in the kidneys. Mercury is excreted mainly by exhalation and in the faeces. (R021, R022)",No data.,1 gram for an adult human (average for inorganic mercurials). (R273),"3, not classifiable as to its carcinogenicity to humans. (R264)",Mercury(I) sulfate is used in the production of batteries. (R270),Chronic Inhalation: 0.0002 mg/m3 (R260),"Mercury mainly affects the nervous system. Exposure to high levels of metallic, inorganic, or organic mercury can permanently damage the brain, kidneys, and developing fetus. Effects on brain functioning may result in irritability, shyness, tremors, changes in vision or hearing, and memory problems. Acrodynia, a type of mercury poisoning in children, is characterized by pain and pink discoloration of the hands and feet. Mercury poisoning can also cause Hunter-Russell syndrome and Minamata disease. (R022)","Common symptoms include peripheral neuropathy (presenting as paresthesia or itching, burning or pain), skin discoloration (pink cheeks, fingertips and toes), edema (swelling), and desquamation (dead skin peels off in layers). (R020)","Mercury poisoning is treated by immediate decontamination and chelation therapy using DMSA, DMPS, DPCN, or dimercaprol. (R023)",P06239;P05186;P29972;P55087;P55064;O14520;O94778;O43315;P30301;P17252;P05771;Q05655;Q02156;P24723;P05129;P41743;Q04759;Q05513;Q9UJT1;Q9UJT0;Q96PS8;Q8NBQ7;Q8IXF9;A6NM10;P41181;Q92482;Q13520;A6NKZ8 ;Q99867;Q9H853;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2;P23258;Q9NRH3
361,T3D0360,2009-03-06 18:58:37 UTC,2009-08-25 21:15:52 UTC,Methylmercuric chloride,Organic Compound;Mercury Compound;Organometallic,Carbocyclic bvdu,"Methylmercuric chloride is an organomercuric compound. Mercury is a heavy, silvery d-block metal and one of six elements that are liquid at or near room temperature and pressure. It is a naturally occuring substance, and combines with other elements such as chlorine, sulfur, or oxygen to form inorganic mercury compounds (salts). Mercury also combines with carbon to make organic mercury compounds. (R005)",,125-09-3,5466678,,"","","","",,,Methylmercuric chloride,,,,,"InChI=1/C12H15BrN2O4/c13-2-1-7-5-15(12(19)14-11(7)18)9-3-8(6-16)10(17)4-9/h1-2,5,8-10,16-17H,3-4,6H2,(H,14,18,19)/b2-1+/t8-,9-,10-/m1/s1","5-[(E)-2-bromoethenyl]-1-[(1R,3R,4R)-3-hydroxy-4-(hydroxymethyl)cyclopentyl]pyrimidine-2,4-dione",http://www.biospider.ca/saved_files/mol/,C1[C@H](C[C@H]([C@H]1CO)O)N2C=C(C(=O)NC2=O)/C=C/Br,C[Hg]Cl,C12H15BrN2O4,330.021520,White crystals.,"","","","","","","","Oral 
Inhalation 
Dermal 
(R022)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Catalase (P04040) 
Hemoglobin subunit alpha (P69905) 
Hemoglobin subunit beta (P68871) 
Hemoglobin subunit gamma-1 (P69891) 
Hemoglobin subunit gamma-2 (P69892) 
Hemoglobin subunit delta (P02042) 
Hemoglobin subunit epsilon (P02100) 
Hemoglobin subunit theta-1 (P09105) 
Hemoglobin subunit zeta (P02008) 
Hemoglobin subunit mu (Q6B0K9) 
(R022, R164) ","High-affinity binding of the divalent mercuric ion to thiol or sulfhydryl groups of proteins is believed to be the major mechanism for the activity of mercury. Through alterations in intracellular thiol status, mercury can promote oxidative stress, lipid peroxidation, mitochondrial dysfunction, and changes in heme metabolism. Mercury is known to bind to microsomal and mitochondrial enzymes, resulting in cell injury and death. For example, mercury is known to inhibit aquaporins, halting water flow across the cell membrane. It also inhibits the protein LCK, which causes decreased T-cell signalling and immune system depression. Mercury is also believed to inhibit neuronal excitability by acting on the postsynaptic neuronal membrane. It also affects the nervous system by inhibiting protein kinase C and alkaline phosphatase, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Organic mercury exerts developmental effects by binding to tubulin, preventing microtubule assembly and causing mitotic inhibition. Mercury also produces an autoimmune response, likely by modification of major histocompatibility complex (MHC) class II molecules, self peptides, T-cell receptors, or cell-surface adhesion molecules. (R022, R025, R066, R067)","Organic mercury is absorbed mainly by the gastrointestinal tract, then distributed throughout the body via the bloodstream. Organic mercury complexes with free cysteine and the cysteine and sulfhydryl groups on proteins such as haemoglobin. These complexes are able to mimic methionine and thus be transported throughout the body, including through the blood-brain barrier and placenta. Organic mercury is metabolized into inorganic mercury, which is eventually excreted in the urine and faeces. (R033)","LD50: 21 mg/kg (Oral, Guinea pig) (R745)
LD50: 11 mg/kg (Intraperitoneal, Rat) (R745)",100 mg for an adult human (average for organic mercurials). (R273),"2B, possibly carcinogenic to humans. (R264)",Methylmercuric chloride is used as fungicide (S272).,Chronic Inhalation: 0.0002 mg/m3 (R260),"Mercury mainly affects the nervous system. Exposure to high levels of metallic, inorganic, or organic mercury can permanently damage the brain, kidneys, and developing fetus. Effects on brain functioning may result in irritability, shyness, tremors, changes in vision or hearing, and memory problems. Acrodynia, a type of mercury poisoning in children, is characterized by pain and pink discoloration of the hands and feet. Mercury poisoning can also cause Hunter-Russell syndrome and Minamata disease. (R022)","Common symptoms include peripheral neuropathy (presenting as paresthesia or itching, burning or pain), skin discoloration (pink cheeks, fingertips and toes), edema (swelling), and desquamation (dead skin peels off in layers). (R020)","Mercury poisoning is treated by immediate decontamination and chelation therapy using DMSA, DMPS, DPCN, or dimercaprol. (R023)",P06239;P05186;P29972;P55087;P55064;O14520;O94778;O43315;P30301;P17252;P05771;Q05655;Q02156;P24723;P05129;P41743;Q04759;Q05513;Q9UJT1;Q9UJT0;Q96PS8;Q8NBQ7;Q8IXF9;A6NM10;P41181;Q92482;Q13520;A6NKZ8 ;Q99867;Q9H853;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2;P23258;Q9NRH3
362,T3D0361,2009-03-06 18:58:37 UTC,2009-08-25 19:52:54 UTC,Dimethyl mercury,Organic Compound;Mercury Compound;Organometallic,(CH3)2HgDimethyl mercuryDimethylmercuryDimethylmercury [mercury and mercury compounds]Methylmercury[HgMe2],"Dimethyl mercury is an organomercuric compound. It is often considered to be the most dangerous mercury compound due to its strong neurotixic effects. Dimethyl mercury has a slightly sweet smell and tends to bioaccumulate due to its slow metabolic elimination rate. Mercury is a heavy, silvery d-block metal and one of six elements that are liquid at or near room temperature and pressure. It is a naturally occuring substance, and combines with other elements such as chlorine, sulfur, or oxygen to form inorganic mercury compounds (salts). Mercury also combines with carbon to make organic mercury compounds. (R005, R481)",,593-74-8,11645,,"","",30786,CPD0-1309,,C073972,Dimethyl mercury,,,,,InChI=1/2CH3.Hg/h2*1H3;,dimethylmercury,http://www.biospider.ca/saved_files/mol/,C[Hg]C,C[Hg]C,C2H6Hg,232.017580,Colorless liquid.,< 25 oC,"","","","","","","Oral 
Inhalation 
Dermal 
(R022)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Catalase (P04040) 
Hemoglobin subunit alpha (P69905) 
Hemoglobin subunit beta (P68871) 
Hemoglobin subunit gamma-1 (P69891) 
Hemoglobin subunit gamma-2 (P69892) 
Hemoglobin subunit delta (P02042) 
Hemoglobin subunit epsilon (P02100) 
Hemoglobin subunit theta-1 (P09105) 
Hemoglobin subunit zeta (P02008) 
Hemoglobin subunit mu (Q6B0K9) 
(R022, R164) ","High-affinity binding of the divalent mercuric ion to thiol or sulfhydryl groups of proteins is believed to be the major mechanism for the activity of mercury. Through alterations in intracellular thiol status, mercury can promote oxidative stress, lipid peroxidation, mitochondrial dysfunction, and changes in heme metabolism. Mercury is known to bind to microsomal and mitochondrial enzymes, resulting in cell injury and death. For example, mercury is known to inhibit aquaporins, halting water flow across the cell membrane. It also inhibits the protein LCK, which causes decreased T-cell signalling and immune system depression. Mercury is also believed to inhibit neuronal excitability by acting on the postsynaptic neuronal membrane. It also affects the nervous system by inhibiting protein kinase C and alkaline phosphatase, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Organic mercury exerts developmental effects by binding to tubulin, preventing microtubule assembly and causing mitotic inhibition. Mercury also produces an autoimmune response, likely by modification of major histocompatibility complex (MHC) class II molecules, self peptides, T-cell receptors, or cell-surface adhesion molecules. (R022, R025, R066, R067)","Organic mercury is absorbed mainly by the gastrointestinal tract, then distributed throughout the body via the bloodstream. Organic mercury complexes with free cysteine and the cysteine and sulfhydryl groups on proteins such as haemoglobin. These complexes are able to mimic methionine and thus be transported throughout the body, including through the blood-brain barrier and placenta. Organic mercury is metabolized into inorganic mercury, which is eventually excreted in the urine and faeces. (R033)",No data.,100 mg for an adult human (average for organic mercurials). (R273),"2B, possibly carcinogenic to humans. (R264)",Dimethylmercury is most often used in toxicology experiments as a fixed point of reference due to its extreme toxicity. It has also been used to calibrate NMR instruments for detection of mercury. (R481),Chronic Inhalation: 0.0002 mg/m3 (R260),"Mercury mainly affects the nervous system. Exposure to high levels of metallic, inorganic, or organic mercury can permanently damage the brain, kidneys, and developing fetus. Effects on brain functioning may result in irritability, shyness, tremors, changes in vision or hearing, and memory problems. Acrodynia, a type of mercury poisoning in children, is characterized by pain and pink discoloration of the hands and feet. Mercury poisoning can also cause Hunter-Russell syndrome and Minamata disease. (R022)","Common symptoms include peripheral neuropathy (presenting as paresthesia or itching, burning or pain), skin discoloration (pink cheeks, fingertips and toes), edema (swelling), and desquamation (dead skin peels off in layers). (R020)","Mercury poisoning is treated by immediate decontamination and chelation therapy using DMSA, DMPS, DPCN, or dimercaprol. (R023)",P06239;P68363;Q13748;P68366;P07437;Q13885;P68371;Q13509;P04350;P23258;P29972;P41181;Q92482;P55087;P55064;Q13520;O14520;O94778;O43315;Q96PS8;Q8NBQ7;Q8IXF9;Q71U36;Q9BQE3;Q6PEY2;Q9NY65;Q9H4B7;Q9BVA1;Q9BUF5;Q3ZCM7;Q9UJT1;Q9UJT0;Q9NRH3;P05186;A6NM10;P30301;P17252;P05771;Q05655;Q02156;P24723;P05129;P41743;Q04759;Q05513;A6NKZ8 ;Q99867;Q9H853;A6NHL2;A6NNZ2
363,T3D0362,2009-03-06 18:58:37 UTC,2009-08-25 19:52:54 UTC,Mercuric potassium iodide,Inorganic Compound;Mercury Compound,"Caswell No. 695Channing's solutionDipotassium tetraiodomercurateK2[HgI4]Kaliumtetraiodomercurat(II)Mayer's reagentMercurate (2-), tetraiodo-, dipotassiumMercurate(2-), tetraiodo-, dipotassiumMercurate(2-), tetraiodo-, dipotassium, (T-4)-Mercurate(2-), tetraiodo-, dipotassium, (beta-4)-Mercuric potassium iodideMercuric potassium iodide, solidMercury potassium iodideMercury potassium iodide (K2HgI4)Mercury potassium iodide [UN1643] [Poison]Mercury(II) chloride - potassium iodide solutionMercury(II) potassium iodideNessler reagentNessler's reagentNesslers reagenzPotassium iodomercuratePotassium mercurIIodidePotassium mercuric iodidePotassium mercury iodinePotassium tetraiodidomercuratePotassium tetraiodidomercurate(II)Potassium tetraiodomercuratePotassium tetraiodomercurate (II)Potassium tetraiodomercurate - potassium hydroxide solutionPotassium tetraiodomercurate(II)Reactivo de nesslerSolution potassium iodohydragyratedipotassium tetraiodomercurate(2-)potassium tetraiodidomercurate(2-)","Mercuric potassium iodide is a chemical compound of mercury, potassium, and iodide. Mercury is a heavy, silvery d-block metal and one of six elements that are liquid at or near room temperature and pressure. It is a naturally occuring substance, and combines with other elements such as chlorine, sulfur, or oxygen to form inorganic mercury compounds (salts). Mercury also combines with carbon to make organic mercury compounds. (R005)",,7783-33-7 ,24542,,"","",51568,"",,C009009,Mercuric potassium iodide,,,,,InChI=1/Hg.4HI.2K/h;4*1H;;/q+2;;;;;2*+1/p-4,dipotassium tetraiodomercury(2-),http://www.biospider.ca/saved_files/mol/,[K+].[K+].I[Hg-2](I)(I)I,[K+].[K+].I[Hg--](I)(I)I,HgI4K2,787.515910,Yellow crystals.,"","","","","","","","Oral 
Inhalation 
Dermal 
(R022)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Catalase (P04040) 
Hemoglobin subunit alpha (P69905) 
Hemoglobin subunit beta (P68871) 
Hemoglobin subunit gamma-1 (P69891) 
Hemoglobin subunit gamma-2 (P69892) 
Hemoglobin subunit delta (P02042) 
Hemoglobin subunit epsilon (P02100) 
Hemoglobin subunit theta-1 (P09105) 
Hemoglobin subunit zeta (P02008) 
Hemoglobin subunit mu (Q6B0K9) 
(R022, R164) ","High-affinity binding of the divalent mercuric ion to thiol or sulfhydryl groups of proteins is believed to be the major mechanism for the activity of mercury. Through alterations in intracellular thiol status, mercury can promote oxidative stress, lipid peroxidation, mitochondrial dysfunction, and changes in heme metabolism. Mercury is known to bind to microsomal and mitochondrial enzymes, resulting in cell injury and death. For example, mercury is known to inhibit aquaporins, halting water flow across the cell membrane. It also inhibits the protein LCK, which causes decreased T-cell signalling and immune system depression. Mercury is also believed to inhibit neuronal excitability by acting on the postsynaptic neuronal membrane. It also affects the nervous system by inhibiting protein kinase C and alkaline phosphatase, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Mercury also produces an autoimmune response, likely by modification of major histocompatibility complex (MHC) class II molecules, self peptides, T-cell receptors, or cell-surface adhesion molecules. (R022, R025, R066, R067)","Mercury is absorbed mainly via ingestion and inhalation, then distributed throughout the body via the bloodstream, where a portion binds to sulfhydryl groups on haemoglobin. Mercury can undergo oxidation to mercuric mercury, which takes place via the catalase-hydrogen peroxide pathway. The mercury atom is able to diffuse down the cleft in the catalase enzyme to reach the active site where the heme ring is located. Oxidation most likely occurs in all tissue, as the catalase hydrogen peroxide pathway is ubiquitous. Following oxidation, mercury tends to accumulate in the kidneys. Mercury is excreted mainly by exhalation and in the faeces. (R021, R022)",Not available.,1 gram for an adult human (average for inorganic mercurials). (R273),"3, not classifiable as to its carcinogenicity to humans. (R264)",In analytical chemistry Nessler's reagent is a reagent used to detect small concentrations of ammonia (S273).,Chronic Inhalation: 0.0002 mg/m3 (R260),"Mercury mainly affects the nervous system. Exposure to high levels of metallic, inorganic, or organic mercury can permanently damage the brain, kidneys, and developing fetus. Effects on brain functioning may result in irritability, shyness, tremors, changes in vision or hearing, and memory problems. Acrodynia, a type of mercury poisoning in children, is characterized by pain and pink discoloration of the hands and feet. Mercury poisoning can also cause Hunter-Russell syndrome and Minamata disease. (R022)","Common symptoms include peripheral neuropathy (presenting as paresthesia or itching, burning or pain), skin discoloration (pink cheeks, fingertips and toes), edema (swelling), and desquamation (dead skin peels off in layers). (R020)","Mercury poisoning is treated by immediate decontamination and chelation therapy using DMSA, DMPS, DPCN, or dimercaprol. (R023)",P06239;P05186;P29972;Q96PS8;Q8NBQ7;Q8IXF9;A6NM10;P41181;Q92482;P55087;P55064;Q13520;O14520;O94778;O43315;P30301;P17252;P05771;Q05655;Q02156;P24723;P05129;P41743;Q04759;Q05513;A6NKZ8 ;Q99867;Q9H853;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2;Q9UJT1;Q9UJT0;P23258;Q9NRH3
364,T3D0363,2009-03-06 18:58:37 UTC,2009-08-05 21:38:45 UTC,Mercury(II) cyanide,Inorganic Compound;Mercury Compound;Cyanide Compound,CianurinaCyanure de mercureCyanure de mercure [french]DicyanomercuryHydrargyrum cyanatumMercuric cyanideMercurius cyanatusMercury cyanideMercury cyanide (Hg(CN)2)Mercury cyanide [UN1636] [Poison]Mercury dicyanideMercury(II) cyanideQuecksilber(II)-cyanid[Hg(CN)2],"Mercuric cyanide is a chemical compound of mercury and cyanide used as a laboratory reagent and occasionally as an antiseptic in veterinary medicine. Mercury is a heavy, silvery d-block metal and one of six elements that are liquid at or near room temperature and pressure. It is a naturally occuring substance, and combines with other elements such as chlorine, sulfur, or oxygen to form inorganic mercury compounds (salts). Mercury also combines with carbon to make organic mercury compounds. (R005, R763)",,592-04-1,11591,,"","",36573,"",,C040189,Mercury(II) cyanide,,,,,InChI=1/2CN.Hg/c2*1-2;,dicyanomercury,http://www.biospider.ca/saved_files/mol/,C(#N)[Hg]C#N,C(#N)[Hg]C#N,C2HgN2,253.976770,White powder.,"","","",71.4 mg/mL [MERCK INDEX (1996)],"","","","Oral 
Inhalation 
Dermal 
(R022)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Catalase (P04040) 
Hemoglobin subunit alpha (P69905) 
Hemoglobin subunit beta (P68871) 
Hemoglobin subunit gamma-1 (P69891) 
Hemoglobin subunit gamma-2 (P69892) 
Hemoglobin subunit delta (P02042) 
Hemoglobin subunit epsilon (P02100) 
Hemoglobin subunit theta-1 (P09105) 
Hemoglobin subunit zeta (P02008) 
Hemoglobin subunit mu (Q6B0K9)
Thiosulfate sulfurtransferase (Q16762) 
3-mercaptopyruvate sulfurtransferase (P25325)  
(R022, R164, R172)","High-affinity binding of the divalent mercuric ion to thiol or sulfhydryl groups of proteins is believed to be the major mechanism for the activity of mercury. Through alterations in intracellular thiol status, mercury can promote oxidative stress, lipid peroxidation, mitochondrial dysfunction, and changes in heme metabolism. Mercury is known to bind to microsomal and mitochondrial enzymes, resulting in cell injury and death. For example, mercury is known to inhibit aquaporins, halting water flow across the cell membrane. It also inhibits the protein LCK, which causes decreased T-cell signalling and immune system depression. Mercury is also believed to inhibit neuronal excitability by acting on the postsynaptic neuronal membrane. It also affects the nervous system by inhibiting protein kinase C and alkaline phosphatase, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Mercury also produces an autoimmune response, likely by modification of major histocompatibility complex (MHC) class II molecules, self peptides, T-cell receptors, or cell-surface adhesion molecules. Cyanide is an inhibitor of cytochrome c oxidase in the fourth complex of the electron transport chain (found in the membrane of the mitochondria of eukaryotic cells). It complexes with the ferric iron atom in this enzyme. The binding of cyanide to this cytochrome prevents transport of electrons from cytochrome c oxidase to oxygen. As a result, the electron transport chain is disrupted and the cell can no longer aerobically produce ATP for energy. Tissues that mainly depend on aerobic respiration, such as the central nervous system and the heart, are particularly affected. Cyanide is also known produce some of its toxic effects by binding to catalase, glutathione peroxidase, methemoglobin, hydroxocobalamin, phosphatase, tyrosinase, ascorbic acid oxidase, xanthine oxidase, succinic dehydrogenase, and Cu/Zn superoxide dismutase. Cyanide binds to the ferric ion of methemoglobin to form inactive cyanmethemoglobin. (R022, R025, R066, R067, R173)","Mercury is absorbed mainly via ingestion and inhalation, then distributed throughout the body via the bloodstream, where a portion binds to sulfhydryl groups on haemoglobin. Mercury can undergo oxidation to mercuric mercury, which takes place via the catalase-hydrogen peroxide pathway. The mercury atom is able to diffuse down the cleft in the catalase enzyme to reach the active site where the heme ring is located. Oxidation most likely occurs in all tissue, as the catalase hydrogen peroxide pathway is ubiquitous. Following oxidation, mercury tends to accumulate in the kidneys. Mercury is excreted mainly by exhalation and in the faeces. Cyanide is rapidly alsorbed through oral, inhalation, and dermal routes and distributed throughout the body. Cyanide is mainly metabolized into thiocyanate by either rhodanese or 3-mercaptopyruvate sulfur transferase. Cyanide metabolites are excreted in the urine. (R021, R022, R172)","LD50: 33 mg/kg (Oral, Mouse) (R263)
LD50: 2710 ug/kg (Subcutaneous, Dog) (R263)",200 to 300 milligrams for an adult human (cyanide salts). (R906),,Mercuric cyanide is used as a laboratory reagent and occasionally as an antiseptic in veterinary medicine. (R763),Chronic Inhalation: 0.0002 mg/m3 (Mercury) (R260),"Mercury mainly affects the nervous system. Exposure to high levels of metallic, inorganic, or organic mercury can permanently damage the brain, kidneys, and developing fetus. Effects on brain functioning may result in irritability, shyness, tremors, changes in vision or hearing, and memory problems. Acrodynia, a type of mercury poisoning in children, is characterized by pain and pink discoloration of the hands and feet. Mercury poisoning can also cause Hunter-Russell syndrome and Minamata disease. Exposure to high levels of cyanide for a short time harms the brain and heart and can even cause coma, seizures, apnea, cardiac arrest and death. Chronic inhalation of cyanide causes breathing difficulties, chest pain, vomiting, blood changes, headaches, and enlargement of the thyroid gland. Skin contact with cyanide salts can irritate and produce sores. (R022, R172, R173)","Common symptoms include peripheral neuropathy (presenting as paresthesia or itching, burning or pain), skin discoloration (pink cheeks, fingertips and toes), edema (swelling), and desquamation (dead skin peels off in layers). Cyanide poisoning is identified by rapid, deep breathing and shortness of breath, general weakness, giddiness, headaches, vertigo, confusion, convulsions/seizures and eventually loss of consciousness. (R020, R172, R173)","Mercury poisoning is treated by immediate decontamination and chelation therapy using DMSA, DMPS, DPCN, or dimercaprol. Antidotes to cyanide poisoning include hydroxocobalamin and sodium nitrite, which release the cyanide from the cytochrome system, and rhodanase, which is an enzyme occurring naturally in mammals that combines serum cyanide with thiosulfate, producing comparatively harmless thiocyanate. Oxygen therapy can also be administered. (R023, R173)",P04040;P06239;P05186;P29972;P55087;P55064;O14520;O94778;O43315;P30301;P17252;P05771;Q05655;Q02156;P24723;P05129;P41743;Q04759;Q05513;Q9UJT1;Q9UJT0;P10696;P24310;P14406;P00395;P00403;P00414;P13073;Q96KJ9;P20674;P10606;P12074;Q02221;P14854;Q6YFQ2;P09669;O60397;P24311;Q8TF08;P15954;P10176;Q7Z4L0;O75715;P08294;P07203;P18283;P22352;P59796;Q96SL4;P00390;P36969;Q8TED1 ;Q99643;O14521;P31040;P21912;P00441;P14679;Q96PS8;Q8NBQ7;Q8IXF9;A6NM10;P41181;Q92482;Q13520;A6NKZ8 ;Q99867;Q9H853;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2;P23258;Q9NRH3
365,T3D0364,2009-03-06 18:58:37 UTC,2009-08-04 21:28:24 UTC,Cadmium acetate,Organic Compound;Cadmium Compound;Organometallic,"ACTACYAcetasolAcetateAcetic Acid Dps 4ch-30chAcetic Acid Liquid(S#223)-LiqAcetic acid (natural)Acetic acid [jan]Acetic acid, aqueous solutionAcetic acid, cadmium saltAcetic acid, cadmium salt dihydrateAcetic acid, cadmium salt, dihydrateAcetic acid, dilutedAcetic acid, glacialAcetic acid, glacial [usan:jan]Acetic acid, water solutionsAceticum acidumAci-jelAcide acetiqueAcide acetique [french]Acido aceticoAcido acetico [italian]AzijnzuurAzijnzuur [dutch]Bis(acetoxy)cadmiumCH3COOHCadmium acetateCadmium acetate [cadmium and cadmium compounds]Cadmium acetate dihydrateCadmium acetate dihydrate (chemical mixture)Cadmium acetate, dihydrateCadmium acetate, trihydrateCadmium di(acetate)Cadmium diacetateCadmium diacetate dihydrateCadmium ethanoateCadmium(II) acetateCaswell No. 003EssigsaeureEssigsaeure [german]EthanoateEthanoic acidEthanoic acid monomerEthylateEthylic acidFEMA No. 2006FEMA Number 2006FMTGlacial acetateGlacial acetic acidHSDB 40Kyselina octovaKyselina octova [czech]MethanecarboxylateMethanecarboxylic acidMixture nameOctowy kwasOctowy kwas [polish]Otic domeboroOtic tridesilonPyroligneous acidShotgunSodium acetateSodium acetate, anhydrous or trihydrateTCLP extraction fluid 2VinegarVinegar acidWLN: QV1acetic acid (ACD/Name 4.0)","Cadmium acetate is a chemical compound of cadmium. It is used for glazing ceramics and pottery, in electroplating baths, in dyeing and printing textiles, and as an analytic reagent for sulfur, selenium and tellurium. Cadmium is a transition metal and chemical element with the symbol Cd and atomic number 48. It is found naturally in the earth's crust, though rarely on it's own. (R019, R755)",,543-90-8,10986,,C00033,"276100
601705",15366,ACET,,C028031,Cadmium acetate,,,,,"InChI=1/C2H4O2/c1-2(3)4/h1H3,(H,3,4)",cadmium(2+) diacetate,http://www.biospider.ca/saved_files/mol/,CC(=O)[O-].CC(=O)[O-].[Cd+2],CC(O)=O,C4H6CdO4,60.021130,Colorless crystals.,16.6 oC,,,"",,,,"Oral 
Inhalation 
Dermal 
(R019)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640)
 Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Serum albumin (P02768) 
(R019, R164)","Cadmium initially binds to metallothionein and is transported to the kidney. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Accumulation of cadmium in the kidney results in increased excretion of vital low and high weight molecular proteins. Cadmium is a high affinity zinc analog and can interfere in its biological processes. It also binds to and activates the estrogen receptor, likely stimulating the growth of certain types of cancer cells and causing other estrogenic effects, such as reproductive dysfunction. Cadmium causes cell apoptosis by activating mitogen-activated protein kinases. (R026, R058, R059, R069)","Cadmium is absorbed from oral, inhalation, and dermal routes. Cadmium initially binds to metallothionein and albumin and is transported mainly to the kidney and liver. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Cadmium is not known to undergo any direct metabolic conversion and is excreted unchanged, mainly in the urine. (R019)","LD50: 225 mg/kg (Oral, Rat) (R757)
LD50: 14 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"1, carcinogenic to humans. (R264)","Cadmium acetate is used for glazing ceramics and pottery, in electroplating baths, in dyeing and printing textiles, and as an analytic reagent for sulfur, selenium and tellurium. (R755)","Acute Inhalation: 0.00003 mg/m3 (R260) 
Chronic Inhalation: 0.00001 mg/m3 (R260) 
Intermediate Oral: 0.0005 mg/kg/day (R260) 
Chronic Oral: 0.0001 mg/kg/day (R260)","Chronic exposure to cadmium fumes can cause chemical pneumonitis, pulmonary edema, and lung diseases such as bronchitis and emphysema. Cadmium also accumulates in the kidneys, causing permanent damage. Loss of bone density also occurs. (R019)","Acute inhalation of cadmium fumes results in metal fume fever, which is characterized by chills, fever, headache, weakness, dryness of the nose and throat, chest pain, and coughing. Ingestion of cadmium causes vomiting and diarrhea. (R019)","Cadmium poisoning is treated by removal from exposure and supportive care. If ingested, induced vomiting or gastric lavage may be performed. (R272)",Q9UQF2;Q13387;Q9UPT6;O60271;P03372;Q92731;P28482;P53779;Q15759;P53778;O15264;Q16539;Q8TD08;P27361;P31152;Q16659;Q13164;P45983;P45984
366,T3D0365,2009-03-06 18:58:37 UTC,2009-08-25 18:02:09 UTC,Cadmium acetate hydrate,Organic Compound;Cadmium Compound;Organometallic,"Acetic acid, cadmium saltAcetic acid, cadmium salt dihydrateAcetic acid, cadmium salt, dihydrateBis(acetoxy)cadmiumCadmium acetateCadmium acetate [cadmium and cadmium compounds]Cadmium acetate dihydrateCadmium acetate dihydrate (chemical mixture)Cadmium acetate, dihydrateCadmium acetate, trihydrateCadmium di(acetate)Cadmium diacetateCadmium diacetate dihydrateCadmium ethanoateCadmium(II) acetate","Cadmium acetate hydrate is a chemical compound of cadmium. Cadmium is a transition metal and chemical element with the symbol Cd and atomic number 48. It is found naturally in the earth's crust, though rarely on it's own. (R019)",,89759-80-8,10986,,"","","","",,,Cadmium acetate hydrate,,,,,"InChI=1/2C2H4O2.Cd/c2*1-2(3)4;/h2*1H3,(H,3,4);/q;;+2/p-2",cadmium(2+) diacetate,http://www.biospider.ca/saved_files/mol/,"",CC(=O)O[Cd]OC(C)=O,C4H6CdO4,231.929970,No data.,"",,,"",,,,"Oral 
Inhalation 
Dermal 
(R019)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640)
 Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Serum albumin (P02768) 
(R019, R164)","Cadmium initially binds to metallothionein and is transported to the kidney. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Accumulation of cadmium in the kidney results in increased excretion of vital low and high weight molecular proteins. Cadmium is a high affinity zinc analog and can interfere in its biological processes. It also binds to and activates the estrogen receptor, likely stimulating the growth of certain types of cancer cells and causing other estrogenic effects, such as reproductive dysfunction. Cadmium causes cell apoptosis by activating mitogen-activated protein kinases. (R026, R058, R059, R069)","Cadmium is absorbed from oral, inhalation, and dermal routes. Cadmium initially binds to metallothionein and albumin and is transported mainly to the kidney and liver. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Cadmium is not known to undergo any direct metabolic conversion and is excreted unchanged, mainly in the urine. (R019)",No data.,No data.,"1, carcinogenic to humans. (R264)",No data.,"Acute Inhalation: 0.00003 mg/m3 (R260) 
Chronic Inhalation: 0.00001 mg/m3 (R260) 
Intermediate Oral: 0.0005 mg/kg/day (R260) 
Chronic Oral: 0.0001 mg/kg/day (R260)","Chronic exposure to cadmium fumes can cause chemical pneumonitis, pulmonary edema, and lung diseases such as bronchitis and emphysema. Cadmium also accumulates in the kidneys, causing permanent damage. Loss of bone density also occurs. (R019)","Acute inhalation of cadmium fumes results in metal fume fever, which is characterized by chills, fever, headache, weakness, dryness of the nose and throat, chest pain, and coughing. Ingestion of cadmium causes vomiting and diarrhea. (R019)","Cadmium poisoning is treated by removal from exposure and supportive care. If ingested, induced vomiting or gastric lavage may be performed. (R272)",P28482;P53779;P27361;P31152;Q16659;Q13164;P45983;P45984;Q9UQF2;Q13387;Q9UPT6;O60271;P03372;Q92731;Q15759;P53778;O15264;Q16539;Q8TD08
367,T3D0366,2009-03-06 18:58:37 UTC,2009-08-19 19:37:32 UTC,Cadmium acetate dihydrate,Organic Compound;Cadmium Compound;Organometallic,"Cadmium acetateCadmium acetate dihydrateCadmium acetate, dihydrateCadmium diacetate dihydrate","Cadmium acetate dihydrate is a chemical compound of cadmium. Cadmium is a transition metal and chemical element with the symbol Cd and atomic number 48. It is found naturally in the earth's crust, though rarely on it's own. (R019)",,5743-04-4,6537495,,"","","","",,,Cadmium acetate dihydrate,,,,,"InChI=1/2C2H4O2.Cd/c2*1-2(3)4;/h2*1H3,(H,3,4);/q;;+2/p-2",cadmium(2+) diacetate dihydrate,http://www.biospider.ca/saved_files/mol/,CC(=O)[O-].CC(=O)[O-].O.O.[Cd+2],O.O.[Cd++].CC([O-])=O.CC([O-])=O,C4H10CdO6,267.951100,White solid (S274).,"",,,"",,,,"Oral 
Inhalation 
Dermal 
(R019)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640)
 Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Serum albumin (P02768) 
(R019, R164)","Cadmium initially binds to metallothionein and is transported to the kidney. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Accumulation of cadmium in the kidney results in increased excretion of vital low and high weight molecular proteins. Cadmium is a high affinity zinc analog and can interfere in its biological processes. It also binds to and activates the estrogen receptor, likely stimulating the growth of certain types of cancer cells and causing other estrogenic effects, such as reproductive dysfunction. Cadmium causes cell apoptosis by activating mitogen-activated protein kinases. (R026, R058, R059, R069)","Cadmium is absorbed from oral, inhalation, and dermal routes. Cadmium initially binds to metallothionein and albumin and is transported mainly to the kidney and liver. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Cadmium is not known to undergo any direct metabolic conversion and is excreted unchanged, mainly in the urine. (R019)","LD50: 360 mg/kg (Oral, Rat) (R756)",No data.,"1, carcinogenic to humans. (R264)",No data.,"Acute Inhalation: 0.00003 mg/m3 (R260) 
Chronic Inhalation: 0.00001 mg/m3 (R260) 
Intermediate Oral: 0.0005 mg/kg/day (R260) 
Chronic Oral: 0.0001 mg/kg/day (R260)","Chronic exposure to cadmium fumes can cause chemical pneumonitis, pulmonary edema, and lung diseases such as bronchitis and emphysema. Cadmium also accumulates in the kidneys, causing permanent damage. Loss of bone density also occurs. (R019)","Acute inhalation of cadmium fumes results in metal fume fever, which is characterized by chills, fever, headache, weakness, dryness of the nose and throat, chest pain, and coughing. Ingestion of cadmium causes vomiting and diarrhea. (R019)","Cadmium poisoning is treated by removal from exposure and supportive care. If ingested, induced vomiting or gastric lavage may be performed. (R272)",P28482;P53779;P27361;P31152;Q16659;Q13164;P45983;P45984;Q9UQF2;Q13387;Q9UPT6;O60271;P03372;Q92731;Q15759;P53778;O15264;Q16539;Q8TD08
368,T3D0367,2009-03-06 18:58:38 UTC,2009-08-25 18:02:14 UTC,Cadmium arsenide,Inorganic Compound;Cadmium Compound;Arsenic Compound,Cadmium arsenide,"Cadmium arsenide is a chemical compound of cadmium and arsenic. It is a semiconductor and is used in infrared detectors, pressure sensors, magnetoresistors, and photodetectors. Cadmium is a transition metal and chemical element with the symbol Cd and atomic number 48. It is found naturally in the earth's crust, though rarely on it's own. Arsenic is a chemical element that has the symbol As and atomic number 33. It is a poisonous metalloid that has many allotropic forms: yellow (molecular non-metallic) and several black and grey forms (metalloi",,12006-15-4,6391215,,"","","","",,,Cadmium arsenide,,,,,InChI=1/2AsH6.3Cd/h2*1H6;;;/q2*-3;3*+2,cadmium; $l^{2}-arsanylidenecadmium,http://www.biospider.ca/saved_files/mol/,[As]=[Cd].[As]=[Cd].[Cd],[Cd][As]=[Cd][As]=[Cd],As2Cd3,491.553270,Dark grey solid.,"","","","","","","","Oral 
Inhalation 
Dermal 
(R019)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Arsenite methyltransferase (Q9HBK9) 
Serum albumin (P02768) 
(R019, R164)","Cadmium initially binds to metallothionein and is transported to the kidney. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Accumulation of cadmium in the kidney results in increased excretion of vital low and high weight molecular proteins. Cadmium is a high affinity zinc analog and can interfere in its biological processes. It also binds to and activates the estrogen receptor, likely stimulating the growth of certain types of cancer cells and causing other estrogenic effects, such as reproductive dysfunction. Cadmium causes cell apoptosis by activating mitogen-activated protein kinases. Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carginogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (R001, R054, R026, R058, R059, R069)","Cadmium and arsenic may be absorbed from oral, inhalation, and dermal routes. Cadmium initially binds to metallothionein and albumin and is transported mainly to the kidney and liver. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Cadmium is not known to undergo any direct metabolic conversion and is excreted unchanged, mainly in the urine.  Arsenic is distributed throughout the body, where it is reduced into arsenite if necessary, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant. (R019, R055)",No data.,No data.,"1, carcinogenic to humans. (R264)","Cadmium arsenide is a semiconductor and is used in infrared detectors, pressure sensors, magnetoresistors, and photodetectors. (R764)","Acute Inhalation: 0.00003 mg/m3 (Cadmium) (R260) 
Chronic Inhalation: 0.00001 mg/m3 (Cadmium) (R260) 
Intermediate Oral: 0.0005 mg/kg/day (Cadmium) (R260) 
Chronic Oral: 0.0001 mg/kg/day (Cadmium) (R260)
Acute Oral: 0.005 mg/kg/day (Arsenic) (R260) 
Chronic Oral: 0.0003 mg/kg/day (Arsenic) (R260) 
Chronic Inhalation: 0.01 mg/m3 (Arsenic) (R260)","Chronic exposure to cadmium fumes can cause chemical pneumonitis, pulmonary edema, and lung diseases such as bronchitis and emphysema. Cadmium also accumulates in the kidneys, causing permanent damage. Loss of bone density also occurs. Arsenic poisoning can lead to death from multi-system organ failure, probably from necrotic cell death, not apoptosis. Arsenic is also a known carcinogen, esepcially in skin, liver, bladder and lung cancers. (R001, R019, R055)","Acute inhalation of cadmium fumes results in metal fume fever, which is characterized by chills, fever, headache, weakness, dryness of the nose and throat, chest pain, and coughing. Ingestion of cadmium causes vomiting and diarrhea. Exposure to lower levels of arsenic can cause nausea and vomiting, decreased production of red and white blood cells, abnormal heart rhythm, damage to blood vessels, and a sensation of ","Cadmium poisoning is treated by removal from exposure and supportive care. If ingested, induced vomiting or gastric lavage may be performed. Arsenic poisoning can be treated by chelation therapy, using chelating agents such as dimercaprol, EDTA or DMSA. Charcoal tablets may also be used for less severe cases. In addition, maintaining a diet high in sulfur helps eliminate arsenic from the body. (R055, R272)",P28482;P53779;P27361;P31152;Q16659;Q13164;P45983;P45984;P68032;P68133;P62736;P60709;P63261;P63267;P10515;P23025;P03372;P04150;P00390;P00738;P69905;P68871;Q14145;P09874;A6NKZ8 ;Q99867;Q9H853;P08559;P29803;P11177;O00330;Q16881;Q9NNW7;Q86VQ6;A6NHL2;Q71U36;P68363;Q9BQE3;Q13748;Q6PEY2;P68366;Q9NY65;P07437;Q9H4B7;Q13885;Q9BVA1;P68371;Q13509;P04350;Q9BUF5;Q3ZCM7;A6NNZ2;Q9UQF2;Q13387;Q9UPT6;O60271;Q92731;Q15759;P53778;O15264;Q16539;Q8TD08
369,T3D0368,2009-03-06 18:58:38 UTC,2009-08-25 18:02:18 UTC,Cadmium bromate,Inorganic Compound;Cadmium Compound;Bromate Compound,Cadmium bromate,"Cadmium bromate is a chemical compound of cadmium and bromine. Cadmium is a transition metal and chemical element with the symbol Cd and atomic number 48. It is found naturally in the earth's crust, though rarely on it's own. Bromine is a halogen element with the symbol Br and atomic number 35. Diatomic bromine does not occur naturally, but bromine salts can be found in crustal rock. (R987, R019)",,14518-94-6,14598111,,"","","","",,,Cadmium bromate,,,,,"InChI=1/2BrHO3.Cd/c2*2-1(3)4;/h2*(H,2,3,4);/q;;+2/p-2",cadmium(2+) dibromate,http://www.biospider.ca/saved_files/mol/,[O-]Br(=O)=O.[O-]Br(=O)=O.[Cd+2],O=Br(=O)[O-][Cd][O-]Br(=O)=O,Br2CdO6,367.709520,White powder.,"",,,"",,,,"Oral 
Inhalation 
Dermal 
(R019)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640)
 Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Serum albumin (P02768) 
(R019, R164)","Cadmium initially binds to metallothionein and is transported to the kidney. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Accumulation of cadmium in the kidney results in increased excretion of vital low and high weight molecular proteins. Cadmium is a high affinity zinc analog and can interfere in its biological processes. It also binds to and activates the estrogen receptor, likely stimulating the growth of certain types of cancer cells and causing other estrogenic effects, such as reproductive dysfunction. Cadmium causes cell apoptosis by activating mitogen-activated protein kinases. Bromine is a powerful oxidizing agent and is able to release oxygen free radicals from the water in mucous membranes. These free radicals are also potent oxidizers and produce tissue damage. In additon, the formation of hydrobromic and bromic acids will result in secondary irritation. The bromide ion is also known to affect the central nervous system, causing bromism. This is believed to be a result of bromide ions substituting for chloride ions in the in actions of neurotransmitters and transport systems, thus affecting numerous synaptic processes. (R989, R990, R991, R026, R058, R059, R069)","Cadmium is absorbed from oral, inhalation, and dermal routes. Cadmium initially binds to metallothionein and albumin and is transported mainly to the kidney and liver. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Cadmium is not known to undergo any direct metabolic conversion and is excreted unchanged, mainly in the urine. Bromine is mainly absorbed via inhalation, but may also enter the body through dermal contact. Bromine salts can be ingested. Due to its reactivity, bromine quickly forms bromide and may be deposited in the tissues, displacing other halogens. (R989, R019)",No data.,No data.,"1, carcinogenic to humans. (R264)",No data.,"Acute Inhalation: 0.00003 mg/m3 (Cadmium) (R260) 
Chronic Inhalation: 0.00001 mg/m3 (Cadmium) (R260) 
Intermediate Oral: 0.0005 mg/kg/day (Cadmium) (R260) 
Chronic Oral: 0.0001 mg/kg/day (Cadmium) (R260)","Chronic exposure to cadmium fumes can cause chemical pneumonitis, pulmonary edema, and lung diseases such as bronchitis and emphysema. Cadmium also accumulates in the kidneys, causing permanent damage. Loss of bone density also occurs. Bromine vapour causes irritation and direct damage to the mucous membranes. Elemental bromine also burns the skin. The bromide ion is a central nervous system depressant and chronic exposure produces neuronal effects. This is called bromism and can result in central reactions reaching from somnolence to coma, cachexia, exicosis, loss of reflexes or pathologic reflexes, clonic seizures, tremor, ataxia, loss of neural sensitivity, paresis, papillar edema of the eyes, abnormal speech, cerebral edema, delirium, aggressiveness, and psychoses. Bromate is also a potential carcinogen. (R987, R989, R990, R019, R1017)","Acute inhalation of cadmium fumes results in metal fume fever, which is characterized by chills, fever, headache, weakness, dryness of the nose and throat, chest pain, and coughing. Ingestion of cadmium causes vomiting and diarrhea. Bromine vapour causes irritation and direct damage to the mucous membranes. Symptoms include lacrimation, rhinorrhoea, eye irritation with mucous secretions from the oropharyngeal and upper airways, coughing, dyspnoea, choking, wheezing, epistaxis, and headache. The bromide ion is a central nervous system depressant producing ataxia, slurred speech, tremor, nausea, vomiting, lethargy, dizziness, visual disturbances, unsteadiness, headaches, impaired memory and concentration, disorientation and hallucinations. This is called bromism. (R989, R990, R019)","Cadmium poisoning is treated by removal from exposure and supportive care. If ingested, induced vomiting or gastric lavage may be performed. Bromine should be washed with water from any areas of dermal or ocular contact. If inhaled, treatment is mainly symptomatic and may include maintaining an adequate airway, administering oxygen, antibronchospasm therapy, and/or antibiotics. (R989, R272)",P28482;P53779;P27361;P31152;Q16659;Q13164;P45983;P45984;Q9UQF2;Q13387;Q9UPT6;O60271;P03372;Q92731;Q15759;P53778;O15264;Q16539;Q8TD08
370,T3D0369,2009-03-06 18:58:38 UTC,2009-08-25 18:02:23 UTC,Cadmium bromide,Inorganic Compound;Cadmium Compound;Bromide Compound,Cadmium bromatumCadmium bromide (CdBr2)Cadmium dibromideCdBr2,"Cadmium bromide is a bromide of cadmium used in photography, engraving and lithography. Cadmium is a transition metal and chemical element with the symbol Cd and atomic number 48. It is found naturally in the earth's crust, though rarely on it's own. Bromine is a halogen element with the symbol Br and atomic number 35. Diatomic bromine does not occur naturally, but bromine salts can be found in crustal rock. (R987, R019, R751)",,7789-42-6,9816930,,"","","","",,,Cadmium bromide,,,,,InChI=1/2BrH.Cd/h2*1H;/q;;+2/p-2,cadmium(2+) dibromide,http://www.biospider.ca/saved_files/mol/,[Br-].[Br-].[Cd+2],Br[Cd]Br,Br2Cd,271.740030,Yellow crystals.,568 °C,,,"",,,,"Oral 
Inhalation 
Dermal 
(R019)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640)
 Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Serum albumin (P02768) 
(R019, R164)","Cadmium initially binds to metallothionein and is transported to the kidney. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Accumulation of cadmium in the kidney results in increased excretion of vital low and high weight molecular proteins. Cadmium is a high affinity zinc analog and can interfere in its biological processes. It also binds to and activates the estrogen receptor, likely stimulating the growth of certain types of cancer cells and causing other estrogenic effects, such as reproductive dysfunction. Cadmium causes cell apoptosis by activating mitogen-activated protein kinases. Bromine is a powerful oxidizing agent and is able to release oxygen free radicals from the water in mucous membranes. These free radicals are also potent oxidizers and produce tissue damage. In additon, the formation of hydrobromic and bromic acids will result in secondary irritation. The bromide ion is also known to affect the central nervous system, causing bromism. This is believed to be a result of bromide ions substituting for chloride ions in the in actions of neurotransmitters and transport systems, thus affecting numerous synaptic processes. (R989, R990, R991, R026, R058, R059, R069)","Cadmium is absorbed from oral, inhalation, and dermal routes. Cadmium initially binds to metallothionein and albumin and is transported mainly to the kidney and liver. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Cadmium is not known to undergo any direct metabolic conversion and is excreted unchanged, mainly in the urine. Bromine is mainly absorbed via inhalation, but may also enter the body through dermal contact. Bromine salts can be ingested. Due to its reactivity, bromine quickly forms bromide and may be deposited in the tissues, displacing other halogens. (R989, R019)","LD50: 225 mg/kg (Acute oral, Rat)",No data.,"1, carcinogenic to humans. (R264)","Cadmium bromide is used in used in photography, lithography and engraving processes. (R751)","Acute Inhalation: 0.00003 mg/m3 (Cadmium) (R260) 
Chronic Inhalation: 0.00001 mg/m3 (Cadmium) (R260) 
Intermediate Oral: 0.0005 mg/kg/day (Cadmium) (R260) 
Chronic Oral: 0.0001 mg/kg/day (Cadmium) (R260)","Chronic exposure to cadmium fumes can cause chemical pneumonitis, pulmonary edema, and lung diseases such as bronchitis and emphysema. Cadmium also accumulates in the kidneys, causing permanent damage. Loss of bone density also occurs. Bromine vapour causes irritation and direct damage to the mucous membranes. Elemental bromine also burns the skin. The bromide ion is a central nervous system depressant and chronic exposure produces neuronal effects. This is called bromism and can result in central reactions reaching from somnolence to coma, cachexia, exicosis, loss of reflexes or pathologic reflexes, clonic seizures, tremor, ataxia, loss of neural sensitivity, paresis, papillar edema of the eyes, abnormal speech, cerebral edema, delirium, aggressiveness, and psychoses. (R987, R989, R990, R019)","Acute inhalation of cadmium fumes results in metal fume fever, which is characterized by chills, fever, headache, weakness, dryness of the nose and throat, chest pain, and coughing. Ingestion of cadmium causes vomiting and diarrhea. (R019)","Cadmium poisoning is treated by removal from exposure and supportive care. If ingested, induced vomiting or gastric lavage may be performed. Bromine should be washed with water from any areas of dermal or ocular contact. If inhaled, treatment is mainly symptomatic and may include maintaining an adequate airway, administering oxygen, antibronchospasm therapy, and/or antibiotics. (R989, R272)",P28482;P53779;P27361;P31152;Q16659;Q13164;P45983;P45984;Q9UQF2;Q13387;Q9UPT6;O60271;P03372;Q92731;Q15759;P53778;O15264;Q16539;Q8TD08
371,T3D0370,2009-03-06 18:58:38 UTC,2009-08-25 19:52:57 UTC,Cadmium carbonate,Inorganic Compound;Cadmium Compound,"Cadmium carbonate (CdCO3)Cadmium carbonate [cadmium and cadmium compounds]Cadmium carbonate, CdCO3Cadmium monocarbonateCarbonic acid, cadmium saltCarbonic acid, cadmium salt (1:1)Carbonic acid, cadmium(2+) salt (1:1)Caswell No. 134AChemcarb (CdCO3)KalcitMikrokalcitOtaviteSupermikrokalcitcarbonic acid (ACD/Name 4.0)","Cadmium carbonate is a chemical compound of cadmium that occurs naturally as the mineral otavite. Cadmium is a transition metal and chemical element with the symbol Cd and atomic number 48. It is found naturally in the earth's crust, though rarely on it's own. (R019, R754)",,513-78-0,10564,,"","","","",,C038075,Cadmium carbonate,,,,,"InChI=1/CH2O3.Cd/c2-1(3)4;/h(H2,2,3,4);/q;+2/p-2",cadmium(2+) carbonate,http://www.biospider.ca/saved_files/mol/,C(=O)([O-])[O-].[Cd+2],C(=O)([O-])[O-].[Cd+2],CCdO3,173.888100,White powder.,"",,,"",,,,"Oral 
Inhalation 
Dermal 
(R019)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640)
 Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Serum albumin (P02768) 
(R019, R164)","Cadmium initially binds to metallothionein and is transported to the kidney. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Accumulation of cadmium in the kidney results in increased excretion of vital low and high weight molecular proteins. Cadmium is a high affinity zinc analog and can interfere in its biological processes. It also binds to and activates the estrogen receptor, likely stimulating the growth of certain types of cancer cells and causing other estrogenic effects, such as reproductive dysfunction. Cadmium causes cell apoptosis by activating mitogen-activated protein kinases. (R026, R058, R059, R069)","Cadmium is absorbed from oral, inhalation, and dermal routes. Cadmium initially binds to metallothionein and albumin and is transported mainly to the kidney and liver. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Cadmium is not known to undergo any direct metabolic conversion and is excreted unchanged, mainly in the urine. (R019)","LD50: 310 mg/kg (Oral, Mouse) (R263)",No data.,"1, carcinogenic to humans. (R264)",Cadmium carbonate ca be used in fungicides and in chemical agents (S275).,"Acute Inhalation: 0.00003 mg/m3 (R260) 
Chronic Inhalation: 0.00001 mg/m3 (R260) 
Intermediate Oral: 0.0005 mg/kg/day (R260) 
Chronic Oral: 0.0001 mg/kg/day (R260)","Chronic exposure to cadmium fumes can cause chemical pneumonitis, pulmonary edema, and lung diseases such as bronchitis and emphysema. Cadmium also accumulates in the kidneys, causing permanent damage. Loss of bone density also occurs. (R019)","Acute inhalation of cadmium fumes results in metal fume fever, which is characterized by chills, fever, headache, weakness, dryness of the nose and throat, chest pain, and coughing. Ingestion of cadmium causes vomiting and diarrhea. (R019)","Cadmium poisoning is treated by removal from exposure and supportive care. If ingested, induced vomiting or gastric lavage may be performed. (R272)",P28482;P53779;P27361;P31152;Q16659;Q13164;P45983;P45984;Q9UQF2;Q13387;Q9UPT6;O60271;P03372;Q92731;Q15759;P53778;O15264;Q16539;Q8TD08
372,T3D0371,2009-03-06 18:58:38 UTC,2009-08-04 21:28:25 UTC,Cadmium chloride,Inorganic Compound;Cadmium Compound,"CaddyCadmium atomic spectroscopy standard concentrate 1.00 g CdCadmium chlorideCadmium chloride (CdCl2)Cadmium chloride (CdCl2) (7CI,8CI,9CI)Cadmium chloride 0.1 M solutionCadmium chloride [cadmium and cadmium compounds]Cadmium chloride solutionCadmium standard concentrate 10.00 g CdCadmium turf fungicideCadmium(II) chlorideCaswell No. 135CdCl2Chloride, cadmiumDichloride, cadmiumDichlorocadmiumKadmiumchloridKadmiumchlorid (german)Kadmiumchlorid [german]Vi-cadWLN: CD G2[CdCl2]cadmium(2+) chloridedichlorocadmium (ACD/Name 4.0)","Cadmium chloride is a chloride of cadmium that is used mainly in the synthesis of other cadmium compounds. Cadmium is a transition metal and chemical element with the symbol Cd and atomic number 48. It is found naturally in the earth's crust, though rarely on it's own. (R019, R750)",,10108-64-2,24947,,C15233,"",35456,CPD0-1355,,D019256,Cadmium chloride,,,,http://en.wikipedia.org/wiki/Cadmium dichloride,InChI=1/Cd.2ClH/h;2*1H/q+2;;/p-2,dichlorocadmium,http://www.biospider.ca/saved_files/mol/40547cccebca260cd1b4f2f3ab49f9d5_1237975059.mol,Cl[Cd]Cl,Cl[Cd]Cl,CdCl2,183.841060,White crystals.,564 °C,,,"",,,,"Oral 
Inhalation 
Dermal 
(R019)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640)
 Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Serum albumin (P02768) 
(R019, R164)","Cadmium initially binds to metallothionein and is transported to the kidney. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Accumulation of cadmium in the kidney results in increased excretion of vital low and high weight molecular proteins. Cadmium is a high affinity zinc analog and can interfere in its biological processes. It also binds to and activates the estrogen receptor, likely stimulating the growth of certain types of cancer cells and causing other estrogenic effects, such as reproductive dysfunction. Cadmium causes cell apoptosis by activating mitogen-activated protein kinases. (R026, R058, R059, R069)","Cadmium is absorbed from oral, inhalation, and dermal routes. Cadmium initially binds to metallothionein and albumin and is transported mainly to the kidney and liver. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Cadmium is not known to undergo any direct metabolic conversion and is excreted unchanged, mainly in the urine. (R019)","LD50: 88 mg/kg (Oral, Rat)  (R263)
LD50: 1800 ug/kg (Intraperitoneal, Rat)  (R263)
LD50: 3200 ug/kg (Subcutaneous, Mouse) (R263)
LD50: 3500 ug/kg Intravenous, Mouse) (R263)",No data.,"1, carcinogenic to humans. (R264)","Cadmium chloride is used in the dyeing and printing of fabrics, in photography, in producing electronics components and in the synthesis of other cadmium compounds. (R750)","Acute Inhalation: 0.00003 mg/m3 (R260) 
Chronic Inhalation: 0.00001 mg/m3 (R260) 
Intermediate Oral: 0.0005 mg/kg/day (R260) 
Chronic Oral: 0.0001 mg/kg/day (R260)","Chronic exposure to cadmium fumes can cause chemical pneumonitis, pulmonary edema, and lung diseases such as bronchitis and emphysema. Cadmium also accumulates in the kidneys, causing permanent damage. Loss of bone density also occurs. (R019)","Acute inhalation of cadmium fumes results in metal fume fever, which is characterized by chills, fever, headache, weakness, dryness of the nose and throat, chest pain, and coughing. Ingestion of cadmium causes vomiting and diarrhea. (R019)","Cadmium poisoning is treated by removal from exposure and supportive care. If ingested, induced vomiting or gastric lavage may be performed. (R272)",P28482;P53779;P27361;P31152;Q16659;Q13164;P45983;P45984;Q9UQF2;Q13387;Q9UPT6;O60271;P03372;Q92731;Q15759;P53778;O15264;Q16539;Q8TD08
373,T3D0372,2009-03-06 18:58:38 UTC,2009-08-25 18:02:27 UTC,Cadmium fluoborate,Inorganic Compound;Cadmium Compound;Fluoride Compound,"CADMIUM FLUOBORATE, 50% SOLN.","Cadmium fluoborate is a chemical compound of cadmium, fluoride, and boron. Cadmium is a transition metal and chemical element with the symbol Cd and atomic number 48. It is found naturally in the earth's crust, though rarely on it's own. (R019)",,14486-19-2,12886773,,"","","","",,,Cadmium fluoborate,,,,,"InChI=1/2BF4.Cd/c2*2-1(3,4)5;/q2*-1;+2",cadmium(2+) ditetrafluoroborate,http://www.biospider.ca/saved_files/mol/,"",F[B](F)(F)(F)[Cd][B](F)(F)(F)F,B2CdF8,287.909200,Colorless liquid.,"",,,"",,,,"Oral 
Inhalation 
Dermal 
(R019)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640)
 Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Serum albumin (P02768) 
(R019, R164)","Cadmium initially binds to metallothionein and is transported to the kidney. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Accumulation of cadmium in the kidney results in increased excretion of vital low and high weight molecular proteins. Cadmium is a high affinity zinc analog and can interfere in its biological processes. It also binds to and activates the estrogen receptor, likely stimulating the growth of certain types of cancer cells and causing other estrogenic effects, such as reproductive dysfunction. Cadmium causes cell apoptosis by activating mitogen-activated protein kinases. (R026, R058, R059, R069)","Cadmium is absorbed from oral, inhalation, and dermal routes. Cadmium initially binds to metallothionein and albumin and is transported mainly to the kidney and liver. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Cadmium is not known to undergo any direct metabolic conversion and is excreted unchanged, mainly in the urine. (R019)","LD50: 250 mg/kg (oral, rat) (S276).",No data.,"1, carcinogenic to humans. (R264)",Cadmium fluoborate is used to prepare electroplating baths. (R270),"Acute Inhalation: 0.00003 mg/m3 (R260) 
Chronic Inhalation: 0.00001 mg/m3 (R260) 
Intermediate Oral: 0.0005 mg/kg/day (R260) 
Chronic Oral: 0.0001 mg/kg/day (R260)","Chronic exposure to cadmium fumes can cause chemical pneumonitis, pulmonary edema, and lung diseases such as bronchitis and emphysema. Cadmium also accumulates in the kidneys, causing permanent damage. Loss of bone density also occurs. (R019)","Acute inhalation of cadmium fumes results in metal fume fever, which is characterized by chills, fever, headache, weakness, dryness of the nose and throat, chest pain, and coughing. Ingestion of cadmium causes vomiting and diarrhea. (R019)","Cadmium poisoning is treated by removal from exposure and supportive care. If ingested, induced vomiting or gastric lavage may be performed. (R272)",P28482;P53779;P27361;P31152;Q16659;Q13164;P45983;P45984;Q9UQF2;Q13387;Q9UPT6;O60271;P03372;Q92731;Q15759;P53778;O15264;Q16539;Q8TD08
374,T3D0373,2009-03-06 18:58:38 UTC,2009-08-25 18:02:31 UTC,Cadmium fluoride,Inorganic Compound;Cadmium Compound;Fluoride Compound,Cadmium fluorideCadmium fluoride (CdF2)Cadmium fluorureCdF2,"Cadmium fluoride is a water-insoluble chemical compound of cadmium used in oxygen-sensitive applications, such as the production of metallic alloys. Cadmium is a transition metal and chemical element with the symbol Cd and atomic number 48. It is found naturally in the earth's crust, though rarely on it's own. (R019, R765)",,7790-79-6,10130045,,"","","","",,,Cadmium fluoride,,,,,InChI=1/Cd.2FH/h;2*1H/q+2;;/p-2,cadmium(2+) difluoride,http://www.biospider.ca/saved_files/mol/,[F-].[F-].[Cd+2],F[Cd]F,CdF2,151.900160,White-grey crystals.,1110 °C,,,"",,,,"Oral 
Inhalation 
Dermal 
(R019)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640)
 Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Serum albumin (P02768) 
(R019, R164)","Cadmium initially binds to metallothionein and is transported to the kidney. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Accumulation of cadmium in the kidney results in increased excretion of vital low and high weight molecular proteins. Cadmium is a high affinity zinc analog and can interfere in its biological processes. It also binds to and activates the estrogen receptor, likely stimulating the growth of certain types of cancer cells and causing other estrogenic effects, such as reproductive dysfunction. Cadmium causes cell apoptosis by activating mitogen-activated protein kinases. (R026, R058, R059, R069)","Cadmium is absorbed from oral, inhalation, and dermal routes. Cadmium initially binds to metallothionein and albumin and is transported mainly to the kidney and liver. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Cadmium is not known to undergo any direct metabolic conversion and is excreted unchanged, mainly in the urine. (R019)",No data.,No data.,"1, carcinogenic to humans. (R264)","Cadmium fluoride is used in the production of metallic alloys, for electronic and optical applications and as a starting material for laser crystals. (R765)","Acute Inhalation: 0.00003 mg/m3 (R260) 
Chronic Inhalation: 0.00001 mg/m3 (R260) 
Intermediate Oral: 0.0005 mg/kg/day (R260) 
Chronic Oral: 0.0001 mg/kg/day (R260)","Chronic exposure to cadmium fumes can cause chemical pneumonitis, pulmonary edema, and lung diseases such as bronchitis and emphysema. Cadmium also accumulates in the kidneys, causing permanent damage. Loss of bone density also occurs. (R019)","Acute inhalation of cadmium fumes results in metal fume fever, which is characterized by chills, fever, headache, weakness, dryness of the nose and throat, chest pain, and coughing. Ingestion of cadmium causes vomiting and diarrhea. (R019)","Cadmium poisoning is treated by removal from exposure and supportive care. If ingested, induced vomiting or gastric lavage may be performed. (R272)",P28482;P53779;P27361;P31152;Q16659;Q13164;P45983;P45984;Q9UQF2;Q13387;Q9UPT6;O60271;P03372;Q92731;Q15759;P53778;O15264;Q16539;Q8TD08
375,T3D0374,2009-03-06 18:58:39 UTC,2009-08-19 19:40:38 UTC,Cadmium fluosilicate,Inorganic Compound;Cadmium Compound;Fluoride Compound,"Cadmium flucsilicateCadmium fluorosilicateCadmium fluosilicateCadmium hexafluorosilicateCadmium hexafluorosilicate (7CI)Cadmium hexafluorosilicate(2-)Cadmium silicon fluorideSilicate(2-), hexafluoro-, cadmium (8CI,9CI)","Cadmium fluosilicate is a chemical compound of cadmium. Cadmium is a transition metal and chemical element with the symbol Cd and atomic number 48. It is found naturally in the earth's crust, though rarely on it's own. (R019)",,17010-21-8,197153,,"","","","",,,Cadmium fluosilicate,,,,,InChI=1/Cd.6FH.Si/h;6*1H;/q+2;;;;;;;+4/p-6,cadmium(2+); silicon(4+); hexafluoride,http://www.biospider.ca/saved_files/mol/,[F-].[F-].[F-].[F-].[F-].[F-].[Si+4].[Cd+2],[F-].[F-].[F-].[F-].[F-].[F-].[Si+4].[Cd++],CdF6Si,255.870700,No data.,"",,,"",,,,"Oral 
Inhalation 
Dermal 
(R019)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640)
 Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Serum albumin (P02768) 
(R019, R164)","Cadmium initially binds to metallothionein and is transported to the kidney. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Accumulation of cadmium in the kidney results in increased excretion of vital low and high weight molecular proteins. Cadmium is a high affinity zinc analog and can interfere in its biological processes. It also binds to and activates the estrogen receptor, likely stimulating the growth of certain types of cancer cells and causing other estrogenic effects, such as reproductive dysfunction. Cadmium causes cell apoptosis by activating mitogen-activated protein kinases. (R026, R058, R059, R069)","Cadmium is absorbed from oral, inhalation, and dermal routes. Cadmium initially binds to metallothionein and albumin and is transported mainly to the kidney and liver. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Cadmium is not known to undergo any direct metabolic conversion and is excreted unchanged, mainly in the urine. (R019)",No data.,No data.,"1, carcinogenic to humans. (R264)",No data.,"Acute Inhalation: 0.00003 mg/m3 (R260) 
Chronic Inhalation: 0.00001 mg/m3 (R260) 
Intermediate Oral: 0.0005 mg/kg/day (R260) 
Chronic Oral: 0.0001 mg/kg/day (R260)","Chronic exposure to cadmium fumes can cause chemical pneumonitis, pulmonary edema, and lung diseases such as bronchitis and emphysema. Cadmium also accumulates in the kidneys, causing permanent damage. Loss of bone density also occurs. (R019)","Acute inhalation of cadmium fumes results in metal fume fever, which is characterized by chills, fever, headache, weakness, dryness of the nose and throat, chest pain, and coughing. Ingestion of cadmium causes vomiting and diarrhea. (R019)","Cadmium poisoning is treated by removal from exposure and supportive care. If ingested, induced vomiting or gastric lavage may be performed. (R272)",P28482;P53779;P27361;P31152;Q16659;Q13164;P45983;P45984;Q9UQF2;Q13387;Q9UPT6;O60271;P03372;Q92731;Q15759;P53778;O15264;Q16539;Q8TD08
376,T3D0375,2009-03-06 18:58:39 UTC,2009-08-25 18:02:36 UTC,Cadmium hydroxide,Inorganic Compound;Cadmium Compound,Cadmium(+2) Cation Dihydroxide,"Cadmium hydroxide is a hydroxide of cadmium. It is used in storage battery anodes, in nickel-cadmium and silver-cadmium storage batteries, in cadmium plating, and to prepare other cadmium salts. Cadmium is a transition metal and chemical element with the symbol Cd and atomic number 48. It is found naturally in the earth's crust, though rarely on it's own. (R019, R766)",,21041-95-2,10313210,,"","","","",,,Cadmium hydroxide,,,,,InChI=1/Cd.2H2O/h;2*1H2/q+2;;/p-2,cadmium(2+) dihydroxide,http://www.biospider.ca/saved_files/mol/,[OH-].[OH-].[Cd+2],O[Cd]O,CdH2O2,147.908840,White solid.,130 °C,,,"",,,,"Oral 
Inhalation 
Dermal 
(R019)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640)
 Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Serum albumin (P02768) 
(R019, R164)","Cadmium initially binds to metallothionein and is transported to the kidney. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Accumulation of cadmium in the kidney results in increased excretion of vital low and high weight molecular proteins. Cadmium is a high affinity zinc analog and can interfere in its biological processes. It also binds to and activates the estrogen receptor, likely stimulating the growth of certain types of cancer cells and causing other estrogenic effects, such as reproductive dysfunction. Cadmium causes cell apoptosis by activating mitogen-activated protein kinases. (R026, R058, R059, R069)","Cadmium is absorbed from oral, inhalation, and dermal routes. Cadmium initially binds to metallothionein and albumin and is transported mainly to the kidney and liver. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Cadmium is not known to undergo any direct metabolic conversion and is excreted unchanged, mainly in the urine. (R019)",No data.,No data.,"1, carcinogenic to humans. (R264)","Cadmium hydroxide is used in storage battery anodes, in nickel-cadmium and silver-cadmium storage batteries, in cadmium plating, and to prepare other cadmium salts. (R766)","Acute Inhalation: 0.00003 mg/m3 (R260) 
Chronic Inhalation: 0.00001 mg/m3 (R260) 
Intermediate Oral: 0.0005 mg/kg/day (R260) 
Chronic Oral: 0.0001 mg/kg/day (R260)","Chronic exposure to cadmium fumes can cause chemical pneumonitis, pulmonary edema, and lung diseases such as bronchitis and emphysema. Cadmium also accumulates in the kidneys, causing permanent damage. Loss of bone density also occurs. (R019)","Acute inhalation of cadmium fumes results in metal fume fever, which is characterized by chills, fever, headache, weakness, dryness of the nose and throat, chest pain, and coughing. Ingestion of cadmium causes vomiting and diarrhea. (R019)","Cadmium poisoning is treated by removal from exposure and supportive care. If ingested, induced vomiting or gastric lavage may be performed. (R272)",P28482;P53779;P27361;P31152;Q16659;Q13164;P45983;P45984;Q9UQF2;Q13387;Q9UPT6;O60271;P03372;Q92731;Q15759;P53778;O15264;Q16539;Q8TD08
377,T3D0376,2009-03-06 18:58:39 UTC,2009-08-25 18:02:40 UTC,Cadmium iodide,Inorganic Compound;Cadmium Compound,Cadmium iodideCadmium iodide (CdI2)CdI2,"Cadmium iodide is an iodide of cadmium that can be made by heating cadmium with iodine. It is used in lithography, photography, electroplating and the manufacturing of phosphors. Cadmium is a transition metal and chemical element with the symbol Cd and atomic number 48. It is found naturally in the earth's crust, though rarely on it's own. (R019, R767)",,7790-80-9,24635,,"","","","",,C073250,Cadmium iodide,,,,,InChI=1/Cd.2HI/h;2*1H/q+2;;/p-2,cadmium(2+) diiodide,http://www.biospider.ca/saved_files/mol/,[Cd+2].[I-].[I-],I[Cd]I,CdI2,367.712290,White or pale yellow crystals.,"387 °C, 660 K, 729 °F",,,"",,,,"Oral 
Inhalation 
Dermal 
(R019)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640)
 Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Serum albumin (P02768) 
(R019, R164)","Cadmium initially binds to metallothionein and is transported to the kidney. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Accumulation of cadmium in the kidney results in increased excretion of vital low and high weight molecular proteins. Cadmium is a high affinity zinc analog and can interfere in its biological processes. It also binds to and activates the estrogen receptor, likely stimulating the growth of certain types of cancer cells and causing other estrogenic effects, such as reproductive dysfunction. Cadmium causes cell apoptosis by activating mitogen-activated protein kinases. (R026, R058, R059, R069)","Cadmium is absorbed from oral, inhalation, and dermal routes. Cadmium initially binds to metallothionein and albumin and is transported mainly to the kidney and liver. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Cadmium is not known to undergo any direct metabolic conversion and is excreted unchanged, mainly in the urine. (R019)","LD50: 4708 mg/kg (Oral, Rat) (R768)",No data.,"1, carcinogenic to humans. (R264)","Cadmium iodide is used in lithography, photography, electroplating and the manufacturing of phosphors. (R767)","Acute Inhalation: 0.00003 mg/m3 (R260) 
Chronic Inhalation: 0.00001 mg/m3 (R260) 
Intermediate Oral: 0.0005 mg/kg/day (R260) 
Chronic Oral: 0.0001 mg/kg/day (R260)","Chronic exposure to cadmium fumes can cause chemical pneumonitis, pulmonary edema, and lung diseases such as bronchitis and emphysema. Cadmium also accumulates in the kidneys, causing permanent damage. Loss of bone density also occurs. (R019)","Acute inhalation of cadmium fumes results in metal fume fever, which is characterized by chills, fever, headache, weakness, dryness of the nose and throat, chest pain, and coughing. Ingestion of cadmium causes vomiting and diarrhea. (R019)","Cadmium poisoning is treated by removal from exposure and supportive care. If ingested, induced vomiting or gastric lavage may be performed. (R272)",P28482;P53779;P27361;P31152;Q16659;Q13164;P45983;P45984;Q9UQF2;Q13387;Q9UPT6;O60271;P03372;Q92731;Q15759;P53778;O15264;Q16539;Q8TD08
378,T3D0377,2009-03-06 18:58:39 UTC,2009-08-25 18:02:45 UTC,Cadmium lactate,Inorganic Compound;Cadmium Compound,"Bis(lactato)cadmiumCadmium dilactateCadmium lactateCadmium, bis(lactato)-Cadmium, bis(lactato)- (8CI)Lactic acid, cadmium salt","Cadmium lactate is a chemical compound of cadmium. Cadmium is a transition metal and chemical element with the symbol Cd and atomic number 48. It is found naturally in the earth's crust, though rarely on it's own. (R019)",,16039-55-7,159769,,"","","","",,,Cadmium lactate,,,,,"InChI=1/2C3H6O3.Cd/c2*1-2(4)3(5)6;/h2*2,4H,1H3,(H,5,6);/q;;+2/p-2",cadmium(2+); 2-hydroxypropanoate,http://www.biospider.ca/saved_files/mol/,CC(C(=O)[O-])O.CC(C(=O)[O-])O.[Cd+2],CC(O)C(=O)O[Cd]OC(=O)C(C)O,C6H10CdO6,291.951100,No data.,"",,,"",,,,"Oral 
Inhalation 
Dermal 
(R019)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640)
 Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Serum albumin (P02768) 
(R019, R164)","Cadmium initially binds to metallothionein and is transported to the kidney. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Accumulation of cadmium in the kidney results in increased excretion of vital low and high weight molecular proteins. Cadmium is a high affinity zinc analog and can interfere in its biological processes. It also binds to and activates the estrogen receptor, likely stimulating the growth of certain types of cancer cells and causing other estrogenic effects, such as reproductive dysfunction. Cadmium causes cell apoptosis by activating mitogen-activated protein kinases. (R026, R058, R059, R069)","Cadmium is absorbed from oral, inhalation, and dermal routes. Cadmium initially binds to metallothionein and albumin and is transported mainly to the kidney and liver. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Cadmium is not known to undergo any direct metabolic conversion and is excreted unchanged, mainly in the urine. (R019)",No data.,No data.,"1, carcinogenic to humans. (R264)",Can be used as chemical reagent. An example is its use for the synthesis of dimethylformamide (S277).,"Acute Inhalation: 0.00003 mg/m3 (R260) 
Chronic Inhalation: 0.00001 mg/m3 (R260) 
Intermediate Oral: 0.0005 mg/kg/day (R260) 
Chronic Oral: 0.0001 mg/kg/day (R260)","Chronic exposure to cadmium fumes can cause chemical pneumonitis, pulmonary edema, and lung diseases such as bronchitis and emphysema. Cadmium also accumulates in the kidneys, causing permanent damage. Loss of bone density also occurs. (R019)","Acute inhalation of cadmium fumes results in metal fume fever, which is characterized by chills, fever, headache, weakness, dryness of the nose and throat, chest pain, and coughing. Ingestion of cadmium causes vomiting and diarrhea. (R019)","Cadmium poisoning is treated by removal from exposure and supportive care. If ingested, induced vomiting or gastric lavage may be performed. (R272)",P28482;P53779;P27361;P31152;Q16659;Q13164;P45983;P45984;Q9UQF2;Q13387;Q9UPT6;O60271;P03372;Q92731;Q15759;P53778;O15264;Q16539;Q8TD08
379,T3D0378,2009-03-06 18:58:39 UTC,2009-08-25 18:02:49 UTC,Cadmium nitrate,Inorganic Compound;Cadmium Compound;Nitrate,"Cadmium dinitrateCadmium nitrate [cadmium and cadmium compounds]Cadmium nitrate, tetrahydrateCadmium(II) nitrateNitric acid, cadmium salt","Cadmium nitrate is a nitrate of cadmium used mainly to prepare other cadmium salts. It is also used for coloring glass and porcelain and as a flash powder in photography. Cadmium is a transition metal and chemical element with the symbol Cd and atomic number 48. It is found naturally in the earth's crust, though rarely on it's own. Nitrite is a toxic compound known to cause methemoglobinemia. (S575, R019, R748)",,10325-94-7,25154,,"","","","",,C035196,Cadmium nitrate,,,,http://en.wikipedia.org/wiki/cadmium nitrate,"InChI=1/Cd.2HNO3/c;2*2-1(3)4/h;2*(H,2,3,4)/q+2;;",cadmium(2+) dinitrate,http://www.biospider.ca/saved_files/mol/,[N+](=O)([O-])[O-].[N+](=O)([O-])[O-].[Cd+2],[O-][N+](=O)O[Cd]O[N+]([O-])=O,CdN2O6,237.878990,White crystals.,59 °C,,,"",,,,"Oral 
Inhalation 
Dermal 
(R019)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640)
 Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Serum albumin (P02768) 
(R019, R164)","Cadmium initially binds to metallothionein and is transported to the kidney. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Accumulation of cadmium in the kidney results in increased excretion of vital low and high weight molecular proteins. Cadmium is a high affinity zinc analog and can interfere in its biological processes. It also binds to and activates the estrogen receptor, likely stimulating the growth of certain types of cancer cells and causing other estrogenic effects, such as reproductive dysfunction. Cadmium causes cell apoptosis by activating mitogen-activated protein kinases. Nitrate's toxicity is a result of it's conversion to nitrite once in the body. Nitrite causes the autocatalytic oxidation of oxyhemoglobin to hydrogen peroxide and methemoglobin. This elevation of methemoglobin levels is a condition known as methemoglobinemia, and is characterized by tissue hypoxia, as methemoglobin cannot bind oxygen. (V305, V306, R026, R058, R059, R069)","Cadmium is absorbed from oral, inhalation, and dermal routes. Cadmium initially binds to metallothionein and albumin and is transported mainly to the kidney and liver. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Cadmium is not known to undergo any direct metabolic conversion and is excreted unchanged, mainly in the urine. Intake of some amount of nitrates and nitrites is a normal part of the nitrogen cycle in humans. In vivo conversion of nitrates to nitrites can occur in the gastrointestional tract under the right conditions, significantly enhancing nitrates' toxic potency. The major metabolic pathway for nitrate is conversion to nitrite, and then to ammonia. Nitrites, nitrates, and their metabolites are excreted in the urine. (S575, R019)","LD50: 100 mg/kg (Oral, Rat) (R747)
LC50: 1925 ppm over 4 hours (Inhalation, Mouse) (R747)",No data.,"1, carcinogenic to humans. (R264)",Cadmium nitrate is used mainly to prepare other cadmium salts. It is also used for coloring glass and porcelain and as a flash powder in photography. (R748),"Acute Inhalation: 0.00003 mg/m3 (R260) 
Chronic Inhalation: 0.00001 mg/m3 (R260) 
Intermediate Oral: 0.0005 mg/kg/day (R260) 
Chronic Oral: 0.0001 mg/kg/day (R260)","Chronic exposure to cadmium fumes can cause chemical pneumonitis, pulmonary edema, and lung diseases such as bronchitis and emphysema. Cadmium also accumulates in the kidneys, causing permanent damage. Loss of bone density also occurs. Nitrate and nitrite poisoning causes methemoglobinemia. Nitrites may cause pregnancy complications and developmental effects. They may also be carcinogenic. (S575, R019)","Acute inhalation of cadmium fumes results in metal fume fever, which is characterized by chills, fever, headache, weakness, dryness of the nose and throat, chest pain, and coughing. Ingestion of cadmium causes vomiting and diarrhea. Nitrate and nitrite poisoning causes methemoglobinemia. Symptoms include cyanosis, cardiac dysrhythmias and circulatory failure, and progressive central nervous system (CNS) effects. CNS effects can range from mild dizziness and lethargy to coma and convulsions. (S575, R019)","Cadmium poisoning is treated by removal from exposure and supportive care. If ingested, induced vomiting or gastric lavage may be performed. Methemoglobinemia can be treated with supplemental oxygen and methylene blue 1% solution administered intravenously slowly over five minutes followed by IV flush with normal saline. Methylene blue restores the iron in hemoglobin to its normal (reduced) oxygen-carrying state. (V306, R272)",P28482;P53779;P27361;P31152;Q16659;Q13164;P45983;P45984;Q9UQF2;Q13387;Q9UPT6;O60271;P03372;Q92731;Q15759;P53778;O15264;Q16539;Q8TD08;P69905;P68871;P02042;P02100;P69891;P69892;Q6B0K9;P09105;P02008
380,T3D0379,2009-03-06 18:58:39 UTC,2009-08-25 18:02:53 UTC,Cadmium nitrate tetrahydrate,Inorganic Compound;Cadmium Compound;Nitrate,"Cadmium dinitrateCadmium nitrateCadmium nitrate [cadmium and cadmium compounds]Cadmium nitrate, tetrahydrateCadmium(II) nitrateNitric acid, cadmium salt","Cadmium nitrate is a nitrate of cadmium used mainly to prepare other cadmium salts. It is also used for coloring glass and porcelain and as a flash powder in photography. Cadmium is a transition metal and chemical element with the symbol Cd and atomic number 48. It is found naturally in the earth's crust, though rarely on it's own. Nitrite is a toxic compound known to cause methemoglobinemia. (S575,  R019, R748)",,10022-68-1,25154,,"","","","",,,Cadmium nitrate tetrahydrate,,,,http://en.wikipedia.org/wiki/Cadmium_nitrate,"InChI=1/Cd.2HNO3/c;2*2-1(3)4/h;2*(H,2,3,4)/q+2;;",cadmium(2+) dinitrate,http://www.biospider.ca/saved_files/mol/,[N+](=O)([O-])[O-].[N+](=O)([O-])[O-].[Cd+2],O[N+](=O)O[Cd]O[N+](O)=O,CdN2O6,237.878990,White crystals.,"",,,"",,,,"Oral 
Inhalation 
Dermal 
(R019)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640)
 Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Serum albumin (P02768) 
(R019, R164)","Cadmium initially binds to metallothionein and is transported to the kidney. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Accumulation of cadmium in the kidney results in increased excretion of vital low and high weight molecular proteins. Cadmium is a high affinity zinc analog and can interfere in its biological processes. It also binds to and activates the estrogen receptor, likely stimulating the growth of certain types of cancer cells and causing other estrogenic effects, such as reproductive dysfunction. Cadmium causes cell apoptosis by activating mitogen-activated protein kinases. Nitrate's toxicity is a result of it's conversion to nitrite once in the body. Nitrite causes the autocatalytic oxidation of oxyhemoglobin to hydrogen peroxide and methemoglobin. This elevation of methemoglobin levels is a condition known as methemoglobinemia, and is characterized by tissue hypoxia, as methemoglobin cannot bind oxygen. (V305, V306, R026, R058, R059, R069)","Cadmium is absorbed from oral, inhalation, and dermal routes. Cadmium initially binds to metallothionein and albumin and is transported mainly to the kidney and liver. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Cadmium is not known to undergo any direct metabolic conversion and is excreted unchanged, mainly in the urine. Intake of some amount of nitrates and nitrites is a normal part of the nitrogen cycle in humans. In vivo conversion of nitrates to nitrites can occur in the gastrointestional tract under the right conditions, significantly enhancing nitrates' toxic potency. The major metabolic pathway for nitrate is conversion to nitrite, and then to ammonia. Nitrites, nitrates, and their metabolites are excreted in the urine. (S575, R019)","LD50: 300 mg/kg (Oral, Rat) (R746)",No data.,"1, carcinogenic to humans. (R264)",Cadmium nitrate is used mainly to prepare other cadmium salts. It is also used for coloring glass and porcelain and as a flash powder in photography. (R748),"Acute Inhalation: 0.00003 mg/m3 (R260) 
Chronic Inhalation: 0.00001 mg/m3 (R260) 
Intermediate Oral: 0.0005 mg/kg/day (R260) 
Chronic Oral: 0.0001 mg/kg/day (R260)",Nitrate and nitrite poisoning causes methemoglobinemia. Nitrites may cause pregnancy complications and developmental effects. They may also be carcinogenic. (S575),"Acute inhalation of cadmium fumes results in metal fume fever, which is characterized by chills, fever, headache, weakness, dryness of the nose and throat, chest pain, and coughing. Ingestion of cadmium causes vomiting and diarrhea. Nitrate and nitrite poisoning causes methemoglobinemia. Symptoms include cyanosis, cardiac dysrhythmias and circulatory failure, and progressive central nervous system (CNS) effects. CNS effects can range from mild dizziness and lethargy to coma and convulsions. (S575, R019)","Cadmium poisoning is treated by removal from exposure and supportive care. If ingested, induced vomiting or gastric lavage may be performed. Methemoglobinemia can be treated with supplemental oxygen and methylene blue 1% solution administered intravenously slowly over five minutes followed by IV flush with normal saline. Methylene blue restores the iron in hemoglobin to its normal (reduced) oxygen-carrying state. (V306, R272)",P28482;P53779;P27361;P31152;Q16659;Q13164;P45983;P45984;Q9UQF2;Q13387;Q9UPT6;O60271;P03372;Q92731;Q15759;P53778;O15264;Q16539;Q8TD08;P69905;P68871;P02042;P02100;P69891;P69892;Q6B0K9;P09105;P02008
381,T3D0380,2009-03-06 18:58:39 UTC,2009-08-04 21:28:27 UTC,Cadmium oxide fume,Inorganic Compound;Cadmium Compound,Aska-ridCDOCadmium fumeCadmium monoxideCadmium oxide (cdo)Cadmium oxide [cadmium and cadmium compounds]Cadmium oxide brownCaswell No. 136AAKadmu tlenekKadmu tlenek [polish],"Cadmium oxide fume is a chemical compound of  cadmium. Cadmium is a transition metal and chemical element with the symbol Cd and atomic number 48. It is found naturally in the earth's crust, though rarely on it's own. (R019)",,1306-19-0,14782,,"","","","",,C029663,Cadmium oxide fume,7174,,,http://en.wikipedia.org/wiki/Cadmium oxide,InChI=1/Cd.O,oxocadmium,http://www.biospider.ca/saved_files/mol/,O=[Cd],O=[Cd],CdO,129.898270,"Dark-brown, infusible powder or cubic crystals (R555).",900-1000 °C (decomposition of amorphous form [ 2 ] ),,,"",,,,"Oral 
Inhalation 
Dermal 
(R019)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640)
 Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Serum albumin (P02768) 
(R019, R164)","Cadmium initially binds to metallothionein and is transported to the kidney. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Accumulation of cadmium in the kidney results in increased excretion of vital low and high weight molecular proteins. Cadmium is a high affinity zinc analog and can interfere in its biological processes. It also binds to and activates the estrogen receptor, likely stimulating the growth of certain types of cancer cells and causing other estrogenic effects, such as reproductive dysfunction. Cadmium causes cell apoptosis by activating mitogen-activated protein kinases. (R026, R058, R059, R069)","Cadmium is absorbed from oral, inhalation, and dermal routes. Cadmium initially binds to metallothionein and albumin and is transported mainly to the kidney and liver. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Cadmium is not known to undergo any direct metabolic conversion and is excreted unchanged, mainly in the urine. (R019)","LD50: 72 mg/kg (oral, rat) (S278); LD50: 72 mg/kg (oral, mouse) (S278).",No data.,"1, carcinogenic to humans. (R264)",High purity cadmium oxide is used as a second polarizer (in addition to silver oxide) in silver-zinc storage batteries. It is also used in nitrile rubbers and plastics such as Teflon to improve their high-temperature properties and heat resistence. Other applications include use as starting material for PVC heat stabilizers and other Cd compounds and as the cadmium source in cyanide electroplating baths (S277). ,"Acute Inhalation: 0.00003 mg/m3 (R260) 
Chronic Inhalation: 0.00001 mg/m3 (R260) 
Intermediate Oral: 0.0005 mg/kg/day (R260) 
Chronic Oral: 0.0001 mg/kg/day (R260)","Chronic exposure to cadmium fumes can cause chemical pneumonitis, pulmonary edema, and lung diseases such as bronchitis and emphysema. Cadmium also accumulates in the kidneys, causing permanent damage. Loss of bone density also occurs. (R019)","Acute inhalation of cadmium fumes results in metal fume fever, which is characterized by chills, fever, headache, weakness, dryness of the nose and throat, chest pain, and coughing. Ingestion of cadmium causes vomiting and diarrhea. (R019)","Cadmium poisoning is treated by removal from exposure and supportive care. If ingested, induced vomiting or gastric lavage may be performed. (R272)",Q9UQF2;Q13387;Q9UPT6;O60271;P03372;Q92731;P28482;P53779;Q15759;P53778;O15264;Q16539;Q8TD08;P27361;P31152;Q16659;Q13164;P45983;P45984
382,T3D0381,2009-03-06 18:58:40 UTC,2009-08-04 21:28:27 UTC,Cadmium phosphate,Inorganic Compound;Cadmium Compound,ARTArsenate ionArsenate ionsArsorateTetraoxoarsenate(v)arsenate(3-)tetraoxidoarsenate(3-)tetraoxoarsenate(3-),"Cadmium phosphate is a chemical compound of cadmium. Cadmium is a transition metal and chemical element with the symbol Cd and atomic number 48. It is found naturally in the earth's crust, though rarely on it's own. (R019)",,13477-1-3 ,24182056,,C11215,"",29125,ARSENATE,,,Cadmium phosphate,,,,,"InChI=1/AsH3O4/c2-1(3,4)5/h(H3,2,3,4,5)","4-N-(7-chloro-3-phenylquinolin-4-yl)-1-N,1-N-diethylpentane-1,4-diamine hydroiodide",http://www.biospider.ca/saved_files/mol/,CCN(CC)CCCC(C)NC1=C2C=CC(=CC2=NC=C1C3=CC=CC=C3)Cl.I,CCN(CC)CCCC(C)NC1=C2C=CC(=CC2=NC=C1C3=CC=CC=C3)Cl.I,C24H31ClIN3,523.125120,No data.,"",,,"",,,,"Oral 
Inhalation 
Dermal 
(R019)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640)
 Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Serum albumin (P02768) 
(R019, R164)","Cadmium initially binds to metallothionein and is transported to the kidney. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Accumulation of cadmium in the kidney results in increased excretion of vital low and high weight molecular proteins. Cadmium is a high affinity zinc analog and can interfere in its biological processes. It also binds to and activates the estrogen receptor, likely stimulating the growth of certain types of cancer cells and causing other estrogenic effects, such as reproductive dysfunction. Cadmium causes cell apoptosis by activating mitogen-activated protein kinases. (R026, R058, R059, R069)","Cadmium is absorbed from oral, inhalation, and dermal routes. Cadmium initially binds to metallothionein and albumin and is transported mainly to the kidney and liver. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Cadmium is not known to undergo any direct metabolic conversion and is excreted unchanged, mainly in the urine. (R019)",No data.,No data.,"1, carcinogenic to humans. (R264)",Cadmium phospahte can be used as soil fertilizer (S279).,"Acute Inhalation: 0.00003 mg/m3 (R260) 
Chronic Inhalation: 0.00001 mg/m3 (R260) 
Intermediate Oral: 0.0005 mg/kg/day (R260) 
Chronic Oral: 0.0001 mg/kg/day (R260)","Chronic exposure to cadmium fumes can cause chemical pneumonitis, pulmonary edema, and lung diseases such as bronchitis and emphysema. Cadmium also accumulates in the kidneys, causing permanent damage. Loss of bone density also occurs. (R019)","Acute inhalation of cadmium fumes results in metal fume fever, which is characterized by chills, fever, headache, weakness, dryness of the nose and throat, chest pain, and coughing. Ingestion of cadmium causes vomiting and diarrhea. (R019)","Cadmium poisoning is treated by removal from exposure and supportive care. If ingested, induced vomiting or gastric lavage may be performed. (R272)",P28482;P53779;P27361;P31152;Q16659;Q13164;P45983;P45984;Q9UQF2;Q13387;Q9UPT6;O60271;P03372;Q92731;Q15759;P53778;O15264;Q16539;Q8TD08
383,T3D0382,2009-03-06 18:58:40 UTC,2009-08-04 21:28:27 UTC,Cadmium selenide,Inorganic Compound;Cadmium Compound;Selenium Compound,"CADMIUM SELENIDE, 99.9%Cadmium selenide (cdse)Cadmium(II) selenidecadmium(2+) selenide","Cadmium selenide is a chemical compound of cadmium and selenium that may be found as the naturally occurring mineral cadmoselite. It is used as a semiconductor. Cadmium is a transition metal and chemical element with the symbol Cd and atomic number 48. It is found naturally in the earth's crust, though rarely on it's own. Selenium is a nonmetal element with the atomic number 34 and the chemical symbol Se. Selenium rarely occurs in its elemental state in nature and is usually found in sulfide ores such as pyrite, partially replacing the sulfur in the ore matrix. It may also be found in silver, copper, lead, and nickel minerals. Though selenium salts are toxic in large amounts, trace amounts of the element are necessary for cellular function in most animals, forming the active center of the enzymes glutathione peroxidase, thioredoxin reductase, and three known deiodinase enzymes. (R976, R019, R769)",,1306-24-7,14784,,"","",50834,"",,C058667,Cadmium selenide,,,,http://en.wikipedia.org/wiki/cadmium selenide,InChI=1/Cd.Se,selanylidenecadmium,http://www.biospider.ca/saved_files/mol/,[Se]=[Cd],[Se]=[Cd],CdSe,193.819880,Greenish-brown or dark red powder.,1268 °C (1541 K),,,"",,,,"Oral 
Inhalation 
Dermal 
(R019)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640)
 Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Serum albumin (P02768) 
(R019, R164)","Cadmium initially binds to metallothionein and is transported to the kidney. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Accumulation of cadmium in the kidney results in increased excretion of vital low and high weight molecular proteins. Cadmium is a high affinity zinc analog and can interfere in its biological processes. It also binds to and activates the estrogen receptor, likely stimulating the growth of certain types of cancer cells and causing other estrogenic effects, such as reproductive dysfunction. Cadmium causes cell apoptosis by activating mitogen-activated protein kinases. Selenium readily substitutes for sulfur in biomolecules and in many biochemical reactions, especially when the concentration of selenium is high and the concentration of sulfur is low. Inactivation of the sulfhydryl enzymes necessary for oxidative reactions in cellular respiration, through effects on mitochondrial and microsomal electron transport, might contribute to acute selenium toxicity. Selenomethionine (a common organic selenium compound) also appears to randomly substitute for methionine in protein synthesis. This substitution may affect the structure and functionability of the protein, for example, by altering disulfide bridges. Inorganic forms of selenium appear to react with tissue thiols by redox catalysis, resulting in formation of reactive oxygen species and causing damage by oxidative stress. (R975, R026, R058, R059, R069)","Cadmium is absorbed from oral, inhalation, and dermal routes. Cadmium initially binds to metallothionein and albumin and is transported mainly to the kidney and liver. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Cadmium is not known to undergo any direct metabolic conversion and is excreted unchanged, mainly in the urine. Selenium may be absorbed through inhalation and ingestion, while some selenium compounds may also be absorbed dermally. Once in the body, selenium is distributed mainly to the liver and kidney. Selenium is an essential micronutrient and is a component of glutathione peroxidase, iodothyronine 5'-deiodinases, and thioredoxin reductase. Organic selenium is first metabolized into inorganic selenium. Inorganic selenium is reduced stepwise to the intermediate hydrogen selenide, which is either incorporated into selenoproteins after being transformed to selenophosphate and selenocysteinyl tRNA or excreted into the urine after being transformed into methylated metabolites of selenide. Elemental selenium is also methylated before excretion. Selenium is primarily eliminated in the urine and feces, but certain selenium compounds may also be exhaled. (R975, R019)",No data.,No data.,"1, carcinogenic to humans. (R264)",Cadmium selenide is used as a semiconductor. It is also found in laser diodes. (R769),"Acute Inhalation: 0.00003 mg/m3 (Cadmium) (R260) 
Chronic Inhalation: 0.00001 mg/m3 (Cadmium) (R260) 
Intermediate Oral: 0.0005 mg/kg/day (Cadmium) (R260) 
Chronic Oral: 0.0001 mg/kg/day (Cadmium) (R260)
Chronic Oral: 0.005 mg/kg/day (Selenium) (R260)","Chronic exposure to cadmium fumes can cause chemical pneumonitis, pulmonary edema, and lung diseases such as bronchitis and emphysema. Cadmium also accumulates in the kidneys, causing permanent damage. Loss of bone density also occurs. Chronic oral exposure to high concentrations of selenium compounds can produce a disease called selenosis. The major signs of selenosis are hair loss, nail brittleness, and neurological abnormalities (such as numbness and other odd sensations in the extremities). Animal studies have shown that selenium may also affect sperm production and the female reproductive cycle. (R975, R019)","Acute inhalation of cadmium fumes results in metal fume fever, which is characterized by chills, fever, headache, weakness, dryness of the nose and throat, chest pain, and coughing. Ingestion of cadmium causes vomiting and diarrhea. Short-term oral exposure to high concentrations of selenium may cause nausea, vomiting, and diarrhea. Brief exposures to high levels of elemental selenium or selenium dioxide in air can result in respiratory tract irritation, bronchitis, difficulty breathing, and stomach pains. Longer-term exposure to either of these air-borne forms can cause respiratory irritation, bronchial spasms, and coughing. (R975, R019)","Cadmium poisoning is treated by removal from exposure and supportive care. If ingested, induced vomiting or gastric lavage may be performed. (R272)",P28482;P53779;P27361;P31152;Q16659;Q13164;P45983;P45984;Q9UQF2;Q13387;Q9UPT6;O60271;P03372;Q92731;Q15759;P53778;O15264;Q16539;Q8TD08
384,T3D0383,2009-03-06 18:58:40 UTC,2009-08-18 16:40:28 UTC,Cadmium succinate,Inorganic Compound;Cadmium Compound,"Butanedioic acid, cadmium salt (1:1)CadminateCadmium succinateCaswell No. 136BSuccinic acid, cadmium saltSuccinic acid, cadmium salt (1:1)","Cadmium succinate is a chemical compound of cadmium. Cadmium is a transition metal and chemical element with the symbol Cd and atomic number 48. It is found naturally in the earth's crust, though rarely on it's own. (R019)",,141-00-4,8828,,"","","","",,C013859,Cadmium succinate,,,,,"InChI=1/C4H6O4.Cd/c5-3(6)1-2-4(7)8;/h1-2H2,(H,5,6)(H,7,8);/q;+2/p-2",butanedioate; cadmium(2+),http://www.biospider.ca/saved_files/mol/,C(CC(=O)[O-])C(=O)[O-].[Cd+2],[O-]C(=O)CCC(=O)[O-][Cd+],C4H4CdO4,229.914320,No data.,"",,,3.67 mg/mL at 40 oC [MERCK INDEX (1996)],,,,"Oral 
Inhalation 
Dermal 
(R019)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640)
 Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Serum albumin (P02768) 
(R019, R164)","Cadmium initially binds to metallothionein and is transported to the kidney. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Accumulation of cadmium in the kidney results in increased excretion of vital low and high weight molecular proteins. Cadmium is a high affinity zinc analog and can interfere in its biological processes. It also binds to and activates the estrogen receptor, likely stimulating the growth of certain types of cancer cells and causing other estrogenic effects, such as reproductive dysfunction. Cadmium causes cell apoptosis by activating mitogen-activated protein kinases. (R026, R058, R059, R069)","Cadmium is absorbed from oral, inhalation, and dermal routes. Cadmium initially binds to metallothionein and albumin and is transported mainly to the kidney and liver. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Cadmium is not known to undergo any direct metabolic conversion and is excreted unchanged, mainly in the urine. (R019)","LD50: 660 mg/kg (oral, rat) (S280); LD50: 312 mg/kg (oral, mouse) (S281).",No data.,"1, carcinogenic to humans. (R264)","Cadmium succinate is used as a pesticide, and also to control turfgrass diseases (S282).","Acute Inhalation: 0.00003 mg/m3 (R260) 
Chronic Inhalation: 0.00001 mg/m3 (R260) 
Intermediate Oral: 0.0005 mg/kg/day (R260) 
Chronic Oral: 0.0001 mg/kg/day (R260)","Chronic exposure to cadmium fumes can cause chemical pneumonitis, pulmonary edema, and lung diseases such as bronchitis and emphysema. Cadmium also accumulates in the kidneys, causing permanent damage. Loss of bone density also occurs. (R019)","Acute inhalation of cadmium fumes results in metal fume fever, which is characterized by chills, fever, headache, weakness, dryness of the nose and throat, chest pain, and coughing. Ingestion of cadmium causes vomiting and diarrhea. (R019)","Cadmium poisoning is treated by removal from exposure and supportive care. If ingested, induced vomiting or gastric lavage may be performed. (R272)",P28482;P53779;P27361;P31152;Q16659;Q13164;P45983;P45984;Q9UQF2;Q13387;Q9UPT6;O60271;P03372;Q92731;Q15759;P53778;O15264;Q16539;Q8TD08
385,T3D0384,2009-03-06 18:58:40 UTC,2009-08-25 19:53:03 UTC,Cadmium sulfate,Inorganic Compound;Cadmium Compound,"CADMIUM SULFATE (1:1) HYDRATE (3:8)Cadmium mesosulfate (CdH2SO5)Cadmium mesosulfate (CdH2SO5) (7CI)Cadmium monosulfateCadmium sulfateCadmium sulfate (1:1)Cadmium sulfate [cadmium and cadmium compounds]Cadmium sulfate monohydrateCadmium sulfate tetrahydrateCadmium sulfate, hydrateCadmium sulfate, tetrahydrateCadmium sulfuricumCadmium sulphateCadmium sulphate (1:1)CadmiumsulfatCaswell No. 136CCdSO4KadmiumsulfatSulfate de cadmiumSulfato de cadmioSulfuric acid, cadmium salt (1:1)Sulfuric acid, cadmium salt (1:1), monohydrate (8CI,9CI)Sulfuric acid, cadmium salt, tetrahydrateSulphuric acid, cadmium salt (1:1)cadmium(2+) sulfate","Cadmium sulfate is a sulfate of cadmium that occurs naturally as the mineral drobecite. It is used mainly in cadmium electroplating. Cadmium is a transition metal and chemical element with the symbol Cd and atomic number 48. It is found naturally in the earth's crust, though rarely on it's own. (R019, R752)",,10124-36-4,24962,,"","",50292,"",,C037123,Cadmium sulfate,,,,,"InChI=1/Cd.H2O4S/c;1-5(2,3)4/h;(H2,1,2,3,4)/q+2;/p-2",cadmium(2+) sulfate,http://www.biospider.ca/saved_files/mol/,[O-]S(=O)(=O)[O-].[Cd+2],[O-]S(=O)(=O)[O-].[Cd+2],CdO4S,209.855090,Colorless crystals.,"",,,"",,,,"Oral 
Inhalation 
Dermal 
(R019)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640)
 Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Serum albumin (P02768) 
(R019, R164)","Cadmium initially binds to metallothionein and is transported to the kidney. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Accumulation of cadmium in the kidney results in increased excretion of vital low and high weight molecular proteins. Cadmium is a high affinity zinc analog and can interfere in its biological processes. It also binds to and activates the estrogen receptor, likely stimulating the growth of certain types of cancer cells and causing other estrogenic effects, such as reproductive dysfunction. Cadmium causes cell apoptosis by activating mitogen-activated protein kinases. (R026, R058, R059, R069)","Cadmium is absorbed from oral, inhalation, and dermal routes. Cadmium initially binds to metallothionein and albumin and is transported mainly to the kidney and liver. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Cadmium is not known to undergo any direct metabolic conversion and is excreted unchanged, mainly in the urine. (R019)","LD50: 280 mg/kg (Oral, Rat) (R263)
LD50: 12 760 ug/kg (Intraperitoneal, Mouse) (R263)",No data.,"1, carcinogenic to humans. (R264)","Cadmium sulfate is used in cadmium electroplating, pigments, and as a nematocide. (R752)","Acute Inhalation: 0.00003 mg/m3 (R260) 
Chronic Inhalation: 0.00001 mg/m3 (R260) 
Intermediate Oral: 0.0005 mg/kg/day (R260) 
Chronic Oral: 0.0001 mg/kg/day (R260)","Chronic exposure to cadmium fumes can cause chemical pneumonitis, pulmonary edema, and lung diseases such as bronchitis and emphysema. Cadmium also accumulates in the kidneys, causing permanent damage. Loss of bone density also occurs. (R019)","Acute inhalation of cadmium fumes results in metal fume fever, which is characterized by chills, fever, headache, weakness, dryness of the nose and throat, chest pain, and coughing. Ingestion of cadmium causes vomiting and diarrhea. (R019)","Cadmium poisoning is treated by removal from exposure and supportive care. If ingested, induced vomiting or gastric lavage may be performed. (R272)",P28482;P53779;P27361;P31152;Q16659;Q13164;P45983;P45984;Q9UQF2;Q13387;Q9UPT6;O60271;P03372;Q92731;Q15759;P53778;O15264;Q16539;Q8TD08
386,T3D0385,2009-03-06 18:58:40 UTC,2009-08-25 19:53:03 UTC,Cadmium sulfate hydrate,Inorganic Compound;Cadmium Compound,"Cadmium sulfateCadmium sulfate (1:1) hydrate (3:8)Cadmium sulfate hydrateCadmium sulfate hydrate (3:8)Cadmium sulfate octahydrateCadmium sulphate octahydrateSulfuric acid, cadmium salt, hydrate","Cadmium sulfate is a sulfate of cadmium that occurs naturally as the mineral drobecite. It is used mainly in cadmium electroplating. Cadmium is a transition metal and chemical element with the symbol Cd and atomic number 48. It is found naturally in the earth's crust, though rarely on it's own. (R019, R752)",,7790-84-3 ,154912,,"","","","",,,Cadmium sulfate hydrate,,,,,"InChI=1/Cd.H2O4S/c;1-5(2,3)4/h;(H2,1,2,3,4)/q+2;/p-2",cadmium(2+) sulfate hydrate,http://www.biospider.ca/saved_files/mol/,O.[O-]S(=O)(=O)[O-].[Cd+2],O.[O-]S(=O)(=O)[O-].[Cd+2],CdH2O5S,227.865650,Colorless crystals.,"",,,"",,,,"Oral 
Inhalation 
Dermal 
(R019)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640)
 Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Serum albumin (P02768) 
(R019, R164)","Cadmium initially binds to metallothionein and is transported to the kidney. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Accumulation of cadmium in the kidney results in increased excretion of vital low and high weight molecular proteins. Cadmium is a high affinity zinc analog and can interfere in its biological processes. It also binds to and activates the estrogen receptor, likely stimulating the growth of certain types of cancer cells and causing other estrogenic effects, such as reproductive dysfunction. Cadmium causes cell apoptosis by activating mitogen-activated protein kinases. (R026, R058, R059, R069)","Cadmium is absorbed from oral, inhalation, and dermal routes. Cadmium initially binds to metallothionein and albumin and is transported mainly to the kidney and liver. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Cadmium is not known to undergo any direct metabolic conversion and is excreted unchanged, mainly in the urine. (R019)","LD50: 27 mg/kg (oral, dog) (S283); LD50: 280 mg/kg (oral, rat) (S283).",No data.,"1, carcinogenic to humans. (R264)","Cadmium sulfate is used in cadmium electroplating, pigments, and as a nematocide. (R752)","Acute Inhalation: 0.00003 mg/m3 (R260) 
Chronic Inhalation: 0.00001 mg/m3 (R260) 
Intermediate Oral: 0.0005 mg/kg/day (R260) 
Chronic Oral: 0.0001 mg/kg/day (R260)","Chronic exposure to cadmium fumes can cause chemical pneumonitis, pulmonary edema, and lung diseases such as bronchitis and emphysema. Cadmium also accumulates in the kidneys, causing permanent damage. Loss of bone density also occurs. (R019)","Acute inhalation of cadmium fumes results in metal fume fever, which is characterized by chills, fever, headache, weakness, dryness of the nose and throat, chest pain, and coughing. Ingestion of cadmium causes vomiting and diarrhea. (R019)","Cadmium poisoning is treated by removal from exposure and supportive care. If ingested, induced vomiting or gastric lavage may be performed. (R272)",P28482;P53779;P27361;P31152;Q16659;Q13164;P45983;P45984;Q9UQF2;Q13387;Q9UPT6;O60271;P03372;Q92731;Q15759;P53778;O15264;Q16539;Q8TD08
387,T3D0386,2009-03-06 18:58:40 UTC,2009-08-04 21:28:28 UTC,Cadmium sulphide,Inorganic Compound;Cadmium Compound,Aurora yellowC.I. Pigment Yellow 37C.P. Golden Yellow 55Cadmium Yellow 000Cadmium Yellow 10G ConcCadmium Yellow 892Cadmium Yellow Primrose 47-4100Cadmium golden 366Cadmium lemon Yellow 527Cadmium monosulfideCadmium orangeCadmium primrose 819Cadmium sulfide (CDS)Cadmium sulfide [cadmium and cadmium compounds]Cadmium sulfide yellowCadmium sulfuratumCadmium sulphideCadmium sulphuratumCadmium yellowCadmium yellow conc. deepCadmium yellow conc. goldenCadmium yellow conc. lemonCadmium yellow conc. primroseCadmium yellow oz darkCadmium(II) sulfideCadmiumsulfidCadmopur golden yellow nCadmopur yellowCapsebonFerro lemon yellowFerro orange yellowFerro yellowGSKGreenockiteJaune brilliantKadmiumsulfidOrange cadmiumPrimrose 1466cadmium(2+) sulfide,"Cadmium sulfide is a sulfide of cadmium that occurs naturally as the minerals greenockite and hawleyite and is also produced by sulfate reducing bacteria. It is used mainly as a semiconductor and pigment. Cadmium is a transition metal and chemical element with the symbol Cd and atomic number 48. It is found naturally in the earth's crust, though rarely on it's own. (R019, R753)",,1306-23-6,14783,,"","",50833,"",,C034939,Cadmium sulphide,,,,http://en.wikipedia.org/wiki/cadmium sulfide,InChI=1/Cd.S,sulfanylidenecadmium,http://www.biospider.ca/saved_files/mol/,S=[Cd],S=[Cd],CdS,145.875430,"Light yellow, orange or brown crystals.",1750 °C at 100 bar (10 MPa),,,"",,,,"Oral 
Inhalation 
Dermal 
(R019)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640)
 Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Serum albumin (P02768) 
(R019, R164)","Cadmium initially binds to metallothionein and is transported to the kidney. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Accumulation of cadmium in the kidney results in increased excretion of vital low and high weight molecular proteins. Cadmium is a high affinity zinc analog and can interfere in its biological processes. It also binds to and activates the estrogen receptor, likely stimulating the growth of certain types of cancer cells and causing other estrogenic effects, such as reproductive dysfunction. Cadmium causes cell apoptosis by activating mitogen-activated protein kinases. (R026, R058, R059, R069)","Cadmium is absorbed from oral, inhalation, and dermal routes. Cadmium initially binds to metallothionein and albumin and is transported mainly to the kidney and liver. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Cadmium is not known to undergo any direct metabolic conversion and is excreted unchanged, mainly in the urine. (R019)","LD50: 1166 mg/kg (Oral, Mouse) (R263)",No data.,"1, carcinogenic to humans. (R264)",Cadmium sulfide is used as a semiconductor and in the electronics industry for photocells and light emitting diodes. It is also found in pigments and solar cells. (R753),"Acute Inhalation: 0.00003 mg/m3 (R260) 
Chronic Inhalation: 0.00001 mg/m3 (R260) 
Intermediate Oral: 0.0005 mg/kg/day (R260) 
Chronic Oral: 0.0001 mg/kg/day (R260)","Chronic exposure to cadmium fumes can cause chemical pneumonitis, pulmonary edema, and lung diseases such as bronchitis and emphysema. Cadmium also accumulates in the kidneys, causing permanent damage. Loss of bone density also occurs. (R019)","Acute inhalation of cadmium fumes results in metal fume fever, which is characterized by chills, fever, headache, weakness, dryness of the nose and throat, chest pain, and coughing. Ingestion of cadmium causes vomiting and diarrhea. (R019)","Cadmium poisoning is treated by removal from exposure and supportive care. If ingested, induced vomiting or gastric lavage may be performed. (R272)",P28482;P53779;P27361;P31152;Q16659;Q13164;P45983;P45984;Q9UQF2;Q13387;Q9UPT6;O60271;P03372;Q92731;Q15759;P53778;O15264;Q16539;Q8TD08
388,T3D0387,2009-03-06 18:58:40 UTC,2009-08-04 21:28:28 UTC,Cadmium telluride,Inorganic Compound;Cadmium Compound,"CADMIUM TELLURIDE, 99.999%Cadmium monotellurideCadmium telluride (cdte)Irtran 6","Cadmium telluride is a chemical compound of cadmium and tellurium. It is used mainly as a semiconductor and in solar cells. Cadmium is a transition metal and chemical element with the symbol Cd and atomic number 48. It is found naturally in the earth's crust, though rarely on it's own. (R019, R770)",,1306-25-8,91501,,"","","","",,C028337,Cadmium telluride,,,,http://en.wikipedia.org/wiki/cadmium telluride,InChI=1/Cd.Te,tellanylidenecadmium,http://www.biospider.ca/saved_files/mol/,[Cd]=[Te],[Cd]=[Te],CdTe,243.809580,Brownish-black crystals.,1092 °C,,,"",,,,"Oral 
Inhalation 
Dermal 
(R019)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640)
 Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Serum albumin (P02768) 
(R019, R164)","Cadmium initially binds to metallothionein and is transported to the kidney. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Accumulation of cadmium in the kidney results in increased excretion of vital low and high weight molecular proteins. Cadmium is a high affinity zinc analog and can interfere in its biological processes. It also binds to and activates the estrogen receptor, likely stimulating the growth of certain types of cancer cells and causing other estrogenic effects, such as reproductive dysfunction. Cadmium causes cell apoptosis by activating mitogen-activated protein kinases. (R026, R058, R059, R069)","Cadmium is absorbed from oral, inhalation, and dermal routes. Cadmium initially binds to metallothionein and albumin and is transported mainly to the kidney and liver. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Cadmium is not known to undergo any direct metabolic conversion and is excreted unchanged, mainly in the urine. (R019)","LD50: 2100 mg/kg (Intraperitoneal, Mouse) (R772)",No data.,"1, carcinogenic to humans. (R264)","Cadmium telluride is used as a semiconductor in solar cells and in infrared, x-ray, and gamma-ray detectors. (R770)","Acute Inhalation: 0.00003 mg/m3 (R260) 
Chronic Inhalation: 0.00001 mg/m3 (R260) 
Intermediate Oral: 0.0005 mg/kg/day (R260) 
Chronic Oral: 0.0001 mg/kg/day (R260)","Chronic exposure to cadmium fumes can cause chemical pneumonitis, pulmonary edema, and lung diseases such as bronchitis and emphysema. Cadmium also accumulates in the kidneys, causing permanent damage. Loss of bone density also occurs. (R019)","Acute inhalation of cadmium fumes results in metal fume fever, which is characterized by chills, fever, headache, weakness, dryness of the nose and throat, chest pain, and coughing. Ingestion of cadmium causes vomiting and diarrhea. (R019)","Cadmium poisoning is treated by removal from exposure and supportive care. If ingested, induced vomiting or gastric lavage may be performed. (R272)",P28482;P53779;P27361;P31152;Q16659;Q13164;P45983;P45984;Q9UQF2;Q13387;Q9UPT6;O60271;P03372;Q92731;Q15759;P53778;O15264;Q16539;Q8TD08
389,T3D0388,2009-03-06 18:58:41 UTC,2009-08-18 16:55:03 UTC,Cadmium tungstate,Inorganic Compound;Cadmium Compound,Cadmium tungstate,"Cadmium tungstate is a chemical compound of cadmium and tungsten used mainly in the detection of gamma rays. Cadmium is a transition metal and chemical element with the symbol Cd and atomic number 48. It is found naturally in the earth's crust, though rarely on it's own. (R019, R771)",,7790-85-4,4985693,,"","","","",,C052547,Cadmium tungstate,,,,,InChI=1/Cd.4O.W/q+2;4*-2;,cadmium; dihydroxy(dioxo)tungsten,http://www.biospider.ca/saved_files/mol/,O[W](=O)(=O)O.[Cd],O[W](=O)(=O)O.[Cd],CdH2O4W,363.849600,White or yellow crystals.,"",,,"",,,,"Oral 
Inhalation 
Dermal 
(R019)","Metallothionein-2 (P02795) 
Metallothionein-1G (P13640)
 Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
Serum albumin (P02768) 
(R019, R164)","Cadmium initially binds to metallothionein and is transported to the kidney. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Accumulation of cadmium in the kidney results in increased excretion of vital low and high weight molecular proteins. Cadmium is a high affinity zinc analog and can interfere in its biological processes. It also binds to and activates the estrogen receptor, likely stimulating the growth of certain types of cancer cells and causing other estrogenic effects, such as reproductive dysfunction. Cadmium causes cell apoptosis by activating mitogen-activated protein kinases. (R026, R058, R059, R069)","Cadmium is absorbed from oral, inhalation, and dermal routes. Cadmium initially binds to metallothionein and albumin and is transported mainly to the kidney and liver. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Cadmium is not known to undergo any direct metabolic conversion and is excreted unchanged, mainly in the urine. (R019)",No data.,No data.,"1, carcinogenic to humans. (R264)","Cadmium tungstate is used in fluorescent paint, x-ray screens, gamma ray detection, and scintillation counters. (R771)","Acute Inhalation: 0.00003 mg/m3 (R260) 
Chronic Inhalation: 0.00001 mg/m3 (R260) 
Intermediate Oral: 0.0005 mg/kg/day (R260) 
Chronic Oral: 0.0001 mg/kg/day (R260)","Chronic exposure to cadmium fumes can cause chemical pneumonitis, pulmonary edema, and lung diseases such as bronchitis and emphysema. Cadmium also accumulates in the kidneys, causing permanent damage. Loss of bone density also occurs. (R019)","Acute inhalation of cadmium fumes results in metal fume fever, which is characterized by chills, fever, headache, weakness, dryness of the nose and throat, chest pain, and coughing. Ingestion of cadmium causes vomiting and diarrhea. (R019)","Cadmium poisoning is treated by removal from exposure and supportive care. If ingested, induced vomiting or gastric lavage may be performed. (R272)",P28482;P53779;P27361;P31152;Q16659;Q13164;P45983;P45984;Q9UQF2;Q13387;Q9UPT6;O60271;P03372;Q92731;Q15759;P53778;O15264;Q16539;Q8TD08
390,T3D0389,2009-03-06 18:58:41 UTC,2009-08-04 21:28:28 UTC,Diphenyl,Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1, 1'-Diphenyl1,1'-Biphenyl1,1'-Biphenyl, butenylated1,1'-Diphenyl1,1'-biphenyl (ACD/Name 4.0)1,1-BiphenylAromatic hydrocarbons, biphenyl-richBNLBibenzeneBiphenyl [bsi:iso]Biphenyl, 1,1-Biphenyl-UL-14CCarolid alCaswell No. 087DiphenylFEMA No. 3129LemonenePHPHPhenador-xPhenylbenzeneTetrosin LYWLN: RRXenenediphenyl, 14C-labeled","Diphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)
",,92-52-4,7095,,C06588,"",17097,CPD-945,,C010574,Diphenyl,162,,,,InChI=1/C12H10/c1-3-7-11(8-4-1)12-9-5-2-6-10-12/h1-10H,phenylbenzene,http://www.biospider.ca/saved_files/mol/a2ab976cd2209a7e7dda15c51bd7eb56_1237976634.mol,C1=CC=C(C=C1)C2=CC=CC=C2,C1=CC=C(C=C1)C2=CC=CC=C2,C12H10,154.078250,White scales (S284).,69 oC,,,"0.00748 mg/mL at 25 oC [YALKOWSKY,SH & HE,Y (2003)]",,,,"Inhalation and dermal/eye contact are the most common routes of exposure. The exposure can also occur trhough inhalation, but to a lesser extent (S286).","",Biphenyl alters the permeability properties of mitochondrial membranes (S289).,"Diphenyl is well absorbed through the gastrointestinal tract. It is rapidly metabolized to 4-hydroxybiphenyl, 4-phenyl-catechol and 4,4'-dihydroxyphenyl, which are excreted in urine and bile as glucuronide and mercapturic conjugates. The metabolites of diphenyl, mainly 4-hydroxybiphenyl, are excreted rapidly and almost exclusively in the urine. Acute oral toxicity is moderate. (S287, S288).","LD50: 3280 mg/kg (oral, rat) (R700); LD50: 2400 mg/kg (oral, rabbit) (R289); LD50: 2500 mg/kg (dermal, rabbit) (R625).",No data.,"2A, probably carcinogenic to humans. (R264)",Organic synthesis; heat transfer agent; fungistat in packaging of citrus fruit; plant disease control; manufacture of benzidine; dyeing assistant for polyesters (S284).,No data.,"Exposure to diphenyl can cause necrosis in the liver and kidney, with regions of cirrhosis in liver; also, degenerative changes in heart muscle, damage to the central and peripheral nervous systems, as well as death can result from diphenyl poisoning (S287).","Symptoms of diphenyl poisoning include headache, fatigue, abdominal pain with nausea or diarrhea and various symptoms, vomiting and bronchitis (S287).","Consider gastric lavage, after ingestion of a potentially life-threatening amount of poison if it can be performed soon after ingestion. In case of inhalation exposure, move patient to fresh air and monitor for
respiratory distress; if cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with inhaled beta2 agonist and oral or parenteral corticosteroids. In case of eye exposure, irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes. I f the exposure occurred through dermal contact, remove contaminated clothing and wash exposed area thoroughly with soap and water (R624).
",P03372;Q92731
391,T3D0390,2009-03-06 18:58:41 UTC,2009-08-11 15:55:22 UTC,2-Chlorobiphenyl,Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, chloro-1-Chloro-2-phenylbenzene2-Chlorbiphenyl2-Chloro-1, 1'-biphenyl2-Chloro-1,1'-biphenyl2-Chlorobiphenyl2-Chlorodiphenyl2-Monochlorobiphenyl2-PCB2-chloro-1,1'-biphenyl (ACD/Name 4.0)Arochlor-1254Biphenyl, 2-chloro-Biphenyl, chloro-Chloro-1,1'-biphenylChlorobiphenylChlorodiphenylChlorodwufenol [polish]DiphenylchlorideMonochlorobiphenylO-chlorobiphenylO-chlorodiphenylPCB 1PCB No 1WLN: GR BR","2-Chlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)
",,2051-60-7,249266,,C14353,"",34269,CPD-946,,C055142,2-Chlorobiphenyl,,,,,InChI=1/C12H9Cl/c13-12-9-5-4-8-11(12)10-6-2-1-3-7-10/h1-9H,1-chloro-2-phenylbenzene,http://www.biospider.ca/saved_files/mol/c16be27a891e474788e1b68088d26aab_1237976786.mol,C1=CC=C(C=C1)C2=CC=CC=C2Cl,C1=CC=C(C=C1)C2=CC=CC=C2Cl,C12H9Cl,188.039280,Oily liquids or solids that are colorless to light yellow. ,34 oC,,,"0.00483 mg/mL at 25 oC [CHIOU,CT et al. (1983)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
392,T3D0391,2009-03-06 18:58:41 UTC,2009-08-11 15:55:22 UTC,3-Chlorobiphenyl,Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 2-chloro-1,1'-Biphenyl, 2-chloro- (9CI)1,1'-Biphenyl, 3-chloro-2-CHLOROBIPHENYL2-Chloro-1,1'-biphenyl2-Chlorodiphenyl2-Monochlorobiphenyl3-Chlorbiphenyl3-Chloro-1,1'-biphenyl3-Chlorobiphenyl3-Chlorodiphenyl3-Monochlorobiphenyl3-PCB3-monochloro-1,1'-biphenylBiphenyl, 2-chloro-Biphenyl, 3-chloro-M-chloro diphenylM-chlorobiphenylO-chlorobiphenylO-chlorodiphenylPCB No 2PCB2","3-Chlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)
",,2051-61-8,16322,,"","",36716,CPD-946,,C034280,3-Chlorobiphenyl,,,,,InChI=1/C12H9Cl/c13-12-8-4-7-11(9-12)10-5-2-1-3-6-10/h1-9H,1-chloro-3-phenylbenzene,http://www.biospider.ca/saved_files/mol/,C1=CC=C(C=C1)C2=CC(=CC=C2)Cl,C1=CC=C(C=C1)C2=CC(=CC=C2)Cl,C12H9Cl,188.039280,Oily liquids or solids that are colorless to light yellow. ,16 oC,,,"0.00363 mg/mL at 25 oC [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
393,T3D0392,2009-03-06 18:58:41 UTC,2009-08-11 15:55:22 UTC,4-Chlorobiphenyl,Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 4-chloro- (9CI)1-Chloro-4-phenylbenzene1-chloro-4-phenyl benzene4-Chlorbiphenyl4-Chloro-1, 1'-biphenyl4-Chloro-1,1'-biphenyl4-Chlorobiphenyl4-Chlorodiphenyl4-Monochloro-biphenyl4-Monochlorobiphenyl4-PCB4-chloro-1,1'-biphenyl (ACD/Name 4.0)Biphenyl, 4-chloro-P-chlorobiphenylP-chlorodiphenylPCB 3PCB No 3WLN: GR DR","4-Chlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)
",,2051-62-9,16323,,C06584,"",27757,CPD-946,,C006983,4-Chlorobiphenyl,,,,,InChI=1/C12H9Cl/c13-12-8-6-11(7-9-12)10-4-2-1-3-5-10/h1-9H,1-chloro-4-phenylbenzene,http://www.biospider.ca/saved_files/mol/298a5d64469e8103b78f33bc3804c466_1237976975.mol,C1=CC=C(C=C1)C2=CC=C(C=C2)Cl,C1=CC=C(C=C1)C2=CC=C(C=C2)Cl,C12H9Cl,188.039280,Oily liquids or solids that are colorless to light yellow. ,78.8 oC,,,"0.00134 mg/mL at 25 oC [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
394,T3D0393,2009-03-06 18:58:41 UTC,2009-08-11 15:55:22 UTC,"2,2'-Dichlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 2,2'-dichloro- (9CI)2,2'-Dichlorbiphenyl2,2'-Dichlorbiphenyl [German]2,2'-Dichloro-1, 1'-biphenyl2,2'-Dichloro-1,1'-biphenyl2,2'-Dichlorobiphenyl2,2'-Dichlorodiphenyl2,2'-dichloro-1,1'-biphenyl (ACD/Name 4.0)Biphenyl, 2,2'-dichloro-O,o'-dichlorobiphenylPCB 4PCB No 4WLN: CR br BG","2,2'-Dichlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)

",,13029-08-8,25622,,"","","",CPD-946,,C012280,"2,2'-Dichlorobiphenyl",,,,,InChI=1/C12H8Cl2/c13-11-7-3-1-5-9(11)10-6-2-4-8-12(10)14/h1-8H,1-chloro-2-(2-chlorophenyl)benzene,http://www.biospider.ca/saved_files/mol/,C1=CC=C(C(=C1)C2=CC=CC=C2Cl)Cl,C1=CC=C(C(=C1)C2=CC=CC=C2Cl)Cl,C12H8Cl2,222.000310,Oily liquids or solids that are colorless to light yellow. ,61.5 oC,,,"0.00185 mg/mL at 25 oC [CHIOU,CT et al. (1983)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
395,T3D0394,2009-03-06 18:58:41 UTC,2009-08-11 15:55:22 UTC,"2,3-Dichlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, dichloro-1,1'-Biphenyl, dichloro- (9CI)2,3-Dichloro-1,1'-biphenyl2,3-DichlorobiphenylBiphenyl, 2,3-dichloro-Biphenyl, dichloro-DICHLORO-1,1'-BIPHENYLDichlorobiphenylDichlorodiphenylPCB 5","2,3-Dichlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)

",,16605-91-7,27959,,"","","",CPD-946,,C030375,"2,3-Dichlorobiphenyl",,,,,InChI=1/C12H8Cl2/c13-11-8-4-7-10(12(11)14)9-5-2-1-3-6-9/h1-8H,"1,2-dichloro-3-phenylbenzene",http://www.biospider.ca/saved_files/mol/,C1=CC=C(C=C1)C2=C(C(=CC=C2)Cl)Cl,C1=CC=C(C=C1)C2=C(C(=CC=C2)Cl)Cl,C12H8Cl2,222.000310,Oily liquids or solids that are colorless to light yellow. ,"",,,0.000997 mg/mL at 25 oC [EPA],,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
396,T3D0395,2009-03-06 18:58:41 UTC,2009-08-11 15:55:23 UTC,"2,3'-Dichlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl 2,3'-dichloro-1,1'-Biphenyl, 2,3'-dichloro-2,3'-DichlorobiphenylPCB 6","2,3'-Dichlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)

",,25569-80-6,33100,,"","","",CPD-946,,C091159,"2,3'-Dichlorobiphenyl",,,,,InChI=1/C12H8Cl2/c13-10-5-3-4-9(8-10)11-6-1-2-7-12(11)14/h1-8H,1-chloro-3-(2-chlorophenyl)benzene,http://www.biospider.ca/saved_files/mol/,C1=CC=C(C(=C1)C2=CC(=CC=C2)Cl)Cl,C1=CC=C(C(=C1)C2=CC(=CC=C2)Cl)Cl,C12H8Cl2,222.000310,Oily liquids or solids that are colorless to light yellow. ,"",,,"0.00058 mg/mL at 20 oC [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
397,T3D0396,2009-03-06 18:58:42 UTC,2009-08-11 15:55:23 UTC,"2,4-Dichlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"2,4-Dichloro-1,1'-biphenyl2,4-Dichloro-1-phenylbenzene2,4-DichlorobiphenylBiphenyl, 2,4-dichloro-PCB 7","2,4-Dichlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)

",,33284-50-3,36399,,"","","",CPD-946,,,"2,4-Dichlorobiphenyl",,,,,InChI=1/C12H8Cl2/c13-10-6-7-11(12(14)8-10)9-4-2-1-3-5-9/h1-8H,"2,4-dichloro-1-phenylbenzene",http://www.biospider.ca/saved_files/mol/,C1=CC=C(C=C1)C2=C(C=C(C=C2)Cl)Cl,C1=CC=C(C=C1)C2=C(C=C(C=C2)Cl)Cl,C12H8Cl2,222.000310,Oily liquids or solids that are colorless to light yellow. ,"",,,"0.00115 mg/mL at 25 oC [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
398,T3D0397,2009-03-06 18:58:42 UTC,2009-08-11 15:55:23 UTC,"2,4'-Dichlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyhl, 2,4'-dichloro-1,1'-Biphenyl, 2,4'-dichloro- (9CI)2,4'-Dichloro-1,1'-biphenyl2,4'-Dichlorobiphenyl2,4'-dichlorobiphenyl, 14C-labeledBCR289_FLUKABiphenyl, 2,4'-dichloro-PCB 8","2,4'-Dichlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)

",,34883-43-7,36982,,C14246,"",34232,CPD-946,,C029907,"2,4'-Dichlorobiphenyl",,,,,InChI=1/C12H8Cl2/c13-10-7-5-9(6-8-10)11-3-1-2-4-12(11)14/h1-8H,1-chloro-4-(2-chlorophenyl)benzene,http://www.biospider.ca/saved_files/mol/7ed4e93d2e49eb707d029786a59c56f2_1237977415.mol,C1=CC=C(C(=C1)C2=CC=C(C=C2)Cl)Cl,C1=CC=C(C(=C1)C2=CC=C(C=C2)Cl)Cl,C12H8Cl2,222.000310,Oily liquids or solids that are colorless to light yellow. ,"",,,"0.00117 mg/mL at 25 oC [CHIOU,CT et al. (1983)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
399,T3D0398,2009-03-06 18:58:42 UTC,2009-08-11 15:55:24 UTC,"2,5-Dichlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"2,5-Dichloro-1,1'-biphenyl2,5-Dichlorobiphenyl3,6-DichlorobiphenylBiphenyl, 2,5-dichloro-PCB 9","2,5-Dichlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)

",,34883-39-1,36980,,C14354,"",34246,CPD-946,,C029905,"2,5-Dichlorobiphenyl",,,,,InChI=1/C12H8Cl2/c13-10-6-7-12(14)11(8-10)9-4-2-1-3-5-9/h1-8H,"1,4-dichloro-2-phenylbenzene",http://www.biospider.ca/saved_files/mol/efb38f9f556561953b78e71d13441cf6_1237977534.mol,C1=CC=C(C=C1)C2=C(C=CC(=C2)Cl)Cl,C1=CC=C(C=C1)C2=C(C=CC(=C2)Cl)Cl,C12H8Cl2,222.000310,Oily liquids or solids that are colorless to light yellow. ,"",,,"0.00112 mg/mL at 25 oC [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
400,T3D0399,2009-03-06 18:58:42 UTC,2009-08-11 15:55:24 UTC,"2,6-Dichlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"2,6-Dichloro-1,1'-biphenyl2,6-DichlorobiphenylBiphenyl, 2,6-dichloro-","2,6-Dichlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)

",,33146-45-1,36342,,C14355,"",34249,CPD-946,,C029908,"2,6-Dichlorobiphenyl",,,,,InChI=1/C12H8Cl2/c13-10-7-4-8-11(14)12(10)9-5-2-1-3-6-9/h1-8H,"1,3-dichloro-2-phenylbenzene",http://www.biospider.ca/saved_files/mol/b927c4099b813f70ca5d74881141cb80_1237977623.mol,C1=CC=C(C=C1)C2=C(C=CC=C2Cl)Cl,C1=CC=C(C=C1)C2=C(C=CC=C2Cl)Cl,C12H8Cl2,222.000310,Oily liquids or solids that are colorless to light yellow. ,"",,,"0.00241 mg/mL at 25 oC [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
401,T3D0400,2009-03-06 18:58:42 UTC,2009-08-11 15:55:24 UTC,"3,3'-Dichlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"3,3'-Dichloro-1,1'-biphenyl3,3'-Dichlorobiphenyl3,3'-DichlorodiphenylBiphenyl, 3,3'-dichloro-Clophen A 30Clophen A-30Clophen A30M,m'-dichlorobiphenylPCB No 11","3,3'-Dichlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)

",,2050-67-1,16307,,"","","",CPD-946,,C029906,"3,3'-Dichlorobiphenyl",,,,,InChI=1/C12H8Cl2/c13-11-5-1-3-9(7-11)10-4-2-6-12(14)8-10/h1-8H,1-chloro-3-(3-chlorophenyl)benzene,http://www.biospider.ca/saved_files/mol/,C1=CC(=CC(=C1)Cl)C2=CC(=CC=C2)Cl,C1=CC(=CC(=C1)Cl)C2=CC(=CC=C2)Cl,C12H8Cl2,222.000310,Oily liquids or solids that are colorless to light yellow. ,29 oC,,,"0.000355 mg/mL at 25 oC [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
402,T3D0401,2009-03-06 18:58:42 UTC,2009-08-11 15:55:25 UTC,"3,4-Dichlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 3,4-dichloro- (9CI)3, 4-Dichlorobiphenyl3,4-Dichloro-1,1'-biphenyl3,4-Dichlorobiphenyl3,4-dichloro-1,1'-biphenyl (ACD/Name 4.0)Biphenyl, 3,4-dichloro-Biphenyl, 3,4-dichloro- (8CI)PCB No 12Polychlorobiphenyl","3,4-Dichlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)

",,2974-92-7,18102,,"","","",CPD-946,,,"3,4-Dichlorobiphenyl",,,,,InChI=1/C12H8Cl2/c13-11-7-6-10(8-12(11)14)9-4-2-1-3-5-9/h1-8H,"1,2-dichloro-4-phenylbenzene",http://www.biospider.ca/saved_files/mol/,C1=CC=C(C=C1)C2=CC(=C(C=C2)Cl)Cl,C1=CC=C(C=C1)C2=CC(=C(C=C2)Cl)Cl,C12H8Cl2,222.000310,Oily liquids or solids that are colorless to light yellow. ,"",,,"9.09e-05 mg/mL at 25 oC [PATIL,GS (1991)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
403,T3D0402,2009-03-06 18:58:42 UTC,2009-08-11 15:55:25 UTC,"3,4'-Dichlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 3,4'-dichloro-3,4'-DICHLOROBIPHENYLDichlorobiphenyl","3,4'-Dichlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)

",,2974-90-5,18101,,"","","",CPD-946,,,"3,4'-Dichlorobiphenyl",,,,,InChI=1/C12H8Cl2/c13-11-6-4-9(5-7-11)10-2-1-3-12(14)8-10/h1-8H,1-chloro-4-(3-chlorophenyl)benzene,http://www.biospider.ca/saved_files/mol/,C1=CC(=CC(=C1)Cl)C2=CC=C(C=C2)Cl,C1=CC(=CC(=C1)Cl)C2=CC=C(C=C2)Cl,C12H8Cl2,222.000310,Oily liquids or solids that are colorless to light yellow. ,"",,,"8.88e-05 mg/mL at 25 oC [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
404,T3D0403,2009-03-06 18:58:43 UTC,2009-08-11 15:55:25 UTC,"3,5-Dichlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"3,5-Dichloro-1,1'-biphenyl3,5-DichlorobiphenylPCB No 14","3,5-Dichlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)

",,34883-41-5,36981,,C14356,"",34326,CPD-946,,C029904,"3,5-Dichlorobiphenyl",,,,,InChI=1/C12H8Cl2/c13-11-6-10(7-12(14)8-11)9-4-2-1-3-5-9/h1-8H,"1,3-dichloro-5-phenylbenzene",http://www.biospider.ca/saved_files/mol/e0183af75947635b28dda8e023591928_1237977948.mol,C1=CC=C(C=C1)C2=CC(=CC(=C2)Cl)Cl,C1=CC=C(C=C1)C2=CC(=CC(=C2)Cl)Cl,C12H8Cl2,222.000310,Oily liquids or solids that are colorless to light yellow. ,"",,,"",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
405,T3D0404,2009-03-06 18:58:43 UTC,2009-08-11 15:55:26 UTC,"4,4'-Dichlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"4, 4'-Dichloro-1,1'-biphenyl4,4'-Dichloro-1,1'-biphenyl4,4'-Dichlorobiphenyl4,4'-Dichlorobiphenyl-UL-14C4,4'-dichloro-1,1'-biphenyl (ACD/Name 4.0)4-DCB cpdBiphenyl, 4,4'-dichloro-Biphenyl, 4,4'-dichloro- (8CI)D9658_SIGMAP,p'-dichlorobiphenylP,p-DCBPPCB No 15Polychlorobiphenyl","4,4'-Dichlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)

",,2050-68-2,16308,,C14248,"",34364,CPD-946,,C029861,"4,4'-Dichlorobiphenyl",,,,,InChI=1/C12H8Cl2/c13-11-5-1-9(2-6-11)10-3-7-12(14)8-4-10/h1-8H,1-chloro-4-(4-chlorophenyl)benzene,http://www.biospider.ca/saved_files/mol/3c9da042f093c4786c7fbdcc426b379e_1237978045.mol,C1=CC(=CC=C1C2=CC=C(C=C2)Cl)Cl,C1=CC(=CC=C1C2=CC=C(C=C2)Cl)Cl,C12H8Cl2,222.000310,Oily liquids or solids that are colorless to light yellow. ,149.3 oC,,,"6.2e-05 mg/mL at 20 oC [CHIOU,CT et al. (1977)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
406,T3D0405,2009-03-06 18:58:43 UTC,2009-08-11 15:55:26 UTC,"2,2',3-Trichlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 2,2',3-trichloro-1,1'-Biphenyl, 2,3,2'-trichloro2,2',3-Trichlorobiphenyl","2,2',3-Trichlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)

",,38444-78-9,38032,,"","","",CPD-946,,,"2,2',3-Trichlorobiphenyl",,,,,InChI=1/C12H7Cl3/c13-10-6-2-1-4-8(10)9-5-3-7-11(14)12(9)15/h1-7H,"1,2-dichloro-3-(2-chlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC=C(C(=C1)C2=C(C(=CC=C2)Cl)Cl)Cl,C1=CC=C(C(=C1)C2=C(C(=CC=C2)Cl)Cl)Cl,C12H7Cl3,255.961330,Oily liquids or solids that are colorless to light yellow. ,"",,,"0.000293 mg/mL at 20 oC [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were uaed as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
407,T3D0406,2009-03-06 18:58:43 UTC,2009-08-11 15:55:26 UTC,"2,2',4-Trichlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 2,2',4-trichloro1,1'-Biphenyl, 2,2',4-trichloro-2,2',4-TrichlorobiphenylPCB No 17","2,2',4-Trichlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,37680-66-3,37804,,"","","",CPD-946,,,"2,2',4-Trichlorobiphenyl",,,,,InChI=1/C12H7Cl3/c13-8-5-6-10(12(15)7-8)9-3-1-2-4-11(9)14/h1-7H,"2,4-dichloro-1-(2-chlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC=C(C(=C1)C2=C(C=C(C=C2)Cl)Cl)Cl,C1=CC=C(C(=C1)C2=C(C=C(C=C2)Cl)Cl)Cl,C12H7Cl3,255.961330,Oily liquids or solids that are colorless to light yellow. ,"",,,"8.33e-05 mg/mL at 25 oC [PATIL,GS (1991)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
408,T3D0407,2009-03-06 18:58:43 UTC,2009-08-11 15:55:27 UTC,"2,2',5-Trichlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"2,2',5'-Trichlorobiphenyl2,2',5-Trichloro-1,1'-biphenyl2,2',5-Trichlorobiphenyl2,5,2'-TrichlorobiphenylPCB No 18","2,2',5-Trichlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,37680-65-2,37803,,"","","",CPD-946,,C078449,"2,2',5-Trichlorobiphenyl",,,,,InChI=1/C12H7Cl3/c13-8-5-6-12(15)10(7-8)9-3-1-2-4-11(9)14/h1-7H,"1,4-dichloro-2-(2-chlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC=C(C(=C1)C2=C(C=CC(=C2)Cl)Cl)Cl,C1=CC=C(C(=C1)C2=C(C=CC(=C2)Cl)Cl)Cl,C12H7Cl3,255.961330,Oily liquids or solids that are colorless to light yellow. ,"",,,"0.0004 mg/mL at 25 oC [SHIU,WY & MACKAY,D (1986)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
409,T3D0408,2009-03-06 18:58:43 UTC,2009-08-11 15:55:27 UTC,"2,2',6-Trichlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"2,2',6-Trichloro-1,1'-biphenyl2,2',6-Trichlorobiphenyl","2,2',6-Trichlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,38444-73-4,38029,,"","","",CPD-946,,,"2,2',6-Trichlorobiphenyl",,,,,InChI=1/C12H7Cl3/c13-9-5-2-1-4-8(9)12-10(14)6-3-7-11(12)15/h1-7H,"1,3-dichloro-2-(2-chlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC=C(C(=C1)C2=C(C=CC=C2Cl)Cl)Cl,C1=CC=C(C(=C1)C2=C(C=CC=C2Cl)Cl)Cl,C12H7Cl3,255.961330,Oily liquids or solids that are colorless to light yellow. ,"",,,0.000324 mg/mL at 25 oC [EPA],,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
410,T3D0409,2009-03-06 18:58:43 UTC,2009-08-11 15:55:27 UTC,"2,3,3'-Trichlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"2,3,3'-Trichloro-1,1'-biphenyl2,3,3'-Trichlorobiphenyl5,5',6-TrichlorobiphenylBCR290_FLUKA","2,3,3'-Trichlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,38444-84-7,38034,,"","","",CPD-946,,C064369,"2,3,3'-Trichlorobiphenyl",,,,,InChI=1/C12H7Cl3/c13-9-4-1-3-8(7-9)10-5-2-6-11(14)12(10)15/h1-7H,"1,2-dichloro-3-(3-chlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=CC(=C1)Cl)C2=C(C(=CC=C2)Cl)Cl,C1=CC(=CC(=C1)Cl)C2=C(C(=CC=C2)Cl)Cl,C12H7Cl3,255.961330,Oily liquids or solids that are colorless to light yellow. ,"",,,"",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
411,T3D0410,2009-03-06 18:58:44 UTC,2009-08-11 15:55:28 UTC,"2,3,4-Trichlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, trichloro-1,1'-Biphenyl, trichloro- (9CI)2,3,4-Trichloro-1,1'-biphenyl2,3,4-TrichlorobiphenylApirolio 1431 CBiphenyl, trichloro-Pyranol 1499Trichloro-1,1'-biphenylTrichlorobiphenylTrichlorodiphenyl","2,3,4-Trichlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,55702-46-0,41541,,C14357,"",34222,CPD-946,,,"2,3,4-Trichlorobiphenyl",,,,,InChI=1/C12H7Cl3/c13-10-7-6-9(11(14)12(10)15)8-4-2-1-3-5-8/h1-7H,"1,2,3-trichloro-4-phenylbenzene",http://www.biospider.ca/saved_files/mol/eeb6ef26ff239aa0f6eac080a381d6d5_1237978611.mol,C1=CC=C(C=C1)C2=C(C(=C(C=C2)Cl)Cl)Cl,C1=CC=C(C=C1)C2=C(C(=C(C=C2)Cl)Cl)Cl,C12H7Cl3,255.961330,Oily liquids or solids that are colorless to light yellow. ,"",,,"0.00017 mg/mL at 25 oC [PATIL,GS (1991)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
412,T3D0411,2009-03-06 18:58:44 UTC,2009-08-11 15:55:28 UTC,"2,3,4'-Trichlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"2,3,4'-Trichloro-1,1'-biphenyl2,3,4'-Trichlorobiphenyl","2,3,4'-Trichlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,38444-85-8,38035,,"","","",CPD-946,,,"2,3,4'-Trichlorobiphenyl",,,,,InChI=1/C12H7Cl3/c13-9-6-4-8(5-7-9)10-2-1-3-11(14)12(10)15/h1-7H,"1,2-dichloro-3-(4-chlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C(=C1)Cl)Cl)C2=CC=C(C=C2)Cl,C1=CC(=C(C(=C1)Cl)Cl)C2=CC=C(C=C2)Cl,C12H7Cl3,255.961330,Oily liquids or solids that are colorless to light yellow. ,"",,,"0.000142 mg/mL at 20 oC [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
413,T3D0412,2009-03-06 18:58:44 UTC,2009-08-11 15:55:28 UTC,"2,3,5-Trichlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 2,3,5-trichloro-2,3,5-TRICHLOROBIPHENYL","2,3,5-Trichlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,55720-44-0,41555,,"","","",DIHYDRO-DIOH-BENZOATE,,,"2,3,5-Trichlorobiphenyl",,,,,InChI=1/C12H7Cl3/c13-9-6-10(12(15)11(14)7-9)8-4-2-1-3-5-8/h1-7H,"1,2,5-trichloro-3-phenylbenzene",http://www.biospider.ca/saved_files/mol/,C1=CC=C(C=C1)C2=CC(=CC(=C2Cl)Cl)Cl,C1=CC=C(C=C1)C2=CC(=CC(=C2Cl)Cl)Cl,C12H7Cl3,255.961330,Oily liquids or solids that are colorless to light yellow. ,"",,,"",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
414,T3D0413,2009-03-06 18:58:44 UTC,2009-08-11 15:55:29 UTC,"2,3,6-Trichlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"2,3,6-Trichloro-1,1'-biphenyl2,3,6-Trichlorobiphenyl","2,3,6-Trichlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,55702-45-9,41540,,C14359,"",34225,CPD-946,,,"2,3,6-Trichlorobiphenyl",,,,,InChI=1/C12H7Cl3/c13-9-6-7-10(14)12(15)11(9)8-4-2-1-3-5-8/h1-7H,"1,2,4-trichloro-3-phenylbenzene",http://www.biospider.ca/saved_files/mol/9559bb1b96350281dc4cd2d25a889777_1237978859.mol,C1=CC=C(C=C1)C2=C(C=CC(=C2Cl)Cl)Cl,C1=CC=C(C=C1)C2=C(C=CC(=C2Cl)Cl)Cl,C12H7Cl3,255.961330,Oily liquids or solids that are colorless to light yellow. ,"",,,8.33e-05 mg/mL at 25 oC [EPA],,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
415,T3D0414,2009-03-06 18:58:44 UTC,2009-08-11 15:55:29 UTC,"2,3',4-Trichlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"2,3',4-Trichloro-1,1'-biphenyl2,3',4-Trichlorobiphenyl","2,3',4-Trichlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,55712-37-3,41551,,"","","",CPD-946,,,"2,3',4-Trichlorobiphenyl",,,,,InChI=1/C12H7Cl3/c13-9-3-1-2-8(6-9)11-5-4-10(14)7-12(11)15/h1-7H,"2,4-dichloro-1-(3-chlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=CC(=C1)Cl)C2=C(C=C(C=C2)Cl)Cl,C1=CC(=CC(=C1)Cl)C2=C(C=C(C=C2)Cl)Cl,C12H7Cl3,255.961330,Oily liquids or solids that are colorless to light yellow. ,"",,,"",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
416,T3D0415,2009-03-06 18:58:44 UTC,2009-08-11 15:55:29 UTC,"2,3',5-Trichlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"2,3',5-Trichloro-1,1'-biphenyl2,3',5-Trichlorobiphenyl2,3,5-Trichlorobiphenyl2,5,3'-Trichlorobiphenyl3,2',5'-Trichlorobiphenyl","2,3',5-Trichlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,38444-81-4,38033,,C14358,"",34215,CPD-946,,C091160,"2,3',5-Trichlorobiphenyl",,,,,InChI=1/C12H7Cl3/c13-9-3-1-2-8(6-9)11-7-10(14)4-5-12(11)15/h1-7H,"1,4-dichloro-2-(3-chlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/49e592e8b54ee4a35f3794aaa4e5ddd6_1237979054.mol,C1=CC(=CC(=C1)Cl)C2=C(C=CC(=C2)Cl)Cl,C1=CC(=CC(=C1)Cl)C2=C(C=CC(=C2)Cl)Cl,C12H7Cl3,255.961330,Oily liquids or solids that are colorless to light yellow. ,"",,,"0.000253 mg/mL at 25 oC [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
417,T3D0416,2009-03-06 18:58:44 UTC,2009-08-11 15:55:30 UTC,"2,3',6-Trichlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 2,3',6-trichloro2,3',6-TRICHLOROBIPHENYL","2,3',6-Trichlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,38444-76-7,38030,,"","","",CPD-946,,,"2,3',6-Trichlorobiphenyl",,,,,InChI=1/C12H7Cl3/c13-9-4-1-3-8(7-9)12-10(14)5-2-6-11(12)15/h1-7H,"1,3-dichloro-2-(3-chlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=CC(=C1)Cl)C2=C(C=CC=C2Cl)Cl,C1=CC(=CC(=C1)Cl)C2=C(C=CC=C2Cl)Cl,C12H7Cl3,255.961330,Oily liquids or solids that are colorless to light yellow. ,"",,,"3.86e-05 mg/mL at 20 oC [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
418,T3D0417,2009-03-06 18:58:45 UTC,2009-08-11 15:55:30 UTC,"2,4,4'-Trichlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"2,4,4'-Trichloro-1,1'-biphenyl2,4,4'-Trichlorobiphenyl2,4,4'-Trichlorobiphenyl solution4,2',4'-TrichlorobiphenylBCR291_FLUKABiphenyl, 2,4,4'-trichloro-PCB No 28PCB No 28 solution","2,4,4'-Trichlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,7012-37-5,23448,,"","","",CPD-946,,C081766,"2,4,4'-Trichlorobiphenyl",,,,,InChI=1/C12H7Cl3/c13-9-3-1-8(2-4-9)11-6-5-10(14)7-12(11)15/h1-7H,"2,4-dichloro-1-(4-chlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=CC=C1C2=C(C=C(C=C2)Cl)Cl)Cl,C1=CC(=CC=C1C2=C(C=C(C=C2)Cl)Cl)Cl,C12H7Cl3,255.961330,Oily liquids or solids that are colorless to light yellow. ,"",,,"0.00027 mg/mL at 25 oC [CHIOU,CT et al. (1983)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
419,T3D0418,2009-03-06 18:58:45 UTC,2009-08-11 15:55:30 UTC,"2,4,5-Trichlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"2,4,5-Trichloro-1,1'-biphenyl2,4,5-Trichloro-1,1-biphenyl2,4,5-TrichlorobiphenylBiphenyl, 2,4,5-trichloro-PCB No 29","2,4,5-Trichlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,15862-07-4,27514,,"","","",CPD-946,,,"2,4,5-Trichlorobiphenyl",,,,,InChI=1/C12H7Cl3/c13-10-7-12(15)11(14)6-9(10)8-4-2-1-3-5-8/h1-7H,"1,2,4-trichloro-5-phenylbenzene",http://www.biospider.ca/saved_files/mol/,C1=CC=C(C=C1)C2=CC(=C(C=C2Cl)Cl)Cl,C1=CC=C(C=C1)C2=CC(=C(C=C2Cl)Cl)Cl,C12H7Cl3,255.961330,Oily liquids or solids that are colorless to light yellow. ,76.3 oC,,,"0.000163 mg/mL at 25 oC [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
420,T3D0419,2009-03-06 18:58:45 UTC,2009-08-11 15:55:31 UTC,"2,4,6-Trichlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"2,4,6-Trichloro-1,1'-biphenyl2,4,6-Trichlorobiphenyl2,4,6-Trichlorobiphenyl solutionPCB No 30 solution","2,4,6-Trichlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,35693-92-6,37247,,"","","",CPD-946,,C102834,"2,4,6-Trichlorobiphenyl",,,,,InChI=1/C12H7Cl3/c13-9-6-10(14)12(11(15)7-9)8-4-2-1-3-5-8/h1-7H,"1,3,5-trichloro-2-phenylbenzene",http://www.biospider.ca/saved_files/mol/,C1=CC=C(C=C1)C2=C(C=C(C=C2Cl)Cl)Cl,C1=CC=C(C=C1)C2=C(C=C(C=C2Cl)Cl)Cl,C12H7Cl3,255.961330,Oily liquids or solids that are colorless to light yellow. ,"",,,"0.000252 mg/mL at 25 oC [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
421,T3D0420,2009-03-06 18:58:45 UTC,2009-08-11 15:55:31 UTC,"2,4',5-Trichlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 2,4',5-trichloro- (9CI)2,4',5-Trichloro-1,1'-biphenyl2,4',5-Trichlorobiphenyl2,5,4'-Trichlorobiphenyl4,2',5'-TrichlorobiphenylBiphenyl, 2,4',5-trichloro-Delor 103PCB No 31","2,4',5-Trichlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,16606-02-3,27960,,"","","",CPD-946,,C015550,"2,4',5-Trichlorobiphenyl",,,,,InChI=1/C12H7Cl3/c13-9-3-1-8(2-4-9)11-7-10(14)5-6-12(11)15/h1-7H,"1,4-dichloro-2-(4-chlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=CC=C1C2=C(C=CC(=C2)Cl)Cl)Cl,C1=CC(=CC=C1C2=C(C=CC(=C2)Cl)Cl)Cl,C12H7Cl3,255.961330,Oily liquids or solids that are colorless to light yellow. ,"",,,"0.000143 mg/mL at 25 oC [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
422,T3D0421,2009-03-06 18:58:45 UTC,2009-08-11 15:55:31 UTC,"2,4',6-Trichlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 2,4',6-trichloro1,1'-Biphenyl, 2,4',6-trichloro-2,4',6-TRICHLOROBIPHENYL","2,4',6-Trichlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,38444-77-8,38031,,"","","",CPD-946,,,"2,4',6-Trichlorobiphenyl",,,,,InChI=1/C12H7Cl3/c13-9-6-4-8(5-7-9)12-10(14)2-1-3-11(12)15/h1-7H,"1,3-dichloro-2-(4-chlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C(=C1)Cl)C2=CC=C(C=C2)Cl)Cl,C1=CC(=C(C(=C1)Cl)C2=CC=C(C=C2)Cl)Cl,C12H7Cl3,255.961330,Oily liquids or solids that are colorless to light yellow. ,"",,,0.000159 mg/mL at 25 oC [EPA],,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
423,T3D0422,2009-03-06 18:58:45 UTC,2009-08-11 15:55:31 UTC,"2,3',4'-Trichlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 2',3,4-trichloro-1,1'-Biphenyl, 2,3',4'-trichloro-2,3',4'-Trichloro-1,1'-biphenyl2,3',4'-Trichlorobiphenyl3,4,2'-TrichlorobiphenylBiphenyl, 2',3,4-trichloro-PCB No 33","2,3',4-Trichlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,38444-86-9,38036,,"","","",DIHYDRO-DIOH-BENZOATE,,,"2,3',4'-Trichlorobiphenyl",,,,,InChI=1/C12H7Cl3/c13-10-4-2-1-3-9(10)8-5-6-11(14)12(15)7-8/h1-7H,"1,2-dichloro-4-(2-chlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC=C(C(=C1)C2=CC(=C(C=C2)Cl)Cl)Cl,C1=CC=C(C(=C1)C2=CC(=C(C=C2)Cl)Cl)Cl,C12H7Cl3,255.961330,Oily liquids or solids that are colorless to light yellow. ,"",,,"0.000133 mg/mL at 20 oC [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
424,T3D0423,2009-03-06 18:58:45 UTC,2009-08-11 15:55:31 UTC,"2,3',5'-Trichlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 2',3,5-trichloro-2',3,5-Trichloro-1,1'-biphenyl2,3',5-TRICHLOROBIPHENYL","2,3',5'-Trichlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,37680-68-5,37805,,"","","",CPD-946,,,"2,3',5'-Trichlorobiphenyl",,,,,InChI=1/C12H7Cl3/c13-9-5-8(6-10(14)7-9)11-3-1-2-4-12(11)15/h1-7H,"1,3-dichloro-5-(2-chlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC=C(C(=C1)C2=CC(=CC(=C2)Cl)Cl)Cl,C1=CC=C(C(=C1)C2=CC(=CC(=C2)Cl)Cl)Cl,C12H7Cl3,255.961330,Oily liquids or solids that are colorless to light yellow. ,"",,,"0.000129 mg/mL at 25 oC [PATIL,GS (1991)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
425,T3D0424,2009-03-06 18:58:45 UTC,2009-08-11 15:55:31 UTC,"3,3',4-Trichlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 3,3',4-trichloro1,1'-Biphenyl, 3,3',4-trichloro-3,3',4-Trichlorobiphenyl3,4,3'-Trichlorobiphenyl","3,3',4-Trichlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,37680-69-6,37806,,"","","",DIHYDRO-DIOH-BENZOATE,,,"3,3',4-Trichlorobiphenyl",,,,,InChI=1/C12H7Cl3/c13-10-3-1-2-8(6-10)9-4-5-11(14)12(15)7-9/h1-7H,"1,2-dichloro-4-(3-chlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=CC(=C1)Cl)C2=CC(=C(C=C2)Cl)Cl,C1=CC(=CC(=C1)Cl)C2=CC(=C(C=C2)Cl)Cl,C12H7Cl3,255.961330,Oily liquids or solids that are colorless to light yellow. ,"",,,"",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
426,T3D0425,2009-03-06 18:58:46 UTC,2009-08-11 15:55:32 UTC,"3,3',5-Trichlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 3,3',5-trichloro-3,3',5-trichlorobiphenylAROCLOR 1016Arochlor 1016Chlorodiphenyl (41% Cl)Polychlorinated biphenyl (aroclor 1016)","3,3',5-Trichlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,38444-87-0,38037,,"","","",DIHYDRO-DIOH-BENZOATE,,,"3,3',5-Trichlorobiphenyl",,,,,InChI=1/C12H7Cl3/c13-10-3-1-2-8(4-10)9-5-11(14)7-12(15)6-9/h1-7H,"1,3-dichloro-5-(3-chlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=CC(=C1)Cl)C2=CC(=CC(=C2)Cl)Cl,C1=CC(=CC(=C1)Cl)C2=CC(=CC(=C2)Cl)Cl,C12H7Cl3,255.961330,Oily liquids or solids that are colorless to light yellow. ,"",,,"",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
427,T3D0426,2009-03-06 18:58:46 UTC,2009-08-11 15:55:32 UTC,"3,4,4'-Trichlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"3,4,4'-Trichloro-1,1'-biphenyl3,4,4'-Trichlorobiphenyl","3,4,4'-Trichlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,38444-90-5,38039,,"","","",CPD-946,,,"3,4,4'-Trichlorobiphenyl",,,,,InChI=1/C12H7Cl3/c13-10-4-1-8(2-5-10)9-3-6-11(14)12(15)7-9/h1-7H,"1,2-dichloro-4-(4-chlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=CC=C1C2=CC(=C(C=C2)Cl)Cl)Cl,C1=CC(=CC=C1C2=CC(=C(C=C2)Cl)Cl)Cl,C12H7Cl3,255.961330,Oily liquids or solids that are colorless to light yellow. ,"",,,"7.19e-05 mg/mL at 20 oC [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
428,T3D0427,2009-03-06 18:58:46 UTC,2009-08-11 15:55:32 UTC,"3,4,5-Tricholobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 3,4,5-trichloro1,1'-Biphenyl, 3,4,5-trichloro-3,4,5-Trichlorobiphenyl","3,4,5-Trichlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,53555-66-1,63099,,"","","",DIHYDRO-DIOH-BENZOATE,,,"3,4,5-Tricholobiphenyl",,,,,InChI=1/C12H7Cl3/c13-10-6-9(7-11(14)12(10)15)8-4-2-1-3-5-8/h1-7H,"1,2,3-trichloro-5-phenylbenzene",http://www.biospider.ca/saved_files/mol/,C1=CC=C(C=C1)C2=CC(=C(C(=C2)Cl)Cl)Cl,C1=CC=C(C=C1)C2=CC(=C(C(=C2)Cl)Cl)Cl,C12H7Cl3,255.961330,Oily liquids or solids that are colorless to light yellow. ,"",,,"",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
429,T3D0428,2009-03-06 18:58:46 UTC,2009-08-11 15:55:32 UTC,"3,4',5-Trichlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 3,4',5-trichloro-3,4',5-TRICHLOROBIPHENYL","3,4',5-Trichlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,38444-88-1,38038,,"","","",DIHYDRO-DIOH-BENZOATE,,,"3,4',5-Trichlorobiphenyl",,,,,InChI=1/C12H7Cl3/c13-10-3-1-8(2-4-10)9-5-11(14)7-12(15)6-9/h1-7H,"1,3-dichloro-5-(4-chlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=CC=C1C2=CC(=CC(=C2)Cl)Cl)Cl,C1=CC(=CC=C1C2=CC(=CC(=C2)Cl)Cl)Cl,C12H7Cl3,255.961330,Oily liquids or solids that are colorless to light yellow. ,"",,,"",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
430,T3D0429,2009-03-06 18:58:46 UTC,2009-08-11 15:55:32 UTC,"2,2',3,3'-Tetrachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"2,2',3,3'-Tetrachloro-1,1'-biphenyl2,2',3,3'-Tetrachlorobiphenyl","2,2',3,3'-Tetrachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)

",,38444-93-8,38040,,"","","",CPD-946,,C068319,"2,2',3,3'-Tetrachlorobiphenyl",,,,,InChI=1/C12H6Cl4/c13-9-5-1-3-7(11(9)15)8-4-2-6-10(14)12(8)16/h1-6H,"1,2-dichloro-3-(2,3-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C(=C1)Cl)Cl)C2=C(C(=CC=C2)Cl)Cl,C1=CC(=C(C(=C1)Cl)Cl)C2=C(C(=CC=C2)Cl)Cl,C12H6Cl4,289.922360,Oily liquids or solids that are colorless to light yellow. ,"",,,"1.56e-05 mg/mL at 25 oC [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
431,T3D0430,2009-03-06 18:58:46 UTC,2009-08-11 15:55:32 UTC,"2,2',3,4-Tetrachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"2,2',3,4-TETRACHLOROBIPHENYL2,2',3,4-Tetrachloro-1,1'-biphenyl","2,2',3,4-Tetrachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,52663-59-9,40467,,"","","",CPD-946,,,"2,2',3,4-Tetrachlorobiphenyl",,,,,InChI=1/C12H6Cl4/c13-9-4-2-1-3-7(9)8-5-6-10(14)12(16)11(8)15/h1-6H,"1,2,3-trichloro-4-(2-chlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC=C(C(=C1)C2=C(C(=C(C=C2)Cl)Cl)Cl)Cl,C1=CC=C(C(=C1)C2=C(C(=C(C=C2)Cl)Cl)Cl)Cl,C12H6Cl4,289.922360,Oily liquids or solids that are colorless to light yellow. ,"",,,4.32e-05 mg/mL at 25 oC [EPA],,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
432,T3D0431,2009-03-06 18:58:46 UTC,2009-08-11 15:55:33 UTC,"2,2',3,4'-Tetrachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 2,2',3',4-tetrachloro2,2',3,4'-Tetrachloro-1,1'-biphenyl2,2',3,4'-TetrachlorobiphenylAroclor 1242","2,2',3,4'-Tetrachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,36559-22-5,63103,,"","","",CPD-946,,C065091,"2,2',3,4'-Tetrachlorobiphenyl",,,,,InChI=1/C12H6Cl4/c13-7-4-5-8(11(15)6-7)9-2-1-3-10(14)12(9)16/h1-6H,"2,4-dichloro-1-(2,3-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C(=C1)Cl)Cl)C2=C(C=C(C=C2)Cl)Cl,C1=CC(=C(C(=C1)Cl)Cl)C2=C(C=C(C=C2)Cl)Cl,C12H6Cl4,289.922360,Oily liquids or solids that are colorless to light yellow. ,"",,,"6.08e-05 mg/mL at 20 oC [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
433,T3D0432,2009-03-06 18:58:47 UTC,2009-08-11 15:55:33 UTC,"2,2',3,5-Tetrachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 2,2',3,5'-tetrachloro-2,2',3',5-TETRACHLOROBIPHENYL2,2',3,5'-TETRACHLOROBIPHENYL2,2',3,5'-Tetrachloro-1,1'-biphenyl2,2',3,5-Tetrachloro-1,1'-biphenyl2,2'3,5'-Tetrachlorobiphenyl","2,2',3,5-Tetrachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,70362-46-8,38875,,"","","",CPD-946,,,"2,2',3,5-Tetrachlorobiphenyl",,,,,InChI=1/C12H6Cl4/c13-7-4-5-10(14)9(6-7)8-2-1-3-11(15)12(8)16/h1-6H,"1,2-dichloro-3-(2,5-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C(=C1)Cl)Cl)C2=C(C=CC(=C2)Cl)Cl,C1=CC(=C(C(=C1)Cl)Cl)C2=C(C=CC(=C2)Cl)Cl,C12H6Cl4,289.922360,Oily liquids or solids that are colorless to light yellow. ,"",,,"0.000172 mg/mL at 25 oC [WAKITA,K et al. (1986)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
434,T3D0433,2009-03-06 18:58:47 UTC,2009-08-11 15:55:33 UTC,"2,2',3,5'-Tetrachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"2,2',3',5-TETRACHLOROBIPHENYL2,2',3,5'-Tetrachloro-1,1'-biphenyl2,2',3,5'-Tetrachlorobiphenyl2,2'3,5'-Tetrachlorobiphenyl2,3,2',5'-Tetrachlorobiphenyl","2,2',3,5'-Tetrachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,41464-39-5,38875,,"","","",CPD-946,,,"2,2',3,5'-Tetrachlorobiphenyl",,,,,InChI=1/C12H6Cl4/c13-7-4-5-10(14)9(6-7)8-2-1-3-11(15)12(8)16/h1-6H,"1,2-dichloro-3-(2,5-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C(=C1)Cl)Cl)C2=C(C=CC(=C2)Cl)Cl,C1=CC(=C(C(=C1)Cl)Cl)C2=C(C=CC(=C2)Cl)Cl,C12H6Cl4,289.922360,Oily liquids or solids that are colorless to light yellow. ,"",,,"0.0001 mg/mL at 20 oC [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
435,T3D0434,2009-03-06 18:58:47 UTC,2009-08-11 15:55:33 UTC,"2,2',3,6-Tetrachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 2,2',3,6-tetrachloro1,1'-Biphenyl, 2,2',3,6-tetrachloro-1,1'-Biphenyl, 2,2',3,6-tetrahloro-1-Methyl-1-(3,5-dimethylcyclohexyl)oxy-1-silacyclopentane1-[(3,5-Dimethylcyclohexyl)oxy]-1-methylsilolane2,2',3,6'-Tetrachlorobiphenyl2,2',3,6-tetrahloro-1,1'-biphenyl","2,2',3,6-Tetrachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,70362-45-7,63108,,"","","",DIHYDRO-DIOH-BENZOATE,,,"2,2',3,6-Tetrachlorobiphenyl",,,,,InChI=1/C12H6Cl4/c13-8-4-2-1-3-7(8)11-9(14)5-6-10(15)12(11)16/h1-6H,"1,2,4-trichloro-3-(2-chlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC=C(C(=C1)C2=C(C=CC(=C2Cl)Cl)Cl)Cl,C1=CC=C(C(=C1)C2=C(C=CC(=C2Cl)Cl)Cl)Cl,C12H6Cl4,289.922360,Oily liquids or solids that are colorless to light yellow. ,"",,,"0.000146 mg/mL at 25 oC [PATIL,GS (1991)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
436,T3D0435,2009-03-06 18:58:47 UTC,2009-08-11 15:55:34 UTC,"2,2',3,6'-Tetrachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 2,2',3,6-tetrachloro1,1'-Biphenyl, 2,2',3,6-tetrachloro-1,1'-Biphenyl, 2,2',3,6-tetrahloro-1-Methyl-1-(3,5-dimethylcyclohexyl)oxy-1-silacyclopentane1-[(3,5-Dimethylcyclohexyl)oxy]-1-methylsilolane2,2',3,6'-Tetrachloro-1,1'-biphenyl2,2',3,6'-Tetrachlorobiphenyl2,2',3,6-tetrahloro-1,1'-biphenyl","2,2',3,6'-Tetrachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,41464-47-5,63108,,"","","",CPD-946,,,"2,2',3,6'-Tetrachlorobiphenyl",,,,,InChI=1/C12H6Cl4/c13-8-4-2-1-3-7(8)11-9(14)5-6-10(15)12(11)16/h1-6H,"1,2,4-trichloro-3-(2-chlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC=C(C(=C1)C2=C(C=CC(=C2Cl)Cl)Cl)Cl,C1=CC=C(C(=C1)C2=C(C=CC(=C2Cl)Cl)Cl)Cl,C12H6Cl4,289.922360,Oily liquids or solids that are colorless to light yellow. ,"",,,"0.000146 mg/mL at 25 oC [PATIL,GS (1991)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
437,T3D0436,2009-03-06 18:58:47 UTC,2009-08-11 15:55:34 UTC,"2,2',4,4'-Tetrachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"2,2',4,4'-Tetrachloro-1,1'-biphenyl2,2',4,4'-Tetrachlorobiphenyl2,2',4,4'-Tetrachlorodiphenyl2,4,2',4'-TetrachlorobiphenylAroclor 1242Biphenyl, 2,2',4,4'-tetrachloro-Chlorierte biphenyle, chlorgehalt 42% [German]Chlorodiphenyl (42% Cl)Chlorodiphenyl (42% chlorine)Chlorodiphenyl, 42% chlorineClorodifenili, cloro 42% [Italian]Diphenyle chlore, 42% de chlore [French]Gechloreerdedifenyl [dutch]Polychlorinated biphenyl (aroclor 1242)Polychlorobiphenyls (42% chlorine)aroclor-1242","2,2',4,4'-Tetrachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,2437-79-8,17097,,C14247,"",34204,CPD-946,,C035976,"2,2',4,4'-Tetrachlorobiphenyl",,,,,InChI=1/C12H6Cl4/c13-7-1-3-9(11(15)5-7)10-4-2-8(14)6-12(10)16/h1-6H,"2,4-dichloro-1-(2,4-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/f4eaed7317c2fa4f1e7a2dbfbf6b6291_1237980868.mol,C1=CC(=C(C=C1Cl)Cl)C2=C(C=C(C=C2)Cl)Cl,C1=CC(=C(C=C1Cl)Cl)C2=C(C=C(C=C2)Cl)Cl,C12H6Cl4,289.922360,Oily liquids or solids that are colorless to light yellow. ,"",,,"5.41e-05 mg/mL at 22 oC [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
438,T3D0437,2009-03-06 18:58:47 UTC,2009-08-11 15:55:34 UTC,"2,2',4,5-Tetrachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 2,2',4,5-tetrachloro2,2',4,5-Tetrachlorobiphenyl2,2'4,5-TETRACHLOROBIPHENYL","2,2',4,5-Tetrachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,70362-47-9,51041,,C14360,"",34205,"",,,"2,2',4,5-Tetrachlorobiphenyl",,,,,InChI=1/C12H6Cl4/c13-9-4-2-1-3-7(9)8-5-11(15)12(16)6-10(8)14/h1-6H,"1,2,4-trichloro-5-(2-chlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/5984e0158edbee8e2f659c5c68e2d483_1237980977.mol,C1=CC=C(C(=C1)C2=CC(=C(C=C2Cl)Cl)Cl)Cl,C1=CC=C(C(=C1)C2=CC(=C(C=C2Cl)Cl)Cl)Cl,C12H6Cl4,289.922360,Oily liquids or solids that are colorless to light yellow. ,"",,,"1.64e-05 mg/mL at 25 oC [SHIU,WY & MACKAY,D (1986)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
439,T3D0438,2009-03-06 18:58:47 UTC,2009-08-11 15:55:35 UTC,"2,2',4,5'-Tetrachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 2,2',4',5-tetrachloro2,2',4,5'-Tetrachloro-1,1'-biphenyl2,2',4,5'-Tetrachlorobiphenyl2,2',4,5-Tetrachlorobiphenyl2,2',4,5-tetrachloro-1,1'-biphenyl2,2',4,5-tetrachlorodiphenyl2,4,2',5'-Tetrachlorobiphenyl","2,2',4,5'-Tetrachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,41464-40-8,38876,,"","","",CPD-946,,C042128,"2,2',4,5'-Tetrachlorobiphenyl",,,,,InChI=1/C12H6Cl4/c13-7-2-4-11(15)10(5-7)9-3-1-8(14)6-12(9)16/h1-6H,"2,4-dichloro-1-(2,5-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C=C1Cl)Cl)C2=C(C=CC(=C2)Cl)Cl,C1=CC(=C(C=C1Cl)Cl)C2=C(C=CC(=C2)Cl)Cl,C12H6Cl4,289.922360,Oily liquids or solids that are colorless to light yellow. ,"",,,"7.81e-05 mg/mL at 20 oC [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
440,T3D0439,2009-03-06 18:58:48 UTC,2009-08-11 15:55:35 UTC,"2,2',4,6-Tetrachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"2,2',4,6-Tetrachloro-1,1'-biphenyl2,2',4,6-Tetrachlorobiphenyl","2,2',4,6-Tetrachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,62796-65-0,44163,,"","","",CPD-946,,,"2,2',4,6-Tetrachlorobiphenyl",,,,,InChI=1/C12H6Cl4/c13-7-5-10(15)12(11(16)6-7)8-3-1-2-4-9(8)14/h1-6H,"1,3,5-trichloro-2-(2-chlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC=C(C(=C1)C2=C(C=C(C=C2Cl)Cl)Cl)Cl,C1=CC=C(C(=C1)C2=C(C=C(C=C2Cl)Cl)Cl)Cl,C12H6Cl4,289.922360,Oily liquids or solids that are colorless to light yellow. ,"",,,"6.54e-05 mg/mL at 25 oC [PATIL,GS (1991)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
441,T3D0440,2009-03-06 18:58:48 UTC,2009-08-11 15:55:35 UTC,"2,2',4,6'-Tetrachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 2,2',4,6'-tetrachloro1,1'-Biphenyl, 2,2',4,6'-tetrachloro-2,2',4,6'-Tetrachlorobiphenyl","2,2',4,6'-Tetrachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,68194-04-7,63106,,"","","",1-AMINO-PROPAN-2-OL,,,"2,2',4,6'-Tetrachlorobiphenyl",,,,,InChI=1/C12H6Cl4/c13-7-4-5-8(11(16)6-7)12-9(14)2-1-3-10(12)15/h1-6H,"2,4-dichloro-1-(2,6-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C(=C1)Cl)C2=C(C=C(C=C2)Cl)Cl)Cl,C1=CC(=C(C(=C1)Cl)C2=C(C=C(C=C2)Cl)Cl)Cl,C12H6Cl4,289.922360,Oily liquids or solids that are colorless to light yellow. ,"",,,"6.54e-05 mg/mL at 25 oC [PATIL,GS (1991)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
442,T3D0441,2009-03-06 18:58:48 UTC,2009-08-11 15:55:36 UTC,"2,2',5,5'-Tetrachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 2,2',5,5'-tetrachloro-2,2 ,5,5 -tetrachlorobiphenyl2,2',5,5'-Tetrachloro-1,1'-biphenyl2,2',5,5'-Tetrachlorobiphenyl (IUPAC No. 52)2,3',5,6'-tetrachlorobiphenyl2,5,2',5'-TetrachlorobiphenylBCR293_FLUKATCBP","2,2',5,5'-Tetrachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,35693-99-3,37248,,C14199,"",34206,1-AMINO-PROPAN-2-ONE-3-PHOSPHATE,,C009407,"2,2',5,5'-Tetrachlorobiphenyl",,,,,InChI=1/C12H6Cl4/c13-7-1-3-11(15)9(5-7)10-6-8(14)2-4-12(10)16/h1-6H,"1,4-dichloro-2-(2,5-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/89cc38b35c6504c781e6ae1773f854cc_1237981354.mol,C1=CC(=C(C=C1Cl)C2=C(C=CC(=C2)Cl)Cl)Cl,C1=CC(=C(C=C1Cl)C2=C(C=CC(=C2)Cl)Cl)Cl,C12H6Cl4,289.922360,Oily liquids or solids that are colorless to light yellow. ,"",,,"1.53e-05 mg/mL at 25 oC [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
443,T3D0442,2009-03-06 18:58:48 UTC,2009-08-11 15:55:36 UTC,"2,2',5,6'-Tetrachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 2,2',5,6-Tetrachloro-2,2',5,6'-Tetrachloro-1,1'-biphenyl2,2',5,6'-Tetrachlorobiphenyl","2,2',5,6'-Tetrachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,41464-41-9,38877,,"","","",CPD-946,,,"2,2',5,6'-Tetrachlorobiphenyl",,,,,InChI=1/C12H6Cl4/c13-7-4-5-9(14)8(6-7)12-10(15)2-1-3-11(12)16/h1-6H,"1,4-dichloro-2-(2,6-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C(=C1)Cl)C2=C(C=CC(=C2)Cl)Cl)Cl,C1=CC(=C(C(=C1)Cl)C2=C(C=CC(=C2)Cl)Cl)Cl,C12H6Cl4,289.922360,Oily liquids or solids that are colorless to light yellow. ,"",,,"4.76e-05 mg/mL at 25 oC [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
444,T3D0443,2009-03-06 18:58:48 UTC,2009-08-11 15:55:37 UTC,"2,2',6,6'-Tetrachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"2,2',6,6'-Tetrachloro-1,1'-biphenyl2,2',6,6'-Tetrachlorobiphenyl2,6,2',6'-TetrachlorobiphenylBiphenyl, 2,2',6,6'-tetrachloro-","2,2',6,6'-Tetrachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,15968-05-5,27588,,"","","",CPD-946,,,"2,2',6,6'-Tetrachlorobiphenyl",,,,,InChI=1/C12H6Cl4/c13-7-3-1-4-8(14)11(7)12-9(15)5-2-6-10(12)16/h1-6H,"1,3-dichloro-2-(2,6-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C(=C1)Cl)C2=C(C=CC=C2Cl)Cl)Cl,C1=CC(=C(C(=C1)Cl)C2=C(C=CC=C2Cl)Cl)Cl,C12H6Cl4,289.922360,Oily liquids or solids that are colorless to light yellow. ,"",,,"1.19e-05 mg/mL at 25 oC [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
445,T3D0444,2009-03-06 18:58:48 UTC,2009-08-11 15:55:37 UTC,"2,3,3',4-Tetrachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 2,3,3',4-tetrachloro1,1'-Biphenyl, 2,3,3',4-tetrachloro-2,3,3',4-Tetrachlorobiphenyl","2,3,3',4-Tetrachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,74338-24-2,63102,,"","","",DIHYDRO-DIOH-BENZOATE,,,"2,3,3',4-Tetrachlorobiphenyl",,,,,InChI=1/C12H6Cl4/c13-8-3-1-2-7(6-8)9-4-5-10(14)12(16)11(9)15/h1-6H,"1,2,3-trichloro-4-(3-chlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=CC(=C1)Cl)C2=C(C(=C(C=C2)Cl)Cl)Cl,C1=CC(=CC(=C1)Cl)C2=C(C(=C(C=C2)Cl)Cl)Cl,C12H6Cl4,289.922360,Oily liquids or solids that are colorless to light yellow. ,"",,,"4.96e-05 mg/mL at 25 oC [PATIL,GS (1991)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
446,T3D0445,2009-03-06 18:58:48 UTC,2009-08-11 15:55:37 UTC,"2,3,3',4'-Tetrachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"2,3,3',4'-TETRACHLOROBIPHENYL2,3,3',4'-Tetrachloro-1,1'-biphenyl","2,3,3',4-Tetrachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,41464-43-1,38879,,"","","",CPD-946,,,"2,3,3',4'-Tetrachlorobiphenyl",,,,,InChI=1/C12H6Cl4/c13-9-5-4-7(6-11(9)15)8-2-1-3-10(14)12(8)16/h1-6H,"1,2-dichloro-4-(2,3-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C(=C1)Cl)Cl)C2=CC(=C(C=C2)Cl)Cl,C1=CC(=C(C(=C1)Cl)Cl)C2=CC(=C(C=C2)Cl)Cl,C12H6Cl4,289.922360,Oily liquids or solids that are colorless to light yellow. ,"",,,"",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
447,T3D0446,2009-03-06 18:58:49 UTC,2009-08-11 15:55:37 UTC,"2,3,3',5-Tetrachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 2,3,3',5-tetrachloro-","2,3,3',5-Tetrachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,70424-67-8,91705,,"","","","",,,"2,3,3',5-Tetrachlorobiphenyl",,,,,InChI=1/C12H6Cl4/c13-8-3-1-2-7(4-8)10-5-9(14)6-11(15)12(10)16/h1-6H,"1,2,5-trichloro-3-(3-chlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=CC(=C1)Cl)C2=CC(=CC(=C2Cl)Cl)Cl,C1=CC(=CC(=C1)Cl)C2=CC(=CC(=C2Cl)Cl)Cl,C12H6Cl4,289.922360,Oily liquids or solids that are colorless to light yellow. ,"",,,"",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
448,T3D0447,2009-03-06 18:58:49 UTC,2009-08-11 15:55:37 UTC,"2,3,3',5'-Tetrachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"2,3,3',5'-Tetrachloro-1,1'-biphenyl2,3,3',5'-Tetrachlorobiphenyl","2,3,3',5'-Tetrachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,41464-49-7,63109,,"","","",CPD-946,,,"2,3,3',5'-Tetrachlorobiphenyl",,,,,InChI=1/C12H6Cl4/c13-8-4-7(5-9(14)6-8)10-2-1-3-11(15)12(10)16/h1-6H,"1,3-dichloro-5-(2,3-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C(=C1)Cl)Cl)C2=CC(=CC(=C2)Cl)Cl,C1=CC(=C(C(=C1)Cl)Cl)C2=CC(=CC(=C2)Cl)Cl,C12H6Cl4,289.922360,Oily liquids or solids that are colorless to light yellow. ,"",,,"",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
449,T3D0448,2009-03-06 18:58:49 UTC,2009-08-11 15:55:38 UTC,"2,3,3',6-Tetrachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 2,3,3',6-tetrachcloro1,1'-Biphenyl, 2,3,3',6-tetrachloro1,1'-Biphenyl, 2,3,3',6-tetrachloro-","2,2',3,3'-Tetrachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,74472-33-6,91718,,"","","","",,,"2,3,3',6-Tetrachlorobiphenyl",,,,,InChI=1/C12H6Cl4/c13-8-3-1-2-7(6-8)11-9(14)4-5-10(15)12(11)16/h1-6H,"1,2,4-trichloro-3-(3-chlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=CC(=C1)Cl)C2=C(C=CC(=C2Cl)Cl)Cl,C1=CC(=CC(=C1)Cl)C2=C(C=CC(=C2Cl)Cl)Cl,C12H6Cl4,289.922360,Oily liquids or solids that are colorless to light yellow. ,"",,,"",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
450,T3D0449,2009-03-06 18:58:49 UTC,2009-08-11 15:55:38 UTC,"2,3,4,4'-Tetrachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"2,3,4,4'-Tetrachloro-1,1'-biphenyl2,3,4,4'-Tetrachlorobiphenyl","2,3,4,4'-Tetrachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,33025-41-1,36304,,C14361,"",34218,CPD-946,,,"2,3,4,4'-Tetrachlorobiphenyl",,,,,InChI=1/C12H6Cl4/c13-8-3-1-7(2-4-8)9-5-6-10(14)12(16)11(9)15/h1-6H,"1,2,3-trichloro-4-(4-chlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/b9cc427ed4252cae5e1f27793e7ec7a7_1237982057.mol,C1=CC(=CC=C1C2=C(C(=C(C=C2)Cl)Cl)Cl)Cl,C1=CC(=CC=C1C2=C(C(=C(C=C2)Cl)Cl)Cl)Cl,C12H6Cl4,289.922360,Oily liquids or solids that are colorless to light yellow. ,"",,,"3.89e-05 mg/mL at 20 oC [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
451,T3D0450,2009-03-06 18:58:49 UTC,2009-08-11 15:55:38 UTC,"2,3,4,5-Tetrachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"2,3,4,5-Tetrachloro-1,1'-biphenyl2,3,4,5-TetrachlorobiphenylBiphenyl, 2,3,4,5-tetrachloro-","2,3,4,5-Tetrachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,33284-53-6,36401,,C14362,"",34221,CPD-946,,,"2,3,4,5-Tetrachlorobiphenyl",,,,,InChI=1/C12H6Cl4/c13-9-6-8(7-4-2-1-3-5-7)10(14)12(16)11(9)15/h1-6H,"1,2,3,4-tetrachloro-5-phenylbenzene",http://www.biospider.ca/saved_files/mol/d7305645fe00fb7b50692bd0b91d6532_1237982147.mol,C1=CC=C(C=C1)C2=CC(=C(C(=C2Cl)Cl)Cl)Cl,C1=CC=C(C=C1)C2=CC(=C(C(=C2Cl)Cl)Cl)Cl,C12H6Cl4,289.922360,Oily liquids or solids that are colorless to light yellow. ,"",,,"1.4e-05 mg/mL at 25 oC [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
452,T3D0451,2009-03-06 18:58:49 UTC,2009-08-11 15:55:38 UTC,"2,3,4,6-Tetrachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 2,3,4,6-tetrachloro-2,3,4,6-Tetrachloro-1,1'-biphenyl","2,3,4,6-Tetrachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,54230-22-7,63105,,"","","","",,,"2,3,4,6-Tetrachlorobiphenyl",,,,,InChI=1/C12H6Cl4/c13-8-6-9(14)11(15)12(16)10(8)7-4-2-1-3-5-7/h1-6H,"1,2,3,5-tetrachloro-4-phenylbenzene",http://www.biospider.ca/saved_files/mol/,C1=CC=C(C=C1)C2=C(C(=C(C=C2Cl)Cl)Cl)Cl,C1=CC=C(C=C1)C2=C(C(=C(C=C2Cl)Cl)Cl)Cl,C12H6Cl4,289.922360,Oily liquids or solids that are colorless to light yellow. ,"",,,"",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
453,T3D0452,2009-03-06 18:58:49 UTC,2009-08-11 15:55:38 UTC,"2,3,4',5-Tetrachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"2,3,4',5-tetrachlorobiphenylPCB No 63","2,3,4',5-Tetrachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,74472-34-7,53035,,"","","","",,,"2,3,4',5-Tetrachlorobiphenyl",,,,,InChI=1/C12H6Cl4/c13-8-3-1-7(2-4-8)10-5-9(14)6-11(15)12(10)16/h1-6H,"1,2,5-trichloro-3-(4-chlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=CC=C1C2=CC(=CC(=C2Cl)Cl)Cl)Cl,C1=CC(=CC=C1C2=CC(=CC(=C2Cl)Cl)Cl)Cl,C12H6Cl4,289.922360,Oily liquids or solids that are colorless to light yellow. ,"",,,"4.96e-05 mg/mL at 25 oC [PATIL,GS (1991)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
454,T3D0453,2009-03-06 18:58:50 UTC,2009-08-11 15:55:39 UTC,"2,3,4',6-Tetrachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"2,3,4',6-Tetrachloro-1,1'-biphenyl2,3,4',6-Tetrachlorobiphenyl","2,3,4',6-Tetrachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,52663-58-8,63110,,"","","",CPD-946,,C052915,"2,3,4',6-Tetrachlorobiphenyl",,,,,InChI=1/C12H6Cl4/c13-8-3-1-7(2-4-8)11-9(14)5-6-10(15)12(11)16/h1-6H,"1,2,4-trichloro-3-(4-chlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=CC=C1C2=C(C=CC(=C2Cl)Cl)Cl)Cl,C1=CC(=CC=C1C2=C(C=CC(=C2Cl)Cl)Cl)Cl,C12H6Cl4,289.922360,Oily liquids or solids that are colorless to light yellow. ,"",,,"",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",,"2A, probably carcinogenic to humans. (R264)","PCBs were as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
455,T3D0454,2009-03-06 18:58:50 UTC,2009-08-11 15:55:39 UTC,"2,3,5,6-Tetrachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"2,3,5,6-Tetrachloro-1,1'-biphenyl2,3,5,6-TetrachlorobiphenylBiphenyl, 2,3,5,6-tetrachloro-","2,3,5,6-Tetrachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,33284-54-7,36402,,C14363,"",34224,CPD-946,,C078132,"2,3,5,6-Tetrachlorobiphenyl",,,,,InChI=1/C12H6Cl4/c13-8-6-9(14)12(16)10(11(8)15)7-4-2-1-3-5-7/h1-6H,"1,2,4,5-tetrachloro-3-phenylbenzene",http://www.biospider.ca/saved_files/mol/3f29fba085b94f76b5e29924ec254659_1237982458.mol,C1=CC=C(C=C1)C2=C(C(=CC(=C2Cl)Cl)Cl)Cl,C1=CC=C(C=C1)C2=C(C(=CC(=C2Cl)Cl)Cl)Cl,C12H6Cl4,289.922360,Oily liquids or solids that are colorless to light yellow. ,"",,,"1.64e-05 mg/mL at 25 oC [PATIL,GS (1991)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
456,T3D0455,2009-03-06 18:58:50 UTC,2009-08-11 15:55:39 UTC,"2,3',4,4'-Tetrachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 2,3',4,4'-tetrachloro- (9CI)2,3',4,4'-Tetrachloro-1,1'-biphenyl2,3',4,4'-Tetrachlorobiphenyl2,4,3',4'-Tetrachlorobiphenyl3,4,2',4'-TetrachlorobiphenylBiphenyl, 2,3',4,4'-tetrachloro-","2,3',4,4'-Tetrachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,32598-10-0,36185,,"","","",CPD-946,,C054482,"2,3',4,4'-Tetrachlorobiphenyl",,,,,InChI=1/C12H6Cl4/c13-8-2-3-9(11(15)6-8)7-1-4-10(14)12(16)5-7/h1-6H,"1,2-dichloro-4-(2,4-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C=C1C2=C(C=C(C=C2)Cl)Cl)Cl)Cl,C1=CC(=C(C=C1C2=C(C=C(C=C2)Cl)Cl)Cl)Cl,C12H6Cl4,289.922360,Oily liquids or solids that are colorless to light yellow. ,"",,,"3.68e-05 mg/mL at 20 oC [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
457,T3D0456,2009-03-06 18:58:50 UTC,2009-08-11 15:55:40 UTC,"2,3',4,5-Tetrachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 2,3',4,5-tetrachloro-","2,3',4,5-Tetrachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,73575-53-8,91717,,"","","","",,,"2,3',4,5-Tetrachlorobiphenyl",,,,,InChI=1/C12H6Cl4/c13-8-3-1-2-7(4-8)9-5-11(15)12(16)6-10(9)14/h1-6H,"1,2,4-trichloro-5-(3-chlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=CC(=C1)Cl)C2=CC(=C(C=C2Cl)Cl)Cl,C1=CC(=CC(=C1)Cl)C2=CC(=C(C=C2Cl)Cl)Cl,C12H6Cl4,289.922360,Oily liquids or solids that are colorless to light yellow. ,"",,,"2.17e-05 mg/mL at 25 oC [PATIL,GS (1991)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
458,T3D0457,2009-03-06 18:58:50 UTC,2009-08-11 15:55:40 UTC,"2,3',4,5'-Tetrachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 2,3',4,5'-tetrachloro2,3',4,5'-TETRACHLOROBIPHENYL","2,3',4,5'-Tetrachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,73575-52-7,51821,,"","","","",,,"2,3',4,5'-Tetrachlorobiphenyl",,,,,InChI=1/C12H6Cl4/c13-8-1-2-11(12(16)6-8)7-3-9(14)5-10(15)4-7/h1-6H,"1,3-dichloro-5-(2,4-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C=C1Cl)Cl)C2=CC(=CC(=C2)Cl)Cl,C1=CC(=C(C=C1Cl)Cl)C2=CC(=CC(=C2)Cl)Cl,C12H6Cl4,289.922360,Oily liquids or solids that are colorless to light yellow. ,"",,,"",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
459,T3D0458,2009-03-06 18:58:50 UTC,2009-08-11 15:55:41 UTC,"2,3',4,6-Tetrachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"2,3',4,6-Tetrachloro-1,1'-biphenyl2,3',4,6-Tetrachlorobiphenyl","2,3',4,6-Tetrachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,60233-24-1,91674,,"","","",CPD-946,,,"2,3',4,6-Tetrachlorobiphenyl",,,,,InChI=1/C12H6Cl4/c13-8-3-1-2-7(4-8)12-10(15)5-9(14)6-11(12)16/h1-6H,"1,3,5-trichloro-2-(3-chlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=CC(=C1)Cl)C2=C(C=C(C=C2Cl)Cl)Cl,C1=CC(=CC(=C1)Cl)C2=C(C=C(C=C2Cl)Cl)Cl,C12H6Cl4,289.922360,Oily liquids or solids that are colorless to light yellow. ,"",,,"2.05e-05 mg/mL at 20 oC [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
460,T3D0459,2009-03-06 18:58:50 UTC,2009-08-11 15:55:41 UTC,"2,3',4',5-Tetrachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"2,3',4',5-Tetrachloro-1,1'-biphenyl2,3',4',5-Tetrachlorobiphenyl2,5,3',4'-TetrachlorobiphenylBiphenyl, 2,3',4',5-tetrachloro-PCB No 70","2,3',4',5-Tetrachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,32598-11-1,36186,,"","","",CPD-946,,,"2,3',4',5-Tetrachlorobiphenyl",,,,,InChI=1/C12H6Cl4/c13-8-2-4-10(14)9(6-8)7-1-3-11(15)12(16)5-7/h1-6H,"1,2-dichloro-4-(2,5-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C=C1C2=C(C=CC(=C2)Cl)Cl)Cl)Cl,C1=CC(=C(C=C1C2=C(C=CC(=C2)Cl)Cl)Cl)Cl,C12H6Cl4,289.922360,Oily liquids or solids that are colorless to light yellow. ,"",,,"4.1e-05 mg/mL at 25 oC [SHIU,WW & MACKAY,D (1986)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
461,T3D0460,2009-03-06 18:58:51 UTC,2009-08-11 15:55:41 UTC,"2,3',4',6-Tetrachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 2',3,4,6'-tetrachloro2,3',4',6-Tetrachloro-1,1'-biphenyl2,3',4',6-tetrachlorobiphenyl2,6,3',4'-Tetrachlorobiphenyl","2,3',4',6-Tetrachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,41464-46-4,38880,,"","","",CPD-946,,,"2,3',4',6-Tetrachlorobiphenyl",,,,,InChI=1/C12H6Cl4/c13-8-5-4-7(6-11(8)16)12-9(14)2-1-3-10(12)15/h1-6H,"1,2-dichloro-4-(2,6-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C(=C1)Cl)C2=CC(=C(C=C2)Cl)Cl)Cl,C1=CC(=C(C(=C1)Cl)C2=CC(=C(C=C2)Cl)Cl)Cl,C12H6Cl4,289.922360,Oily liquids or solids that are colorless to light yellow. ,"",,,"2.79e-05 mg/mL at 25 oC [PATIL,GS (1991)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
462,T3D0461,2009-03-06 18:58:51 UTC,2009-08-11 15:55:42 UTC,"2,3',5,5'-Tetrachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"2,3',5,5'-Tetrachloro-1,1'-biphenyl2,3',5,5'-Tetrachlorobiphenyl","2,3',5,5'-Tetrachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,41464-42-0,38878,,"","","",CPD-946,,,"2,3',5,5'-Tetrachlorobiphenyl",,,,,InChI=1/C12H6Cl4/c13-8-1-2-12(16)11(6-8)7-3-9(14)5-10(15)4-7/h1-6H,"1,3-dichloro-5-(2,5-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C=C1Cl)C2=CC(=CC(=C2)Cl)Cl)Cl,C1=CC(=C(C=C1Cl)C2=CC(=CC(=C2)Cl)Cl)Cl,C12H6Cl4,289.922360,Oily liquids or solids that are colorless to light yellow. ,"",,,"",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
463,T3D0462,2009-03-06 18:58:51 UTC,2009-08-11 15:55:42 UTC,"2,3',5',6-Tetrachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 2,3',5',6-tetrachloro1,1'-Biphenyl, 2,3',5',6-tetrachloro-2,3',5',6-Tetrachlorobiphenyl","2,3',5',6-Tetrachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,74338-23-1,63100,,"","","","",,,"2,3',5',6-Tetrachlorobiphenyl",,,,,InChI=1/C12H6Cl4/c13-8-4-7(5-9(14)6-8)12-10(15)2-1-3-11(12)16/h1-6H,"1,3-dichloro-5-(2,6-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C(=C1)Cl)C2=CC(=CC(=C2)Cl)Cl)Cl,C1=CC(=C(C(=C1)Cl)C2=CC(=CC(=C2)Cl)Cl)Cl,C12H6Cl4,289.922360,Oily liquids or solids that are colorless to light yellow. ,"",,,"",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
464,T3D0463,2009-03-06 18:58:51 UTC,2009-08-11 15:55:42 UTC,"2,4,4',5-Tetrachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 2,4,4',5-tetrachloro1,1'-Biphenyl, 2,4,4',5-tetrachloro-2,4,4',5-Tetrachloro-1,1'-biphenyl2,4,4',5-tetrachlorobiphenyl","2,4,4',5-Tetrachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,32690-93-0,36218,,"","","",CPD-945,,,"2,4,4',5-Tetrachlorobiphenyl",,,,,InChI=1/C12H6Cl4/c13-8-3-1-7(2-4-8)9-5-11(15)12(16)6-10(9)14/h1-6H,"1,2,4-trichloro-5-(4-chlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=CC=C1C2=CC(=C(C=C2Cl)Cl)Cl)Cl,C1=CC(=CC=C1C2=CC(=C(C=C2Cl)Cl)Cl)Cl,C12H6Cl4,289.922360,Oily liquids or solids that are colorless to light yellow. ,"",,,"4.96e-06 mg/mL at 25 oC [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
465,T3D0464,2009-03-06 18:58:51 UTC,2009-08-11 15:55:43 UTC,"2,4,4',6-Tetrachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"2,4,4',6-Tetrachloro-1,1'-biphenyl2,4,4',6-Tetrachlorobiphenyl2,4,4'6-Tetrachlorobiphenyl2,4,6,4'-tetrachlorobiphenyl","2,4,4',6-Tetrachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,32598-12-2,63107,,C14364,"",34233,CPD-946,,,"2,4,4',6-Tetrachlorobiphenyl",,,,,InChI=1/C12H6Cl4/c13-8-3-1-7(2-4-8)12-10(15)5-9(14)6-11(12)16/h1-6H,"1,3,5-trichloro-2-(4-chlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/89488596517cb8b09571f4705d80982a_1237983273.mol,C1=CC(=CC=C1C2=C(C=C(C=C2Cl)Cl)Cl)Cl,C1=CC(=CC=C1C2=C(C=C(C=C2Cl)Cl)Cl)Cl,C12H6Cl4,289.922360,Oily liquids or solids that are colorless to light yellow. ,65 oC,,,"9.11e-05 mg/mL at 25 oC [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
466,T3D0465,2009-03-06 18:58:51 UTC,2009-08-11 15:55:43 UTC,"2,3',4',5'-Tetrachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 2,3',4',5'-tetrachloro-2',3,4,5-Tetrachlorobiphenyl2,3',4',5'-TETRACHLOROBIPHENYL","2,3',4',5'-Tetrachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,70362-48-0,51042,,"","","","",,,"2,3',4',5'-Tetrachlorobiphenyl",,,,,InChI=1/C12H6Cl4/c13-9-4-2-1-3-8(9)7-5-10(14)12(16)11(15)6-7/h1-6H,"1,2,3-trichloro-5-(2-chlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC=C(C(=C1)C2=CC(=C(C(=C2)Cl)Cl)Cl)Cl,C1=CC=C(C(=C1)C2=CC(=C(C(=C2)Cl)Cl)Cl)Cl,C12H6Cl4,289.922360,Oily liquids or solids that are colorless to light yellow. ,106.0 oC,,,"3.62e-05 mg/mL at 20 oC [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
467,T3D0466,2009-03-06 18:58:51 UTC,2009-08-11 15:55:43 UTC,"3,3',4,4'-Tetrachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 3,3',4,4'-tetrachloro- (9CI)3,3',4,4'-Tetrachloro(14C-U)biphenyl3,3',4,4'-Tetrachloro-1,1'-biphenyl3,3',4,4'-Tetrachloro-1,1'-biphenyl labeled with carbon-143,3',4,4'-Tetrachlorobiphenyl3,3',4,4'-tetrachlorobinphenyl3,4,3',4'-Tetra coplanar polychlorinated biphenyl3,4,3',4'-Tetrachloro-biphenyl3,4,3',4'-Tetrachlorobiphenyl3,4,3',4'-tetrachlorobiphenyl, 4,4'-(36)Cl-labeledBiphenyl, 3,3',4,4'-tetrachloro-TCB","3,3',4,4'-Tetrachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,32598-13-3,36187,,C11057,"",1367,CPD-946,,C028451,"3,3',4,4'-Tetrachlorobiphenyl",,,,,InChI=1/C12H6Cl4/c13-9-3-1-7(5-11(9)15)8-2-4-10(14)12(16)6-8/h1-6H,"1,2-dichloro-4-(3,4-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/6e3b8ce0f214af4e2907ab054762c846_1237983421.mol,C1=CC(=C(C=C1C2=CC(=C(C=C2)Cl)Cl)Cl)Cl,C1=CC(=C(C=C1C2=CC(=C(C=C2)Cl)Cl)Cl)Cl,C12H6Cl4,289.922360,Oily liquids or solids that are colorless to light yellow. ,"",,,"5.69e-07 mg/mL at 25 oC [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
468,T3D0467,2009-03-06 18:58:52 UTC,2009-08-11 15:55:43 UTC,"3,3',4,5-Tetrachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 3,3',4,5-tetrachloro-3,3',4,5-Tetrachlorobiphenyl","3,3',4,5-Tetrachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,70362-49-1,63101,,"","","","",,,"3,3',4,5-Tetrachlorobiphenyl",,,,,InChI=1/C12H6Cl4/c13-9-3-1-2-7(4-9)8-5-10(14)12(16)11(15)6-8/h1-6H,"1,2,3-trichloro-5-(3-chlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=CC(=C1)Cl)C2=CC(=C(C(=C2)Cl)Cl)Cl,C1=CC(=CC(=C1)Cl)C2=CC(=C(C(=C2)Cl)Cl)Cl,C12H6Cl4,289.922360,Oily liquids or solids that are colorless to light yellow. ,"",,,"",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
469,T3D0468,2009-03-06 18:58:52 UTC,2009-08-11 15:55:43 UTC,"3,3',4,5'-Tetrachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"3,3',4,5'-Tetrachloro-1,1'-biphenyl3,3',4,5'-Tetrachlorobiphenyl","3,3',4,5'-Tetrachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,41464-48-6,63104,,"","","",CPD-946,,,"3,3',4,5'-Tetrachlorobiphenyl",,,,,InChI=1/C12H6Cl4/c13-9-3-8(4-10(14)6-9)7-1-2-11(15)12(16)5-7/h1-6H,"1,2-dichloro-4-(3,5-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C=C1C2=CC(=CC(=C2)Cl)Cl)Cl)Cl,C1=CC(=C(C=C1C2=CC(=CC(=C2)Cl)Cl)Cl)Cl,C12H6Cl4,289.922360,Oily liquids or solids that are colorless to light yellow. ,"",,,"",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
470,T3D0469,2009-03-06 18:58:52 UTC,2009-08-11 15:55:44 UTC,"3,3',5,5'-Tetrachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 3,3',5, 5'-tetrachloro-1,1'-Biphenyl, 3,3',5,5'-tetrachloro- (9CI)3,3',5, 5'-Tetrachlorodiphenyl3,3',5,5'-Tetrachloro-1,1'-biphenyl3,3',5,5'-Tetrachlorobiphenyl3,3',5,5'-Tetrachlorodiphenyl3,3',5,5'-tetrachloro-1,1'-biphenyl (ACD/Name 4.0)3,5,3',5'-TetrachlorobiphenylAroclor 1248Biphenyl, 3,3',5,5'-tetrachloro-Biphenyl, 3,3',5,5'-tetrachloro- (8CI)Kanechlor 400Kaneclor 400Polychlorinated biphenyl (kanechlor 400)","3,3',5,5'-Tetrachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,33284-52-5,36400,,"","",35445,CPD-946,,C029860,"3,3',5,5'-Tetrachlorobiphenyl",,,,,InChI=1/C12H6Cl4/c13-9-1-7(2-10(14)5-9)8-3-11(15)6-12(16)4-8/h1-6H,"1,3-dichloro-5-(3,5-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=C(C=C(C=C1Cl)Cl)C2=CC(=CC(=C2)Cl)Cl,C1=C(C=C(C=C1Cl)Cl)C2=CC(=CC(=C2)Cl)Cl,C12H6Cl4,289.922360,Oily liquids or solids that are colorless to light yellow. ,"",,,"1.23e-06 mg/mL at 25 oC [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
471,T3D0470,2009-03-06 18:58:52 UTC,2009-08-11 15:55:44 UTC,"3,4,4',5-Tetrachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 3,4,4',5-tetrachloro1,1'-Biphenyl, 3,4,4',5-tetrachloro-3,4,4',5-Tetrachlorobiphenyl","3,4,4',5-Tetrachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,70362-50-4,51043,,"","","",DIHYDRO-DIOH-BENZOATE,,,"3,4,4',5-Tetrachlorobiphenyl",,,,,InChI=1/C12H6Cl4/c13-9-3-1-7(2-4-9)8-5-10(14)12(16)11(15)6-8/h1-6H,"1,2,3-trichloro-5-(4-chlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=CC=C1C2=CC(=C(C(=C2)Cl)Cl)Cl)Cl,C1=CC(=CC=C1C2=CC(=C(C(=C2)Cl)Cl)Cl)Cl,C12H6Cl4,289.922360,Oily liquids or solids that are colorless to light yellow. ,"",,,"",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
472,T3D0471,2009-03-06 18:58:52 UTC,2009-08-11 15:55:44 UTC,"2,2',3,3',4-Pentachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"2,2',3,3',4'-Pentachlorobiphenyl2,2',3,3',4-Pentachloro-1,1'-biphenyl2,2',3,3',4-pentachlorobiphenyl2,2',3,3'4-Pentachlorobiphenyl2,2',3,4,5-PENTACHLOROBIPHENYL2,3,4,2',3'-PentachlorobiphenylAROCLOR 1254Arclor1254Arochlor 1254Aroclor-1254Chlorierte biphenyle, chlorgehalt 54% [German]Chlorodiphenyl (54% Chlorine)Chlorodiphenyl (54% Cl)Chlorodiphenyl, 54% chlorineClorodifenili, cloro 54% [Italian]Diphenyle chlore, 54% de chlore [French]PCBPCB's (54% Cl)PCBs (54%Cl)Polychlorinated biphenyl (aroclor 1254)Polychlorobiphenyls (54% chlorine)polychlorinated biphenyl 1254","2,2',3,3',4-Pentachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,52663-62-4,40470,,"","","",CPD-946,,,"2,2',3,3',4-Pentachlorobiphenyl",,,,,InChI=1/C12H5Cl5/c13-8-3-1-2-6(10(8)15)7-4-5-9(14)12(17)11(7)16/h1-5H,"1,2,3-trichloro-4-(2,3-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C(=C1)Cl)Cl)C2=C(C(=C(C=C2)Cl)Cl)Cl,C1=CC(=C(C(=C1)Cl)Cl)C2=C(C(=C(C=C2)Cl)Cl)Cl,C12H5Cl5,323.883390,Oily liquids or solids that are colorless to light yellow. ,"",,,"2.91e-05 mg/mL at 20 oC [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
473,T3D0472,2009-03-06 18:58:52 UTC,2009-08-11 15:55:45 UTC,"2,2',3,3',5-Pentachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"2,2',3,3',5-Pentachloro-1,1'-biphenyl2,2',3,3',5-PentachlorobiphenylBiphenyl, 2,2',3,3',5-pentachloro-","2,2',3,3',5-Pentachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,60145-20-2,63093,,"","","",CPD-946,,,"2,2',3,3',5-Pentachlorobiphenyl",,,,,InChI=1/C12H5Cl5/c13-6-4-8(12(17)10(15)5-6)7-2-1-3-9(14)11(7)16/h1-5H,"1,2,5-trichloro-3-(2,3-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C(=C1)Cl)Cl)C2=CC(=CC(=C2Cl)Cl)Cl,C1=CC(=C(C(=C1)Cl)Cl)C2=CC(=CC(=C2Cl)Cl)Cl,C12H5Cl5,323.883390,Oily liquids or solids that are colorless to light yellow. ,"",,,"",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
474,T3D0473,2009-03-06 18:58:52 UTC,2009-08-11 15:55:45 UTC,"2,2',3,3',6-Pentachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"2,2',3,3',6-PENTACHLOROBIPHENYL2,2',3,3',6-Pentachloro-1,1'-biphenyl","2,2',3,3',6-Pentachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,52663-60-2,40468,,"","","",CPD-946,,C032902,"2,2',3,3',6-Pentachlorobiphenyl",,,,,InChI=1/C12H5Cl5/c13-7-4-5-9(15)12(17)10(7)6-2-1-3-8(14)11(6)16/h1-5H,"1,2,4-trichloro-3-(2,3-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C(=C1)Cl)Cl)C2=C(C=CC(=C2Cl)Cl)Cl,C1=CC(=C(C(=C1)Cl)Cl)C2=C(C=CC(=C2Cl)Cl)Cl,C12H5Cl5,323.883390,Oily liquids or solids that are colorless to light yellow. ,"",,,5.42e-05 mg/mL at 25 oC [EPA],,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
475,T3D0474,2009-03-06 18:58:53 UTC,2009-08-11 15:55:45 UTC,"2,2',3,4,4'-Pentachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 2,2',3,4,4'-pentachloro1,1'-Biphenyl, 2,2',3,4,4'-pentachloro-2,2',3,4,4'-PENTACHLOROBIPHENYL","2,2',3,4,4'-Pentachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,65510-45-4,47651,,"","","",DIHYDRO-DIOH-BENZOATE,,,"2,2',3,4,4'-Pentachlorobiphenyl",,,,,InChI=1/C12H5Cl5/c13-6-1-2-7(10(15)5-6)8-3-4-9(14)12(17)11(8)16/h1-5H,"1,2,3-trichloro-4-(2,4-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C=C1Cl)Cl)C2=C(C(=C(C=C2)Cl)Cl)Cl,C1=CC(=C(C=C1Cl)Cl)C2=C(C(=C(C=C2)Cl)Cl)Cl,C12H5Cl5,323.883390,Oily liquids or solids that are colorless to light yellow. ,"",,,7.83e-06 mg/mL at 25 oC [EPA],,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
476,T3D0475,2009-03-06 18:58:53 UTC,2009-08-11 15:55:46 UTC,"2,2',3,4,5-Pentachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"2,2',3,4,5-Pentachloro-1,1'-biphenyl2,2',3,4,5-Pentachlorobiphenyl","2,2',3,4,5-Pentachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,55312-69-1,41404,,"","","",CPD-946,,,"2,2',3,4,5-Pentachlorobiphenyl",,,,,InChI=1/C12H5Cl5/c13-8-4-2-1-3-6(8)7-5-9(14)11(16)12(17)10(7)15/h1-5H,"1,2,3,4-tetrachloro-5-(2-chlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC=C(C(=C1)C2=CC(=C(C(=C2Cl)Cl)Cl)Cl)Cl,C1=CC=C(C(=C1)C2=CC(=C(C(=C2Cl)Cl)Cl)Cl)Cl,C12H5Cl5,323.883390,Oily liquids or solids that are colorless to light yellow. ,"",,,"9.8e-06 mg/mL at 25 oC [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
477,T3D0476,2009-03-06 18:58:53 UTC,2009-08-11 15:55:46 UTC,"2,2',3,4,5'-Pentachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"2,2',3,4,5'-Pentachloro-1,1'-biphenyl2,2',3,4,5'-Pentachlorobiphenyl2,2',3,4,5'-Pentachlorodiphenyl2,3,4,2',5'-Pentachlorobiphenyl2,5,2',3',4'-Pentachlorobiphenyl","2,2',3,4,5'-Pentachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,38380-02-8,38014,,"","","",CPD-946,,,"2,2',3,4,5'-Pentachlorobiphenyl",,,,,InChI=1/C12H5Cl5/c13-6-1-3-9(14)8(5-6)7-2-4-10(15)12(17)11(7)16/h1-5H,"1,2,3-trichloro-4-(2,5-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C=C1Cl)C2=C(C(=C(C=C2)Cl)Cl)Cl)Cl,C1=CC(=C(C=C1Cl)C2=C(C(=C(C=C2)Cl)Cl)Cl)Cl,C12H5Cl5,323.883390,Oily liquids or solids that are colorless to light yellow. ,"",,,"2.94e-05 mg/mL at 20 oC [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
478,T3D0477,2009-03-06 18:58:53 UTC,2009-08-11 15:55:46 UTC,"2,2',3,4,6-Pentachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"2,2',3,4,6-Pentachloro-1,1'-biphenyl2,2',3,4,6-Pentachlorobiphenyl","2,2',3,4,6-Pentachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,55215-17-3,41362,,"","","",CPD-946,,,"2,2',3,4,6-Pentachlorobiphenyl",,,,,InChI=1/C12H5Cl5/c13-7-4-2-1-3-6(7)10-8(14)5-9(15)11(16)12(10)17/h1-5H,"1,2,3,5-tetrachloro-4-(2-chlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC=C(C(=C1)C2=C(C(=C(C=C2Cl)Cl)Cl)Cl)Cl,C1=CC=C(C(=C1)C2=C(C(=C(C=C2Cl)Cl)Cl)Cl)Cl,C12H5Cl5,323.883390,Oily liquids or solids that are colorless to light yellow. ,"",,,"1.2e-05 mg/mL at 25 oC [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
479,T3D0478,2009-03-06 18:58:53 UTC,2009-08-11 15:55:47 UTC,"2,2',3,4,6'-Pentachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 2,2',3,4,6'-pentachloro1,1'-Biphenyl, 2,2',3,4,6'-pentachloro-2,2',3,4,6'-PENTACHLOROBIPHENYL2,3,4,2',6'-Pentachlorobiphenyl","2,2',3,4,6'-Pentachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,73575-57-2,51822,,"","","","",,,"2,2',3,4,6'-Pentachlorobiphenyl",,,,,InChI=1/C12H5Cl5/c13-7-2-1-3-8(14)10(7)6-4-5-9(15)12(17)11(6)16/h1-5H,"1,2,3-trichloro-4-(2,6-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C(=C1)Cl)C2=C(C(=C(C=C2)Cl)Cl)Cl)Cl,C1=CC(=C(C(=C1)Cl)C2=C(C(=C(C=C2)Cl)Cl)Cl)Cl,C12H5Cl5,323.883390,Oily liquids or solids that are colorless to light yellow. ,"",,,"5.42e-05 mg/mL at 25 oC [PATIL,GS (1991)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
480,T3D0479,2009-03-06 18:58:53 UTC,2009-08-11 15:55:47 UTC,"2,2',3,4',5-Pentachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 2,2',3,4',5-pentachloro-2,2',3,4',5-PENTACHLOROBIPHENYL","2,2',3,4',5-Pentachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,68194-07-0,50100,,"","","","",,,"2,2',3,4',5-Pentachlorobiphenyl",,,,,InChI=1/C12H5Cl5/c13-6-1-2-8(10(15)4-6)9-3-7(14)5-11(16)12(9)17/h1-5H,"1,2,5-trichloro-3-(2,4-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C=C1Cl)Cl)C2=CC(=CC(=C2Cl)Cl)Cl,C1=CC(=C(C=C1Cl)Cl)C2=CC(=CC(=C2Cl)Cl)Cl,C12H5Cl5,323.883390,Oily liquids or solids that are colorless to light yellow. ,"",,,"4.94e-06 mg/mL at 25 oC [PATIL,GS (1991)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
481,T3D0480,2009-03-06 18:58:53 UTC,2009-08-11 15:55:47 UTC,"2,2',3,4',6-Pentachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 2,2',3,4',6-pentachloro1,1'-Biphenyl, 2,2',3,4',6-pentachloro-2,2',3,4',6-PENTACHLOROBIPHENYL","2,2',3,4',6-Pentachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,68194-05-8,50099,,"","","",DIHYDRO-DIOH-BENZOATE,,,"2,2',3,4',6-Pentachlorobiphenyl",,,,,InChI=1/C12H5Cl5/c13-6-1-2-7(10(16)5-6)11-8(14)3-4-9(15)12(11)17/h1-5H,"1,2,4-trichloro-3-(2,4-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C=C1Cl)Cl)C2=C(C=CC(=C2Cl)Cl)Cl,C1=CC(=C(C=C1Cl)Cl)C2=C(C=CC(=C2Cl)Cl)Cl,C12H5Cl5,323.883390,Oily liquids or solids that are colorless to light yellow. ,"",,,"2.21e-05 mg/mL at 25 oC [PATIL,GS (1991)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
482,T3D0481,2009-03-06 18:58:54 UTC,2009-08-11 15:55:48 UTC,"2,2',3,5,5'-Pentachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"2,2',3,5,5'-PENTACHLOROBIPHENYL2,2',3,5,5'-Pentachloro-1,1'-biphenyl2,2',4,5,5'-Pentachlorobiphenyl","2,2',3,5,5'-Pentachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,52663-61-3,40469,,"","","",CPD-946,,,"2,2',3,5,5'-Pentachlorobiphenyl",,,,,InChI=1/C12H5Cl5/c13-6-1-2-10(15)8(3-6)9-4-7(14)5-11(16)12(9)17/h1-5H,"1,2,5-trichloro-3-(2,5-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C=C1Cl)C2=CC(=CC(=C2Cl)Cl)Cl)Cl,C1=CC(=C(C=C1Cl)C2=CC(=CC(=C2Cl)Cl)Cl)Cl,C12H5Cl5,323.883390,Oily liquids or solids that are colorless to light yellow. ,"",,,4.94e-06 mg/mL at 25 oC [EPA],,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
483,T3D0482,2009-03-06 18:58:54 UTC,2009-08-11 15:55:48 UTC,"2,2',3,5,6-Pentachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"2,2',3,5,6-Pentachloro-1,1'-biphenyl2,2',3,5,6-Pentachlorobiphenyl","2,2',3,5,6-Pentachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,73575-56-1,63084,,"","","",CPD-946,,,"2,2',3,5,6-Pentachlorobiphenyl",,,,,InChI=1/C12H5Cl5/c13-7-4-2-1-3-6(7)10-11(16)8(14)5-9(15)12(10)17/h1-5H,"1,2,4,5-tetrachloro-3-(2-chlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC=C(C(=C1)C2=C(C(=CC(=C2Cl)Cl)Cl)Cl)Cl,C1=CC=C(C(=C1)C2=C(C(=CC(=C2Cl)Cl)Cl)Cl)Cl,C12H5Cl5,323.883390,Oily liquids or solids that are colorless to light yellow. ,"",,,"1.3e-05 mg/mL at 25 oC [PATIL,GS (1991)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
484,T3D0483,2009-03-06 18:58:54 UTC,2009-08-11 15:55:48 UTC,"2,2',3,5,6'-Pentachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl 2,2',3,5,6'-pentachloro-1,1'-Biphenyl, 2,2',3,5,6'-pentachloro1,1'-Biphenyl, 2,2',3,5,6'-pentachloro-2,2',3,5,6'-Pentachlorobiphenyl","2,2',3,5,6'-Pentachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,73575-55-0,63095,,"","","","",,,"2,2',3,5,6'-Pentachlorobiphenyl",,,,,InChI=1/C12H5Cl5/c13-6-4-7(12(17)10(16)5-6)11-8(14)2-1-3-9(11)15/h1-5H,"1,2,5-trichloro-3-(2,6-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C(=C1)Cl)C2=CC(=CC(=C2Cl)Cl)Cl)Cl,C1=CC(=C(C(=C1)Cl)C2=CC(=CC(=C2Cl)Cl)Cl)Cl,C12H5Cl5,323.883390,Oily liquids or solids that are colorless to light yellow. ,"",,,"",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
485,T3D0484,2009-03-06 18:58:54 UTC,2009-08-11 15:55:48 UTC,"2,2',3,5',6-Pentachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"2,2',3,5',6-Pentachloro-1,1'-biphenyl2,2',3,5',6-Pentachlorobiphenyl2,3,6,2',5'-Pentachlorobiphenyl2,5,2',3',6'-Pentachlorobiphenyl","2,2',3,5',6-Pentachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,38379-99-6,38012,,"","","",CPD-946,,C032904,"2,2',3,5',6-Pentachlorobiphenyl",,,,,InChI=1/C12H5Cl5/c13-6-1-2-8(14)7(5-6)11-9(15)3-4-10(16)12(11)17/h1-5H,"1,2,4-trichloro-3-(2,5-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C=C1Cl)C2=C(C=CC(=C2Cl)Cl)Cl)Cl,C1=CC(=C(C=C1Cl)C2=C(C=CC(=C2Cl)Cl)Cl)Cl,C12H5Cl5,323.883390,Oily liquids or solids that are colorless to light yellow. ,"",,,"2.11e-05 mg/mL at 20 oC [PATIL,GS (1991)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
486,T3D0485,2009-03-06 18:58:54 UTC,2009-08-11 15:55:49 UTC,"2,2',3,6,6'-Pentachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 2,2',3,6,6'-pentachloro-2,2',3,6,6'-Pentachlorobiphenyl","2,2',3,6,6'-Pentachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,73575-54-9,63089,,"","","","",,,"2,2',3,6,6'-Pentachlorobiphenyl",,,,,InChI=1/C12H5Cl5/c13-6-2-1-3-7(14)10(6)11-8(15)4-5-9(16)12(11)17/h1-5H,"1,2,4-trichloro-3-(2,6-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C(=C1)Cl)C2=C(C=CC(=C2Cl)Cl)Cl)Cl,C1=CC(=C(C(=C1)Cl)C2=C(C=CC(=C2Cl)Cl)Cl)Cl,C12H5Cl5,323.883390,Oily liquids or solids that are colorless to light yellow. ,"",,,"",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
487,T3D0486,2009-03-06 18:58:54 UTC,2009-08-11 15:55:49 UTC,"2,2',3,4',5'-Pentachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 2,2',3,4',5'-pentachloro-2,2',3',4,5-Pentachloro-1,1'-biphenyl2,2',3',4,5-Pentachlorobiphenyl2,2',3',4,5-Pentachlorodiphenyl2,2',3,4',5'-Pentachloro-1,1'-biphenyl2,4,5,2',3'-Pentachlorobiphenyl","2,2',3,4',5'-Pentachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,41464-51-1,38881,,"","","",CPD-946,,,"2,2',3,4',5'-Pentachlorobiphenyl",,,,,InChI=1/C12H5Cl5/c13-8-3-1-2-6(12(8)17)7-4-10(15)11(16)5-9(7)14/h1-5H,"1,2,4-trichloro-5-(2,3-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C(=C1)Cl)Cl)C2=CC(=C(C=C2Cl)Cl)Cl,C1=CC(=C(C(=C1)Cl)Cl)C2=CC(=C(C=C2Cl)Cl)Cl,C12H5Cl5,323.883390,Oily liquids or solids that are colorless to light yellow. ,"",,,"2.84e-05 mg/mL at 20 oC [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
488,T3D0487,2009-03-06 18:58:54 UTC,2009-08-11 15:55:49 UTC,"2,2',3,4',6'-Pentachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 2,2',3,4',6'-Pentachloro-1,1'-Biphenyl, 2,3,2',4',6'-pentachloro-2,2',3,4',6'-PENTACHLOROBIPHENYL2,2',3,4',6'-Pentachloro-1,1'-biphenyl2,3,2',4',6'-Pentachlorobiphenyl","2,2',3,4',6'-Pentachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,60233-25-2,43238,,"","","",CPD-946,,,"2,2',3,4',6'-Pentachlorobiphenyl",,,,,InChI=1/C12H5Cl5/c13-6-4-9(15)11(10(16)5-6)7-2-1-3-8(14)12(7)17/h1-5H,"1,3,5-trichloro-2-(2,3-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C(=C1)Cl)Cl)C2=C(C=C(C=C2Cl)Cl)Cl,C1=CC(=C(C(=C1)Cl)Cl)C2=C(C=C(C=C2Cl)Cl)Cl,C12H5Cl5,323.883390,Oily liquids or solids that are colorless to light yellow. ,"",,,"1.3e-05 mg/mL at 25 oC [PATIL,GS (1991)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
489,T3D0488,2009-03-06 18:58:55 UTC,2009-08-11 15:55:49 UTC,"2,2',4,4',5-Pentachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"2,2',4,4',5-PENTACHLOROBIPHENYL2,2',4,4',5-Pentachloro-1,1'-biphenyl2,2',4,4'5-Pentachlorobiphenyl","2,2',4,4',5-Pentachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,38380-01-7,38013,,"","","",CPD-946,,,"2,2',4,4',5-Pentachlorobiphenyl",,,,,InChI=1/C12H5Cl5/c13-6-1-2-7(9(14)3-6)8-4-11(16)12(17)5-10(8)15/h1-5H,"1,2,4-trichloro-5-(2,4-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C=C1Cl)Cl)C2=CC(=C(C=C2Cl)Cl)Cl,C1=CC(=C(C=C1Cl)Cl)C2=CC(=C(C=C2Cl)Cl)Cl,C12H5Cl5,323.883390,Oily liquids or solids that are colorless to light yellow. ,"",,,"3.66e-06 mg/mL at 25 oC [PATIL,GS (1991)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
490,T3D0489,2009-03-06 18:58:55 UTC,2009-08-11 15:55:49 UTC,"2,2',4,4',6-Pentachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"2,2',4,4',6-Pentachloro-1,1'-biphenyl2,2',4,4',6-Pentachlorobiphenyl","2,2',4,4',6-Pentachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,39485-83-1,38277,,"","","",CPD-946,,,"2,2',4,4',6-Pentachlorobiphenyl",,,,,InChI=1/C12H5Cl5/c13-6-1-2-8(9(15)3-6)12-10(16)4-7(14)5-11(12)17/h1-5H,"1,3,5-trichloro-2-(2,4-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C=C1Cl)Cl)C2=C(C=C(C=C2Cl)Cl)Cl,C1=CC(=C(C=C1Cl)Cl)C2=C(C=C(C=C2Cl)Cl)Cl,C12H5Cl5,323.883390,Oily liquids or solids that are colorless to light yellow. ,"",,,"7.14e-06 mg/mL at 25 oC [PATIL,GS (1991)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
491,T3D0490,2009-03-06 18:58:55 UTC,2009-08-11 15:55:50 UTC,"2,2',4,5,5'-Pentachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 2,2',4,5',6-Pentachloro-1,1'-Biphenyl, 2,2',4,5,5'-pentachloro-2,2',4,5,5'-PENTACHLOROBIPHENYL2,2',4,5,5'-Pentachloro-1,1'-biphenyl2,2',4,5,5'Pentachlorobiphenyl2,4,5,2',5'-pentachlorobiphenyl","2,2',4,5,5'-Pentachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,37680-73-2,37807,,"","","",1-AMINO-PROPAN-2-OL,,C009828,"2,2',4,5,5'-Pentachlorobiphenyl",,,,,InChI=1/C12H5Cl5/c13-6-1-2-9(14)7(3-6)8-4-11(16)12(17)5-10(8)15/h1-5H,"1,2,4-trichloro-5-(2,5-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C=C1Cl)C2=CC(=C(C=C2Cl)Cl)Cl)Cl,C1=CC(=C(C=C1Cl)C2=CC(=C(C=C2Cl)Cl)Cl)Cl,C12H5Cl5,323.883390,Oily liquids or solids that are colorless to light yellow. ,"",,,"1.54e-05 mg/mL at 25 oC [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
492,T3D0491,2009-03-06 18:58:55 UTC,2009-08-11 15:55:50 UTC,"2,2',4,5,6'-Pentachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"2,2',4,5,6'-Pentachloro-1,1'-biphenyl2,2',4,5,6'-Pentachlorobiphenyl","2,2',4,5,6'-Pentachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,68194-06-9,63096,,"","","",CPD-946,,,"2,2',4,5,6'-Pentachlorobiphenyl",,,,,InChI=1/C12H5Cl5/c13-7-2-1-3-8(14)12(7)6-4-10(16)11(17)5-9(6)15/h1-5H,"1,2,4-trichloro-5-(2,6-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C(=C1)Cl)C2=CC(=C(C=C2Cl)Cl)Cl)Cl,C1=CC(=C(C(=C1)Cl)C2=CC(=C(C=C2Cl)Cl)Cl)Cl,C12H5Cl5,323.883390,Oily liquids or solids that are colorless to light yellow. ,"",,,"",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
493,T3D0492,2009-03-06 18:58:55 UTC,2009-08-11 15:55:50 UTC,"2,2',4,5',6-Pentachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"2,2',4,5',6-Pentachlorobiphenyl2,2',4,5,5'-Pentachloro-1,1'-biphenyl2,2',4,5,5'-Pentachlorobiphenyl","2,2',4,5',6-Pentachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)
",,60145-21-3,63086,,"","","",CPD-946,,,"2,2',4,5',6-Pentachlorobiphenyl",,,,,InChI=1/C12H5Cl5/c13-6-1-2-9(15)8(3-6)12-10(16)4-7(14)5-11(12)17/h1-5H,"1,3,5-trichloro-2-(2,5-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C=C1Cl)C2=C(C=C(C=C2Cl)Cl)Cl)Cl,C1=CC(=C(C=C1Cl)C2=C(C=C(C=C2Cl)Cl)Cl)Cl,C12H5Cl5,323.883390,Oily liquids or solids that are colorless to light yellow. ,"",,,"1.11e-05 mg/mL at 25 oC [PATIL,GS (1991)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
494,T3D0493,2009-03-06 18:58:55 UTC,2009-08-11 15:55:50 UTC,"2,2',4,6,6'-Pentachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"2,2',4,6,6'-Pentachloro-1,1'-biphenyl2,2',4,6,6'-Pentachlorobiphenyl2,4,6,2',6'-pentachlorobiphenyl","2,2',4,6,6'-Pentachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,56558-16-8,91662,,"","","",CPD-946,,,"2,2',4,6,6'-Pentachlorobiphenyl",,,,,InChI=1/C12H5Cl5/c13-6-4-9(16)12(10(17)5-6)11-7(14)2-1-3-8(11)15/h1-5H,"1,3,5-trichloro-2-(2,6-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C(=C1)Cl)C2=C(C=C(C=C2Cl)Cl)Cl)Cl,C1=CC(=C(C(=C1)Cl)C2=C(C=C(C=C2Cl)Cl)Cl)Cl,C12H5Cl5,323.883390,Oily liquids or solids that are colorless to light yellow. ,85.0 oC,,,"1.58e-05 mg/mL at 25 oC [YALKOWSKY,SH & DANNENFELSER,RM (1992)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
495,T3D0494,2009-03-06 18:58:55 UTC,2009-08-11 15:55:50 UTC,"2,3,3',4,4'-Pentachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 2,3,3'4,4'-pentachloro-1,1'-Biphenyl, 2,3,3'4,4'-pentachloro- (9CI)2,3,3',4,4'-Pentachloro-1,1'-biphenyl2,3,3',4,4'-Pentachlorobiphenyl2,3,3'4,4'-Pentachloro-1,1'-biphenyl2,3,4,3',4'-Pentachlorobiphenyl3,4,2',3',4'-PentachlorobiphenylBiphenyl, 2,3,3',4,4'-pentachloro-PCB No 105Pencb","2,3,3',4,4'-Pentachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,32598-14-4,36188,,"","","",CPD-946,,C067940,"2,3,3',4,4'-Pentachlorobiphenyl",,,,,InChI=1/C12H5Cl5/c13-8-3-1-6(5-10(8)15)7-2-4-9(14)12(17)11(7)16/h1-5H,"1,2,3-trichloro-4-(3,4-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C=C1C2=C(C(=C(C=C2)Cl)Cl)Cl)Cl)Cl,C1=CC(=C(C=C1C2=C(C(=C(C=C2)Cl)Cl)Cl)Cl)Cl,C12H5Cl5,323.883390,Oily liquids or solids that are colorless to light yellow. ,"",,,"3.4e-06 mg/mL at 25 oC [OZRETICH,RJ et al. (1995)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
496,T3D0495,2009-03-06 18:58:56 UTC,2009-08-11 15:55:51 UTC,"2,3,3',4,5-Pentachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"2,3,3',4,5-PENTACHLOROBIPHENYL2,3,3',4,5-pentachloro-1,1'-biphenyl2,3,4,5,3'-pentachlorobiphenyl","2,3,3',4,5-Pentachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,70424-69-0,51075,,C14365,"",34216,"",,,"2,3,3',4,5-Pentachlorobiphenyl",,,,,InChI=1/C12H5Cl5/c13-7-3-1-2-6(4-7)8-5-9(14)11(16)12(17)10(8)15/h1-5H,"1,2,3,4-tetrachloro-5-(3-chlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/d749e17726ebf9cefb1cc66edc73ef3c_1237985894.mol,C1=CC(=CC(=C1)Cl)C2=CC(=C(C(=C2Cl)Cl)Cl)Cl,C1=CC(=CC(=C1)Cl)C2=CC(=C(C(=C2Cl)Cl)Cl)Cl,C12H5Cl5,323.883390,Oily liquids or solids that are colorless to light yellow. ,"",,,"",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
497,T3D0496,2009-03-06 18:58:56 UTC,2009-08-11 15:55:51 UTC,"2,3,3',4',5-Pentachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"2,3,3',4',5-PENTACHLOROBIPHENYL","2,3,3',4',5-Pentachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,70424-68-9,51074,,"","","","",,,"2,3,3',4',5-Pentachlorobiphenyl",,,,,InChI=1/C12H5Cl5/c13-7-4-8(12(17)11(16)5-7)6-1-2-9(14)10(15)3-6/h1-5H,"1,2,5-trichloro-3-(3,4-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C=C1C2=CC(=CC(=C2Cl)Cl)Cl)Cl)Cl,C1=CC(=C(C=C1C2=CC(=CC(=C2Cl)Cl)Cl)Cl)Cl,C12H5Cl5,323.883390,Oily liquids or solids that are colorless to light yellow. ,"",,,"",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
498,T3D0497,2009-03-06 18:58:56 UTC,2009-08-11 15:55:51 UTC,"2,3,3',4,5'-Pentachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 2,3,3',4,5'-pentachloro-","2,3,3',4,5'-Pentachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,70362-41-3,91704,,"","","","",,,"2,3,3',4,5'-Pentachlorobiphenyl",,,,,InChI=1/C12H5Cl5/c13-7-3-6(4-8(14)5-7)9-1-2-10(15)12(17)11(9)16/h1-5H,"1,2,3-trichloro-4-(3,5-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C(=C1C2=CC(=CC(=C2)Cl)Cl)Cl)Cl)Cl,C1=CC(=C(C(=C1C2=CC(=CC(=C2)Cl)Cl)Cl)Cl)Cl,C12H5Cl5,323.883390,Oily liquids or solids that are colorless to light yellow. ,"",,,"",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
499,T3D0498,2009-03-06 18:58:56 UTC,2009-08-11 15:55:51 UTC,"2,3,3',4,6-Pentachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"2,3,3',4,6-Pentachloro-1,1'-biphenyl","2,3,3',4,6-Pentachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,74472-35-8,93440,,"","","",CPD-946,,,"2,3,3',4,6-Pentachlorobiphenyl",,,,,InChI=1/C12H5Cl5/c13-7-3-1-2-6(4-7)10-8(14)5-9(15)11(16)12(10)17/h1-5H,"1,2,3,5-tetrachloro-4-(3-chlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=CC(=C1)Cl)C2=C(C(=C(C=C2Cl)Cl)Cl)Cl,C1=CC(=CC(=C1)Cl)C2=C(C(=C(C=C2Cl)Cl)Cl)Cl,C12H5Cl5,323.883390,Oily liquids or solids that are colorless to light yellow. ,"",,,"",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
500,T3D0499,2009-03-06 18:58:56 UTC,2009-08-11 15:55:52 UTC,"2,3,3',4',6-Pentachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"2,3,3',4',6-Pentachloro-1,1'-biphenyl2,3,3',4',6-PentachlorobiphenylChlorobiphenyl 110","2,3,3',4',6-Pentachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,38380-03-9,38015,,"","","",CPD-946,,C032903,"2,3,3',4',6-Pentachlorobiphenyl",,,,,InChI=1/C12H5Cl5/c13-7-2-1-6(5-10(7)16)11-8(14)3-4-9(15)12(11)17/h1-5H,"1,2,4-trichloro-3-(3,4-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C=C1C2=C(C=CC(=C2Cl)Cl)Cl)Cl)Cl,C1=CC(=C(C=C1C2=C(C=CC(=C2Cl)Cl)Cl)Cl)Cl,C12H5Cl5,323.883390,Oily liquids or solids that are colorless to light yellow. ,"",,,7.31e-06 mg/mL at 25 oC [EPA],,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
501,T3D0500,2009-03-06 18:58:56 UTC,2009-08-11 15:55:52 UTC,"2,3,3',5,5'-Pentachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 2,3,3',5,5'-pentachloro-2,3,3',5,5'-Pentachlorobiphenyl","2,3,3',5,5'-Pentachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,39635-32-0,63091,,"","","","",,,"2,3,3',5,5'-Pentachlorobiphenyl",,,,,InChI=1/C12H5Cl5/c13-7-1-6(2-8(14)3-7)10-4-9(15)5-11(16)12(10)17/h1-5H,"1,2,5-trichloro-3-(3,5-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=C(C=C(C=C1Cl)Cl)C2=CC(=CC(=C2Cl)Cl)Cl,C1=C(C=C(C=C1Cl)Cl)C2=CC(=CC(=C2Cl)Cl)Cl,C12H5Cl5,323.883390,Oily liquids or solids that are colorless to light yellow. ,"",,,"",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data.,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
502,T3D0501,2009-03-06 18:58:56 UTC,2009-08-11 15:55:52 UTC,"2,3,3',5,6-Pentachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 2,3,3',5,6-pentachloro-","2,3,3',5,6-Pentachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,74472-36-9,91719,,"","","","",,,"2,3,3',5,6-Pentachlorobiphenyl",,,,,InChI=1/C12H5Cl5/c13-7-3-1-2-6(4-7)10-11(16)8(14)5-9(15)12(10)17/h1-5H,"1,2,4,5-tetrachloro-3-(3-chlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=CC(=C1)Cl)C2=C(C(=CC(=C2Cl)Cl)Cl)Cl,C1=CC(=CC(=C1)Cl)C2=C(C(=CC(=C2Cl)Cl)Cl)Cl,C12H5Cl5,323.883390,Oily liquids or solids that are colorless to light yellow. ,"",,,"5.67e-06 mg/mL at 25 oC [PATIL,GS (1991)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be inducing the expression of hepatic Phase I and Phase II enzymes, especially of the cytochrome P450 family. Most of the toxic effects of PCBs are believed to be results of Ah receptor binding. Other PBCs are believed to interfere with calcium channels and/or change brain dopamine levels. PCBs can also cause endocrine disurption by altering the production of thyroid hormones and binding to estrogen receptors, which can stimulate the growth of certain cancer cells and produce other estrogenic effects, such as reproductive dysfunction. They will bioaccumulate by binding to receptor proteins such as uteroglobin. (R013, R015, R071, R203)","PCBs are absorbed via inhalation, oral, and dermal routes of exposure. They are trasported in the blood, often bound to albumin. Due to their lipophilic nature they tend to accumulate in lipid-rich tissues, such as the liver, adipose, and skin. Metabolism of PCBs is very slow and varies based on the degree and position of chlorination. PCBs are metabolized by the microsomal monooxygenase system catalyzed by cytochrome P-450 enzymes to polar metabolites that can undergo conjugation with glutathione and glucuronic acid. The major metabolites are hydroxylated products which are excreted in the bile and faeces. The slow metabolism of PCBs means they tend to accumulate in body tissues. (R012, R014)","LD50: 1010 mg/kg (Oral, Rat) (R263) LD50: 880 mg/kg (Intraperitoneal, Mouse) (R263)",No data,"2A, probably carcinogenic to humans. (R264)","PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical devices (such as fluorescent lights and refridgerators) produced before 1977. PCBs may contaminate the air and water near hazardous waste sites. In addition, PCBs bioaccumulate in the environment and may be found in fish, meat, and dairy products. (R012)",Intermediate Oral: 0.03 ug/kg/day (R260),"The most common health effects of PCBs are skin conditions such as chloracne and rashes. Chronic PCB exposure has also been shown to cause liver, stomach and kidney, damage, jaundice, edema, anemia, changes in the immune system, behavioral alterations, and impaired reproduction. (R012)","Chronic PCB exposure results in symptoms such as abdominal pain, nausea, vomiting, diarrhea, headache, dizziness, depression, nervousness, dermal and ocular lesions, fatigue, irregular menstrual cycles and a lowered immune response. (R013)","There are no specific treatments for PCB poisoning, since it is not usually recognized until after substantial chronic exposure. Only preventing further exposure and treating the observed symptons can be done. Acute inhalation can be treated by administering oxygen. (R012)",P20711;P35869;P03372;Q92731;P49888;P07101;P11684
503,T3D0502,2009-03-06 18:58:57 UTC,2009-08-11 15:55:53 UTC,"2,3,3',5',6-Pentachlorobiphenyl",Organic Compound;Coolant;Plasticizer;Polychlorinated Biphenyl;Aromatic Hydrocarbon;Organochloride,"1,1'-Biphenyl, 2,3,3',5',6-pentachloro1,1'-Biphenyl, 2,3,3',5',6-pentachloro-2,3,3',5',6-pentachlorobiphenyl","2,3,3',5',6-Pentachlorobiphenyl is one of 209 polychlorinated biphenyls (PCBs). PCBs are a group of synthetic organic compounds with 1-10 chlorine atoms attached to biphenyl. They were manufactured as commercial mixtures but banned in the 1970's because they were found to bioaccumulate and cause harmful health effects. However, PCBs do not break down readily and are still found in the environment. (R012)",,68194-10-5,63087,,"","","",DIHYDRO-DIOH-BENZOATE,,,"2,3,3',5',6-Pentachlorobiphenyl",,,,,InChI=1/C12H5Cl5/c13-7-3-6(4-8(14)5-7)11-9(15)1-2-10(16)12(11)17/h1-5H,"1,2,4-trichloro-3-(3,5-dichlorophenyl)benzene",http://www.biospider.ca/saved_files/mol/,C1=CC(=C(C(=C1Cl)C2=CC(=CC(=C2)Cl)Cl)Cl)Cl,C1=CC(=C(C(=C1Cl)C2=CC(=CC(=C2)Cl)Cl)Cl)Cl,C12H5Cl5,323.883390,Oily liquids or solids that are colorless to light yellow. ,"",,,"3.66e-06 mg/mL at 25 oC [PATIL,GS (1991)]",,,,"Oral
 Inhalation
 Dermal
 (R012)","Cytochrome P450 1A1 (P04798) 
Cytochrome P450 1A2 (P05177) 
Cytochrome P450 2B6 (P20813) 
Serum albumin (P02768) 
(R012)","The mechanism of action varies with the specific PCB. Dioxin-like PCBs bind to the aryl hydrocarbon receptor, which disrupts cell function by altering the transcription of genes, mainly be induci