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This chemical does not meet GHS hazard criteria for 18.8% (3 of 16) of reports.

Warning

H371 (75%): May cause damage to organs [Warning Specific target organ toxicity, single exposure]

P260, P264, P270, P308+P316, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 16 reports by companies from 3 notifications to the ECHA C&L Inventory.

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. (L10, L23, A27, A32)

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. (L10)

Found in the mineral pendletonite; A byproduct of hydrocarbon combustion; Used in charge-coupled devices as an ultraviolet phosphor; [Merck Index]

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. (L10)