Non-enzymic activation of polycyclic aromatic hydrocarbons as mutagens

Gibson, Thomas L.; Smart, Vera B.; Smith, Leland L.

doi:10.1016/0027-5107(78)90152-5

Cited by 53 publications

(12 citation statements)

References 5 publications

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“…Photochemical oxidation of a number of PAHs has been reported with the formation of nitrated PAHs, quinones, phenols, and dihydrodiols (Holloway et al 1987;Kamens et al 1986). Some of these breakdown products are mutagenic (Gibson et al 1978). Reaction with ozone or peroxyacetylnitrate yields diones; nitrogen oxide reactions yield intro and dinitro PAHs.…”

Section: Airmentioning

confidence: 99%

The Gulf Oil Spill

2011

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Section: Airmentioning

confidence: 99%

The Gulf Oil Spill

2011

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“…Photochemical oxidation of a number of PAHs has been reported with the formation of nitrated PAHs, quinones, phenols, and dihydrodiols (Holloway et al, 1987;Kamens et al, 1986). Some of these breakdown products are mutagenic (Gibson et al, 1978). Reaction with ozone or peroxyacetylnitrate yields diones; nitrogen oxide reactions yield nitro and dinitro PAHs.…”

Section: Transformation and Degradationmentioning

confidence: 99%

Atsdr Evaluation of Health Effects of Chemicals. Iv. Polycyclic Aromatic Hydrocarbons (PAHs): Understanding a Complex Problem

et al. 1996

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Polycyclic Aromatic Hydrocarbons (PAHs) are a group of chemicals that are formed during the incomplete burning of coal, oil, gas, wood, garbage, or other organic substances, such as tobacco and charbroiled meat. There are more than 100 PAHs. PAHs generally occur as complex mixtures (for example, as part of products such as soot), not as single compounds. PAHs are found throughout the environment in the air, water, and soil. As part of its mandate, the Agency for Toxic Substances and Disease Registry (ATSDR) prepares toxicological profiles on hazardous chemicals, including PAHs (ATSDR, 1995), found at facilities on the Comprehensive Environmental Response, Compensation, and Liability Act (CERCLA) National Priorities List (NPL) and which pose the most significant potential threat to human health, as determined by ATSDR and the Environmental Protection Agency (EPA). These profiles include information on health effects of chemicals from different routes and durations of exposure, their potential for exposure, regulations and advisories, and the adequacy of the existing database. Assessing the health effects of PAHs is a major challenge because environmental exposures to these chemicals are usually to complex mixtures of PAHs with other chemicals. The biological consequences of human exposure to mixtures of PAHs depend on the toxicity, carcinogenic and noncarcinogenic, of the individual components of the mixture, the types of interactions among them, and confounding factors that are not thoroughly understood. Also identified are components of exposure and health effects research needed on PAHs that will allow estimation of realistic human health risks posed by exposures to PAHs. The exposure assessment component of research should focus on (1) development of reliable analytical methods for the determination of bioavailable PAHs following ingestion, (2) estimation of bioavailable PAHs from environmental media, particularly the determination of particle-bound PAHs, (3) data on ambient levels of PAHs metabolites in tissues/fluids of control populations, and (4) the need for a critical evaluation of current levels of PAHs found in environmental media including data from hazardous waste sites. The health effects component should focus on obtaining information on (1) the health effects of mixtures of PAHs particularly their noncarcinogenic effects in humans, and (2) their toxicokinetics. This report provides excerpts from the toxicological profile of PAHs (ATSDR, 1995) that contains more detailed information.

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“…Florin et al (1980) did not detect any mutagenic activity in tester strains TA 98, TA 100, TA 1535 and TA 1537 with and without metabolic activation. Gibson et al (1978) also found no mutagenicity in TA 98, TA 1535 and TA 1537 and TA 1538 after activation by gamma radiation. In contrast, Platt et al (1990) found weak mutagenic activity of picene in TA 100 after metabolic activation as well as tumors in mice after treatment with picene.…”

Section: Ames Fluctuation Test (Mutagenicity)mentioning

confidence: 82%

“…Chrysene was repeatedly found to induce mutagenicity in TA 100 after metabolic activation (Cheung et al, 1993;Florin et al, 1980;Salamone et al, 1979) and Gibson et al (1978) reported mutagenic activity in TA 98 after non-enzymatic activation by gamma radiation. The reports on picene are ambiguous.…”

Section: Ames Fluctuation Test (Mutagenicity)mentioning

confidence: 99%