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INTRODUCTION <br />Several polycyclic aromatic hydrocarbons (PAHs) are among the most potent <br />carcinogens known to exist, producing tumors in some organisms through single <br />exposures to microgram quantities. PAHs act at both the site of application <br />and at organs distant to the site of absorption; their effects have been <br />demonstrated in nearly every tissue and species tested, regardless of the <br />route of administration (Lee and Grant 1981). The evidence implicating PAHs <br />as an inducer of cancerous and precancerous lesions is becoming overwhelming, <br />and this class of substances is probably a major contributor to the recent <br />increase in cancer rates reported for industrialized nations (Cooke and Dennis <br />1984). PAHs were the first compounds known to be associated with <br />carcinogenesis (Lee and Grant 1981). Occupational skin cancer was first <br />documented in London chimney sweeps in 1775 and in German coal tar workers in <br />the late 1800's. By the early 1900's, soot, coal tar, and pitch were all <br />found to be carcinogenic to humans. By 1918, it was shown that topical <br />applications of coal tar produced skin tumors in mice and rabbits; <br />benzo(a)pyrene, a PAH, was identified as one of the most carcinogenic <br />compounds in coal tar (Dipple 1985). The carcinogenic activity to man of <br />soots, tars, and oils is beyond dispute. In addition to the skin cancers <br />noted initially, higher 'incidences of respiratory tract and upper <br />gastrointestinal tract tumors were associated with occupational exposures to <br />these carcinogens (Dipple 1985). PAH-induced cancers in laboratory animals is <br />well documented. Benzo(a)pyrene, for example, has produced tumors in mice, <br />rats, hamsters, guinea pigs, rabbits, ducks, and monkeys following <br />administration by oral, dermal, and intraperitoneal routes (Pucknat 1981). <br />Teratogenic or carcinogenic responses have been induced in sponges, <br />planarians, echinoderm larvae, teleosts, amphibians, and plants by exposure to <br />carcinogenic PAHs (Neff 1979, 1982b). An unusually high prevalence of oral, <br />dermal, and hepatic neoplasms have been observed in bottom-dwelling fish from <br />polluted sediments containing grossly-elevated PAH levels (Couch and <br />Harshbarger 1985). PAH compounds have damaged chromosomes in cytogenetic <br />tests, have produced mutations in mammalian cell culture systems, and have <br />induced DNA repair synthesis in human fibroblast cultures (EPA 1980). While <br />some PAHs are potent mutagens and carcinogens, others are less active or <br />suspected carcinogens. Some, especially those of biological origin, are <br />probably not carcinogens (Jackim and Lake 1978). Certain lower molecular <br />weight, noncarcinogenic PAHs, at environmentally realistic levels, were <br />acutely toxic to aquatic organisms, or produced deleterious sublethal