Introduction

The most significant endpoint of PAH toxicity is cancer.

PAHs generally have a low degree of acute toxicity to humans. Some studies have shown noncarcinogenic effects that are based on PAH exposure dose [Gupta et al. 1991].

After chronic exposure, the non-carcinogenic effects of PAHs involve primarily the

• pulmonary,
• gastrointestinal,
• renal, and dermatologic systems.

Many PAHs are only slightly mutagenic or even nonmutagenic in vitro; however, their metabolites or derivatives can be potent mutagens.

Carcinogenicity

The carcinogenicity of certain PAHs is well established in laboratory animals. Researchers have reported increased incidences of skin, lung, bladder, liver, and stomach cancers, as well as injection-site sarcomas, in animals. Animal studies show that certain PAHs also can affect the hematopoietic and immune systems and can produce reproductive, neurologic, and developmental effects [Blanton 1986, 1988; Dasgupta and Lahiri 1992; Hahon and Booth 1986; Malmgren et al. 1952; Philips et al. 1973; Szczeklik et al. 1994; Yasuhira 1964; Zhao 1990].

It is difficult to ascribe observed health effects in epidemiological studies to specific PAHs because most exposures are to PAH mixtures.

Increased incidences of lung, skin, and bladder cancers are associated with occupational exposure to PAHs. Epidemiologic reports of PAH-exposed workers have noted increased incidences of skin, lung, bladder, and gastrointestinal cancers. These reports, however, provide only qualitative evidence of the carcinogenic potential of PAHs in humans because of the presence of multiple PAH compounds and other suspected carcinogens. Some of these reports also indicate the lack of quantitative monitoring data [Hammond et al. 1976; Lloyd 1971; Mazumdar 1975; Redmond et al. 1972; Redmond and Strobino 1976].

The earliest human PAH-related epidemiologic study was reported in 1936 by investigators in Japan and England who studied lung cancer mortality among workers in coal carbonization and gasification processes. Subsequent U.S. studies among coke oven workers confirmed an excess of lung cancer mortality, with the suggestion of excessive genitourinary system cancer mortality. Later experimental studies showed that PAHs in soot were probably responsible for the increased incidence of scrotal cancer noted by Percival Pott among London chimney sweeps in his 1775 treatise [Zedeck 1980].

Research

Continued research regarding the mutagenic and carcinogenic effects from chronic exposure to PAHs and metabolites is needed. The following table indicates the carcinogenic classifications of selected PAHs by specific agencies.

Progress Check