Hannukesela-Svahn et al. (1999) analyzed basal-cell carcinomas and other nonmelanoma skin cancers assembled in the Finnish Cancer Registry over 4 decades by linking to subjects’ stated occupations in the 1970 census. For “transportation and communication” (a nonspecific, self-reported occupation code at a single time), the estimated risk of basal-cell carcinoma among men was 1.0 (95% CI 1.0–1.1), which suggests that the risk was not increased. There were only about 15% as many cases of the other types of nonmelanoma skin cancers (predominantly squamous-cell carcinomas) as there were cases of basal-cell carcinoma, so the confidence intervals associated with the estimated risks were wider; the estimated risk in men was slightly below unity, that in women somewhat above.
As discussed above in connection with exposures to fuels, Kubasiewicz et al. (1991) presented an analysis of occupational exposure of 376 skin-cancer subjects (primarily with basal-cell carcinoma) and their 752 population and 752 hospital controls to PAHs. Full work histories had been gathered, but exposure to PAHs was determined on the basis of self-reported exposure to each of 17 possible sources of PAHs. The cases were compared independently (apparently without adjustment beyond matching on age) with both the population and hospital controls, and the results were virtually identical (the statistics related to the population controls are reported here). There was a slight increase in risk in those who had ever been exposed to any of the sources of PAHs (OR 1.15, 95% CI 0.90–1.51; 95% CI calculated with standard methods from the observed and expected numbers presented in the original paper), but there was no indication of a dose-response relationship with duration of exposure.
In the case-control study of squamous-cell carcinoma and basal-cell carcinoma from the Alberta Cancer Registry, Gallagher et al. (1996) presented the results related to several potentially PAH-containing exposures (determined by self-report) in addition to the fuel-related exposure reported above. After adjustment for age, pigmentation, ethnicity, and exposure to sunlight, but not smoking, the risk of squamous-cell carcinoma after exposure to diesel fumes was increased (OR 1.7, 95% CI 1.1–2.5). For basal-cell carcinoma, only a modestly increased PAH-related risk was seen after exposure to diesel fumes (OR 1.1, 95% CI 0.8–1.6).
The committee recognizes that PAHs (present in soot and numerous similar complex mixtures, mostly originating from combustion processes) have long been accepted to be skin carcinogens in animals and humans (ATSDR 1995; IARC 1985). IARC limited the scope of its consideration to chimney soot, so the subjects of the studies on which its conclusions were based were all chimney sweeps. Similarly, the epidemiologic bases of the Agency for Toxic Substances and Disease Registry (ATSDR) conclusions were shale-oil workers and chimney sweeps. As explained in Chapter 2, in planning its approach to its task, the committee considered those types of exposure as too dissimilar to the exposure scenarios in the Persian Gulf to base its conclusions on combustion products and nonmelanoma skin cancers on the conclusions of IARC and ATSDR.
Dermal application of individual PAHs to animals has been shown to lead to skin tumors in a number of studies. Mechanistic studies have demonstrated that some PAHs are genotoxic and can act as initiators, promoters, and complete carcinogens. Despite strong evidence that PAHs are carcinogenic in animal models and that they are genotoxic, the committee used