Industrial Chemicals and Occupational Cancers

The chemicals and industrial processes that have a known or suspected etiologic role in the development of cancer are listed in Table 3-6. As noted above, about 2%-5% of all cancer deaths are attributed to occupational hazards. Of those agents listed as carcinogenic for humans, a number were identified because of their close association between an abnormal clustering of certain cancers and exposure to an industrial chemical or process. For example, epidemiologic studies of workers occupationally exposed to industrial levels of 4-aminobiphenyl have a higher incidence of bladder cancer.80 Occupational exposure to asbestos fibers results in a higher incidence of lung cancer, mesotheliomas, gastrointestinal tract cancers, and laryngeal cancers.81 As mentioned earlier, cigarette smoking and occupational exposure to asbestos act synergistically to increase the incidence of lung cancer. Several epidemiologic studies have shown increased frequency of leukemia in workers exposed to benzene.81-83 Two studies of workers exposed to bis(chlorome-thyl) ether have indicated an increased risk of lung cancer, primarily small-cell carcinoma.81 There is also an increased risk of lung cancer among workers in chromium industries. Occupational exposure to 2-naphthylamine has long been known to be associated with urinary bladder cancer.81 Since the time of Percival Pott and his study of chimney sweeps (see Chapter 2), coal soot has been known as a cause of skin cancer. Since that time, occupational exposure to soot, coal tar, pitch, coal fumes, and some crude shale and cutting oils has been shown to be associated with cancers of the skin, lung, bladder, and gastrointestinal tract. The carcinogenicity of these latter agents is probably related to their content of polycyclic aromatic hydrocarbons (PAH).

The highest levels of human exposure to PAH occur in industrial processes involving the use of coal tar and pitch and in the production of coke from coke ovens.84 Epidemiological data indicate that ambient coal tar and pitch in iron and steel foundries contains carcinogenic substances and may lead to an increased incidence of lung cancer, particularly in smokers who work in such environments. A study by van Schooten et al.84 showed that coke-oven workers were exposed to substantial concentrations of PAH in the air, including benzo[a]pyrene and pyrene. Forty-seven percent had detectable levels of PAH-DNA adducts in their white blood cells, compared to 30% of control subjects who worked in another part of the plant. In both groups, smokers had significantly higher levels of PAH adducts than nonsmokers. Since the carcinogenic mechanisms of PAH involves metabolic activation and alteration of DNA function (see Chapter 2), these data suggest that exposure to various carcinogens and/or susceptibility to their DNA-damaging effects could be monitored by measuring DNA-adduct formation in peripheral white blood cells or perhaps in urine, if sensitive and specific enough assays could be developed. It should be noted that such measurements would be subject to individual variations relating to variation in daily exposure levels, genetic differences in metabolic activation of PAH and DNA repair mechanisms, smoking habits, amount of air pollution with PAH in the place of residence, and amount of PAH in the drinking water and diet.

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