T Sabo Attwood M Ramos Nino and Brooke T Mossman

Environmental carcinogens are broadly defined as compounds that humans are exposed to through diet, lifestyle, infectious agents, and occupation.1 They are considered as nongenetic factors that contribute to cancer risk. A subset of known and reasonably anticipated human carcinogens can be classified as environmental carcinogens and include such compounds as dioxins, metals, components of pesticides, the polyaromatic hydrocarbon (PAH) benzo(a)pyrene (BaP), and mineral fibers such as erionite and asbestos2 (Table 18.1). These contaminants are major constituents of indoor and outdoor air pollution, water, soil, and food products.

Criteria for deciding whether a substance is a carcinogen are constantly being modified as technology and our understanding of carcinogenesis evolve. Definitively linking exposure to environmental contaminants and cancer is difficult because parameters such as dose, duration, composition, and routes of exposure are indeterminate. Currently, the U.S. Environmental Protection Agency (EPA) relies on data from human epidemiologic, animal, and mechanistic studies to classify compounds as carcinogens. Individually, these approaches have limitations, and therefore, these assays should complement each other in defining which compounds have the ability to cause cancer in humans.

One of the major hurdles in assessing the ability of environmental contaminants to cause disease is defining the dose of exposure. Contact with suspected compounds is commonly at low levels over long periods of time. In many cases, the latency period can last decades, masking our ability to realize the cancerous potential of compounds until many people are already sick; this is the case for asbestos-related diseases that have latency periods of greater than 20 to 40 years.3 Thus, a causal link between exposure to asbestos and malignancies was not realized until long after thousands of people were exposed.

Another difficulty in assessing the exposure dose of compounds found in the environment is their ability to bioaccu-mulate in both environmental media and human tissues. Many potential carcinogens have lipophilic properties whereby smaller doses accumulate in human tissues over time.4 Biomagnification through the food chain is also another way small doses of chemicals are amplified. For example, there is increasing concern regarding compounds termed hormonally active agents (HAA) that have the ability to act as natural hormones such as estrogen, androgens, and thyroidal proteins. Although much controversy exists regarding the carcinogenic potential of HAAs, they have been implicated in a variety of reproductive diseases including breast and prostate cancers.5,6 Enough scientific data have convinced the EPA to mandate the testing of all active ingredients of pesticides for endocrine disrupting effects through the Food Quality Protection Act (P.L. 104-170, 1996).

It is also difficult to causally link carcinogenesis to a single compound because environmental contaminants are frequently present as complex mixtures. Interactions of a single compound with other chemicals and elements may greatly increase or decrease the carcinogenic potential to human populations.

As exposure to target compounds can vary greatly among individuals, much of the information available today regarding human cancer risk stems from occupational and accidental exposures. In these situations, information regarding the dose, composition, and duration of the exposure is readily available. A classic example is the industrial accident in Seveso, Italy, where in 1976 an explosion at an industrial plant released large quantities of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) into the air.7 Populations residing in the vicinity of the plant have been studied to try and elucidate the direct effect of TCDD exposure on human health, specifically the development of cancers. Although controversial, evidence from epidemiologic, animal, and mechanistic studies support the National Toxicology Program (NTP) classification of TCDD as a known human carcinogen.8

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