Abstract

DETECTION AND CHARACTERIZATION OF RISK FACTORS It is generally acknowledged that environmental factors play a significant role in the causation of cancer (4-9, 19). In principle, therefore, cancer should be preventable to the extent that its causal factors can be identified and either removed from the environment or counteracted (1,4,5,7-9,11,13,14,16-18,20). Recognition of this possibility, in the face of the rising incidence of cancer, challenges us to intensify our efforts to identify the causal factors, to clarify their mechanisms of action, and to formulate appropriate countermeasures. Growing public demand for such efforts is reflected in the recent legislation reauthorizing the U.S. National Cancer Program, which increased the priority given to activities for cancer prevention. Strategies for the detection of carcinogenic risk factors comprise a spectrum of epidemiological and experimental approaches (5,9,12,16,20). Altogether these approaches have thus far implicated some dozens of exogenous agents or exposure conditions as being carcinogenic for humans and some hundreds as carcinogenic for experimental animals (12,15). included are various lifestyle factors (such as ultraviolet radiation, tobacco, and alcohol), dietary factors (such as aflatoxin, safrole, and bracken fern), drugs (such as diethylstibestrol and chlornaphazine), and occupational factors (such as ionizing radiation, vinyl chloride, and asbestos). Also relevant are various preneoplastic conditions predisposing to the development of cancer, such as familial polyposis of the colon, xeroderma pigmentosum, Down’s disease, Fanconi’s anemia, atrophic gastritis, and leukoplakia (Table 1). While proof that a given agent causes cancer in man rests on epidemiologic evidence demonstrating carcinogenic effects in humans themselves, extrapolation from effects in animals can serve to prevent new carcinogens from entering the environment and to prevent continued exposure of humans to otherwise unsuspected risks. Hence, it is the combined use of epidemiologic and laboratory studies, complementing and reinforcing each other, that provides the best foundation for a successful cancer prevention program. Since human beings are exposed throughout life to myriad substances in small amounts and in complex and changing combinations, it is likely that the cancer incidence patterns characteristic for different cultures reflect the interactive effects of prolonged low-level exposure to a multiplicity of carcinogens, cocarcino-

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