Conclusions

Identification and understanding the mechanisms of cancer induction and/or development induced by environmental carcinogens are critical for both cancer prevention and therapeutic approaches. As emphasized at a recent workshop,127 removal or reduction of carcinogens in the environment is the most effective way to reduce future cancer risks. In this regard, clinicians and basic scientists should be advocates in the public health arena.

This chapter illustrates the complexities of action of diverse groups of environmental/occupational carcinogens, but also indicates common modes of action that might be modeled in bioassays using human cells to predict carcino-genicity (Table 18.3); these include assays for DNA damage or repair and carcinogenic adduct formation and assays for activation of key proto-oncogenes or inhibition of tumor suppressor genes. It is important to realize that agents in combination, for example, asbestos and cigarette smoke, may be more carcinogenic than individual agents; thus, modeling and revealing additive or multiplicative risks from mixtures of carcinogens are critical future tasks. Defining gene-environment interactions will also be important in defining genetic predisposition to suspect agents.

A recent volume128 presents the challenges of diagnosis and treatment of occupational cancers to the physician, which include the necessity for thorough patient questionnaires emphasizing smoking habits and working histories. The identity of prototypic cancers, such as mesothelioma, may pinpoint asbestos exposures, but these tumors are difficult to diagnose. A multidisciplinary clinical team is advocated to address genetic factors, diagnosis of tumors, treatment options, and follow-up of patients.

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