Multiple factors in carcinogenesis were discussed. The historical background in which the multifactorial nature of occupational cancer was recognized was outlined. Multiple host factors affecting carcinogens were considered. Genetic factors such as enzymes, immune defenses, and hormonal imbalances were described. Aryl- hydrocarbon-hydroxylase (AHH) an enzyme that metabolizes benzo(a)pyrene (50328) and other polycyclic aromatic hydrocarbons was mentioned as an example of a genetic factor. Clinical and in- vivo studies have shown that higher inducible levels of AHH activity are associated with an increased susceptibility to lung cancer. Lifestyle factors that may modify the susceptibility of the host to carcinogens such as smoking, diet, and environmental exposures were discussed. Epidemiological studies have indicated that smoking increases the incidence of lung cancer in asbestos workers and uranium miners. A study in rats found that high dietary intake of riboflavin decreased the carcinogenic activity of 4- dimethylaminoazobenzene (60117). The influence of health status factors such as prior exposure to industrial chemicals, medication use, aging, and infections on host risk factors was discussed. The roles of physical and occupational agents in occupational cancer was considered. Cocarcinogens and their influence on chemical carcinogenesis were discussed. It was noted that certain agents that are noncarcinogenic or weakly carcinogenic may, when combined with carcinogens, increase the yield of tumors and their rate of appearance. The effects of benzo(a)pyrene on sulfur-dioxide (7446095) and benz(a)anthracene (56553) were cited as examples. The carcinogenicity of complex mixtures such as petroleum, coal-tar, and shale-oil was discussed. The authors conclude that because of the multiplicity of factors involved in carcinogenesis, causal relationships and correlations may be difficult to define conclusively. A negative result in an epidemiological evaluation does not always mean that an agent is noncarcinogenic. Risk assessments of low concentrations or weak carcinogens are very difficult. At present the philosophy of setting standards for exposure to carcinogens should be that there is no safe level.