Commentary. Concluding remarks on Session II

The assessment of human cancer risk from exposure to chemicals in aquatic environments includes understanding such factors as chemical inputs, bioaccumulation, metabolism, foodchain transfer and biological effects. The estimation of the risk to humans is dependent on being able to evaluate the net effect of these complementary parameters on human populations, recognizing that humans are ultimately affected by chemical changes that have occurred in the aquatic environment. The task we face is obviously profoundly difficult. It is particularly so because almost all aquatic environments are comprised of complex mixtures of chemicals that can act synergistically or antagonistically to produce a given effect. These effects can range from subtle biochemical changes to alterations in behavior. However, exactly how these events relate to cancer, per se, is shrouded in mystery. The difficult task ofhuman risk assessment is exacerbated by large gaps in knowledge embracing virtually every area necessary for the attainment of validjudgments. Chemical inputs are only partially understood, as is the actual chemical composition of sediments and tissues. While we often operate on the assumption that these matrices from urban areas are composed of simple suites ofchemicals, such as certain metals, PCBs, and aromatic hydrocarbons, we know that this is not actually true. Scores ofother contaminants cannot simply be dismissed as influencing toxicity just because we do not or cannot analyze for them. Neither can we assume (as we sometimes do) that an individual compound that fascinates us scientifically, or otherwise catches our attention, is necessarily singularly important in the manifestation of toxic effects. Benzo(a)pyrene, for example, is an interesting model. It has been studied extensively, but are BaP and its metabolites especially important in assessing toxicity in the presence of scores of other environmentally derived compounds in tissues? One suspects not, but there is little information upon which to base an argument either way. Further, how reasonable is it to dismiss the contributions of agents, such as free radicals arising from environmental chemicals, in the induction ofcancer? Such compounds may be necrogenic, for example, and thus play a major role in cell proliferation. Free radicals are only one example in this context scores of other chemicals present in sediments and tissues of aquatic species are potential candidates for influencing (e.g., promoting) the effects of carcinogenic chemicals. So where do we stand in our attempts to relate the contamina-