Abstract
Has mutation research contributed sufficiently to the genetic risk assessment of chemicals? The answer may be “No”. Although it has contributed much to predict carcinogenicity, how much benefit has exposure prevention of those mutagens brought to public health? It is suggested that the proportion of human carcinogenesis related to environmental chemicals is less than 10%. The main causes for cancer are tobacco smoking, diet, and aging. As genetic toxicologists, we have become too satisfied with a qualitative evaluation of mutation assay results and try to detect as many “carcinogens” as possible. This approach ignores the quantitative evaluation, which is more important in risk assessment. Many “carcinogens”, especially socalled non-genotoxic carcinogens, do not cause cancer at the human exposure level. The “genotoxic non-carcinogens”, if they exist, may be more important because cancer is not the only toxicological outcome of genotoxicity. We should pay more attention to heritable genetic effects of chemicals. An increasing incidence of smoking among young women alerts us to investigate the genetic effects of smoking in their progeny.
The paradigm shift from hazard identification to risk assessment is important in mutation research. In this regard, quantitative, mechanism-based, and humanized mutation assays are required.
