Abstract
Polymorphisms in metabolism and DNA-repair genes can increase the risks of cancer associated with exposure to chemical and physical agents in the environment. These types of gene-environment interactions may alter our view of dose–response patterns and how to characterize risk in an exposed population. Depending upon the action of the different forms of these genes, differing patterns of dose–response may be seen in a study population and these patterns can effect our interpretation of the degree of hazard as well as the risk in the general population. This short report describes some of the key issues associated with how variation in genetic make-up can result in different dose–response patterns for cancer following exposure to environmental agents.
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