Estimations of human risk are generally based on animal studies, and thus require a species-to-species extrapolation. Such data are usually obtained at exposure levels much higher than those ordinarily encountered by humans; consequently, estimates of low-dose risk require a consideration of how the animal dose-response can be extrapolated to lower exposures. Information on mechanisms and rates of DNA repair and on similarities and differences among different cell types and species is important in the development of biologically based extrapolation models for quantitative risk assessment. Such information serves to guide or to provide insight into predicted shapes of dose-response curves at low exposures and how to extrapolate risk across species. The paper will present a conceptual outline for considering how information on DNA damage and repair mechanism may be applicable to the assessment of health risks, particularly those posed by exposure to carcinogens and mutagens.