Although biomarkers have been used for sometime in epidemiology, recent advances in molecular biologic techniques have made it possible to detect biologic changes at low levels of exposure. Biomarkers can be used to identify exposures, effects of those exposures, and populations that may be at increased risk. Measurement of DNA adducts from polycyclic aromatic hydrocarbons, atlatoxint and alkylating agents have been used to monitor exposure to these agents in smokers, workers, and those with environmental exposure. Lipid peroxidation produces high levels of malondialdehyde DNA adducts which are highly mutagenic. Oxidative DNA damage is also present at high levels. Thus, DNA damage from endogenous sources may be an important factor in tumor development. Data on the relationship between DNA damage (or protein damage as a surrogate) and risk for cancer have demonstrated that these assays can predict development of disease in populations exposed to aflatoxin. Genetic susceptibility factors related to ability to metabolize carcinogens influence DNA damage levels and cancer risk. Biomarkers of effect measure mutations (HPRT or glycophorin A) or cytogenetic damage and are useful to help bridge the continuum of exposure to disease. Many of the biomarkers of exposure and early effects are reversible and can be used as tools to monitor reductions in workplace exposure or the efficacy of chemoprevention studies. The rapid expansion of large banks of stored blood samples will make possible nested case-control studies evaluating the relationship between biomarkers and disease risk and gene-environment interactions.
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