Molecular and genomic biomarkers of arsenic-induced health hazards: Gene-environment interactions

摘要

Humans are exposed to ingested and inhaled arsenic through the environment, occupation, diet and medicines. Long-term exposure to arsenic causes systemic health hazards including characteristic skin hyperpigmentation or depigmentation, hyperkeratosis in palms and soles, Bowen's disease, circulatory diseases, goiter, diabetes mellitus, cataract, pterygium, neurological disorder, retarded development, and cancers of the skin, lung, urinary bladder, kidney and liver. Many molecular and genomic biomarkers for internal dose and biologically effective dose of exposure, early biological effects, preclinical lesions, and genetic and acquired susceptibility to arsenic-caused diseases have been developed and validated. These biomarkers are useful for the molecular dosimetry of arsenic exposure from various sources, the prediction and early detection of arsenic-induced diseases, the prevention or intervention of development of end-stage diseases caused by arsenic. Variation in individual susceptibility to chronic arsenic poisoning is determined by gene-environment interactions.