Health hazards and susceptibility biomarkers of arsenic in the environment: Gene-environment interactions

摘要

Humans are exposed to arsenic in the environment through ingestion and inhalation. Environmental exposure to arsenic has been well documented to cause multiple health hazards including skin lesions (hyperpigmentation/depigmentation, palmosolar hyperkeratosis, Bowen's disease and skin cancers), blackfoot disease, ischemic heart disease, cerebral infarction, peripheral vascular disease, microvascular diseases, abnormal peripheral microcirculation, carotid atherosclerosis, QT prolongation in electrocardiography, hypertension, goiter, diabetes mellitus, posterior subcapsular lens opacity, pterygium, slow neural conduction, retarded neurobehavioral development, erectile dysfunction, as well as cancers of the lung, kidney, bladder, liver and prostate. Several susceptibility biomarkers, either genetic or acquired, have been reported to modify arsenic-induced health effects. They include arsenic methylation capability, folate and carotenoids intake, and genetic polymorphisms of enzymes involved in xenobiotic metabolism, DNA repair, and oxidative stress. Further exploration of epigenetic changes, gene-environment interactions, and toxicological mechanisms in the development of arsenic-induced heath hazards is in urgent need.