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Polymorphisms of AS3MT influence adverse health effects in adults, but little is known about their role in iAs metabolism in pregnant women and infants.
These associations were strongly dependent upon the male sex of the fetus but independent of fetal genotype for AS3MT. These data highlight a potential sex-dependence of the relationships among maternal genotype, iAs metabolism and infant health outcomes.
Inorganic arsenic iAs is a developmental toxicant that crosses the placenta reaching fetal organs [ 1 — 3 ]. Exposure to iAs during pregnancy has been associated with adverse health and infant outcomes including increased risk of spontaneous abortion, stillbirth, infant mortality, low birth weight, decreased head and chest circumferences, and increased risk of infection in infants [ 4 ].
In addition to being associated with adverse outcomes in early life, prenatal and early childhood exposures to iAs have been associated with higher rates of mortality in adulthood [ 5 ]. There is increasing information that the detrimental health impacts of prenatal iAs exposure are associated not only with levels of exposure to iAs but also its biotransformation.
In humans, ingested iAs is biotransformed via multiple consecutive methylation steps into the methylated metabolites, monomethyl-arsenic MMAs and dimethyl-arsenic DMAs , a process that has been described as enhancing removal and thus decreasing the overall toxicity of arsenic [ 6 ]. Both inorganic and methylated arsenicals have been detected in trivalent As III and pentavalent As V oxidation states in the urine of subjects chronically exposed to arsenic [ 6 , 7 ].