Arsenic Exposure and Reproductive Toxicity

A number of epidemiological studies have indicated significant associations between maternal exposure to naturally occurring arsenic and adverse pregnancy outcomes, such as increased spontaneous abortion and infant mortality. Recent studies have also reported arsenic-associated male sexual dysfunctions, such as lower sperm quality. Animal studies suggest that a variety of cell types and systems are involved in such dysfunctions as the targets of arsenic. In vivo and in vitro experiments have shown that arsenic exposure causes defects in oocytes or embryos leading to embryonic growth retardation. Vasculogenesis in placentas and steroidogenesis in ovarian follicular cells are also implicated as the targets of arsenic. Animal studies in males have reported lower sperm quality and defects in the testis, epididymis, and Leydig cells, all of which are pivotal in spermatogenesis, are caused by arsenic exposure. Arsenic-induced changes in the levels of sex hormones in males have also been reported. As a background mechanism, an arsenic-induced increase in the levels of reactive oxygen species (ROS) is shared between males and females. In addition to infant adverse outcomes, late- or adult-onset outcomes of gestational arsenic exposure, which are not obvious at birth, are also reported by epidemiological and animal studies. Furthermore, multigenerational effects of gestational arsenic exposure have emerged as concerns.