Effects of prenatal exposure to endocrine disruptors and toxic metals on the fetal epigenome

Abstract

Exposure to environmental contaminants during pregnancy has been linked to adverse outcomes at birth and later in life. The link between prenatal exposures and latent health outcomes suggests that these exposures may result in long-term epigenetic reprogramming. Toxic metals and endocrine disruptors are two major classes of contaminants that are ubiquitously present in the environment and represent threats to human health. In this review, we present evidence that prenatal exposures to these contaminants result in fetal epigenomic changes, including altered global DNA methylation, gene-specific CpG methylation and microRNA expression. Importantly, these changes may have functional cellular consequences, impacting health outcomes later in life. Therefore, these epigenetic changes represent a critical mechanism that warrants further study.

Keywords: DNA methylation; endocrine disruptors; environmental exposure; epigenetics; fetal epigenome; in utero; prenatal; toxic metals.

Figure 1.. Schematic of environmentally-induced fetal epigenomic reprogramming.

Exposure to toxic metals and endocrine disruptors occurring during the prenatal period may result in fetal epigenomic reprogramming. The impacts of exposure on the fetal epigenome depend, in part, on factors such as nutrition and fetal sex. There is evidence that fetal epigenomic reprogramming is associated with altered disease susceptibility and may increase the incidence of adverse health outcomes in exposed populations. Finally, if germ cells are exposed to toxic metals and/or endocrine disruptors and undergo epigenomic reprogramming, multi- and transgenerational effects may be noted following prenatal exposure in the F1.