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Review
. 2017 Mar;9(3):333-350.
doi: 10.2217/epi-2016-0112. Epub 2017 Feb 17.

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

Affiliations
Review

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

Paige A Bommarito et al. Epigenomics. 2017 Mar.

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.

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Conflict of interest statement

Financial & competing interests disclosure

This research was supported by grants from the National Institute of Environmental Health Sciences (T32ES007018 and P42ES005948). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Figures

<b>Figure 1.</b>
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.

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