Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2018 Sep 7;4(3):dvy022.
doi: 10.1093/eep/dvy022. eCollection 2018 Jul.

Impacts of bisphenol A (BPA) and phthalate exposures on epigenetic outcomes in the human placenta

Affiliations

Impacts of bisphenol A (BPA) and phthalate exposures on epigenetic outcomes in the human placenta

Rita S Strakovsky et al. Environ Epigenet. .

Abstract

The placenta guides fetal growth and development. Bisphenol A (BPA) and phthalates are widespread environmental contaminants and endocrine disruptors, and the placental epigenetic response to these chemicals is an area of growing research interest. Therefore, our objective was to summarize research linking BPA or phthalate exposure to placental outcomes in human pregnancies, with a particular focus on epigenetic endpoints. In PubMed, studies were selected for review (without limiting start date and ending on 1 May 2018) if they reported any direct effects of BPA or phthalates on the placenta in humans. Collectively, available studies suggest that BPA and phthalate exposures are associated with changes to placental micro-RNA expression, DNA methylation, and genomic imprinting. Furthermore, several studies suggest that fetal sex may be an important modifier of placental outcomes in response to these chemicals. Studies in humans demonstrate associations of BPA and phthalate exposure with adverse placental outcomes. Moving forward, more studies should consider sex differences (termed "placental sex") in the measured outcomes, and should utilize appropriate statistical approaches to assess modification by fetal sex. Furthermore, more consistent sample collection and molecular outcome assessment paradigms will be indispensable for making progress in the field. These advances, together with improved non-invasive tools for measuring placental function and outcomes across pregnancy, will be critical for understanding the mechanisms driving placental epigenetic disruption in response to BPA and phthalates, and how these disruptions translate into placental and fetal health.

Keywords: BPA; endocrine disrupting chemicals; epigenetics; phthalates; placenta.

PubMed Disclaimer

Similar articles

Cited by

References

    1. Kaufmann P, Black S, Huppertz B.. Endovascular trophoblast invasion: implications for the pathogenesis of intrauterine growth retardation and preeclampsia. Biol Reprod 2003;69:1–7. - PubMed
    1. Desforges M, Sibley CP.. Placental nutrient supply and fetal growth. Int J Dev Biol 2010;54:377–90. - PubMed
    1. Lacroix MC, Guibourdenche J, Frendo JL, Muller F, Evain-Brion D.. Human placental growth hormone – a review. Placenta 2002;23(Suppl A):S87–S94. - PubMed
    1. Newbern D, Freemark M.. Placental hormones and the control of maternal metabolism and fetal growth. Curr Opin Endocrinol Diabetes Obes 2011;18:409–16. - PubMed
    1. Albrecht ED, Pepe GJ.. Estrogen regulation of placental angiogenesis and fetal ovarian development during primate pregnancy. Int J Dev Biol 2010;54:397–408. - PMC - PubMed

LinkOut - more resources