The impact of prenatal insults on the human placental epigenome: A systematic review

Neurotoxicol Teratol. 2018 Mar-Apr:66:80-93. doi: 10.1016/j.ntt.2018.01.001. Epub 2018 Jan 4.

Abstract

The placenta is the first human organ to reach full development during pregnancy. It serves as a barrier but also as an interchange surface. Epigenetic changes observed in placental tissue may reflect intrauterine insults while also pointing to physiological pathways altered under exposure to such environmental threats. By means of a systematic search of the literature, 39 papers assessing human placental epigenetic signatures in association with either (i) psychosocial stress, (ii) maternal psychopathology, (iii) maternal smoking during pregnancy, and (iv) exposure to environmental pollutants, were identified. Their findings revealed placental tissue as a unique source of epigenetic variability that does not correlate with epigenetic patterns observed in maternal or newborn blood, tissues which are typically analyzed regarding prenatal stress. Studies regarding prenatal stress and psychopathology during pregnancy were scarce and exploratory in nature revealing inconsistent findings. Of note, there was a marked tendency towards placental hypomethylation in studies assessing either tobacco use during pregnancy or exposure to environmental pollutants suggesting the interaction between contaminant-derived metabolites and epigenetic machinery. This review highlights the need for further prospective longitudinal studies assessing long-term health effects of placental epigenetic signatures derived from exposure to several prenatal stressors.

Keywords: Environmental pollutants; Epigenetics; Maternal smoking during pregnancy; Placenta; Prenatal stress.

Publication types

  • Research Support, Non-U.S. Gov't
  • Systematic Review

MeSH terms

  • Animals
  • DNA Methylation / drug effects*
  • Environmental Pollutants / toxicity*
  • Epigenesis, Genetic / drug effects*
  • Female
  • Humans
  • Placenta / metabolism*
  • Pregnancy
  • Prenatal Exposure Delayed Effects / chemically induced
  • Prenatal Exposure Delayed Effects / genetics*
  • Prenatal Exposure Delayed Effects / metabolism
  • Smoking / adverse effects*

Substances

  • Environmental Pollutants