DNA methylation: A mechanism linking environmental chemical exposures to risk of autism spectrum disorders?

Kimberly P. Keil, Pamela J. Lein

Research output: Contribution to journalReview articlepeer-review

Abstract

There is now compelling evidence that gene by environment interactions are important in the etiology of autism spectrum disorders (ASDs). However, the mechanisms by which environmental factors interact with genetic susceptibilities to confer individual risk for ASD remain a significant knowledge gap in the field. The epigenome, and in particular DNA methylation, is a critical gene expression regulatory mechanism in normal and pathogenic brain development. DNA methylation can be influenced by environmental factors such as diet, hormones, stress, drugs, or exposure to environmental chemicals, suggesting that environmental factors may contribute to adverse neurodevelopmental outcomes of relevance to ASD via effects on DNA methylation in the developing brain. In this review, we describe epidemiological and experimental evidence implicating altered DNA methylation as a potential mechanism by which environmental chemicals confer risk for ASD, using polychlorinated biphenyls (PCBs), lead, and bisphenol A (BPA) as examples. Understanding how environmental chemical exposures influence DNA methylation and how these epigenetic changes modulate the risk and/or severity of ASD will not only provide mechanistic insight regarding gene-environment interactions of relevance to ASD but may also suggest potential intervention strategies for these and potentially other neurodevelopmental disorders.

Original languageEnglish (US)
JournalEnvironmental Epigenetics
Volume2
Issue number1
DOIs
StatePublished - Jan 1 2016

Keywords

  • autism
  • bisphenol A
  • epigenetics
  • lead
  • neurodevelopment
  • PCBs

ASJC Scopus subject areas

  • Genetics
  • Molecular Biology
  • Health, Toxicology and Mutagenesis
  • Genetics(clinical)

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