Environmentally induced epigenetic toxicity: potential public health concerns

Emma L. Marczylo*, Miriam Jacobs, Timothy Gant

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

69 Citations (Scopus)


Throughout our lives, epigenetic processes shape our development and enable us to adapt to a constantly changing environment. Identifying and understanding environmentally induced epigenetic change(s) that may lead to adverse outcomes is vital for protecting public health. This review, therefore, examines the present understanding of epigenetic mechanisms involved in the mammalian life cycle, evaluates the current evidence for environmentally induced epigenetic toxicity in human cohorts and rodent models and highlights the research considerations and implications of this emerging knowledge for public health and regulatory toxicology. Many hundreds of studies have investigated such toxicity, yet relatively few have demonstrated a mechanistic association among specific environmental exposures, epigenetic changes and adverse health outcomes in human epidemiological cohorts and/or rodent models. While this small body of evidence is largely composed of exploratory in vivo high-dose range studies, it does set a precedent for the existence of environmentally induced epigenetic toxicity. Consequently, there is worldwide recognition of this phenomenon, and discussion on how to both guide further scientific research towards a greater mechanistic understanding of environmentally induced epigenetic toxicity in humans, and translate relevant research outcomes into appropriate regulatory policies for effective public health protection.

Original languageEnglish
Pages (from-to)676-700
Number of pages25
JournalCritical Reviews in Toxicology
Issue number8
Publication statusPublished - 13 Sept 2016

Bibliographical note

Publisher Copyright:
© 2016, Crown Copyright 2016. Reproduced with the permission of Public Health England. Published by Informa UK Limited, trading as Taylor & Francis Group.


  • Adverse outcomes
  • DNA methylation
  • environmental exposures
  • epigenetic machinery
  • histone modification
  • human cohorts
  • non-coding RNA
  • rodent models


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