Environmental toxicants--induced epigenetic alterations and their reversers

J Environ Sci Health C Environ Carcinog Ecotoxicol Rev. 2012;30(4):323-67. doi: 10.1080/10590501.2012.731959.


Epigenetics has been emphasized in the postgenome era to clarify obscure health risks of environmental toxicants including endocrine disrupting chemicals (EDCs). In addition, mixed exposure in real life can modify health consequences of the toxicants. Particularly, some nutritional and dietary materials modify individual susceptibility through changes in the epigenome. Therefore, we focused on some environmental toxicants that induce epigenetic alterations, and introduced chemopreventive materials to reverse the toxicants-induced epigenetic alterations. Methodologically, we used global and specific DNA methylation as epigenetic end points and searched epigenetic modulators in food. We reviewed various epigenetic end points induced by environmental toxicants including alcohol, asbestos, nanomaterials, benzene, EDCs, metals, and ionizing radiation. The epigenetic end points can be summarized into global hypomethylation and specific hypermethylation at diverse tumor suppress genes. Exposure timing, dose, sex, or organ specificity should be considered to use the epigenetic end points as biomarkers for exposure to the epimutagenic toxicants. Particularly, neonatal exposure to the epimutagens can influence their future adult health because of characteristics of the epimutagens, which disrupt epigenetic regulation in imprinting, organogenesis, development, etc. Considering interaction between epimutagenic toxicants and their reversers in food, we suggest that multiple exposures to them can alleviate or mask epigenetic toxicity in real life. Our present review provides useful information to find new end points of environmental toxicants and to prevention from environment-related diseases.

Publication types

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

MeSH terms

  • Animals
  • Antimutagenic Agents / therapeutic use*
  • Biomarkers / analysis
  • DNA Methylation / drug effects
  • DNA Methylation / radiation effects
  • Environmental Exposure*
  • Environmental Pollutants / toxicity
  • Epigenesis, Genetic / drug effects*
  • Epigenesis, Genetic / radiation effects*
  • Genes, Tumor Suppressor / drug effects
  • Genes, Tumor Suppressor / radiation effects
  • Humans
  • Mice
  • Mutagens / toxicity*
  • Radiation Injuries*
  • Radiation, Ionizing*
  • Rats


  • Antimutagenic Agents
  • Biomarkers
  • Environmental Pollutants
  • Mutagens