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Reviews on Environmental Health

Editor-in-Chief: Carpenter, David O. / Sly, Peter

Editorial Board: Brugge, Doug / Edwards, John W. / Field, R.William / Garbisu, Carlos / Hales, Simon / Horowitz, Michal / Lawrence, Roderick / Maibach, H.I. / Shaw, Susan / Tao, Shu / Tchounwou, Paul B.

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Volume 32, Issue 1-2


Impact of nutrition on pollutant toxicity: an update with new insights into epigenetic regulation

Jessie B. Hoffman
  • Superfund Research Center, University of Kentucky, Lexington, KY 40536, USA
  • Department of Pharmacology and Nutritional Sciences, College of Medicine, University of Kentucky, Lexington, KY 40536, USA
  • Other articles by this author:
  • De Gruyter OnlineGoogle Scholar
/ Michael C. Petriello
  • Superfund Research Center, University of Kentucky, Lexington, KY 40536, USA
  • Department of Animal and Food Sciences, College of Agriculture, Food and Environment, University of Kentucky, Lexington, KY 40536, USA
  • Other articles by this author:
  • De Gruyter OnlineGoogle Scholar
/ Bernhard Hennig
  • Corresponding author
  • Department of Animal and Food Sciences, College of Agriculture, Food and Environment, University of Kentucky, Lexington, KY 40536, USA
  • Superfund Research Center, University of Kentucky, 900 S. Limestone Street, Lexington, KY 40536, USA, Tel.: +1 859-218-1343, Fax: +1 859-257-1811
  • Email
  • Other articles by this author:
  • De Gruyter OnlineGoogle Scholar
Published Online: 2017-01-11 | DOI: https://doi.org/10.1515/reveh-2016-0041


Exposure to environmental pollutants is a global health problem and is associated with the development of many chronic diseases, including cardiovascular disease, diabetes and metabolic syndrome. There is a growing body of evidence that nutrition can both positively and negatively modulate the toxic effects of pollutant exposure. Diets high in proinflammatory fats, such as linoleic acid, can exacerbate pollutant toxicity, whereas diets rich in bioactive and anti-inflammatory food components, including omega-3 fatty acids and polyphenols, can attenuate toxicant-associated inflammation. Previously, researchers have elucidated direct mechanisms of nutritional modulation, including alteration of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling, but recently, increased focus has been given to the ways in which nutrition and pollutants affect epigenetics. Nutrition has been demonstrated to modulate epigenetic markers that have been linked either to increased disease risks or to protection against diseases. Overnutrition (i.e. obesity) and undernutrition (i.e. famine) have been observed to alter prenatal epigenetic tags that may increase the risk of offspring developing disease later in life. Conversely, bioactive food components, including curcumin, have been shown to alter epigenetic markers that suppress the activation of NF-κB, thus reducing inflammatory responses. Exposure to pollutants also alters epigenetic markers and may contribute to inflammation and disease. It has been demonstrated that pollutants, via epigenetic modulations, can increase the activation of NF-κB and upregulate microRNAs associated with inflammation, cardiac injury and oxidative damage. Importantly, recent evidence suggests that nutritional components, including epigallocatechin gallate (EGCG), can protect against pollutant-induced inflammation through epigenetic regulation of proinflammatory target genes of NF-κB. Further research is needed to better understand how nutrition can modulate pollutant toxicity through epigenetic regulation. Therefore, the objective of this review is to elucidate the current evidence linking epigenetic changes to pollutant-induced diseases and how this regulation may be modulated by nutrients allowing for the development of future personalized lifestyle interventions.

Keywords: anti-inflammatory nutrients; antioxidant response; environmental pollutants; epigenetics; nutrition


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About the article

Received: 2016-08-09

Accepted: 2016-11-09

Published Online: 2017-01-11

Published in Print: 2017-03-01

Research funding: This work was supported by the National Institute of Environmental Health Sciences at the National Institutes of Health [P42ES007380], and the University of Kentucky Agricultural Experiment Station.

Conflict of interests: The authors declare that there are no competing financial interests.

Citation Information: Reviews on Environmental Health, Volume 32, Issue 1-2, Pages 65–72, ISSN (Online) 2191-0308, ISSN (Print) 0048-7554, DOI: https://doi.org/10.1515/reveh-2016-0041.

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