Epigenomics in environmental health

Our plain-English summary of Epigenomics in environmental health, by B.C. Christensen, C.J. Marsit (Frontiers in Genetics, 2011).

The study

• Authors: B.C. Christensen, C.J. Marsit
• Journal: Frontiers in Genetics
• Published: 2011;2:84
• Cited by: 82 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

This review considers the emerging relationships between environmental factors and epigenetic alterations and the application of genome-wide assessments to better define these relationships. First we will briefly cover epigenetic programming in development, one-carbon metabolism, and exposures that may disrupt normal developmental programming of epigenetic states. In addition, because a large portion of epigenetic research has focused on cancer, we discuss exposures associated with carcinogenesis including asbestos, alcohol, radiation, arsenic, and air pollution. Research on other exposures that may affect epigenetic states such as endocrine disruptors is also described, and we also review the evidence for epigenetic alterations associated with aging that may reflect cumulative effects of exposures. From this evidence, we posit potential mechanisms by which exposures modify epigenetic states, noting that understanding the true effect of environmental exposures on the human epigenome will require additional research with appropriate epidemiologic studies and application of novel technologies. With a more comprehensive understanding of the affects of exposures on the epigenome, including consideration of genetic background, the prediction of the toxic potential of new compounds may be more readily achieved, and may lead to the development of more personalized disease prevention and treatment strategies.

In plain English

This article was a review, not a new study. The authors summarized published research, focusing on human studies, on how environmental exposures may be linked to epigenetic changes. These include DNA methylation (a chemical mark on DNA), changes to histone proteins and changes in microRNA levels, which affect gene activity without changing the DNA sequence. The exposures covered included asbestos, alcohol, arsenic, other metals, air pollution, endocrine disruptors, benzene and radiation, as well as aging. On asbestos, the review cited a report that about 80% of malignant pleural mesothelioma cases report a known asbestos exposure, and stated that asbestos is known to be a weak mutagen. It described earlier studies, including some by these authors, in which asbestos exposure among people with mesothelioma was associated with methylation at certain genes. In one of these, a quantitative measure of asbestos exposure was associated with over 100 DNA sites, and at 94% of those sites higher exposure went with more methylation. The authors also mentioned unpublished observations in pleural tissue. The authors concluded that the ways exposures alter epigenetic marks are not yet understood and require further research.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: review of published research
• Who was studied: Published studies (in vitro, animal and human), with a focus on human studies; no new participants were studied
• Exposure: Exposures linked to cancer, including asbestos, alcohol, radiation, arsenic and air pollution; also other metals, endocrine disruptors, benzene, and aging. No asbestos fiber types are named.
• Main results:
  • Citing Robinson and Lake (2005), the review stated that about 80% of malignant pleural mesothelioma cases report a known asbestos exposure
  • Citing Sugarbaker et al. (2008), the review stated that asbestos is known to be a weak mutagen
  • Citing Tsou et al. (2007): in patients with mesothelioma, self-reported asbestos exposure was significantly associated with methylation at the MT1A and MT2A genes, among 28 genes examined
  • Citing Christensen et al. (2008): an increasing number of methylated cell cycle control genes was significantly associated with a quantitative asbestos burden measure
  • Citing Christensen et al. (2009a): a quantitative measure of asbestos exposure was associated with over 100 CpG sites in mesotheliomas. At 94% of these sites, higher exposure went with increased methylation.
  • The authors described unpublished observations from pleural tissue grouped by asbestos exposure history. Methylation at CpG-island sites decreased with exposure, and methylation at sites outside CpG islands increased with exposure.
• The authors' conclusion: The authors concluded that the mechanisms by which toxicants and the environment change epigenetic marks are not yet clear and require further research, including population-based epidemiologic studies
• Limitations the authors state:
  • The authors noted that the detailed analysis behind the pleural-tissue asbestos observation had not been published

Topics

Medical terms in this study, explained in our Lexicon: Carcinogenesis, Environmental Exposure.

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