domingo, 12 de octubre de 2014

American Public Health Association - Epigenome: Biosensor of Cumulative Exposure to Chemical and Nonchemical Stressors Related to Environmental Justice

American Public Health Association - Epigenome: Biosensor of Cumulative Exposure to Chemical and Nonchemical Stressors Related to Environmental Justice

American Public Health Association





Accepted on: Jun 13, 2014

Epigenome: Biosensor of Cumulative Exposure to Chemical and Nonchemical Stressors Related to Environmental Justice

Kenneth OldenPhD, ScDYu-Sheng LinScDDavid GruberPhD, and Babasaheb SonawanePhD

Kenneth Olden, Yu-Sheng Lin, and Babasaheb Sonawane are with National Center for Environmental Assessment, Office of Research and Development, US Environmental Protection Agency, Washington, DC. David Gruber is with Department of Natural Sciences, Baruch College, City University of New York, New York, NY.
Correspondence should be sent to Kenneth Olden, PhD, ScD, National Center for Environmental Assessment, Office of Research and Development, US Environmental Protection Agency, Washington, DC 20460 (e-mail: ). Reprints can be ordered athttp://www.ajph.org by clicking the “Reprints” link.
Note. The findings and conclusions in this article are those of the authors and do not necessarily represent the views of the US Environmental Protection Agency.
Contributors
K. Olden conceptualized and supervised the work. Y.-S. Lin, D. Gruber, and B. Sonawane conducted a systematic literature review and co-wrote the article.
Peer Reviewed


ABSTRACT
Understanding differential disease susceptibility requires new tools to quantify the cumulative effects of environmental stress. Evidence suggests that social, physical, and chemical stressors can influence disease through the accumulation of epigenetic modifications.
Geographically stable epigenetic alterations could identify plausible mechanisms for health disparities among the disadvantaged and poor. Relations between neighborhood-specific epigenetic markers and disease would identify the most appropriate targets for medical and environmental intervention. Complex interactions among genes, the environment, and disease require the examination of how epigenetic changes regulate susceptibility to environmental stressors. Progress in understanding disparities in disease susceptibility may depend on assessing the cumulative effect of environmental stressors on genetic substrates.
We highlight key concepts regarding the interface between environmental stress, epigenetics, and chronic disease.

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