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Environmental epigenetics: prospects for studying epigenetic mediation of exposure–response relationships

Victoria K. Cortessis, Duncan C. Thomas, A. Joan Levine, Carrie V. Breton, Thomas M. Mack, Kimberly D. Siegmund, Robert W. Haile, Peter W. Laird

Human Genetics · 2012 · ▲ 314 citations

Abstract

Changes in epigenetic marks such as DNA methylation and histone acetylation are associated with a broad range of disease traits, including cancer, asthma, metabolic disorders, and various reproductive conditions. It seems plausible that changes in epigenetic state may be induced by environmental exposures such as malnutrition, tobacco smoke, air pollutants, metals, organic chemicals, other sources of oxidative stress, and the microbiome, particularly if the exposure occurs during key periods of development. Thus, epigenetic changes could represent an important pathway by which environmental factors influence disease risks, both within individuals and across generations. We discuss some of the challenges in studying epigenetic mediation of pathogenesis and describe some unique opportunities for exploring these phenomena.

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OpenAlex
DOI
10.1007/s00439-012-1189-8
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2026-06-09 MST

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APA
Cortessis, V.K., Thomas, D.C., Levine, A.J., Breton, C.V., Mack, T.M., Siegmund, K.D., Haile, R.W., &amp; Laird, P.W. (2012). Environmental epigenetics: prospects for studying epigenetic mediation of exposure–response relationships. <em>Human Genetics</em>. https://doi.org/10.1007/s00439-012-1189-8
Vancouver
Cortessis VK, Thomas DC, Levine AJ, Breton CV, Mack TM, Siegmund KD, et al. Environmental epigenetics: prospects for studying epigenetic mediation of exposure–response relationships. Human Genetics. 2012. doi:10.1007/s00439-012-1189-8.
BibTeX
@article{victoria2012Enviro, title = {Environmental epigenetics: prospects for studying epigenetic mediation of exposure–response relationships}, author = {Victoria K. Cortessis and Duncan C. Thomas and A. Joan Levine and Carrie V. Breton and Thomas M. Mack and Kimberly D. Siegmund and Robert W. Haile and Peter W. Laird}, journal = {Human Genetics}, year = {2012}, doi = {10.1007/s00439-012-1189-8}, }

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