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.
Am J Public Health. 2014 Oct;104(10):1816-21. doi: 10.2105/AJPH.2014.302130. Epub 2014 Aug 14.
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.
了解不同疾病易感性需要新的工具来量化环境应激的累积效应。有证据表明,社会、物理和化学应激源可以通过表观遗传修饰的积累来影响疾病。在地理上稳定的表观遗传改变可以为劣势和贫困人群中的健康差异找到合理的机制。特定于邻里的表观遗传标记物与疾病之间的关系将确定医学和环境干预的最适当目标。基因、环境和疾病之间的复杂相互作用需要研究表观遗传变化如何调节对环境应激源的易感性。了解疾病易感性差异方面的进展可能取决于评估环境应激源对遗传基质的累积效应。我们强调了环境应激、表观遗传学和慢性疾病之间界面的关键概念。