Abstract
Current risk assessment practices and toxicity information are hard to utilize for assessing the health impact of combined or cumulative exposure to multiple chemical and non-chemical stressors encountered in the “real world” environment. Non-chemical stressors such as heat, radiation, noise, humidity, bacterial and viral agents, and social factors, like stress related to violence and socioeconomic position generally cannot be currently incorporated into the risk assessment paradigm. The Science and Decisions report released by the National Research Council (NRC) in 2009 emphasized the need to characterize the effects of multiple stressors, both chemical and non-chemical exposures. One impediment to developing information relating such non-chemical stressors to health effects and incorporating them into cumulative assessment has been the lack of analytical tools to easily and quantitatively monitor the cumulative exposure to combined effects of stressors over the life course.
Highlights
Progress in environmental health research has greatly expanded our understanding of the role of the environment in human health and disease
There is broad consensus that where people live and work makes a difference in their health; that is, neighborhood characteristics or place matters for human health and disease
Some markers, such as changes in the methylation of certain genes (e.g., AHRR) reflect exposures early in life and persist long into later life [23,44]. Other markers, such as histone modifications or the expressions of noncoding RNA, seem to be more transient. While this complicates the formation of broad generalizations about epigenetic changes, it creates opportunities for investigators to study the effects of all different types of epigenetic modifications, and by doing so, obtain information about likely exposures at different times and life stages—some indicating whether exposures occurred or not in early life exposures, some indicating there have been recent exposures, and some perhaps increasing in their degree of change as concentration and duration increases [45]
Summary
Progress in environmental health research has greatly expanded our understanding of the role of the environment in human health and disease. Olden et al (2011, 2014) [17,19] earlier suggested that advantaged and disadvantaged neighborhoods differentially “imprint” the epigenome, and these durable modifications can be detected as an exposure signature in population studies to assess cumulative impact of lifetime exposures The objective of this commentary is to explore the plausibility that environment-induced epigenetic signatures can be used as a biomarker to assess the combined or cumulative exposure to multiple chemical and non-chemical stressors over the life course. It was found that several loci in both blood and buccal cell samples, repeatedly collected from the same individuals (age 14–62 years old) over a period of up to 20 years, generally remain stable [39] Some markers, such as changes in the methylation of certain genes (e.g., AHRR) reflect exposures early in life and persist long into later life (e.g., infants exposed to second-hand smoking) [23,44]. While this complicates the formation of broad generalizations about epigenetic changes, it creates opportunities for investigators to study the effects of all different types of epigenetic modifications, and by doing so, obtain information about likely exposures at different times and life stages—some indicating whether exposures occurred or not in early life exposures, some indicating there have been recent exposures, and some perhaps increasing in their degree of change as concentration and duration increases (as epidemiologists often phrase “cumulative exposure” discussing a single factor over time) [45]
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