TY - JOUR
T1 - Early life stress, air pollution, inflammation, and disease
T2 - An integrative review and immunologic model of social-environmental adversity and lifespan health
AU - Olvera Alvarez, Hector A.
AU - Kubzansky, Laura D.
AU - Campen, Matthew J.
AU - Slavich, George M.
N1 - Funding Information:
Preparation of this review was supported by a JPB Environmental Health Fellowship and Grant 5G12MD007592 from the National Institutes on Minority Health and Health Disparities (NIMHD) , a component of the National Institutes of Health (NIH) to Hector Olvera Alvarez; by NIEHS Virtual Consortium for Translational/Transdisciplinary Environmental Research (ViCTER) grant 3R01ES014639-09S1 and grant R01 ES014639 to Matthew Campen; and by a Society in Science—Branco Weiss Fellowship , NARSAD Young Investigator Grant # 23958 from the Brain & Behavior Research Foundation , and NIH grant K08 MH103443 to George Slavich. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.
Publisher Copyright:
© 2018 Elsevier Ltd
PY - 2018/9
Y1 - 2018/9
N2 - Socially disadvantaged individuals are at greater risk for simultaneously being exposed to adverse social and environmental conditions. Although the mechanisms underlying joint effects remain unclear, one hypothesis is that toxic social and environmental exposures have synergistic effects on inflammatory processes that underlie the development of chronic diseases, including cardiovascular disease, diabetes, depression, and certain types of cancer. In the present review, we examine how exposure to two risk factors that commonly occur with social disadvantage—early life stress and air pollution—affect health. Specifically, we identify neuroimmunologic pathways that could link early life stress, inflammation, air pollution, and poor health, and use this information to propose an integrated, multi-level model that describes how these factors may interact and cause health disparity across individuals based on social disadvantage. This model highlights the importance of interdisciplinary research considering multiple exposures across domains and the potential for synergistic, cross-domain effects on health, and may help identify factors that could potentially be targeted to reduce disease risk and improve lifespan health.
AB - Socially disadvantaged individuals are at greater risk for simultaneously being exposed to adverse social and environmental conditions. Although the mechanisms underlying joint effects remain unclear, one hypothesis is that toxic social and environmental exposures have synergistic effects on inflammatory processes that underlie the development of chronic diseases, including cardiovascular disease, diabetes, depression, and certain types of cancer. In the present review, we examine how exposure to two risk factors that commonly occur with social disadvantage—early life stress and air pollution—affect health. Specifically, we identify neuroimmunologic pathways that could link early life stress, inflammation, air pollution, and poor health, and use this information to propose an integrated, multi-level model that describes how these factors may interact and cause health disparity across individuals based on social disadvantage. This model highlights the importance of interdisciplinary research considering multiple exposures across domains and the potential for synergistic, cross-domain effects on health, and may help identify factors that could potentially be targeted to reduce disease risk and improve lifespan health.
KW - Cytokine
KW - Early adversity
KW - Inflammation
KW - Inflammatory reactivity
KW - Pro-inflammatory phenotype
KW - Stress responsivity
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U2 - 10.1016/j.neubiorev.2018.06.002
DO - 10.1016/j.neubiorev.2018.06.002
M3 - Review article
C2 - 29874545
AN - SCOPUS:85048855900
VL - 92
SP - 226
EP - 242
JO - Neuroscience and Biobehavioral Reviews
JF - Neuroscience and Biobehavioral Reviews
SN - 0149-7634
ER -