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Long-Term Ambient Air Pollution Exposures and Circulating and Stimulated Inflammatory Mediators in a Cohort of Midlife Adults
Journal article   Open access   Peer reviewed

Long-Term Ambient Air Pollution Exposures and Circulating and Stimulated Inflammatory Mediators in a Cohort of Midlife Adults

Sheila Tripathy, Anna L. Marsland, Ellen J. Kinnee, Brett J. Tunno, Stephen B. Manuck, Peter J. Gianaros and Jane E. Clougherty
Environmental health perspectives, v 129(5), pp 57007-57007
01 May 2021
PMID: 34014775
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Long-Term Ambient Air Pollution Exposures and Circulating and Stimulated Inflammatory Mediators in a Cohort of Midlife Adults779.58 kBDownloadView
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https://doi.org/10.1289/ehp7089View
Published, Version of Record (VoR)access removed by US government, 1 Dec 2025Open Access (License Unspecified) Restricted
url
https://doi.org/10.1289/EHP7089View
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Abstract

Environmental Sciences Environmental Sciences & Ecology Life Sciences & Biomedicine Public, Environmental & Occupational Health Science & Technology Toxicology
BACKGROUND: Chronic exposure to air pollution may prime the immune system to be reactive, increasing inflammatory responses to immune stimulation and providing a pathway to increased risk for inflammatory diseases, including asthma and cardiovascular disease. Although long-term exposure to ambient air pollution has been associated with increased circulating markers of inflammation, it is unknown whether it also relates to the magnitude of inflammatory response. OBJECTIVES: The aim of this study was to examine associations between chronic ambient pollution exposures and circulating and stimulated levels of inflammatory mediators in a cohort of healthy adults. METHODS: Circulating interleukin (IL)-6,C-reactive protein (CRP) (n = 392), and lipopolysaccharide stimulated production of IL-beta, IL-6, and tumor necrosis factor (TNF)-alpha (n = 379) were measured in the Adult Health and Behavior II cohort. Fine particulate matter [particulate matter with aerodynamic diameter less than or equal to 2.5 mu m (PM2.5)] and constituents [black carbon (BC), and lead (Pb), manganese (Mn), zinc (Zn), and iron (Fe)] were estimated for each residential address using hybrid dispersion land use regression models. Associations between pollutant exposures and inflammatory measures were examined using linear regression; models were adjusted for age, sex, race, education, smoking, body mass index, and month of blood draw. RESULTS: There were no significant correlations between circulating and stimulated measures of inflammation. Significant positive associations were found between exposure to PM2.5 and BC with stimulated production of IL-6, IL-beta, and TNF-alpha. Pb, Mn, Fe, and Zn exposures were positively associated with stimulated production of IL-beta and TNF-alpha. No pollutants were associated with circulating IL-6 or CRP levels. DISCUSSION: Exposure to PM2.5, BC, Pb, Mn, Fe, and Zn was associated with increased production of inflammatory mediators by stimulated immune cells. In contrast, pollutant exposure was not related to circulating markers of inflammation. These results suggest that chronic exposure to some pollutants may prime immune cells to mount larger inflammatory responses, possibly contributing to increased risk for inflammatory disease.

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UN Sustainable Development Goals (SDGs)

This publication has contributed to the advancement of the following goals:

#3 Good Health and Well-Being
#11 Sustainable Cities and Communities

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Collaboration types
Domestic collaboration
Web of Science research areas
Environmental Sciences
Public, Environmental & Occupational Health
Toxicology
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