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

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 a...

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Autores principales: Tripathy, Sheila, Marsland, Anna L., Kinnee, Ellen J., Tunno, Brett J., Manuck, Stephen B., Gianaros, Peter J., Clougherty, Jane E.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Environmental Health Perspectives 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8136520/
https://www.ncbi.nlm.nih.gov/pubmed/34014775
http://dx.doi.org/10.1289/EHP7089
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author Tripathy, Sheila
Marsland, Anna L.
Kinnee, Ellen J.
Tunno, Brett J.
Manuck, Stephen B.
Gianaros, Peter J.
Clougherty, Jane E.
author_facet Tripathy, Sheila
Marsland, Anna L.
Kinnee, Ellen J.
Tunno, Brett J.
Manuck, Stephen B.
Gianaros, Peter J.
Clougherty, Jane E.
author_sort Tripathy, Sheila
collection PubMed
description 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) ([Formula: see text]), and lipopolysaccharide stimulated production of [Formula: see text] , IL-6, and tumor necrosis factor [Formula: see text] ([Formula: see text]) 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 μm ([Formula: see text])] 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 [Formula: see text] and BC with stimulated production of IL-6, [Formula: see text] , and [Formula: see text]. Pb, Mn, Fe, and Zn exposures were positively associated with stimulated production of [Formula: see text] and [Formula: see text]. No pollutants were associated with circulating IL-6 or CRP levels. DISCUSSION: Exposure to [Formula: see text] , 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. https://doi.org/10.1289/EHP7089
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spelling pubmed-81365202021-05-21 Long-Term Ambient Air Pollution Exposures and Circulating and Stimulated Inflammatory Mediators in a Cohort of Midlife Adults Tripathy, Sheila Marsland, Anna L. Kinnee, Ellen J. Tunno, Brett J. Manuck, Stephen B. Gianaros, Peter J. Clougherty, Jane E. Environ Health Perspect Research 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) ([Formula: see text]), and lipopolysaccharide stimulated production of [Formula: see text] , IL-6, and tumor necrosis factor [Formula: see text] ([Formula: see text]) 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 μm ([Formula: see text])] 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 [Formula: see text] and BC with stimulated production of IL-6, [Formula: see text] , and [Formula: see text]. Pb, Mn, Fe, and Zn exposures were positively associated with stimulated production of [Formula: see text] and [Formula: see text]. No pollutants were associated with circulating IL-6 or CRP levels. DISCUSSION: Exposure to [Formula: see text] , 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. https://doi.org/10.1289/EHP7089 Environmental Health Perspectives 2021-05-17 /pmc/articles/PMC8136520/ /pubmed/34014775 http://dx.doi.org/10.1289/EHP7089 Text en https://ehp.niehs.nih.gov/about-ehp/licenseEHP is an open-access journal published with support from the National Institute of Environmental Health Sciences, National Institutes of Health. All content is public domain unless otherwise noted.
spellingShingle Research
Tripathy, Sheila
Marsland, Anna L.
Kinnee, Ellen J.
Tunno, Brett J.
Manuck, Stephen B.
Gianaros, Peter J.
Clougherty, Jane E.
Long-Term Ambient Air Pollution Exposures and Circulating and Stimulated Inflammatory Mediators in a Cohort of Midlife Adults
title Long-Term Ambient Air Pollution Exposures and Circulating and Stimulated Inflammatory Mediators in a Cohort of Midlife Adults
title_full Long-Term Ambient Air Pollution Exposures and Circulating and Stimulated Inflammatory Mediators in a Cohort of Midlife Adults
title_fullStr Long-Term Ambient Air Pollution Exposures and Circulating and Stimulated Inflammatory Mediators in a Cohort of Midlife Adults
title_full_unstemmed Long-Term Ambient Air Pollution Exposures and Circulating and Stimulated Inflammatory Mediators in a Cohort of Midlife Adults
title_short Long-Term Ambient Air Pollution Exposures and Circulating and Stimulated Inflammatory Mediators in a Cohort of Midlife Adults
title_sort long-term ambient air pollution exposures and circulating and stimulated inflammatory mediators in a cohort of midlife adults
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8136520/
https://www.ncbi.nlm.nih.gov/pubmed/34014775
http://dx.doi.org/10.1289/EHP7089
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