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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...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Environmental Health Perspectives
2021
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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 |
format | Online Article Text |
id | pubmed-8136520 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Environmental Health Perspectives |
record_format | MEDLINE/PubMed |
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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