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Association between gaseous air pollutants and inflammatory, hemostatic and lipid markers in a cohort of midlife women.

ABSTRACT: BACKGROUND:Exposures to ambient gaseous pollutants have been linked to cardiovascular diseases (CVDs), but the biological mechanisms remain uncertain. OBJECTIVES:This study examined the changes in CVD marker levels resulting from elevated exposure to ambient gaseous pollutants in midlife women. METHODS:Annual repeated measurements of several inflammatory, hemostatic and lipid makers were obtained from 2306 midlife women enrolled in the longitudinal Study of Women's Health Across the Nation (SWAN) between 1999 and 2004. Ambient carbon monoxide (CO), nitrogen dioxide (NO2), and sulfur dioxide (SO2) data were assigned to each woman based on proximity of the monitoring station to her residential address. Short- and long-term exposures were calculated, and their associations with markers were examined using linear mixed-effects regression models, adjusted for demographic, health and other factors. RESULTS:Short-term CO exposure was associated with increased fibrinogen, i.e., every interquartile increase of average prior one-week exposure to CO was associated with 1.3% (95% CI: 0.6%, 2.0%) increase in fibrinogen. Long-term exposures to NO2 and SO2 were associated with reduced high-density lipoproteins and apolipoprotein A1, e.g., 4.0% (1.7%, 6.3%) and 4.7% (2.8%, 6.6%) decrease per interquartile increment in prior one-year average NO2 concentration, respectively. Fine particle (PM2.5) exposure confounded associations between CO/NO2 and inflammatory/hemostatic markers, while associations with lipoproteins were generally robust to PM2.5 adjustment. CONCLUSIONS:Exposures to these gas pollutants at current ambient levels may increase thrombotic potential and disrupt cholesterol metabolism, contributing to greater risk of CVDs in midlife women. Caution should be exercised in evaluating the confounding by PM2.5 exposure.

SUBMITTER: Wu XM

PROVIDER: S-EPMC5584622 | biostudies-literature | 2017 Oct

REPOSITORIES: biostudies-literature

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Association between gaseous air pollutants and inflammatory, hemostatic and lipid markers in a cohort of midlife women.

Wu Xiangmei May XM Basu Rupa R Malig Brian B Broadwin Rachel R Ebisu Keita K Gold Ellen B EB Qi Lihong L Derby Carol C Green Rochelle S RS

Environment international 20170726

<h4>Background</h4>Exposures to ambient gaseous pollutants have been linked to cardiovascular diseases (CVDs), but the biological mechanisms remain uncertain.<h4>Objectives</h4>This study examined the changes in CVD marker levels resulting from elevated exposure to ambient gaseous pollutants in midlife women.<h4>Methods</h4>Annual repeated measurements of several inflammatory, hemostatic and lipid makers were obtained from 2306 midlife women enrolled in the longitudinal Study of Women's Health A ...[more]

PMID: 28732305

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Project description:BackgroundChronic 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.ObjectivesThe 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.MethodsCirculating interleukin (IL)-6, C-reactive protein (CRP) (n=392), and lipopolysaccharide stimulated production of IL-1β, IL-6, and tumor necrosis factor (TNF)-α (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 μm (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.ResultsThere 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-1β, and TNF-α. Pb, Mn, Fe, and Zn exposures were positively associated with stimulated production of IL-1β and TNF-α. No pollutants were associated with circulating IL-6 or CRP levels.DiscussionExposure 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. https://doi.org/10.1289/EHP7089.

Dataset Information

Association between gaseous air pollutants and inflammatory, hemostatic and lipid markers in a cohort of midlife women.

Publications

Association between gaseous air pollutants and inflammatory, hemostatic and lipid markers in a cohort of midlife women.

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