Vascular Responses to Long- and Short-Term Exposure to Fine Particulate Matter: MESA Air (Multi-Ethnic Study of Atherosclerosis and Air Pollution)
Peer Reviewed
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2012/11/20
Details
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Personal Author:Adar SD ; Barr RG ; Herrington DM ; Jorgensen NW ; Kaufman JD ; Krishnan RM ; O'Neill MS ; Polak JF ; Szpiro AA ; Van Hee VC
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Description:Objectives: This study evaluated the association of long- and short-term air pollutant exposures with flow-mediated dilation (FMD) and baseline arterial diameter (BAD) of the brachial artery using ultrasound in a large multicity cohort. Background: Exposures to ambient air pollution, especially long-term exposure to particulate matter <2.5 um in aerodynamic diameter (PM2.5), are linked with cardiovascular mortality. Short-term exposure to PM2.5 has been associated with decreased FMD and vasoconstriction, suggesting that adverse effects of PM2.5 may involve endothelial dysfunction. However, long-term effects of PM2.5 on endothelial dysfunction have not been investigated. Methods: FMD and BAD were measured by brachial artery ultrasound at the initial examination of the Multi-Ethnic Study of Atherosclerosis. Long-term PM2.5 concentrations were estimated for the year 2000 at each participant's residence (n = 3,040) using a spatio-temporal model informed by cohort-specific monitoring. Short-term PM2.5 concentrations were based on daily central-site monitoring in each of the 6 cities. Results: An interquartile increase in long-term PM2.5 concentration (3 ug/m3) was associated with a 0.3% decrease in FMD (95% confidence interval CI of difference: -0.6 to -0.03; p = 0.03), adjusting for demographic characteristics, traditional risk factors, sonographers, and 1/BAD. Women, nonsmokers, younger participants, and those with hypertension seemed to show a greater association of PM2.5 with FMD. FMD was not significantly associated with short-term variation in PM2.5 (-0.1% per 12 ug/m3 daily increase 95% CI: -0.2 to 0.04 on the day before examination). Conclusions: Long-term PM2.5 exposure was significantly associated with decreased endothelial function according to brachial ultrasound results. These findings may elucidate an important pathway linking air pollution and cardiovascular mortality. Description provided by NIOSH
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ISSN:0735-1097
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Volume:60
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Issue:21
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NIOSHTIC Number:nn:20054982
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Citation:J Am Coll Cardiol 2010 Nov; 60(21):2158-2166
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Contact Point Address:Dr. Ranjini M. Krishnan, University of Washington, Box Number 354695, 4225 Roosevelt Way NE, Suite 100, Seattle, Washington 98105
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Email:ranjik@u.washington.edu
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Federal Fiscal Year:2013
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Performing Organization:University of Washington
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Peer Reviewed:True
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Start Date:20050701
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Source Full Name:Journal of the American College of Cardiology
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End Date:20250630
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Main Document Checksum:urn:sha-512:eedc7023f9576fc89c871ffbb75c0d33469506f1a5025783ffb2f2166ebc4ade759f33511a39fb8946364dbb26c6c49cf7dcc59039e71ce61fb9185294d85f5b
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