The initiation and acceleration of atherosclerosis is hypothesized as a physiologic mechanism underlying associations between air pollution and cardiovascular effects. Despite toxicologic evidence, epidemiologic data are limited.
In this cross-sectional analysis we investigated exposure to fine particulate matter (PM2.5) and residential proximity to major roads in relation to abdominal aortic calcification, a sensitive indicator of systemic atherosclerosis. Aortic calcification was measured by computed tomography among 1147 persons, in 5 US metropolitan areas, enrolled in the Multi-Ethnic Study of Atherosclerosis. The presence and quantity of aortic calcification were modeled using relative risk regression and linear regression, respectively, with adjustment for potential confounders.
We observed a slightly elevated risk of aortic calcification (RR = 1.06; 95% confidence interval = 0.96–1.16) with a 10 μg/m3 contrast in PM2.5. The PM2.5-associated risk of aortic calcification was stronger among participants with long-term residence near a PM2.5 monitor (RR = 1.11; 1.00–1.24) and among participants not recently employed outside the home (RR = 1.10; 1.00–1.22). PM2.5 was not associated with an increase in the quantity of aortic calcification (Agatston score) and no roadway proximity effects were noted. There was indication of PM2.5 effect modification by lipid-lowering medication use, with greater effects among users, and PM2.5 associations were observed most consistently among Hispanics.
Although we did not find persuasive associations across our full study population, associations were stronger among participants with less exposure misclassification. These findings support the hypothesis of a relationship between particulate air pollution and systemic atherosclerosis.
From the aFaculty of Health Sciences, Simon Fraser University, Burnaby, BC, Canada; bDepartment of Family and Preventive Medicine, University of California at San Diego, San Diego, CA; cDepartment of Epidemiology, University of Michigan, Ann Arbor, MI; dDepartments of Medicine and Epidemiology, Columbia University, New York, NY; eDepartment of Radiological Sciences, University of California at Irvine, Irvine, CA; fDepartment of Environmental and Occupational Health Sciences, University of Washington, Seattle, WA; gDepartment of Biostatistics, University of Washington, Seattle, WA; and hDepartment of Cardiology, University of California at Irvine, Irvine, CA.
Submitted 9 February 2008; accepted 27 May 2008; posted 5 January 2009.
Supported by grants N01-HC-95159–N01-HC-95161, N01-HC-95163–N01-HC-95165, and N01-HC-95169 from the National Heart, Lung, and Blood Institute (NHLBI), and grants HL72403 (NHLBI), ES013195 and K24ES013195 (NIEHS), and R830543 and R831697 (US EPA).
Correspondence: Ryan Allen, Simon Fraser University, 8888 University Drive, Burnaby, BC V5A 1S6, Canada. E-mail: email@example.com.