Background: 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.
Methods: 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.
Results: 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.
Conclusions: 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.