Exposure to ambient air pollution as a potential explanation of ethnic disparities in atherosclerosis severity and progression
Jones, Miranda Renee
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Disparities in atherosclerosis and other cardiovascular outcomes by race/ethnicity persist in the United States even after accounting for clinical risk factors. Exposure to ambient air pollution, which is associated with increased risk for subclinical and clinical cardiovascular disease, is markedly different by race/ethnicity. However, the contribution of air pollution exposure to racial/ethnic differences in atherosclerosis has not been evaluated. The objective of this dissertation was to investigate the role of exposure to ambient air pollution, measured by household-level concentrations of fine particulate matter (PM2.5) and oxides of nitrogen (NOX), to racial/ethnic differences in atherosclerosis severity and progression in the Multi-Ethnic Study of Atherosclerosis (MESA). We first examined associations of race/ethnicity, neighborhood racial/ethnic composition and neighborhood residential segregation with concentrations of PM2.5 and NOX across 5,870 White, Black, Hispanic, and Chinese MESA participants from 6 different U.S. communities (Baltimore, Maryland; Chicago, Illinois; Forsyth County (Winston-Salem), North Carolina; Los Angeles County, California; New York, New York and St. Paul, Minnesota). We found that Black and Hispanic race/ethnicity, living in majority Hispanic neighborhoods and living in segregated Hispanic neighborhoods were associated with higher air pollution concentrations and living in majority White neighborhoods with lower air pollution concentrations. We then estimated the contribution of differences in PM2.5 and NOX exposure to racial/ethnic differences in common carotid intima media thickness (IMT) and coronary artery calcification (CAC) at MESA Exam 1 (2000- 2002). After adjusting for demographics and cardiovascular risk factors, exposure to PM2.5 exposure was associated with significant increases in carotid IMT for Black, Hispanic and Chinese women compared to White women. These differences were not observed in men and were no longer statistically significant for women after adjustment for metropolitan area. Air pollution exposure did not contribute to ethnic differences in the amount of coronary calcium. Finally, we estimated the contribution of PM2.5 and NOX exposure to racial/ethnic differences in progression of coronary artery calcification from MESA Exam 1 (2000- 2012) through MESA Exam 5 (2010– 2012). Our outcomes of interest were the development of incident CAC in participants without coronary calcium at Exam 1 and annual change in coronary calcium in participants with coronary calcium at Exam 1. After adjusting for demographics and cardiovascular risk factors, risk for incident CAC increased for Black women in connection with NOX exposure. For Chinese women risk for incident CAC decreased in connection with PM2.5 exposure. These differences were no longer statistically significant after adjustment for metropolitan area. Exposure to air pollution did not contribute to risk for incident CAC among men nor did contribute to ethnic differences in the annual change in coronary calcium. This dissertation provides novel information regarding ethnic differences in air pollution exposure and the role of these exposures to differences in atherosclerosis by race/ethnicity. Although air pollution did not significantly contribute to racial/ethnic differences in atherosclerosis severity and progression in MESA after adjustment for metropolitan area, we cannot discard the possibility of cardiovascular disease disparities related to differential air pollution exposure in women. Also, additional studies are needed to evaluate whether air pollution related cardiovascular disparities are related to the triggering of cardiovascular events rather than changes in long-term subclinical atherosclerosis.