Association Between Air Pollution and Coronary Artery Calcification
Is there an association between long-term exposure to ambient air pollution, defined as fine particulate matter <2.5 μm in diameter (PM2.5), and progression of coronary artery calcium (CAC) and common carotid artery intima-media thickness (CIMT)?
In this prospective 10-year cohort study, baseline enrollment was between 2000 and 2002. CAC scores (CACS) were measured by computed tomography (CT) in 6,795 participants ages 45–84 years in the MESA Air study (Multi-Ethnic Study of Atherosclerosis and Air Pollution) in six metropolitan areas in the United States. Repeated scans were done in nearly all between 2002 and 2005, for a subset of participants between 2005 and 2007, and for one half of all participants between 2010 and 2012. CIMT was measured by ultrasound at baseline in all and in 2010–2012 for 3,459 participants. Residence-specific spatiotemporal pollution concentration models, incorporating community-specific measurements, agency monitoring data, and geographical predictors, estimated concentrations of PM2.5, and nitrogen oxides (NOX) between 1999 and 2012. The primary aim was to examine the association between both progression of CAC and mean CIMT and long-term exposure to ambient air pollutant concentrations (PM2.5, NOX, and black carbon) between examinations and within the six metropolitan areas, adjusting for baseline age, sex, ethnicity, socioeconomic characteristics, cardiovascular (CV) risk factors, site, and CT scanner technology.
Mean age was 62 years and 53% were female. Mean follow-up for those with a CACS was 6.2 years (standard deviation [SD], 3.5 years). At baseline, mean CACS were 145 Agatston units (407). CACS increased on average by 24 Agatston units per year (SD, 58), and CIMT by 12 μm per year (10), before adjusting for risk factors or air pollutant exposures. Participant-specific pollutant concentrations averaged over the 10 years ranged from 9.2–22.6 μg PM2.5/m3 and 7.2–139.2 parts per billion (ppb) NOX. For each 5 μg PM2.5/m3 increase, CACS progressed by 4.1 Agatston units per year and for each 40 ppb, NOX CACS progressed by 4.8 Agatston units per year. Pollutant exposures were not associated with CIMT change. Results were not affected by diabetes or hypertension.
Increased concentrations of PM2.5 and traffic-related air pollution within metropolitan areas, in ranges commonly encountered worldwide, are associated with progression in coronary calcification, consistent with acceleration of atherosclerosis. This study supports the case for global efforts of pollution reduction in prevention of CV diseases.
The relationship between ambient air pollution, CACS, CV risk factors, CV events, and mortality has been well described. But as the authors acknowledged, calcification may represent maturation of atherosclerotic plaque and not an increase in soft or vulnerable plaques. The increase in progression of CAC in the MESA sites was obtained in regions of the United States with the mean exposure of 14.2 μg/m3, which is only minimally higher than the 12 μg/m³ annual average PM2.5 permitted in the United States. The concentrations in highly populated industrialized countries are much higher.
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