Long-Term Exposure to Air Pollution and Vascular Damage in Young Adults

Background: Long-term exposure to ambient air pollution has recently been linked to atherosclerosis and cardiovascular events. There are, however, very limited data in healthy young people. We examined the association between air pollutants and indicators of vascular damage in a cohort of young adults. Methods: We used data from the Atherosclerosis Risk in Young Adults study. We estimated exposure to nitrogen dioxide (NO2), particulate matter less than 2.5 mu m in aerodynamic diameter (PM2.5), black smoke, sulfur dioxide (SO2), and various traffic indicators for participants' 2000 home addresses. Exposure for the year 2000 was estimated by land-use regression models incorporating regional background annual air pollution levels, land-use variables, population densities, and traffic intensities on nearby roads. Outcomes were common carotid artery intima-media thickness (n = 745), aortic pulse wave velocity (n = 524), and augmentation index (n = 729). Results: Exposure contrasts were substantial for NO2, SO2, and black smoke (5th-95th percentiles = 19.7 to 44.9, 2.5 to 5.2, and 8.6 to 19.4 mu g/m(3), respectively) and smaller for PM2.5 (16.5 to 19.9 mu g/m3). The variability of carotid artery intima-media thickness was less than for pulse wave velocity and especially augmentation index (5-95th percentiles = 0.42 to 0.58 mm, 4.9 to 7.4 m/s and -12.3% to 27.3%, respectively). No associations were found between any of the pollutants or traffic indicators and carotid artery intima-media thickness, although PM2.5 effect estimates were in line with previous studies. We observed a 4.1% (95% confidence interval = 0.1% to 8.0%) increase in pulse wave velocity and a 37.6% (2.2% to 72.9%) increase in augmentation index associated with a 25 mu g/m(3) increase in NO2, and a 5.3% (0.1% to 10.4%) increase in pulse wave velocity with a 5 mu g/m(3) increase in SO2. PM2.5 and black smoke were not associated with either of these 2 outcomes. Conclusions: Air pollution may accelerate arterial-wall stiffening in young adults. Small outcome variability and lack of residential mobility data may have limited the power to detect an effect on intima-media thickness.