TPS 683: Short-term health effects of air pollutants 2, Exhibition Hall, Ground floor, August 28, 2019, 3:00 PM - 4:30 PM Ambient air pollution is a complex mixture of particulate matter (PM2.5), gases and metals. Epidemiological evidence suggests that exposure to air pollution is one of the leading risk factors for cardiovascular disease (CVD). While the association between PM2.5 exposure and CVD is particularly strong, the pathophysiologic mechanisms underlying this association are not completely understood. We conducted a cross-sectional study of 100 participants, recruited from the University of Louisville. Peripheral endothelial function in these subjects was assessed by calculating a reactive hyperemia index (RHI) using the EndoPAT device. Urine samples were used to measure isoprostanes (n=90) while 14 cytokines, 2 adhesion molecules, and 2 matrix metalloproteinases were measured in plasma using a Luminex (n=77). Ambient levels of PM2.5 were obtained by calculating the daily average of all regional EPA-validated monitoring stations in the Louisville, KY region. Adjusted associations with ambient PM2.5 levels were tested using generalized linear models. The average age of our participants was 48 years, with 44% male, 62% white, 52% with diagnosed hypertension, and 44% having Type-2 diabetes. Average daily PM2.5 levels were 11.5 ± 5.1 μg/m3. We found that there was a 12.4% decrease in RHI with every 10μg/m3 PM2.5 increase (95% CI: -21.0, -2.7). F-2 isoprostane metabolite, a measure of oxidative stress, showed a positive association of 28.4% (95% CI: 2.7, 60.3) per 10μg/m3 PM2.5. We also observed positive associations with angiopoietin 1 (17.4%; 95% CI: 2.8, 33.8), VEGF (10.4%; 95% CI: 0.6, 21.0), PiGf (31.7%; 95% CI: 12.2, 54.5), ICAM-1 (24.6%; 95% CI: 1.6, 52.8), and MMP-9 (30.3%; 95% CI: 8.0, 57.5) per 10μg/m3 PM2.5. Additionally, we observed a negative association between PM2.5 and VCAM-1 of -15.9% per 10μg/m3 (95% CI:-28.3, -1.3). Exposure to PM2.5 was associated with impaired vascular function, which may result from oxidative stress and inflammation, and lead to a pro-atherogenic state.