Particulate and gaseous pollutants on inflammation, thrombosis, and autonomic imbalance in subjects at risk for cardiovascular disease

This study examined effects of short-term urban air pollution exposures on inflammation, thrombosis, and autonomic imbalance in subjects at risk for cardiovascular disease (CVD). We enrolled 61 patients with multiple CVD risk factors and measured high sensitive C-reactive protein (hs-CRP), fibrinogen, D-dimer, and heart rate variability (HRV) indices. Two health examinations for each participant were performed during December 2002 through September 2003. Changes in inflammation and thrombotic markers and HRV indices with exposures to PM2.5, organic carbon (OC), elemental carbon (EC), sulfur dioxide (SO2), nitrogen dioxide (NO2), and carbon monoxide (CO) at 1- to 3-day lags were analyzed using mixed models. The results showed inflammatory and thrombotic markers increased with 1- to 3-day lagged PM2.5 components and gaseous pollutants exposures. hs-CRP maximally increased 0.19 [95% confidence interval (CI): 0.07–0.31] and 0.15 (95% CI: 0.05–0.24) mg/L for an interquartile range (IQR) of 1-day lagged SO2 (2.3 ppb) and CO (0.5 ppm), respectively. D-dimer maximally increased 1.05 (95% CI: 0.13–1.75), 0.72 (95% CI: 0.09–1.21), 0.92 (95% CI: 0.13–1.50), and 0.90 (95% CI: 0.07–1.61) mg/dL for an IQR of 1-day lagged OC (3.9 μg/m3), EC (2.0 μg/m3), SO2, and NO2 (13.4 ppb), respectively. The HRV indices, including low frequency, very low frequency, and the ratio of low frequency to high frequency decreased 19.8 (95% CI: 4.4–32.7), 12.9 (95% CI: 0.8–23.4), and 17.6 (95% CI: 5.4–28.2)% for an IQR of 1-day lagged PM2.5 (20.2 μg/m3), respectively. Our findings demonstrated PM2.5 components and gaseous pollutants exert prolonged inflammatory and thrombotic reactions, while PM2.5 exert an immediate autonomic imbalance.