The Effect of Urban Air Pollution on Inflammation, Oxidative Stress, Coagulation, and Autonomic Dysfunction in Young Adults

作者：Kai-Jen Chuang, Chang‐Chuan Chan, Ta‐Chen Su, Chung-Te Lee, Chin-Sheng Tang · 发表于：American Journal of Respiratory and Critical Care Medicine · 年份：2007 · DOI：10.1164/rccm.200611-1627oc · 被引用次数：694 · 研究领域：Air Quality and Health Impacts、Indoor Air Quality and Microbial Exposure、Biomarkers in Disease Mechanisms

RATIONALE: The biological mechanisms linking air pollution to cardiovascular events still remain largely unclear. OBJECTIVES: To investigate whether biological mechanisms linking air pollution to cardiovascular events occurred concurrently in human subjects exposed to urban air pollutants. METHODS: We recruited a panel of 76 young, healthy students from a university in Taipei. Between April and June of 2004 or 2005, three measurements were made in each participant of high-sensitivity C-reactive protein (hs-CRP), 8-hydroxy-2'-deoxyguanosine (8-OHdG), plasminogen activator fibrinogen inhibitor-1 (PAI-1), tissue-type plasminogen activator (tPA) in plasma, and heart rate variability (HRV). Gaseous air pollutants were measured at one air-monitoring station inside their campus, and particulate air pollutants were measured at one particulate matter supersite monitoring station 1 km from their campus. We used linear mixed-effects models to associate biological endpoints with individual air pollutants averaged over 1- to 3-day periods before measurements were performed. MEASUREMENTS AND MAIN RESULTS: We found that increases in hs-CRP, 8-OHdG, fibrinogen, and PAI-1, and decreases in HRV indices were associated with increases in levels of particles with aerodynamic diameters less than 10 microm and 2.5 microm, sulfate, nitrate, and ozone (O(3)) in single-pollutant models. The increase in 8-OHdG, fibrinogen, and PAI-1, and the reduction in HRV remained significantly associated with 3-day...