Published ahead of print on April 26, 2007, doi:10.1164/rccm.200611-1627OC
© 2007 American Thoracic Society doi: 10.1164/rccm.200611-1627OC
The Effect of Urban Air Pollution on Inflammation, Oxidative Stress, Coagulation, and Autonomic Dysfunction in Young Adults1 Institute of Occupational Medicine and Industrial Hygiene, College of Public Health, and 2 Department of Internal Medicine, National Taiwan University Hospital and College of Medicine, National Taiwan University, Taipei, Taiwan; 3 Graduate Institute of Environmental Engineering, National Central University, Taoyuan, Taiwan; and 4 Department of Public Health, College of Medicine, Fu Jen Catholic University, Taipei, Taiwan Correspondence and requests for reprints should be addressed to Chang-Chuan Chan, Sc.D., Room 722, No.17, Xu-Zhou Rd., Taipei 100, Taiwan. E-mail: ccchan{at}ntu.edu.tw Rationale: The biological mechanisms linking air pollution to cardiovascular events still remain largerly 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 µm and 2.5 µm, sulfate, nitrate, and ozone (O3) in single-pollutant models. The increase in 8-OHdG, fibrinogen, and PAI-1, and the reduction in HRV remained significantly associated with 3-day averaged sulfate and O3 levels in two-pollutant models. There were moderate correlations (r = -0.3) between blood markers of hs-CRP, fibrinogen, PAI-1, and HRV indices. Conclusions: Urban air pollution is associated with inflammation, oxidative stress, blood coagulation and autonomic dysfunction simultaneously in healthy young humans, with sulfate and O3 as two major traffic-related pollutants contributing to such effects.
Key Words: air pollution • inflammation • oxidative stress • blood coagulation • heart rate variability
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