Published ahead of print on April 26, 2007, doi:10.1164/rccm.200611-1627OC
Am. J. Respir. Crit. Care Med., Volume 176, Number 4, August 2007, 370-376
A more recent version of this article appeared on August 15, 2007
Submitted on November 12, 2006
Accepted on April 25, 2007
Urban Air Pollution on Inflammation, Oxidative Stress, Coagulation and Autonomic Dysfunction
Kai-Jen Chuang1, Chang-Chuan Chan1*, Ta-Chen Su2, Chung-Te Lee3, and Chin-Sheng Tang4
1 Institute of Occupational Medicine and Industrial Hygiene, College of Public Health, National Taiwan University, Taipei, Taiwan,
2 Institute of Occupational Medicine and Industrial Hygiene, College of Public Health, National Taiwan University, Taipei, Taiwan; Department of Internal Medicine, College of Medicine, National Taiwan University Hospital, Taipei, Taiwan,
3 Graduate Institute of Environmental Engineering, National Central University, Taoyuan, Taiwan,
4 Department of Public Health, College of Medicine, Fu Jen Catholic University, Taipei, Taiwan
* To whom correspondence should be addressed. E-mail: ccchan{at}ntu.edu.tw.
Background. 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 and 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). Particles with aerodynamic diameters less than 10 µm (PM10) and gaseous air pollutants were measured at one air-monitoring station inside their campus, and particles with aerodynamic diameters less than 2.5 µm (PM2.5) and particulate components were measured at one particulate matter Supersite monitoring station 1km from their campus. We used linear mixed-effects models to associate biological endpoints with individual air pollutants averaged over 1-day to 3-day periods prior to measurements.
Results. We found increases in hs-CRP, 8-OHdG, fibrinogen, PAI-1, and decreases in HRV indices were associated with increases in levels of PM10, PM2.5, sulfate, nitrate and ozone (O3) in single-pollutant models. The increase in 8-OHdG, fibrinogen and PAI-1, and HRV reduction remained significantly associated with 3-day averaged sulfate and O3 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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