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

¹ 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

AT A GLANCE COMMENTARY Scientific Knowledge on the Subject The mechanisms linking air pollution to cardiovascular diseases involve direct effects of air pollution on the lung and cardiovascular system and indirect effects mediated through pulmonary inflammation and oxidative stress. What This Study Adds to the Field 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.

 

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