The effect of urban air pollution on inflammation, oxidative stress, coagulation, and autonomic dysfunction in young adults

Am J Respir Crit Care Med. 2007 Aug 15;176(4):370-6. doi: 10.1164/rccm.200611-1627OC. Epub 2007 Apr 26.


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 averaged sulfate and O(3) 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 O(3) as two major traffic-related pollutants contributing to such effects.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 8-Hydroxy-2'-Deoxyguanosine
  • Adolescent
  • Adult
  • Air Pollutants / chemistry
  • Air Pollution / adverse effects*
  • Biomarkers / blood
  • Blood Coagulation / physiology*
  • C-Reactive Protein / analysis
  • Deoxyguanosine / analogs & derivatives
  • Deoxyguanosine / blood
  • Environmental Monitoring
  • Female
  • Fibrinogen / analysis
  • Heart Rate / physiology*
  • Humans
  • Inflammation / physiopathology*
  • Male
  • Oxidative Stress / physiology*
  • Particle Size
  • Plasminogen Activator Inhibitor 1 / blood
  • Taiwan
  • Tissue Plasminogen Activator / blood
  • Urban Health*
  • Urban Population


  • Air Pollutants
  • Biomarkers
  • Plasminogen Activator Inhibitor 1
  • 8-Hydroxy-2'-Deoxyguanosine
  • Fibrinogen
  • C-Reactive Protein
  • Tissue Plasminogen Activator
  • Deoxyguanosine