PM2.5, oxidant defence and cardiorespiratory health: a review

Environ Health. 2013 May 4;12:40. doi: 10.1186/1476-069X-12-40.


Airborne fine particle mass concentrations (PM2.5) are used for ambient air quality management worldwide based in part on known cardiorespiratory health effects. While oxidative stress is generally thought to be an important mechanism in determining these effects, relatively few studies have specifically examined how oxidant defence may impact susceptibility to particulate air pollution. Here we review studies that explore the impact of polymorphisms in anti-oxidant related genes or anti-oxidant supplementation on PM2.5-induced cardiorespiratory outcomes in an effort to summarize existing evidence related to oxidative stress defence and the health effects of PM2.5. Recent studies of PM-oxidative burden were also examined. In total, nine studies were identified and reviewed and existing evidence generally suggests that oxidant defence may modify the impact of PM2.5 exposure on various health outcomes, particularly heart rate variability (a measure of autonomic function) which was the most common outcome examined in the studies reviewed. Few studies examined interactions between PM2.5 and oxidant defence for respiratory outcomes, and in general studies focused primarily on acute health effects. Therefore, further evaluation of the potential modifying role of oxidant defence in PM2.5-induced health effects is required, particularly for chronic outcomes. Similarly, while an exposure metric that captures the ability of PM2.5 to cause oxidative stress may offer advantages over traditional mass concentration measurements, little epidemiological evidence is currently available to evaluate the potential benefits of such an approach. Therefore, further evaluation is required to determine how this metric may be incorporated in ambient air quality management.

Publication types

  • Review

MeSH terms

  • Air Pollutants / toxicity*
  • Antioxidants / metabolism
  • Cardiovascular Diseases / chemically induced
  • Cardiovascular Diseases / epidemiology*
  • Environmental Exposure*
  • Environmental Monitoring
  • Humans
  • Incidence
  • Oxidative Stress / drug effects*
  • Particulate Matter / toxicity*
  • Polymorphism, Genetic*
  • Respiratory Tract Infections / chemically induced
  • Respiratory Tract Infections / epidemiology*


  • Air Pollutants
  • Antioxidants
  • Particulate Matter