Although it is now well established that air pollution is a risk factor for cardiovascular disease (CVD), the mechanisms by which air pollution leads to CVD are not well understood. Postulated mechanisms include systemic inflammation and thrombosis or endothelial dysfunction. However, pollution-associated increases in these biomarkers have been inconsistent, partly due to inherent limitations of panel study designs that assessed biomarker changes in relation to concentrations of air pollutants. Therefore this innovative study used the greatly restricted air pollution emissions enforced during the Beijing Olympics to measure various biomarkers that would inform the physiological effect of decreased atmospheric pollution.
Particulate (-13%) and gaseous (-60%) pollutants decreased substantially during the Olympic games. In the 125 healthy young adults studied, statistically significant improvements were seen in sCD62P levels (a platelet activation marker) and von Willebrand factor were seen. The percentage of participants with high levels of CRP decreased during the Olympics, from 55% to 46%, and fell further during the post-Olympic period to 36%. Furthermore, interquartile range increases in pollution were consistently associated with significant increases in fibrinogen, von Willebrand factor, heart rate, sCD62P, and sCD40L concentrations.
In this study changes in the level of air pollution were found to cause acute changes in biomarkers of inflammation and thrombosis, as well as measures of cardiovascular physiology, in healthy young people.
- Rich DQ, Kipen HM, Huang W, et al. Association Between Changes in Air Pollution Levels During the Beijing Olympics and Biomarkers of Inflammation and Thrombosis in Healthy Young Adults. JAMA 2012;307:2068-2078.