Air Pollution Level Changes in Beijing Linked With Biomarkers of Cardiovascular Disease
During the 2008 Beijing Olympics, changes in air pollution were associated with changes in biomarkers of systemic inflammation and thrombosis (formation of blood clot) as well as measures of cardiovascular physiology in healthy young persons, according to a study in the May 16 issue of JAMA, a theme issue on Global Health.
"Air pollution is a risk factor for cardiovascular diseases (CVD), but the mechanisms by which air pollution leads to CVD is not well understood. Hypothesized mechanisms with associated biomarkers include systemic inflammation and thrombosis or endothelial [thin layer of cells that line the heart and certain vessels and cavities within the body] dysfunction," according to background information in the article. "As a condition for hosting the 2008 Olympic Games, the Chinese government agreed to temporarily and substantially improve air quality in Beijing for the Olympics and subsequent Paralympics. This provided a unique opportunity to use a quasi-experimental design in which exposures and biomarkers were measured at baseline (pre-Olympics), following a change in pollution (during-Olympics), and then repeated after an expected return to baseline (post-Olympics)."
David Q. Rich, Sc.D., of the University of Rochester, New York, and colleagues conducted a study to determine whether markers related to CVD pathophysiological pathways (biomarkers for systemic inflammation and thrombosis, heart rate, and blood pressure) are sensitive to changes in air pollution. The researchers measured environmental air pollutants daily and also measured various biomarkers and other measures (heart rate, blood pressure) in 125 healthy young adults before, during, and after the 2008 Olympics (June 2-October 30). The biomarkers measured included those associated with systemic inflammation (fibrinogen, C-reactive protein [CRP], white blood cell [WBC] count) and thrombosis or endothelial dysfunction (platelet activation markers P-selectin [sCD62P] and soluble CD40 ligand [sCD40L] as well as the adhesive endothelial glycoprotein von Willebrand factor).
Concentrations of particulate and gaseous pollutants decreased substantially (-13 percent to -60 percent) from the pre-Olympic period to the during-Olympic period. There were reductions in the average concentration of sulfur dioxide (-60 percent), carbon monoxide (-48 percent), nitrogen dioxide (-43 percent), elemental carbon (-36 percent), PM2.5 (-27 percent), organic carbon (-22 percent) and sulfate (-13 percent) from the pre-Olympic to the during-Olympic period. "In contrast, ozone concentrations increased (24 percent). Pollutant concentrations generally increased substantially from the during- to post-Olympic period for all the pollutants (21 percent to 197 percent) except ozone (-61 percent) and sulfate (-47 percent)," the authors write.
The researchers observed statistically significant improvements in SCD62P levels (by -34.0 percent), and von Willebrand factor (by -13.1 percent). Changes in the other outcomes were not statistically significant after adjustments for multiple comparisons. In the post-Olympic period when pollutant concentrations increased, most outcomes approximated pre-Olympic levels, but only sCD62P and systolic blood pressure were significantly worsened from the during-Olympic period. "The fraction of above-detection-limit values for CRP was reduced from 55 percent in the pre-Olympic period to 46 percent in the during-Olympic period and reduced further to 36 percent in the post-Olympic period. Interquartile range increases in pollutant concentrations were consistently associated with statistically significant increases in fibrinogen, von Willebrand factor, heart rate, sCD62P, and SCD40L concentrations."
"Although these findings are of uncertain clinical significance, this study provides quasi-experimental, mechanistic data to support the argument that air pollution may be a global risk factor for CVD."