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Study links air pollution to CVD biomarker changes

Tuesday May 15, 2012
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During the 2008 Beijing Olympics, changes in air pollution were associated with changes in biomarkers of thrombosis in healthy young people, according to a study.

Writing in the May 16 issue of JAMA, researchers said that "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."

In background information for the study, the researchers wrote that "air pollution is a risk factor for cardiovascular diseases, but the mechanisms by which air pollution leads to CVD [are] not well understood. Hypothesized mechanisms with associated biomarkers include systemic inflammation and thrombosis or endothelial dysfunction."

The researchers noted that as a condition for hosting the 2008 Summer Olympics and Paralympics, the Chinese government agreed to temporarily and substantially improve air quality in Beijing. "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 the Olympics) and then repeated after an expected return to baseline (post-Olympics)," they wrote.

David Q. Rich, ScD, of the University of Rochester (N.Y.) 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-Oct. 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], and the adhesive endothelial glycoprotein von Willebrand factor).

Concentrations of particulate and gaseous pollutants such as sulfur dioxide and carbon monoxide decreased substantially (by 13% to 60%, depending on the particle) from before the Olympics to during the Olympics. Ozone concentrations increased, however. The researchers observed statistically significant improvements in two of the three biomarkers for blood clotting they measured: SCD62P levels (by -34%), and von Willebrand factor (by -13.1%).

Changes in the other outcomes, including indicators of inflammation such as WBC count and CRP, were not statistically significant after adjustments for multiple comparisons.

Between the Olympics and the post-Olympic period in the study, pollutant concentrations increased substantially except for ozone and sulfate, which decreased. Among outcomes, only sCD62P and systolic blood pressure were significantly worsened from the period during the Olympics.

To read the study, visit http://bit.ly/JmgGL6.

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