Air pollution linked to CV risk markers

Air Pollution Linked to Cardiovascular Disease Markers
Air Pollution Linked to Cardiovascular Disease Markers

HealthDay News -- Beijing's ban on emissions during the 2008 Olympics is associated with a reduction in biomarkers for cardiovascular risk in healthy young people, study results indicate.

Levels of P-selectin and von Willebrand factor dropped significantly when the restrictions were in place (P<0.001 for both), Jim Zhang, PhD, of the University of Southern California in Los Angeles, and colleagues reported in the the Journal of the American Medical Association.

"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 cardiovascular disease," they wrote.

Despite findings from several studies linking air pollution to CVD, the underlying biological mechanisms at play are not well understood, the researchers explained.

To determine which biomarkers are sensitive to air pollution, the researchers analyzed levels of several among 125 study participants before, during and after the 2008 Olympics. These included C-reactive protein (CRP), fibrinogen, von Willebrand factor, soluble CD40 ligand (sCD40L), soluble P-selectin (sCD26P) concentrations, white blood cell count, heart rate and BP.

Efforts from the Chinese government to restrict air pollution during the games consisted of limiting the operation of industrial and commercial combustion facilities in the city and using alternate-day driving to remove about 1.5 million cars from the road each day between July 20 and Sept. 17, 2008.

After these measures were implemented, concentrations of particulate and gaseous pollutants decreased substantially (−13 to −60 percent) during-Olympic period, the researchers found. During this time period sCD62P levels fell 34% (from 6.29 ng/mL to 4.16 ng/mL; P<0.001), and von Willebrand factor levels fell 13.1% (from 106.4% to 92.6%; P<0.001).

Changes in the other outcomes were not statistically significant after adjusting for multiple comparisons. In the post-Olympic period, when pollutant concentrations increased, only sCD62P and systolic BP were significantly worsened, compared with the during-Olympic period.

The fraction of above-detection-limit values for CRP decreased from 55% to 46% to 36% for the pre-Olympic, during-Olympic, and post-Olympic periods, respectively. Interquartile range increases in pollutant concentrations were consistently associated with statistically significant increases in fibrinogen, von Willebrand factor, heart rate, sCD62P and sCD40L concentrations.

Study limitations included air pollution measurements obtained from only a single location in China and lack of data on exposure to specific pollutants at the individual patient level, the researchers acknowledged.

Francesca Dominici, PhD, and Murray Mittleman, MD, DrPH, of Harvard, called the study "compelling," in an accompanying editorial, because it "provides evidence supporting the hypothesis that exposure to higher levels of air pollution leads to a prothrombotic response."

They went on to warn that if air pollution in China and other Asian countries is left unchecked, it could go on to spread to other continents, jeopardizing the health of people as far away as the United States.

But reconciling the need to reduce air pollution with rapid economic growth from industry presents a dilemma, according to Dominici and Mittleman. China's heavy reliance on coal, lack of political incentives to trade slower growth for less air pollution, the fact that pollution fines are currently lower than the cost of implementing pollution control are several factors that contribute to the challenge.

"Clean air is a shared global resource. It is in the common interest to maintain air quality for the promotion of global health," Dominici and Mittleman concluded.

Rich DQ et al. JAMA. 2012; 307(19): 2068-2078.

Dominici F, Mittleman MA. JAMA. 2012; 307(19): 2100-2102.

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