Association between changes in air pollution levels during the Beijing Olympics and biomarkers of inflammation and thrombosis in healthy young adults

Abstract

Context: Air pollution is a risk factor for cardiovascular diseases (CVD), but the underlying biological mechanisms are not well understood.

Objective: 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.

Design, setting, and participants: Using a quasi-experimental opportunity offered by greatly restricted air pollution emissions during the Beijing Olympics, we measured pollutants daily and the outcomes listed below in 125 healthy young adults before, during, and after the 2008 Olympics (June 2-October 30). We used linear mixed-effects models to estimate the improvement in outcome levels during the Olympics and the anticipated reversal of outcome levels after pollution controls ended to determine whether changes in outcome levels were associated with changes in pollutant concentrations.

Main outcome measures: C-reactive protein (CRP), fibrinogen, von Willebrand factor, soluble CD40 ligand (sCD40L), soluble P-selectin (sCD62P) concentrations; white blood cell count (WBC); heart rate; and blood pressure.

Results: Concentrations of particulate and gaseous pollutants decreased substantially (-13% to -60%) from the pre-Olympic period to the during-Olympic period. Using 2-sided tests conducted at the .003 level, we observed statistically significant improvements in sCD62P levels by -34.0% (95% CI, -38.4% to -29.2%; P < .001) from a pre-Olympic mean of 6.29 ng/mL to a during-Olympic mean of 4.16 ng/mL and von Willebrand factor by -13.1% (95% CI, -18.6% to -7.5%; P < .001) from 106.4% to 92.6%. After adjustments for multiple comparisons, changes in the other outcomes were not statistically significant. 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 (percentage ≥ 0.3 mg/L) was reduced from 55% in the pre-Olympic period to 46% in the during-Olympic period and reduced further to 36% 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.

Conclusions: Changes in air pollution levels during the Beijing Olympics were associated with acute changes in biomarkers of inflammation and thrombosis and measures of cardiovascular physiology in healthy young persons. These findings are of uncertain clinical significance.

Figure 1

Percentage Changes in sCD62P and sCD40L Associated With Each IQR Change in Pollutant Concentration Data markers represent the percentage change (error bars are 95% confidence intervals) associated with each interquartile range (IQR) increase in pollutant concentration, by 24-hour lag period. Zero lag represents 0 to 23 hours; lag 1, 24 to 47 hours; lag 2, 48 to 71 hours; lag 3, 72 to 95 hours; lag 4, 96 to 119 hours; lag 5, 120 to 143 hours; and lag 6, 144 to 167 hours before a clinic visit. sCD62P indicates soluble P-selectin; sCD40L, soluble CD40 ligand.

Figure 2

Percentage Changes in von Willebrand Factor and Fibrinogen Associated With Each IQR Change in Pollutant Concentration See Figure 1 legend for definitions.

Figure 3

Percentage Changes in White Blood Cell Count and Heart Rate Associated With Each IQR Change in Pollutant Concentration See Figure 1 legend for definitions.

Figure 4

Percentage Changes in Systolic and Diastolic Blood Pressure Associated With Each IQR Change in Pollutant Concentration See Figure 1 legend for definitions.