Air pollution and markers of inflammation and coagulation in patients with coronary heart disease

Rationale: Ambient air pollution has been shown to be associated with cardiovascular morbidity and mortality. Objectives: A prospective panel study was conducted to study the early physiologic reactions characterized by blood biomarkers of inflammation, endothelial dysfunction, and coagulation in response to daily changes in air pollution in Erfurt, Germany. Methods: Blood parameters were repeatedly measured in 57 male patients with coronary heart disease during the winter of 2000/2001. Fixed-effects linear and logistic regression models were applied, adjusting for trend, weekday, and meteorologic parameters. Measurements: Hourly data on ultrafine particles (UFPs; number concentration of particles from 0.01 to 0.1 mu m), mass concentration of particles less than 10 (PM10) and 2.5 mu m in diameter, elemental and organic carbon, gaseous pollutants, and meteorologic data were collected at central monitoring sites. Main Results: Increased levels of C-reactive protein above the 90th percentile were observed for an increase in air pollution concentrations of one interquartile range. The effect was strongest for accumulation mode particles, with a delay of 2 d (odds ratio [OR], 3.2; confidence interval [CI], 1.7, 6.0). Results were consistent for UFIPs and PM10, which also showed a 2-d delayed response (OR, 2.3; CI, 1.3, 3.8; and OR, 2.2; CI, 1.2, 3.8, respectively). However, not all of the blood markers of endothelial dysfunction and coagulation increased consistently in association with air pollutants. Conclusion: These results suggest that inflammation as well as parts of the coagulation pathway may contribute to the association between particulate air pollution and coronary events.