Short-term effects of air pollution: a panel study of blood markers in patients with chronic pulmonary disease

Abstract

Background: Growing evidence indicates that ambient air pollution is associated with exacerbation of chronic diseases like chronic pulmonary disease. A prospective panel study was conducted to investigate short-term changes of blood markers of inflammation and coagulation in response to daily changes in air pollution in Erfurt, Germany. 12 clinical visits were scheduled and blood parameters were measured in 38 male patients with chronic pulmonary disease during winter 2001/2002. Additive mixed models with random patient intercept were applied, adjusting for trend, weekday, and meteorological parameters. Hourly data on ultrafine particles (UFP, 0.01-0.1 mum), accumulation mode particles (ACP, 0.1-1.0 mum), PM10 (particulate matter <10 mum in diameter), elemental (EC) and organic carbon (OC), gaseous pollutants (nitrogen monoxide [NO], nitrogen dioxide [NO2], carbon monoxide [CO], and sulphur dioxide [SO2]) were collected at a central monitoring site and meteorological data were received from an official network. For each person and visit the individual 24-hour average of pollutants immediately preceding the blood withdrawal (lag 0) up to day 5 (lag1-4) and 5-day running means were calculated.

Results: Increased levels of fibrinogen were observed for an increase in one interquartile range of UFP, PM10, EC, OC, CO, and NO revealing the strongest effect for lag 3. E-selectin increased in association with ACP and PM10 with a delay of one day. The ACP effect was also seen with the 5-day-mean. The pattern found for D-dimer was inconsistent. Prothrombin fragment 1+2 decreased with lag 4 consistently for all particulate pollutants. Von Willebrand factor antigen (vWF) showed a consistent decrease in association with almost all air pollutants with all lags except for lag 0. No associations were found for C-reactive protein, soluble intercellular adhesion molecule 1, serum amyloid A and factor VII.

Conclusion: These results suggest that elevated concentrations of air pollution are associated with changes in some blood markers of inflammation and coagulation in patients with chronic pulmonary disease. The clinical implications of these findings need further investigation.

Figure 1

Time series of number concentrations of particles sized 0.01 to 0.1 μm (ultra fine particles, UFP) and mass concentrations of particles less than 10 μm in diameter (PM₁₀) with air temperature in Erfurt, Germany between October 2001 and May 2002.

Figure 2

Effects of particulate ambient air pollutants on fibrinogen, prothrombin fragment 1+2, and von Willebrand factor antigen (vWF), lag 0 to lag 4 and 5-day-mean exposure. 38 men with chronic pulmonary disease in Erfurt, Germany, between October 2001 and May 2002. IQR, interquartile range; UFP, ultrafine particles number concentration of particles with a size range of 0.01 to 0.1 μm in diameter; ACP, accumulation mode particles, particles with a size range of 0.1 to 1.0 μm; PM₁₀, mass concentration of particles less than 10 μm in diameter; OC, organic carbon; EC, elemental carbon; lag 0 (1, 2, 3, 4, 5-day-mean) = average pollutant concentration 0-23 (24-47; 48-71, 72-95, 96-119, 0-119) hours prior to blood withdrawal.

Figure 3

Comparison of associations between blood markers and PM₁₀ for all observations (black circle) and observations without smokers (black square) for fibrinogen, E-selectin and prothrombin fragment 1+2 lag 0 to lag 4 and 5-day-mean exposure. 31 male non-smokers and 7 male smokers with chronic pulmonary disease in Erfurt, Germany, between October 2001 and May 2002. IQR, interquartile range; PM₁₀, mass concentration of particles less than 10 μm in diameter; lag 0 (1, 2, 3, 4, 5-day-mean) = average pollutant concentration 0-23 (24-47; 48-71, 72-95, 96-119, 0-119) hours prior to blood withdrawal.