Abstract
BackgroundEpidemiological studies on health effects of air pollution have consistently shown adverse cardiovascular effects. Toxicological studies have provided evidence for thrombogenic effects of particles.A prospective panel study in a susceptible population was conducted in Erfurt, Germany, to study the effects of daily changes in ambient particles on various blood cells and soluble CD40ligand (sCD40L, also known as CD154), a marker for platelet activation that can cause increased coagulation and inflammation.Blood cells and plasma sCD40L levels were repeatedly measured in 57 male patients with coronary heart disease (CHD) during winter 2000/2001. Fixed effects linear regression models were applied, adjusting for trend, weekday and meteorological parameters.Hourly data on ultrafine particles (UFP, number concentration of particles from 0.01 to 0.1 μm), mass concentration of particles less than 10 and 2.5 μm in diameter (PM10, PM2.5), accumulation mode particle counts (AP, 0.1–1.0 μm), elemental and organic carbon, gaseous pollutants and meteorological data were collected at central monitoring sites.ResultsAn immediate increase in plasma sCD40L was found in association with UFP and AP (% change from geometric mean: 7.1; CI: [0.1, 14.5] and 6.9; CI: [0.5, 13.8], respectively). Platelet counts decreased in association with UFP showing an immediate, a three days delayed (lag 3) and a 5-day average response (% change from the mean: -1.8; CI: [-3.4,-0.2]; -2.4; CI: [-4.5,-0.3] and -2.2; CI: [-4.0,-0.3] respectively).ConclusionThe increased plasma sCD40L levels support the hypothesis that higher levels of ambient air pollution lead to an inflammatory response in patients with CHD thus providing a possible explanation for the observed association between air pollution and cardiovascular morbidity and mortality in susceptible parts of the population.
Highlights
Epidemiological studies on health effects of air pollution have consistently shown adverse cardiovascular effects
An immediate increase in plasma soluble CD40L (sCD40L) was found in association with UFP and AP (% change from geometric mean: 7.1; CI: [0.1, 14.5] and 6.9; CI: [0.5, 13.8], respectively)
Increased inflammation would increase the likelihood of serious arterial vascular thrombotic events in susceptible individuals such as patients with coronary heart disease (CHD), possibly explaining, in part, the observed association between air pollution and cardiovascular morbidity and mortality
Summary
Epidemiological studies on health effects of air pollution have consistently shown adverse cardiovascular effects. Recent toxicological studies have demonstrated a prothrombogenic effect of diesel exhaust particles in hamsters, as well as an activation of platelets [7], providing one possible explanation for the observed effects. Nemmar et al [10] demonstrated in hamster models that ultrafine polystyrene particles can modulate thrombus formation and Suwa et al [11] observed a systemic inflammatory response and a progression of the atherosclerotic process in hyperlipidemic rabbits in association with PM10 (mass concentration of particles < 10 μm in diameter). We previously observed a delayed increase in levels of Creactive protein (CRP) and intercellular adhesion molecule 1 (ICAM-1) above the 90th percentile for an increase in accumulation mode particles (AP, 0.1–1.0 μm), UFP and PM10 in the same patients with coronary heart disease (CHD) we report about here [12]. For FVII clear and consistent negative associations were observed [12]
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