gms | German Medical Science

51. Jahrestagung der Deutschen Gesellschaft für Medizinische Informatik, Biometrie und Epidemiologie

Deutsche Gesellschaft für Medizinische Informatik, Biometrie und Epidemiologie e. V. (gmds)

10. - 14.09.2006, Leipzig

Long-Term Personal Exposure to Traffic and Coronary Calcification

Meeting Abstract

  • Barbara Hoffmann - Institut für Med. Informatik, Biometrie und Epidemiologie, Essen
  • Susanne Moebus - Institut für Med. Informatik, Biometrie und Epidemiologie, Essen
  • Andreas Stang - Institut für Med. Epidemiologie, Biometrie und Informatik, Halle
  • Nils Lehmann - Institut für Med. Informatik, Biometrie und Epidemiologie, Essen
  • Raimund Erbel - Westdeutsches Herzzentrum, Essen
  • Karl-Heinz Jöckel - Institut für Med. Epidemiologie, Biometrie und Informatik, Essen

Deutsche Gesellschaft für Medizinische Informatik, Biometrie und Epidemiologie e.V. (gmds). 51. Jahrestagung der Deutschen Gesellschaft für Medizinische Informatik, Biometrie und Epidemiologie. Leipzig, 10.-14.09.2006. Düsseldorf, Köln: German Medical Science; 2006. Doc06gmds018

The electronic version of this article is the complete one and can be found online at:

Published: September 1, 2006

© 2006 Hoffmann et al.
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Epidemiological evidence suggests that long-term exposure to particulate matter (PM) air pollution accelerates atherogenesis and increases cardiopulmonary mortality [1], [2]. We examined the relationship between long-term personal exposure to traffic, a major source of urban air pollution, and the degree of coronary artery calcification (CAC), controlling for major risk factors for arteriosclerosis and background PM air pollution.


We used baseline data from the German Heinz Nixdorf Recall study, an ongoing population-based, prospective cohort study of 4814 inhabitants of the Rhein-Ruhr area [3]. Participants´ addresses were geocoded with a geographic information system (GIS). To assess personal long-term traffic exposure, the major source of ambient ultrafine particles (UFP, < 100 nm), distances between residence and major roads, namely autobahn (mean daily vehicle count >30,000) and federal highways (mean daily vehicle count >10,000 to ≤30,000) were calculated with the GIS. Distance to major roads is a useful surrogate for UFP-exposure, because UFP exhibit a steep decline in number concentration with increasing distance from major motorways [4]. Annual mean values for PM2.5 mass concentration on a spatial scale of 1 km were estimated with the EURAD-model for the year 2002 (midpoint of baseline examination) and assigned to each address [5]. The main outcome was the degree of coronary artery calcification (CAC), assessed quantitatively by electron-beam computer tomography [6]. CAC is a highly reproducible and accurate measure of clinical and subclinical coronary atherosclerosis that correlates well with cardiovascular risk factors and clinical events. We evaluated the association between the logarithm of proximity to major roads and log(CAC+1) with linear regression, controlling for background PM2.5 and individual level risk factors for coronary arteriosclerosis (age, sex, educational attainment, smoking status, number of cigarettes per day, environmental tobacco smoke exposure, hip-to-waist ratio, hypertension, systolic blood pressure, diabetes mellitus, HBA1c, LDL, HDL).


We performed the analysis on 4464 out of 4814 participants for which information on all explanatory variables were available. 677 of 4464 participants (15.2%) lived within 200 m of a major road. Exposure values for background PM2.5 ranged from 19.8 to 26.8 μg/m3 (mean 22.8). Mean CAC-values were strongly dependent on age, sex and smoking status. Reducing the distance to a major road by half is associated with an increase in CAC by 1.13 (95% CI 1.01-1.26) in women and 1.09 (95% CI 0.97-1.23) in men in the crude model and by 1.06 (95% CI 0.96-1.17) in women and 1.07 (95% CI 0.96-1.20) in men in the adjusted model. In a subgroup analysis of 4167 participants without clinically manifest coronary artery disease (no history of myocardial infarction, bypass surgery, angioplasty or implantation of a coronary stent), the observed effects were similar (women: 1.09; 0.99-1.20 and men: 1.05; 0.94-1.17). The effect is comparable in size to the estimated increase in CAC due to six months of aging (1.06; 95% CI 1.05-1.07).


We could observe a substantial effect of long-term residential traffic exposure on CAC. This finding is in agreement with the results from a Dutch study, where cardiopulmonary mortality was shown to be associated with an indicator variable for residential traffic exposure [2]. Pathogenetic factors within the complex mixture of traffic emissions, including UFP, chemical composition of particles and noise, could be responsible for this effect.


This study provides epidemiological evidence that long-term exposure to traffic-related emissions is associated with coronary artery calcification. More research is needed to identify the factors responsible for the adverse health effects of urban air pollution.


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