Does traffic noise explain the association of residential proximity to traffic with coronary artery calcification?

A Viehmann; S Moebus; S Möhlenkamp; M Nonnemacher; N Dragano; H Jakobs; C Kessler; R Erbel; K Jöckel; B Hoffmann

doi:10.1055/s-0030-1266411

Does traffic noise explain the association of residential proximity to traffic with coronary artery calcification?

A Viehmann ¹, S Moebus ¹, S Möhlenkamp ², M Nonnemacher ¹, N Dragano ³, H Jakobs ⁴, C Kessler ⁴, R Erbel ², K Jöckel ¹ B Hoffmann ¹, on behalf of the Heinz Nixdorf Recall Investigator Group

¹Institute for Medical Informatics, Biometry and Epidemiology, University Hospital of Essen, Essen
²Department of Cardiology, West German Heart Centre of Essen, University Hospital of Essen, Essen
³Institute of Medical Sociology, Medical Faculty, University of Düsseldorf, Düsseldorf
⁴Rhenish Institute for Environmental Research at the University of Cologne, Cologne

Abstract

Introduction: Residential proximity to high traffic, a major source of noise and fine particle exposure, has been linked to atherosclerosis. We investigate, whether the association of traffic proximity and coronary atherosclerosis can be explained by chronic traffic noise exposure. Methods: We used baseline data (2000–2003) from the Heinz Nixdorf Recall-Study, a population-based cohort of 4814 participants living in three cities in Germany. We calculated the distances between participants' home address and federal and state highways. For long-term traffic noise exposure we used categorical noise map values (according to the EU-directive; 2002/49/EC) and assigned these to the participants' home addresses. Main outcome was coronary artery calcification (CAC) measured by electron-beam computed tomography. We used multiple linear regression to investigate the association of exposure to traffic noise with CAC, controlling for gender, age, education, occupation, smoking, waist-hip ratio, physical activity, LDL, statins, urban background PM2.5 and city. Results: Distance to federal and state highways and exposure to traffic noise were only weakly correlated in this urban setting (r=0.3).No consistent association was observed for weighted daily mean (Lden) or night-time traffic noise exposure with CAC (N=4249). We estimated CAC to be 3.2% higher (95% CI –26.0–43.9%) for the highest traffic noise category (Lden >70 dB; n=192) compared to the reference group (<55 dB). When noise was included in the model for distance to major roads, the estimate for distance and CAC did not change substantially [without noise: 12.3% increase (95% CI 2–21.5%) in CAC for a reduction of the distance by half; including noise in the model: 14.5% (95% CI 3.7–24.1%)]. Discussion: With our current traffic noise exposure data we were unable to show the effect of traffic noise on the biological variability of CAC. Further analyses including residential characteristics and investigation of more refined noise exposure data are necessary. Funded by DFG JO 170/8–1 and by the Heinz Nixdorf foundation, Germany