Harris Héritier1,2, Danielle Vienneau1,2, Maria Foraster1,2,3, Ikenna C Eze1,2, Emmanuel Schaffner1,2, Kees de Hoogh1,2, Laurie Thiesse4,5, Franziska Rudzik4,5, Manuel Habermacher6, Micha Köpfli6, Reto Pieren7, Mark Brink8, Christian Cajochen4,5, Jean Marc Wunderli7, Nicole Probst-Hensch1,2, Martin Röösli1,2. 1. Department of Epidemiology and Public Health, Swiss Tropical and Public Health Institute, Socinstrasse 57, Basel, Switzerland. 2. University of Basel, Petersplatz 1, Basel, Switzerland. 3. ISGlobal, Universitat Pompeu Fabra (UFP), Barcelona Biomedical Research Park (PRBB), Doctor Aiguader, 88, 08003 Barcelona, Spain; CIBER Epidemiología y Salud Pública (CIBERESP); Av. Monforte de Lemos, 3-5. Pabellón 11. Planta 0, Madrid, Spain. 4. Centre for Chronobiology, Psychiatric Hospital of the University of Basel, Wilhelm Klein-Strasse 27, Basel, Switzerland. 5. Transfaculty Research Platform Molecular and Cognitive Neurosciences, University of Basel, Birmannsgasse 8, Basel, Switzerland. 6. n-sphere AG, Räffelstrasse 29, Zürich, Switzerland. 7. Empa, Laboratory for Acoustics/Noise control, Swiss Federal Laboratories for Materials Science and Technology, Überlandstrase 129, Dübendorf, Switzerland. 8. Federal Office for the Environment, Division of Noise and Non-Ionizing Radiation, Bern, Switzerland.
Abstract
AIMS: The present study aimed to disentangle the risk of the three major transportation noise sources-road, railway, and aircraft traffic-and the air pollutants NO2 and PM2.5 on myocardial infarction (MI) mortality in Switzerland based on high quality/fine resolution exposure modelling. METHODS AND RESULTS: We modelled long-term exposure to outdoor road traffic, railway, and aircraft noise levels, as well as NO2 and PM2.5 concentration for each address of the 4.40 million adults (>30 years) in the Swiss National Cohort (SNC). We investigated the association between transportation noise/air pollution exposure and death due to MI during the follow-up period 2000-08, by adjusting noise [Lden(Road), Lden(Railway), and Lden(Air)] estimates for NO2 and/or PM2.5 and vice versa by multipollutant Cox regression models considering potential confounders. Adjusting noise risk estimates of MI for NO2 and/or PM2.5 did not change the hazard ratios (HRs) per 10 dB increase in road traffic (without air pollution: 1.032, 95% CI: 1.014-1.051, adjusted for NO2 and PM2.5: 1.034, 95% CI: 1.014-1.055), railway traffic (1.020, 95% CI: 1.007-1.033 vs. 1.020, 95% CI: 1.007-1.033), and aircraft traffic noise (1.025, 95% CI: 1.006-1.045 vs. 1.025, 95% CI: 1.005-1.046). Conversely, noise adjusted HRs for air pollutants were lower than corresponding estimates without noise adjustment. Hazard ratio per 10 μg/m³ increase with and without noise adjustment were 1.024 (1.005-1.043) vs. 0.990 (0.965-1.016) for NO2 and 1.054 (1.013-1.093) vs. 1.019 (0.971-1.071) for PM2.5. CONCLUSION: Our study suggests that transportation noise is associated with MI mortality, independent from air pollution. Air pollution studies not adequately adjusting for transportation noise exposure may overestimate the cardiovascular disease burden of air pollution. Published on behalf of the European Society of Cardiology. All rights reserved.
AIMS: The present study aimed to disentangle the risk of the three major transportation noise sources-road, railway, and aircraft traffic-and the air pollutants NO2 and PM2.5 on myocardial infarction (MI) mortality in Switzerland based on high quality/fine resolution exposure modelling. METHODS AND RESULTS: We modelled long-term exposure to outdoor road traffic, railway, and aircraft noise levels, as well as NO2 and PM2.5 concentration for each address of the 4.40 million adults (>30 years) in the Swiss National Cohort (SNC). We investigated the association between transportation noise/air pollution exposure and death due to MI during the follow-up period 2000-08, by adjusting noise [Lden(Road), Lden(Railway), and Lden(Air)] estimates for NO2 and/or PM2.5 and vice versa by multipollutant Cox regression models considering potential confounders. Adjusting noise risk estimates of MI for NO2 and/or PM2.5 did not change the hazard ratios (HRs) per 10 dB increase in road traffic (without air pollution: 1.032, 95% CI: 1.014-1.051, adjusted for NO2 and PM2.5: 1.034, 95% CI: 1.014-1.055), railway traffic (1.020, 95% CI: 1.007-1.033 vs. 1.020, 95% CI: 1.007-1.033), and aircraft traffic noise (1.025, 95% CI: 1.006-1.045 vs. 1.025, 95% CI: 1.005-1.046). Conversely, noise adjusted HRs for air pollutants were lower than corresponding estimates without noise adjustment. Hazard ratio per 10 μg/m³ increase with and without noise adjustment were 1.024 (1.005-1.043) vs. 0.990 (0.965-1.016) for NO2 and 1.054 (1.013-1.093) vs. 1.019 (0.971-1.071) for PM2.5. CONCLUSION: Our study suggests that transportation noise is associated with MI mortality, independent from air pollution. Air pollution studies not adequately adjusting for transportation noise exposure may overestimate the cardiovascular disease burden of air pollution. Published on behalf of the European Society of Cardiology. All rights reserved.
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