Harris Héritier1, Danielle Vienneau1, Maria Foraster1, Ikenna C Eze1, Emmanuel Schaffner1, Laurie Thiesse2, Franziska Ruzdik2, Manuel Habermacher3, Micha Köpfli3, Reto Pieren4, Arno Schmidt-Trucksäss5, Mark Brink6, Christian Cajochen2, Jean Marc Wunderli4, Nicole Probst-Hensch1, Martin Röösli7. 1. Swiss Tropical and Public Health Institute, Socinstrasse 57,4051 Basel, Switzerland; University of Basel, Petersplatz 1, 4001 Basel, Switzerland. 2. Centre for Chronobiology, Psychiatric Hospital of the University of Basel, Wilhelm Klein-Strasse 27, 4012 Basel, Switzerland. 3. N-sphere AG, Räffelstrasse 29, 8045 Zürich, Switzerland. 4. Empa, Laboratory for Acoustics/Noise control, Swiss Federal Laboratories for Materials Science and Technology, Überland Str. 129, 8600 Dübendorf, Switzerland. 5. Department of Sport, Exercise and Health, Division of Sports and Exercise Medicine, University of Basel, Birsstrasse 320, 4052 Basel, Switzerland. 6. Federal Office for The Environment, Papiermühlestrasse 172, 3063 Ittigen, Switzerland. 7. Swiss Tropical and Public Health Institute, Socinstrasse 57,4051 Basel, Switzerland; University of Basel, Petersplatz 1, 4001 Basel, Switzerland. Electronic address: martin.roosli@swisstph.ch.
Abstract
BACKGROUND: Most epidemiological noise studies consider 24 h average noise exposure levels. Our aim was to exploratively analyze the impact of noise exposure at different time windows during day and night on cardiovascular mortality. METHODS: We generated Switzerland-wide exposure models for road traffic, railway and aircraft noise for different time windows for the year 2001. Combined noise source equivalent continuous sound levels (Leq) for different time windows at the most exposed façade were assigned to each of the 4.41 million Swiss National Cohort adult participants. Follow-up period was from 2000 to 2008. Hazard ratios (HR) of noise effects on various cardiovascular primary causes of death were computed by Cox regression models adjusted for potential confounders and NO2 levels. RESULTS: For most cardiovascular causes of death we obtained indications for a diurnal pattern. For ischemic heart disease the highest HR was observed for the core night hours from 01 h to 05 h (HR per standard deviation of Leq: 1.025, 95% CI: 1.016-1.034) and lower HR for the daytime 07 h to 19 h (1.018 [1.009-1.028]). Heart failure and daytime Leq yielded the highest HR (1.047 [1.027-1.068]). CONCLUSION: For acute cardiovascular diseases, nocturnal intermittent noise exposure tended to be more relevant than daytime exposure, whereas it was the opposite for chronic conditions such as heart failure most strongly associated with continuous daytime noise. This suggests that for acute diseases sleep is an important mediator for health consequences of transportation noise.
BACKGROUND: Most epidemiological noise studies consider 24 h average noise exposure levels. Our aim was to exploratively analyze the impact of noise exposure at different time windows during day and night on cardiovascular mortality. METHODS: We generated Switzerland-wide exposure models for road traffic, railway and aircraft noise for different time windows for the year 2001. Combined noise source equivalent continuous sound levels (Leq) for different time windows at the most exposed façade were assigned to each of the 4.41 million Swiss National Cohort adult participants. Follow-up period was from 2000 to 2008. Hazard ratios (HR) of noise effects on various cardiovascular primary causes of death were computed by Cox regression models adjusted for potential confounders and NO2 levels. RESULTS: For most cardiovascular causes of death we obtained indications for a diurnal pattern. For ischemic heart disease the highest HR was observed for the core night hours from 01 h to 05 h (HR per standard deviation of Leq: 1.025, 95% CI: 1.016-1.034) and lower HR for the daytime 07 h to 19 h (1.018 [1.009-1.028]). Heart failure and daytime Leq yielded the highest HR (1.047 [1.027-1.068]). CONCLUSION: For acute cardiovascular diseases, nocturnal intermittent noise exposure tended to be more relevant than daytime exposure, whereas it was the opposite for chronic conditions such as heart failure most strongly associated with continuous daytime noise. This suggests that for acute diseases sleep is an important mediator for health consequences of transportation noise.
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