Façades, floors and maps - Influence of exposure measurement error on the association between transportation noise and myocardial infarction.

BACKGROUND: Epidemiological research on transportation noise uses different exposure assessment strategies based on façade point estimates or regulatory noise maps. The degree of exposure measurement error and subsequent potentially biased risk estimates related to exposure definition is unclear. We aimed to evaluate associations between transportation noise exposure and myocardial infarction (MI) mortality considering: assumptions about residential floor, façade point selection (loudest, quietest, nearest), façade point vs. noise map estimates, and influence of averaging exposure at coarser spatial scales (e.g. in ecological health studies). METHODS: Lden from the façade points were assigned to >4 million eligible adults in the Swiss National Cohort for the best match residential floor (reference), middle floor, and first floor. For selected floors, the loudest and quietest exposed façades per dwelling, plus the nearest façade point to the residential geocode, were extracted. Exposure was also assigned from 10 × 10 m noise maps, using "buffers" from 50 to 500 m derived from the maps, and by aggregating the maps to larger areas. Associations between road traffic and railway noise and MI mortality were evaluated by multi-pollutant Cox regression models, adjusted for aircraft noise, NO2 and socio-demographic confounders, following individuals from 2000 to 2008. Bias was calculated to express differences compared to the reference. RESULTS: Hazard ratios (HRs) for the best match residential floor were 1.05 (1.02-1.07) and 1.03 (1.01-1.05) per IQR (11.3 and 15.0 dB) for road traffic and railway noise, respectively. In most situations, comparing the alternative exposure definitions to this reference resulted in attenuated HRs. For example, assuming everyone resided on the middle or everyone on first floor introduced little bias (%Bias in excess risk: -1.9 to 4.4 road traffic and -4.4 to 10.7 railway noise). Using the noise grids generated a bias of approximately -26% for both sources. Averaging the maps at a coarser spatial scale led to bias from -19.4 to -105.1% for road traffic and 17.6 to -34.3% for railway noise and inflated the confidence intervals such that some HRs were no longer statistically significant. CONCLUSION: Changes in spatial scale introduced more bias than changes in residential floor. Use of noise maps to represent residential exposure may underestimate noise-induced health effects, in particular for small-scale heterogeneously distributed road traffic noise in urban settings.

A systematic analysis of mutual effects of transportation noise and air pollution exposure on myocardial infarction mortality: a nationwide cohort study in Switzerland.

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.

Diurnal variability of transportation noise exposure and cardiovascular mortality: A nationwide cohort study from Switzerland.

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.

Transportation noise exposure and cardiovascular mortality: a nationwide cohort study from Switzerland.

Most studies published to date consider single noise sources and the reported noise metrics are not informative about the peaking characteristics of the source under investigation. Our study focuses on the association between cardiovascular mortality in Switzerland and the three major transportation noise sources-road, railway and aircraft traffic-along with a novel noise metric termed intermittency ratio (IR), expressing the percentage contribution of individual noise events to the total noise energy from all sources above background levels. We generated Swiss-wide exposure models for road, railway and aircraft noise for 2001. Noise from the most exposed façade was linked to geocodes at the residential floor height for each of the 4.41 million adult (>30 y) Swiss National Cohort participants. For the follow-up period 2000-2008, we investigated the association between all noise exposure variables [Lden(Road), Lden(Rail), Lden(Air), and IR at night] and various cardiovascular primary causes of death by multipollutant Cox regression models adjusted for potential confounders including NO2. The most consistent associations were seen for myocardial infarction: adjusted hazard ratios (HR) (95% CI) per 10 dB increase of exposure were 1.038 (1.019-1.058), 1.018 (1.004-1.031), and 1.026 (1.004-1.048) respectively for Lden(Road), Lden(Rail), and Lden(Air). In addition, total IR at night played a role: HRs for CVD were non-significant in the 1st, 2nd and 5th quintiles whereas they were 1.019 (1.002-1.037) and 1.021 (1.003-1.038) for the 3rd and 4th quintiles. Our study demonstrates the impact of all major transportation noise sources on cardiovascular diseases. Mid-range IR levels at night (i.e. between continuous and highly intermittent) are potentially more harmful than continuous noise levels of the same average level.