Department of Epidemiology and Public Health, Swiss Tropical and Public Health Institute, Socinstrasse 57, Basel, Switzerland.
University of Basel, Petersplatz 1, Basel, Switzerland.
Eur Heart J. 2019 Feb 14;40(7):598-603. doi: 10.1093/eurheartj/ehy650.
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.
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.
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.
本研究旨在基于高质量/精细分辨率的暴露建模，厘清道路交通、铁路和航空交通这三大交通噪声源以及空气污染物二氧化氮（NO2）和细颗粒物（PM2.5）对瑞士心肌梗死（MI）死亡率的风险。
我们为瑞士国家队列（SNC）中 440 万（>30 岁）成年人的每个地址建模了长期的室外道路交通、铁路和航空噪声水平以及 NO2 和 PM2.5 浓度。在 2000-08 年的随访期间，我们通过多污染物 Cox 回归模型，考虑潜在混杂因素，根据 NO2 和/或 PM2.5 调整噪声[Lden（道路）、Lden（铁路）和 Lden（航空）]估计值，反之亦然，以此来研究交通噪声/空气污染暴露与 MI 死亡之间的相关性。调整了道路交通（无空气污染：1.032，95%CI：1.014-1.051，考虑了 NO2 和 PM2.5 的调整风险估计值：1.034，95%CI：1.014-1.055）、铁路交通（1.020，95%CI：1.007-1.033 与 1.020，95%CI：1.007-1.033）和航空交通噪声（1.025，95%CI：1.006-1.045 与 1.025，95%CI：1.005-1.046）每增加 10dB 时，MI 的危险比（HR）不会改变。而调整空气污染物的噪声 HR 低于未调整噪声的相应估计值。NO2 每增加 10μg/m³，调整噪声后的 HR 为 1.024（1.005-1.043），而未调整噪声后的 HR 为 0.990（0.965-1.016）；PM2.5 每增加 10μg/m³，调整噪声后的 HR 为 1.054（1.013-1.093），而未调整噪声后的 HR 为 1.019（0.971-1.071）。
本研究表明，交通噪声与 MI 死亡率有关，与空气污染无关。空气污染研究如果没有充分调整交通噪声暴露，可能会高估空气污染对心血管疾病的负担。
