Traffic pollution and the incidence of cardiorespiratory outcomes in an adult cohort in London.
Traffic pollution and the incidence of cardiorespiratory outcomes in an adult cohort in London.
复制标题
DOI：
10.1136/oemed-2015-103531
复制
发表时间：
2016-12
影响因子：
4.9
通讯作者：
Kelly FJ
中科院分区：
文献类型：
--
作者：
Carey IM;Anderson HR;Atkinson RW;Beevers S;Cook DG;Dajnak D;Gulliver J;Kelly FJ
关于长期暴露于空气和交通噪音污染对健康产生不利影响的流行病学证据并不一致。此外，背景与附近的交通污染浓度在这一过程中的相对作用还不清楚。我们调查了伦敦交通噪声污染和突发心肺疾病的空气浓度模型之间的关系。在2005年至2011年期间在75个大伦敦诊所登记的211016名40-79岁的成年人中，从初级保健和医院记录中确定了一系列心血管和呼吸结局的首次诊断。 氮氧化物（NOx）、排气和非排气源产生的空气动力学直径中值<2.5 μm的颗粒物（PM2.5）、交通强度和噪声的年度基线浓度是根据分散模型以20 m2的分辨率估算的，并通过住宅邮政编码与临床数据相关联。 HR调整混杂因素，包括吸烟和区域剥夺。观察到的最大关联是交通相关的空气污染和心力衰竭之间的关联（对于20 μg/m3的NOx变化，HR=1.10，95% CI 1.01至1.21）。 然而，没有其他结果与任何污染指标（包括噪音）一致相关。不同做法之间的交通造成的模拟空气污染差异较大，妨碍了有意义的精细空间尺度分析。观察到的与心力衰竭的相关性可能提示加重效应，而不是潜在的慢性疾病。然而，总体上未能观察到与交通污染的更广泛的关联，这可能反映出基于居住地的暴露估计不足以代表个人暴露的相关模式，未来的研究必须解决这个问题。
The epidemiological evidence for adverse health effects of long-term exposure to air and noise pollution from traffic is not coherent. Further, the relative roles of background versus near traffic pollution concentrations in this process are unclear. We investigated relationships between modelled concentrations of air and noise pollution from traffic and incident cardiorespiratory disease in London. Among 211 016 adults aged 40–79 years registered in 75 Greater London practices between 2005 and 2011, the first diagnosis for a range of cardiovascular and respiratory outcomes were identified from primary care and hospital records. Annual baseline concentrations for nitrogen oxide (NOx), particulate matter with a median aerodynamic diameter <2.5 μm (PM2.5) attributable to exhaust and non-exhaust sources, traffic intensity and noise were estimated at 20 m2 resolution from dispersion models, linked to clinical data via residential postcode. HRs were adjusted for confounders including smoking and area deprivation. The largest observed associations were between traffic-related air pollution and heart failure (HR=1.10 for 20 μg/m3 change in NOx, 95% CI 1.01 to 1.21). However, no other outcomes were consistently associated with any of the pollution indicators, including noise. The greater variations in modelled air pollution from traffic between practices, versus within, hampered meaningful fine spatial scale analyses. The associations observed with heart failure may suggest exacerbatory effects rather than underlying chronic disease. However, the overall failure to observe wider associations with traffic pollution may reflect that exposure estimates based on residence inadequately represent the relevant pattern of personal exposure, and future studies must address this issue.