Huang Jing, Yang Teng, Gulliver John, Hansell Anna L, Mamouei Mohammad, Cai Yutong Samuel, Rahimi Kazem
Department of Occupational and Environmental Health Sciences, School of Public Health, Peking University, Beijing, China.
Deep Medicine, Nuffield Department of Women's and Reproductive Health, University of Oxford, Oxford, United Kingdom.
JACC Adv. 2023 Mar;2(2):None. doi: 10.1016/j.jacadv.2023.100262.
The quality of evidence regarding the associations between road traffic noise and hypertension is low due to the limitations of cross-sectional study design, and the role of air pollution remains to be further clarified.
The purpose of this study was to evaluate the associations of long-term road traffic noise exposure with incident primary hypertension; we conducted a prospective population-based analysis in UK Biobank.
Road traffic noise was estimated at baseline residential address using the common noise assessment method model. Incident hypertension was ascertained through linkage with medical records. Cox proportional hazard models were used to estimate hazard ratios (HRs) for association in an analytical sample size of over 240,000 participants free of hypertension at baseline, adjusting for covariates determined via directed acyclic graph.
During a median of 8.1 years follow-up, 21,140 incident primary hypertension (International Classification of Diseases-10th Revision [ICD-10]: I10) were ascertained. The HR for a 10 dB[A] increment in mean weighted average 24-hour road traffic noise level ( ) exposure was 1.07 (95% CI: 1.02-1.13). A dose-response relationship was found, with HR of 1.13 (95% CI: 1.03-1.25) for >65 dB[A] vs ≤55 dB[A] ( for trend <0.05). The associations were all robust to adjustment for fine particles (PM) and nitrogen dioxide (NO). Furthermore, high exposure to both road traffic noise and air pollution was associated with the highest hypertension risk.
Long-term exposure to road traffic noise was associated with increased incidence of primary hypertension, and the effect estimates were stronger in presence of higher air pollution.
由于横断面研究设计的局限性,关于道路交通噪声与高血压之间关联的证据质量较低,空气污染的作用仍有待进一步阐明。
本研究旨在评估长期道路交通噪声暴露与原发性高血压发病之间的关联;我们在英国生物银行进行了一项基于人群的前瞻性分析。
使用常见噪声评估方法模型在基线居住地址估算道路交通噪声。通过与医疗记录的关联确定高血压发病情况。在基线时无高血压的超过240,000名参与者的分析样本中,使用Cox比例风险模型估计关联的风险比(HR),并对通过有向无环图确定的协变量进行调整。
在中位8.1年的随访期间,确定了21,140例原发性高血压发病(国际疾病分类第10版[ICD - 10]:I10)。平均加权平均24小时道路交通噪声水平()暴露每增加10 dB[A],HR为1.07(95% CI:1.02 - 1.13)。发现了剂量反应关系,>65 dB[A]与≤55 dB[A]相比,HR为1.13(95% CI:1.03 - 1.25)(趋势P<0.05)。这些关联在调整细颗粒物(PM)和二氧化氮(NO)后均具有稳健性。此外,道路交通噪声和空气污染的高暴露与最高的高血压风险相关。
长期暴露于道路交通噪声与原发性高血压发病率增加相关,在空气污染较高的情况下效应估计更强。