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代谢综合征在长期道路交通噪声、空气污染共同暴露与 2 型糖尿病发病风险之间的中介作用。

Mediation of metabolic syndrome in the association between long-term co-exposure to road traffic noise, air pollution and incident type 2 diabetes.

机构信息

Department of Occupational and Environmental Health Sciences, Peking University School of Public Health, 38 Xueyuan Road, Haidian District, Beijing 100191, China.

Deep Medicine, Nuffield Department of Women's and Reproductive Health, University of Oxford, Oxford OX1 2BQ, UK.

出版信息

Ecotoxicol Environ Saf. 2023 Jun 15;258:114992. doi: 10.1016/j.ecoenv.2023.114992. Epub 2023 May 9.

Abstract

OBJECTIVES

Recent studies have linked exposure to road traffic noise or air pollution with incident type 2 diabetes (T2D), but investigation on their co-exposure was limited and underlying mechanisms remain unclear. We hypothesized that long-term co-exposure to road traffic noise and air pollution increases the risk of incident T2D via the development of metabolic syndrome (MetS).

METHODS

This prospective study included 390,834 participants in UK Biobank. Cumulative risk index (CRI), the health-based weighted levels of multiple exposures, was applied to characterize the co-exposure to 24-hour road traffic noise (L), particulate matter with aerodynamic diameter ≤ 2.5 µm (PM), and nitrogen dioxide (NO). L was modeled by the Common Noise Assessment Methods in Europe and air pollutant levels were measured by the Land Use Regression model at participants' residential addresses. Incident T2D was ascertained through linkages to inpatient hospital records. MetS was defined by five (central obesity, triglycerides, HDL cholesterol, glucose, and blood pressure) or six factors (C-reactive protein additionally). Cox proportional hazard models were used to assess the association between environmental exposures and incident T2D, and mediation analyses were applied to investigate the role of MetS.

RESULTS

After a median of 10.9 years of follow-up, 13,214 (3.4%) incident T2D cases were ascertained. The exposure to L, PM, and NO, as well as their co-exposure, were significantly associated with an elevated risk of incident T2D, with HRs of 1.03 (95%CI: 1.00, 1.05) per 3.5 dB(A) increase in L, 1.05 (95%CI: 1.01, 1.10) per 1.3 μg/m increase in PM, 1.07 (95%CI: 1.02, 1.11) per 9.8 μg/m increase in NO, and 1.06 (95%CI: 1.02, 1.09) per interquartile range increase in CRI. MetS significantly mediated 43.5%- 54.7% of the CRI-T2D relationship.

CONCLUSIONS

Long-term co-exposure to road traffic noise and air pollution is associated with an elevated risk of incident T2D, which may partly be mediated by MetS.

摘要

目的

最近的研究表明,道路交通噪声或空气污染暴露与 2 型糖尿病(T2D)的发生有关,但对两者共同暴露的研究有限,其潜在机制尚不清楚。我们假设,长期共同暴露于道路交通噪声和空气污染会通过代谢综合征(MetS)的发展增加 T2D 的发病风险。

方法

这项前瞻性研究纳入了英国生物银行的 390834 名参与者。应用累积风险指数(CRI),即多种暴露的基于健康的加权水平,来描述 24 小时道路交通噪声(L)、空气动力学直径≤2.5μm 的颗粒物(PM)和二氧化氮(NO)的共同暴露情况。L 通过欧洲共同噪声评估方法进行建模,空气污染物水平则通过居住地址的土地利用回归模型进行测量。T2D 的发病情况通过与住院患者记录的关联来确定。代谢综合征定义为五项(中心性肥胖、甘油三酯、高密度脂蛋白胆固醇、血糖和血压)或六项因素(另外加上 C 反应蛋白)。采用 Cox 比例风险模型评估环境暴露与 T2D 发病的关系,并进行中介分析以探讨 MetS 的作用。

结果

中位随访 10.9 年后,共确定了 13214 例(3.4%)T2D 发病病例。L、PM 和 NO 的暴露以及它们的共同暴露与 T2D 的发病风险升高显著相关,L 每增加 3.5dB(A),风险比(HR)为 1.03(95%CI:1.00,1.05);PM 每增加 1.3μg/m,HR 为 1.05(95%CI:1.01,1.10);NO 每增加 9.8μg/m,HR 为 1.07(95%CI:1.02,1.11);CRI 每增加一个四分位间距,HR 为 1.06(95%CI:1.02,1.09)。代谢综合征显著介导了 CRI-T2D 关系的 43.5%-54.7%。

结论

长期共同暴露于道路交通噪声和空气污染与 T2D 的发病风险升高有关,这可能部分是通过代谢综合征介导的。

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