Environmental Epidemiology Group, Institute of Occupational, Social and Environmental Medicine, Centre for Health and Society, Medical Faculty, Heinrich-Heine University Düsseldorf, Düsseldorf, Germany; Institute for Medical Statistics, Medical Faculty, Heinrich-Heine University Düsseldorf, Düsseldorf, Germany.
Environmental Epidemiology Group, Institute of Occupational, Social and Environmental Medicine, Centre for Health and Society, Medical Faculty, Heinrich-Heine University Düsseldorf, Düsseldorf, Germany.
Environ Int. 2020 Mar;136:105493. doi: 10.1016/j.envint.2020.105493. Epub 2020 Jan 25.
An increasing number of studies have been published recently on the association between ambient air pollution (AP) and incident diabetes mellitus (DM), but studies investigating source-specific AP toxicity and potential mediating pathways are rare. We investigated the associations of all-source, traffic-specific, and industry-specific outdoor AP exposure with 10-year incidence of DM and potential mediation via inflammation-associated biomarkers.
Data from participants of the prospective Heinz Nixdorf Recall cohort study who attended the baseline (t; 2000-2003), 5-year follow-up (t; 2006-2008), and 10-year follow-up (t; 2011-2015) examinations was used. For participants without DM at baseline (determined using information on physician diagnosis and glucose-lowering medication), residential long-term exposure (total, traffic-specific, and industry-specific) to particulate matter (PM, PM), nitrogen dioxide (NO), and accumulation mode particle number concentration (PN) were estimated using a chemistry transport model. Covariate-adjusted modified Poisson regression models with robust standard errors were applied to estimate relative risks (RR) for the associations between baseline AP and incident DM at t. Mediation analyses for adiponectin, high-sensitivity C-reactive protein (hsCRP), and interleukin-1 receptor antagonist (IL-1RA) were conducted to estimate natural direct and indirect effects.
Of the 4,814 participants at t, 2,451 participants (mean baseline age: 58.2 years) were included in the main analysis. Interquartile range (IQR) increases in total PM and PN were associated with increased risk of DM (e.g., RR: 1.25 [95% Confidence Interval (CI): 1.02, 1.53] per 3.8 µg/m PM). Whereas traffic-specific exposures were associated with DM risk for all air pollutants (e.g., RR: 1.24 [95% CI: 1.06, 1.46] per 0.3 µg/m PM), significant associations for industry exposures were limited to NO and PN (e.g., RR: 1.24 [95% CI: 1.03, 1.49] per 230 particles/mL PN). Potential mediation of the association between AP and DM was observed for adiponectin but not for hsCRP and IL-1RA.
Our study shows that long-term exposure to total and source-specific ambient AP may increase DM risk, with consistent results observed across traffic-specific exposures. Decreases in adiponectin may play a potential role along the causal pathway.
最近发表了越来越多关于环境空气污染 (AP) 与糖尿病 (DM) 发病之间关系的研究，但研究特定来源的 AP 毒性及其潜在的中介途径的研究很少。我们调查了全源、交通特定和工业特定户外 AP 暴露与 10 年 DM 发病的关联，并通过炎症相关生物标志物进行潜在的中介作用。
本研究使用了前瞻性 Heinz Nixdorf 召回队列研究参与者的数据，他们参加了基线 (t；2000-2003 年)、5 年随访 (t；2006-2008 年) 和 10 年随访 (t；2011-2015 年)。对于基线时没有 DM 的参与者（通过医生诊断和降血糖药物的信息确定），使用化学传输模型估算了长期居住地暴露于颗粒物 (PM、PM)、二氧化氮 (NO) 和积聚模式粒子数浓度 (PN) 的总暴露、交通特定暴露和工业特定暴露。应用调整了协变量的修正泊松回归模型和稳健标准差来估计 AP 与 t 时新发 DM 之间的关联的相对风险 (RR)。为了估计脂联素、高敏 C 反应蛋白 (hsCRP) 和白细胞介素 1 受体拮抗剂 (IL-1RA) 的中介作用，进行了自然直接和间接效应的估计。
在 t 时的 4814 名参与者中，有 2451 名参与者（平均基线年龄：58.2 岁）纳入了主要分析。总 PM 和 PN 的四分位距 (IQR) 升高与 DM 风险增加相关（例如，每 3.8μg/m PM 增加 1.25 [95%置信区间 (CI)：1.02, 1.53]）。交通特定暴露与所有空气污染物的 DM 风险相关（例如，每增加 0.3μg/m PM，RR：1.24 [95% CI：1.06, 1.46]），但工业暴露与 NO 和 PN 相关（例如，每增加 230 个粒子/mL PN，RR：1.24 [95% CI：1.03, 1.49]）。AP 与 DM 之间的关联存在潜在的中介作用，脂联素可能发挥了作用，但 hsCRP 和 IL-1RA 则没有。
我们的研究表明，长期暴露于总源和特定来源的环境 AP 可能会增加 DM 风险，交通特定暴露的结果一致。脂联素的降低可能在因果途径中发挥潜在作用。
