State Key Joint Laboratory for Environmental Simulation and Pollution Control, College of Environmental Sciences and Engineering, Peking University, Beijing, China.
Hebei Xiongan Green-Research Inspection and Certification Co., Ltd., Shenzhen Institute of Building Research Co., Ltd., Shenzhen, China.
Environ Health Perspect. 2020 Jun;128(6):67004. doi: 10.1289/EHP4906. Epub 2020 Jun 1.
Accumulating evidence suggests that individuals with glucose metabolism disorders are susceptible to mortality associated with fine particles. However, the mechanisms remain largely unknown.
We examined whether particle-associated respiratory inflammation differed between individuals with prediabetes and healthy control participants.
Based on a panel study [A prospective Study COmparing the cardiometabolic and respiratory effects of air Pollution Exposure on healthy and prediabetic individuals (SCOPE)] conducted in Beijing between August 2013 and February 2015, fractional exhaled nitric oxide (FeNO) was measured from 112 participants at two to seven visits to indicate respiratory inflammation. Particulate pollutants-including particulate matter with an aerodynamic diameter of (), black carbon (BC), ultrafine particles (UFPs), and accumulated-mode particles-were monitored continuously at a single central monitoring site. Linear mixed-effects models were used to estimate associations between ln-FeNO with pollutant concentrations at individual 1-h lags (up to 24 h) and with average concentrations at 8 and 24 h before the clinical visit. We evaluated glucose metabolism disorders as a potential modifier by comparing associations between participants with high vs. low average fasting blood glucose (FBG) and homeostasis model assessment insulin resistance (HOMA-IR) levels.
FeNO was positively associated with all pollutants, with the strongest associations for an interquartile range increase in 1-h lagged exposures (ranging from 21.3% for to 74.7% for BC). Associations differed significantly according to average HOMA-IR values when lagged 6-18 h for , 15-19 h for BC, and 6-15 h for UFPs, with positive associations among those with while associations were closer to the null or inverse among those with . Associations between and FeNO were consistently higher among individuals with average vs. low FBG, with significant differences for multiple hourly lags.
Glucose metabolism disorders may aggravate respiratory inflammation following exposure to ambient particulate matter. https://doi.org/10.1289/EHP4906.
越来越多的证据表明,葡萄糖代谢紊乱的个体易受到与细颗粒物相关的死亡率的影响。然而,其机制在很大程度上尚不清楚。
我们研究了前驱糖尿病患者和健康对照者之间,颗粒相关的呼吸炎症是否存在差异。
基于 2013 年 8 月至 2015 年 2 月在北京进行的一项前瞻性研究(比较空气污染暴露对健康和前驱糖尿病个体的心血管代谢和呼吸影响的研究(SCOPE)),在两次至七次就诊中,从 112 名参与者中测量了呼出气一氧化氮分数(FeNO)以指示呼吸炎症。连续监测了包括空气动力学直径()在内的颗粒污染物、黑碳(BC)、超细颗粒(UFPs)和累积模式颗粒)在一个单一的中央监测点。使用线性混合效应模型来估计 ln-FeNO 与个体 1 小时滞后(最长 24 小时)的污染物浓度之间的关联,以及临床就诊前 8 小时和 24 小时的平均浓度之间的关联。我们通过比较高平均空腹血糖(FBG)和稳态模型评估胰岛素抵抗(HOMA-IR)水平的参与者与低平均 FBG 参与者之间的关联,评估了葡萄糖代谢紊乱作为潜在修饰物的作用。
FeNO 与所有污染物呈正相关,与 1 小时滞后暴露的中值范围增加呈最强相关(范围从 1 小时滞后的中值范围增加的 21.3%到 BC 的 74.7%)。当滞后 6-18 小时时,BC 的滞后 15-19 小时,UFPs 的滞后 6-15 小时时,根据平均 HOMA-IR 值,关联差异显著,与高 HOMA-IR 水平的参与者呈正相关,而与低 HOMA-IR 水平的参与者呈接近零或负相关。在平均 与低 FBG 的参与者中,与 FeNO 之间的关联始终高于高 与 FeNO 之间的关联,多个小时滞后均有显著差异。
葡萄糖代谢紊乱可能会加重暴露于环境细颗粒物后的呼吸炎症。