Traffic-related air pollution is associated with cardio-metabolic biomarkers in general residents

Traffic-related air pollution is associated with cardio-metabolic biomarkers in general residents
复制标题

交通相关空气污染与普通居民的心脏代谢生物标志物相关

DOI:
10.1007/s00420-016-1129-3
复制
发表时间:
2016-08-01
影响因子:
3
通讯作者:
Zhao, Jinzhuo
Zhao, Jinzhuo
中科院分区:
医学3区
文献类型:
--
作者:
Jiang, Shuo;Bo, Liang;Zhao, Jinzhuo

文献摘要

被引文献

相似文献

目的探讨交通空气污染与心脏代谢风险的关系机制。方法研究对象为371名年龄在45 ~ 75岁之间的上海城市居民。根据住宅与主要道路的距离,将参与者分为≤50、51-100、101-200和100 - 200米四类。此外,从上午8:00至下午6:00测量个人细颗粒物(PM2.5),以评估一般居民的PM2.5暴露情况。然后,检测与心脏代谢紊乱相关的连续亚临床测量和生物学效应。应用广义线性回归分析估计与交通相关空气污染相关的心脏代谢紊乱的校正危险比。结果居住在距离主干道50 m范围内的居民人均PM2.5为111.1 μg/m3,显著高于居住在距离主干道200 m范围内的居民人均PM2.5为68.2 μg/m3。居住在距离主干道50米以内的参与者心率(HR)比200米以外的参与者高1.15倍,空腹胰岛素高1.95倍,胰岛素抵抗稳态模型评估(HOMA-IR)高1.30倍,低密度脂蛋白胆固醇(LDL-C)高1.56倍,白细胞介素6 (IL-6)高8.39倍,增强指数(AI)高4.30倍。收缩压(SBP)高1.60倍,舒张压(DBP)高1.91倍。与上述生物效应的增加相反,低频(LF)降低1.06倍,高频(HF)降低1.05倍,IL-10降低2.54倍,一氧化氮(NO)降低4.61倍,超氧化物歧化酶(SOD)降低1.19倍,总抗氧化能力(T-AOC)降低1.85倍。在空腹血糖、LF/HF、胆固醇和高密度脂蛋白(HDL)中未观察到明显的暴露-反应关系。结论长期暴露于交通相关的空气污染可能导致心代谢疾病的发生或加重。空气污染与心脏代谢紊乱之间的联系机制可能与全身炎症和氧化应激增加、胰岛素敏感性降低、动脉僵硬度和血压升高有关。
PurposeThe study was conducted to explore the mechanisms linking traffic-related air pollution and cardio-metabolic risk.MethodsThe participants included 371 men and women aged from 45 to 75 in an urban residential area in Shanghai, China. The participants were divided into four categories (≤50, 51–100, 101–200 and >200 m) according to the residential distance to major road. Additionally, the personal fine particulate matter (PM2.5) was measured from 8:00 am to 6:00 pm to assess the PM2.5exposure in general residents. Then, the continuous subclinical measurements and biological effects related to cardio-metabolic disorders were detected. The generalized linear regression analysis was applied for estimating the adjusted hazards ratio for cardio-metabolic disorders relative to traffic-related air pollution.ResultsThe average personal PM2.5is 111.1 μg/m3in the participants living within 50 m to major road, which is significantly higher than the personal PM2.5(68.2 μg/m3) in the participants living more than 200 m away from the major road. The participants living within 50 m to major road compared with those living more than 200 m away have 1.15 times higher of heart rate (HR), 1.95 times higher of fasting insulin, 1.30 times higher of homeostasis model assessment of insulin resistance (HOMA-IR), 1.56 times higher of low-density lipoprotein cholesterol (LDL-C), 8.39 times higher of interleukin 6 (IL-6), 4.30 times higher of augmentation index (AI), 1.60 times higher of systolic blood pressure (SBP) and 1.91 times higher of diastolic blood pressure (DBP). Contrary to the increase in above biological effects, there were 1.06 times lower of low frequency (LF), 1.05 times lower of high frequency (HF), 2.54 times lower of IL-10, 4.61 times lower of nitric oxide (NO), 1.19 times lower of superoxide dismutase (SOD) and 1.85 times lower of total antioxidant capacity (T-AOC). There was no clear exposure–response relationship can be observed in the fasting glucose, LF/HF, cholesterol and high-density lipoprotein (HDL).ConclusionLong-term exposure to traffic-related air pollution may contribute to the development or exacerbation of cardio-metabolic disorders. The mechanisms linking air pollution and cardio-metabolic disorders may be associated with the increased systemic inflammation and oxidative stress, reduced insulin sensitivity and elevated arterial stiffness and blood pressure.