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Association between Air Pollution Exposure and Inflammation in Chronic Obstructive Pulmonary Disease Patients in Beijing, China

机译:北京地区慢性阻塞性肺疾病患者的空气污染与炎症之间的关系

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Background/Aim: Chronic obstructive pulmonary disease (COPD), characterized by chronic inflammation, is one of the leading causes of death worldwide. The biological mechanism of inflammation associated with exposure to air pollution in COPD patients are not well understood. To elucidate the association between air pollution exposure and inflammatory response in COPD patients, 135 subjects, including 53 stable COPD patients and 82 healthy controls, were recruited in a panel study in Beijing, China. Methods: Fractional exhaled nitric oxide (FeNO) and serum cytokines were repeatedly measured from each subject during 4 visits. Levels of air pollutants, including mass and number concentration of fine particulate matter, mass concentration of black carbon/organic carbon (OC)/elemental carbon/ heavy metals, gaseous pollutants, were online monitored. Linear mixed-effect models were used to estimate the different inflammatory responses to the air pollution exposure between COPD patients and healthy controls. Results: Exposures to SO2, OC and ultrafine particles (UFP) were positively associated with the levels of FeNO, which were more significant in COPD patients. Increases in levels of IL-6 associated with CO, Mn and Cu exposures in COPD patients were significantly higher than those in healthy controls. Exposures to UFP and Acc were associated with increasing levels of IL-15, which were more significant in COPD patients. Exposure to CO was associated with decreasing levels of IL-1B, IL-4, IL-10, IL-13 and IL-17A in healthy controls, which was not observed in COPD patients. Conclusions: In summary, COPD patients are susceptible to the acute respiratory inflammation associated with air pollution exposure, and their capabilities to regulate inflammation are weaker than healthy controls. Acknowledgement: The study was funded by National Program on Key Basic Research Project (2015CB553401). We thank all the volunteers, students and staff involved in COPD for their contributions.
机译:背景/目的:慢性阻塞性肺疾病(COPD)以慢性炎症为特征,是全世界主要的死亡原因之一。与COPD患者暴露于空气污染有关的炎症的生物学机制尚未得到很好的了解。为了阐明COPD患者的空气污染暴露与炎症反应之间的关系,在中国北京的一项小组研究中招募了135名受试者,包括53名稳定的COPD患者和82名健康对照。方法:在4次就诊期间,对每名受试者重复测量其呼出气一氧化氮(FeNO)和血清细胞因子。在线监测了空气污染物的水平,包括细颗粒物的质量和数量浓度,黑碳/有机碳(OC)/元素碳/重金属,气态污染物的质量浓度。线性混合效应模型用于估计COPD患者和健康对照者对空气污染暴露的不同炎症反应。结果:接触SO2,OC和超细颗粒(UFP)与FeNO含量呈正相关,在COPD患者中更为明显。 COPD患者中与CO,Mn和Cu暴露相关的IL-6水平升高明显高于健康对照组。暴露于UFP和Acc与IL-15水平升高有关,IL-15水平在COPD患者中更为显着。健康对照组中CO暴露与IL-1B,IL-4,IL-10,IL-13和IL-17A水平降低有关,而COPD患者未观察到。结论:总之,COPD患者易患与空气污染相关的急性呼吸道炎症,其调节炎症的能力比健康对照组弱。致谢:该研究由国家关键基础研究计划(2015CB553401)资助。我们感谢参与COPD的所有志愿者,学生和员工的贡献。

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