BIC-ESAT and SKL-ESPC, College of Environmental Sciences and Engineering, Peking University, Beijing 100871, China; GRiC, Shenzhen Institute of Building Research Co., Ltd., Xiong'an 071700, China.
Peking University First Hospital, Peking University, Beijing 100034, China.
Sci Total Environ. 2021 Sep 20;788:147760. doi: 10.1016/j.scitotenv.2021.147760. Epub 2021 May 15.
The underlying mechanism on the susceptibility of chronic obstructive pulmonary disease (COPD) patients to air pollution has yet to be clarified.
Based on the COPD in Beijing (COPDB) study, we examined whether lung dysfunction contributed to pollutant-associated systemic inflammation in COPD patients.
Proinflammatory biomarkers including interleukin-8 (IL-8) and tumor necrosis factor α (TNFα) were measured in serum samples collected from 53 COPD and 82 healthy participants. Concentrations of particulate matter with aerodynamic diameter ≤ 2.5 μm (PM), carbonaceous components in PM, and PM size distribution were continuously monitored. Linear mixed effects models were used to examine the associations of biomarker differences with particle exposure, between COPD and healthy participants, and across subgroups with different levels of lung dysfunction.
COPD patients showed higher differences in IL-8 and TNFα levels associated with exposure to measured pollutants, comparing to healthy controls. In advanced analysis, particle-associated differences in IL-8 and TNFα levels were higher in participants with poorer lung ventilation and diffusion capacity, and higher ratio of residual volume. For example, an interquartile range increase in average PM concentration 2 weeks before visits was associated with a 15.7% difference in IL-8 level in participants with the lowest ratio of measured value to predicted value of forced expiratory volume in 1 s (FEV1%pred) (65.2%), and the association decreased monotonically with increasing FEV1%pred. Associations between differences in TNFα level and average ultrafine particle concentration 1 week before visits increased gradually with increasing ratio of measured value to predicted value of residual volume/total lung capacity.
COPD patients, especially those with poorer lung function, are more susceptible to systemic inflammation associated with fine particle exposure.
慢性阻塞性肺疾病（COPD）患者对空气污染易感性的潜在机制尚不清楚。
基于 COPD 在北京（COPDB）研究，我们研究了肺功能障碍是否导致 COPD 患者与污染物相关的全身炎症。
从 53 例 COPD 患者和 82 例健康对照者的血清样本中检测了促炎生物标志物白细胞介素-8（IL-8）和肿瘤坏死因子-α（TNFα）。连续监测了空气动力学直径≤2.5μm（PM）的颗粒物浓度、PM 中的碳质成分和 PM 粒径分布。采用线性混合效应模型，检验生物标志物差异与颗粒物暴露、COPD 患者与健康对照者之间、以及不同肺功能障碍水平亚组之间的关系。
与健康对照组相比，COPD 患者暴露于测量污染物时，IL-8 和 TNFα 水平的差异更大。在进一步分析中，肺通气和弥散功能较差、残气量与肺总量比值较高的患者，与颗粒物相关的 IL-8 和 TNFα 水平差异更大。例如，在访视前 2 周平均 PM 浓度的一个四分位距增加，与用力呼气量 1 秒率（FEV1%pred）最低的患者（65.2%）IL-8 水平差异 15.7%相关，且这种关联随着 FEV1%pred 的增加而呈单调递减。访视前 1 周平均超细颗粒浓度与 TNFα 水平差异的相关性随着残气量/肺总量比值的增加而逐渐增加。
COPD 患者，尤其是肺功能较差的患者，更容易受到细颗粒物暴露引起的全身炎症反应。
