UBC James Hogg Research Centre, Heart and Lung Institute, St. Paul's Hospital, University of British Columbia, Vancouver, BC, Canada.
UBC James Hogg Research Centre, Heart and Lung Institute, St. Paul's Hospital, University of British Columbia, Vancouver, BC, Canada.
Chest. 2011 Dec;140(6):1540-1549. doi: 10.1378/chest.10-2281. Epub 2011 Jun 9.
Particulate matter (PM) is present in lung tissues of smokers and urban dwellers. This study was designed to quantify the burden of PM in different lung tissues of subjects with COPD and determine its relationship to disease severity.
Surgical lung tissue samples from nonsmokers (control subjects) were compared with those from smokers with normal spirometry and subjects in the four other categories of the GOLD (Global Initiative for Obstructive Lung Disease) classification of COPD severity using quantitative histologic techniques.
PM was present in the lung parenchyma, blood vessel walls, airways, lymphoid follicles, and alveolar macrophages. The total burden of PM (volume fraction [Vv]) in all tissues of the lung was higher in smokers than nonsmokers (P < .001) and also in smokers with airflow obstruction compared with the smokers with normal spirometry (P < .01). There was an incremental increase in total PM burden with increased COPD severity that peaked in GOLD II and then trended downward in GOLD III and IV COPD. This same pattern of PM retention was also observed in alveolar walls. The total burden of PM in lung tissues correlated with a decline in FEV(1)/FVC as well as pack-years smoking. mRNA expression of fibrinogen (γ chain) correlated with total lung burden of PM and burden of PM in lung parenchyma (r(2) = 0.22, P < .001).
We conclude that retained PM is widely distributed in lung tissues of subjects with COPD and that cigarette smoke exposure and airflow obstruction are associated with retention of PM in lung tissues. We attribute the downward trend in PM burden in severe COPD to either less deposition and retention or selective removal of PM containing tissues by emphysematous destruction.
颗粒物(PM)存在于吸烟者和城市居民的肺部组织中。本研究旨在定量评估 COPD 患者不同肺部组织中 PM 的负担,并确定其与疾病严重程度的关系。
使用定量组织学技术,将非吸烟者(对照者)的手术肺组织样本与正常肺功能的吸烟者以及 GOLD(全球倡议阻塞性肺病)分类中其他四类 COPD 严重程度的患者进行比较。
PM 存在于肺实质、血管壁、气道、淋巴滤泡和肺泡巨噬细胞中。所有肺部组织中 PM 的总负担(体积分数 [Vv])在吸烟者中高于非吸烟者(P <.001),在气流受限的吸烟者中也高于肺功能正常的吸烟者(P <.01)。随着 COPD 严重程度的增加,总 PM 负担呈递增趋势,在 GOLD II 达到峰值,然后在 GOLD III 和 IV COPD 中呈下降趋势。这种 PM 保留的模式也在肺泡壁中观察到。肺组织中 PM 的总负担与 FEV1/FVC 下降以及吸烟包年数呈正相关。纤维蛋白原(γ 链)的 mRNA 表达与肺组织中 PM 的总负担以及肺实质中 PM 的负担呈正相关(r2 = 0.22,P <.001)。
我们得出结论,保留的 PM 广泛分布在 COPD 患者的肺部组织中,并且吸烟暴露和气流受限与 PM 在肺部组织中的保留有关。我们将严重 COPD 中 PM 负担的下降趋势归因于 PM 沉积和保留减少,或通过肺气肿破坏选择性清除含 PM 的组织。