National Clinical Research Center for Respiratory Disease, State Key Laboratory of Respiratory Disease, Guangzhou Institute of Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou, China.
Respirology. 2018 Feb;23(2):198-205. doi: 10.1111/resp.13176. Epub 2017 Sep 14.
Chronic exposure to biomass smoke (BS) can significantly compromise pulmonary function and lead to chronic obstructive pulmonary disease (COPD). To determine whether BS exposure induces a unique phenotype of COPD from an early stage, with different physiopathological features compared with COPD associated with smoking (cigarette-smoke (CS) COPD), we assessed the physiopathology of early COPD associated with BS exposure (BS COPD) by incorporating spirometry, high-resolution computed tomography (HRCT) imaging, bronchoscopy and pathological examinations.
In this cross-sectional study, we recruited 29 patients with BS COPD, 31 patients with CS COPD and 22 healthy controls, including 12 BS-exposed subjects who did not smoke and 10 healthy smokers without BS exposure. Spirometry, HRCT scans, bronchoscopy and bronchial mucosa biopsies were performed to assess lung function, emphysema and air trapping, as well as the pathological characteristics and levels of inflammatory cells in bronchoalveolar lavage fluid (BALF).
Among COPD patients with mild-to-moderate airflow limitation, BS exposure caused greater small airway dysfunction in BS COPD patients, although these patients had less emphysema and air trapping, as detected by HRCT (P < 0.05). We also observed significantly thicker basement membranes and greater endobronchial pigmentation in BS COPD than in CS COPD (P < 0.05). Moreover, patients with BS COPD exhibited greater macrophage and lymphocyte infiltration but reduced neutrophil infiltration in their BALF (P < 0.05).
We used both radiology and pathology to document a distinct COPD phenotype associated with BS exposure. This is characterized by small airway disease.
慢性暴露于生物质烟雾（BS）会显著损害肺功能，导致慢性阻塞性肺疾病（COPD）。为了确定 BS 暴露是否会从早期就引起一种独特的 COPD 表型，与与吸烟相关的 COPD（香烟烟雾（CS）COPD）相比具有不同的生理病理学特征，我们通过纳入肺功能测定、高分辨率计算机断层扫描（HRCT）成像、支气管镜检查和病理检查，评估了与 BS 暴露相关的早期 COPD（BS COPD）的生理病理学。
在这项横断面研究中，我们招募了 29 名 BS COPD 患者、31 名 CS COPD 患者和 22 名健康对照者，包括 12 名不吸烟的 BS 暴露者和 10 名无 BS 暴露的健康吸烟者。进行肺功能测定、HRCT 扫描、支气管镜检查和支气管黏膜活检，以评估肺功能、肺气肿和气腔潴留，以及支气管肺泡灌洗液（BALF）中炎症细胞的病理特征和水平。
在有轻度至中度气流受限的 COPD 患者中，BS 暴露导致 BS COPD 患者的小气道功能障碍更大，尽管这些患者的肺气肿和气腔潴留较少，HRCT 检测结果显示（P<0.05）。我们还观察到 BS COPD 患者的支气管内膜色素沉着和基底膜较厚，明显大于 CS COPD 患者（P<0.05）。此外，BS COPD 患者的 BALF 中巨噬细胞和淋巴细胞浸润显著增加，中性粒细胞浸润减少（P<0.05）。
我们使用放射学和病理学来记录与 BS 暴露相关的独特 COPD 表型。其特征为小气道疾病。
