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Small airway disease: A different phenotype of early stage COPD associated with biomass smoke exposure
Author(s) -
Zhao Dongxing,
Zhou Yumin,
Jiang Changbin,
Zhao Zhuxiang,
He Fang,
Ran Pixin
Publication year - 2018
Publication title -
respirology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 85
eISSN - 1440-1843
pISSN - 1323-7799
DOI - 10.1111/resp.13176
Subject(s) - medicine , copd , airway , phenotype , smoke , pulmonary disease , disease , stage (stratigraphy) , immunology , gene , anesthesia , genetics , biology , paleontology , physics , meteorology
Background and objective 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. Methods 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 ). Results 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). Conclusion We used both radiology and pathology to document a distinct COPD phenotype associated with BS exposure. This is characterized by small airway disease.