• Int J Chron Obstruct Pulmon Dis · Jan 2012

    Comparative Study

    Bronchial hyperresponsiveness in women with chronic obstructive pulmonary disease related to wood smoke.

    • Mauricio González-García, Carlos A Torres-Duque, Adriana Bustos, Claudia Jaramillo, and Darío Maldonado.
    • Fundación Neumológica Colombiana, Bogotá, Colombia. mgonzalez@neumologica.org
    • Int J Chron Obstruct Pulmon Dis. 2012 Jan 1; 7: 367-73.

    PurposeChronic obstructive pulmonary disease (COPD) related to wood smoke exposure is characterized by important inflammation of the central and peripheral airways without significant emphysema. The objective of this study is to describe the bronchial hyperresponsiveness (BHR) level in women with COPD related to wood smoke exposure and to compare it with the BHR in women with COPD related to tobacco smoking.Materials And MethodsTWO GROUPS OF WOMEN WITH STABLE COPD WERE STUDIED: (1) wood smoke exposed (WS-COPD); and (2) tobacco smoke exposed (TS-COPD). A methacholine challenge test (MCT) was performed in all patients according to American Thoracic Society criteria. BHR levels were compared using the methacholine concentration, which caused a 20% fall in the FEV1 (PC20).ResultsThirty-one patients, 19 with WS-COPD and 12 with TS-COPD, were included. There were no significant differences between the groups in baseline FVC, FEV1, IC, FEF25-75, and FEF25-75/FVC. All 31 patients had a positive MCT (PC20<16 mg/mL) and the fall in the FEV1 and IC was similar in both groups. The severity of BHR was significantly higher in the WS-COPD patients (PC20: 0.39 mg/mL) than in the TS-COPD patients (PC20: 1.24 mg/mL) (P=0.028). The presence of cough, phlegm, and dyspnea during the test were similar in both groups.ConclusionWe found moderate to severe BHR in women with WS-COPD, which was more severe than in the TS-COPD women with similar age and airflow obstruction. This paper suggests that the structural and inflammatory changes induced by the chronic exposure to wood smoke, described in other studies, can explain the differences with TS-COPD patients. Future studies may clarify our understanding of the impact of BHR on COPD physiopathology, phenotypes, and treatment strategies.

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