To the Editor:
We read with interest the article by Camp et al. [1] published in the European Respiratory Journal. In this study, based on both qualitative and quantitative computed tomography (CT) scan measures, the authors established that women exposed to biomass smoke had less emphysema than women exposed to tobacco smoke with similar obstruction observed by spirometry [1]. In addition, they described the presence of bronchiectasis in 14% of the biomass-exposed women compared to 0% of the tobacco-exposed women, without differences between the groups in the quantitative measures of air trapping or airway thickness on the inspiratory scans [1]. Finally, the authors concluded that this is the first study showing differences in chronic obstructive pulmonary disease (COPD) phenotypes in living women with biomass- versus tobacco-smoke exposure [1]. However, there have been previous studies investigating the differences in clinical presentation, pulmonary function tests and CT scan findings between COPD related to wood smoke and tobacco smoke [[2–5]. In 2008, a review by Torres-Duque et al. [6] of evidence on biomass fuels and respiratory diseases presented the existing information about the similarities and differences between COPD related to cigarette smoking and biomass smoke.
A recent study from Colombia [3] compared the CT scans and functional findings in severe COPD related to wood smoke and tobacco smoke. The airflow obstruction observed by spirometry, the hyperinflation in lung volumes and the increase of the airway resistance were similar in both groups. Based on the CT scans, we demonstrated that, unlike women with smoking-related COPD, those with wood smoke-related COPD and severe obstruction did not have emphysema, but did have significant airway involvement that manifested as peribronchial thickening (75% versus 10%, p=0,008) and bronchial dilation (67% versus 10%, p=0,024). In addition, they had tree-in-bud pattern (25%) and subsegmental atelectasis (33%), neither of which were found in those with tobacco smoke-related COPD. In concordance with the CT findings, women with wood smoke-related COPD had less decrease in the diffusing capacity for carbon monoxide (DLCO) and the DLCO/alveolar volume ratio than women with smoking related-COPD and a similar grade of obstruction [3]. This functional finding has been reported in patients with obstruction without emphysema and is probably due to severe bronchial obstruction and incomplete mixing of inspired gas during the determination of single breath DLCO. With these results, we postulated that the airflow obstruction in wood smoke COPD is mainly caused by severe airway involvement rather than by a loss of elastic recoil due to emphysema. Similar to our results, a recent study from Brazil [4] showed that the most common findings on CT scans in a wood smoke-exposed COPD group were bronchial wall thickening (66.7%), bronchiectasis (54.8%), mosaic perfusion pattern (45.2%), parenchymal bands, tree-in-bud pattern and laminar atelectasis (p<0.001 versus the control group for all) and, in contrast, emphysema was uncommon. The authors described a positive association between bronchial wall thickening and hour-years of wood smoke exposure [4].
In another study in women with similar age and baseline airflow obstruction, it was demonstrated that the bronchial hyperresponsiveness level was more severe in wood smoke COPD than in tobacco smoke COPD using the methacholine challenge test (p<0.028) [5]. With these findings, it was suggested that the observed greater airway involvement induced by the chronic exposure to wood smoke could explain the differences in bronchial hyperresponsiveness between the two groups [5].
In conclusion, the study from Camp et al. [1] complements the existing information about the significant differences in the clinical presentation, pulmonary function test and CT findings between wood smoke- and tobacco smoke-related COPD, reinforcing the fact that wood smoke COPD could configure a different phenotype. The information from these studies [[1–5] contributes to a better understanding of COPD and suggests that pathophysiologically distinct diseases, caused by a different irritant that shares airflow obstruction, could be included within the term COPD.
Footnotes
Conflict of interest: None declared.
- Received December 20, 2013.
- Accepted January 11, 2014.
- © ERS 2014