Special
attention has emerged towards
biomass smoke-induced
chronic obstructive pulmonary disease (
COPD), providing new
knowledge for prevention and
therapeutic approach of
non-smoker COPD patients. However, the
understanding of
biomass smoke COPD is still limited and somewhat controversial. The aim of the present study was to compare
COPD exclusively caused by
tobacco smoking with
COPD exclusively caused by environmental or
occupational exposures. For this
cross-sectional study,
COPD patients were recruited from
outpatient clinics and formed two groups
non-smoker COPD group (n=16) with exposure to
biomass smoke who did not
smoke cigarette and
tobacco smoker COPD group (n=15) with people
who did not
report biomass smoke exposure. Subjects underwent
pulmonary function tests, thoracic high-resolution computed
tomography,
6-min walk test, and
sputum induction. The
non-smoker COPD group had
biomass smoke exposure of 133.3±86 hour-years. The tobacco
COPD group smoked 48.5±27.4 pack-years.
Women were 62.5 and 66.7%, respectively, of
non-smokers and
smokers. The
non-smoker COPD group showed higher
prevalence of
dyspnea, lower arterial
oxygen tension (PaO2), and lower arterial
oxygen saturation (SaO2%) with
similar spirometry results,
lung volumes, and
diffusion capacity. Regarding inflammatory
biomarkers, differences were detected in
sputum number of lymphomononuclear
cells and in
sputum concentrations of
interleukin (IL)-6 and
IL-8 with higher values in the
smoker group.
Emphysema was more prevalent in the
tobacco smoker group, which also showed higher relative bronchial wall thickness and lower
lung density by
quantitative analysis.
Biomass smoke induced more
hypoxemia compared to tobacco in
COPD patients with
similar severity.