Biomass smoke COPD has less tomographic abnormalities but worse hypoxemia compared with tobacco COPD
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...
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| Published in: | Brazilian journal of medical and biological research Vol. 52; no. 5; p. e8233 |
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Brazil
Associacao Brasileira de Divulgacao Cientifica (ABDC)
01-01-2019
Revista Brasileira de Pesquisas Medicas Associação Brasileira de Divulgação Científica |
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| Abstract | 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. |
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| AbstractList | 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. 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 crosssectional 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 [+ or -]86 hour- years. The tobacco COPD group smoked 48.5 [+ or -]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 (Pa[O.sub.2]), and lower arterial oxygen saturation (Sa[O.sub.2]%) 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. 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 (PaO 2 ), and lower arterial oxygen saturation (SaO 2 %) 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. 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.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. 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 crosssectional 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. 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 crosssectional 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 [+ or -]86 hour- years. The tobacco COPD group smoked 48.5 [+ or -]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 (Pa[O.sub.2]), and lower arterial oxygen saturation (Sa[O.sub.2]%) 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. Key words: Chronic obstructive pulmonary disease; Biomass; Tobacco |
| Audience | Academic |
| Author | Cunha, F Q Koenigkam-Santos, M Menezes, M B de Tonidandel, P R Pereira, M C Vianna, E O Meneghini, A C Terra-Filho, J |
| AuthorAffiliation | Universidade de São Paulo Universidade Estadual de Campinas |
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| CitedBy_id | crossref_primary_10_2147_COPD_S397996 crossref_primary_10_2147_COPD_S439064 crossref_primary_10_1167_iovs_64_11_24 crossref_primary_10_1007_s13665_023_00318_9 crossref_primary_10_2147_COPD_S267114 crossref_primary_10_1080_17476348_2021_1835476 crossref_primary_10_3389_fmed_2021_700836 crossref_primary_10_3390_medicina57090911 |
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| Keywords | Tobacco Chronic obstructive pulmonary disease Biomass |
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| References_xml | – volume: 139 start-page: 752 year: 2011 ident: ref6 article-title: COPD in never smokers publication-title: Chest doi: 10.1378/chest.10-1253 contributor: fullname: Lamprecht B – volume: 12 start-page: 1092 year: 2008 ident: ref5 article-title: Wood smoke-associated lung disease: a clinical, functional, radiological and pathological description publication-title: Int J Tuberc Lung Dis contributor: fullname: Moran-Mendoza O – volume: 54 start-page: 192 year: 2014 ident: ref22 article-title: Evaluation of respiratory impairment in patients with systemic lupus erythematosus with the six-min walk test publication-title: Rev Bras Reumatol contributor: fullname: Leite MA – volume: 151 start-page: 686 year: 2017 ident: ref3 article-title: Improving the management of COPD in women publication-title: Chest doi: 10.1016/j.chest.2016.10.031 contributor: fullname: Jenkins CR – volume: 123 start-page: 185 year: 1981 ident: ref17 article-title: Standardized single breath normal 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obstructive pulmonary disease publication-title: Thorax contributor: fullname: Bestall, JC; Paul, EA; Garrod, R; Garnham, R – volume: 103 start-page: 57 year: 1971 end-page: 67 article-title: Spirometric standards for healthy non-smoking adults publication-title: Am Rev Respir Dis contributor: fullname: Morris, JF; Koski, A; Johnson, LC – volume: 43 start-page: 659 year: 2014 end-page: 661 article-title: The “other” COPD publication-title: Eur Respir J contributor: fullname: Han, MK – volume: 160 start-page: 1525 year: 1999 end-page: 1531 article-title: Arterial blood gas reference values for sea level an altitude of 1400 meters publication-title: Am J Resp Crit Care Med contributor: fullname: Crapo, RO; Jensen, RL; Hegewald, M; Tashkin, DP – volume: 151 start-page: 686 year: 2017 end-page: 696 article-title: Improving the management of COPD in women publication-title: Chest contributor: fullname: Jenkins, CR; Chapman, KR; Donohue, JF; Roche, N; Tsiligianni, I; Han, MK – volume: 39 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Tuberc Lung Dis contributor: fullname: Moran-Mendoza, O; Pérez-Padilla, JR; Salazar-Flores, M; Vazquez-Alfaro, F – volume: 123 start-page: 185 year: 1981 end-page: 189 article-title: Standardized single breath normal values for carbon monoxide diffusing capacity publication-title: Am Rev Respir Dis contributor: fullname: Crapo, RO; Morris, AH – volume: 5 start-page: e000246 year: 2018 article-title: Chronic obstructive pulmonary disease associated with biomass fuel use in women: a systematic review and meta-analysis publication-title: BMJ Open Resp Res contributor: fullname: Sana, A; Sonda, SMA; Meda, N; Bouland, C – volume: 54 start-page: 192 year: 2014 end-page: 199 article-title: Evaluation of respiratory impairment in patients with systemic lupus erythematosus with the six-min walk test publication-title: Rev Bras Reumatol contributor: fullname: Leite, MA; Pereira, MC; Costalat, LT; Villaba Wde, O; Moreira, MM; Paschoal, IA – volume: 29 start-page: 17 year: 2004 end-page: 25 article-title: Enfermedad pulmonar obstructiva crónica (EPOC) por humo de leãa en mujeres: comparación con la EPOC por tabaquismo [in Spanish] publication-title: Acta Med Colomb contributor: fullname: González-García, M; Páez, S; Jaramillo, C; Barrero, M; Maldonado, D – volume: 44 start-page: 261 year: 2014 end-page: 262 article-title: Wood smoke COPD: a new description of a COPD phenotype? publication-title: Eur Respir J contributor: fullname: González-García, M; Torres-Duque, C – volume: 39 start-page: 155 year: 2013 end-page: 163 article-title: Pulmonary changes on HRCT scans in nonsmoking females with COPD due to wood smoke exposure publication-title: J Bras Pneumol contributor: fullname: Moreira, MA; Barbosa, MA; Queiroz, MC; Teixeira, KI; Torres, PP; Santana Júnior, PJ – volume: 43 start-page: 725 year: 2014 end-page: 734 article-title: COPD phenotypes in biomass smoke- versus tobacco smoke-exposed mexican women publication-title: Eur Respir J contributor: fullname: Camp, PG; Ramirez-Venegas, A; Sansores, RH; Alva, LF; McDougall, JE; Sin, DD – volume: 23 start-page: 198 year: 2018 end-page: 205 article-title: Small airway disease: A different phenotype of early stage COPD associated with biomass smoke exposure publication-title: Respirology contributor: fullname: Zhao, D; Zhou, Y; Jiang, C; Zhao, Z; He, F; Ran, P – volume: 139 start-page: 752 year: 2011 end-page: 763 article-title: COPD in never smokers publication-title: Chest contributor: fullname: Lamprecht, B; Mcburnie, MA; Vollmer, WM; Gudmundsson, G; Welte, T; Nizankowska-Mogilnicka, E |
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| Title | Biomass smoke COPD has less tomographic abnormalities but worse hypoxemia compared with tobacco COPD |
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