Meneghini A C, Koenigkam-Santos M, Pereira M C, Tonidandel P R, Terra-Filho J, Cunha F Q, Menezes M B de, Vianna E O
Departamento de Medicina Social, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, SP, Brasil.
Departamento de Clínica Médica, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, SP, Brasil.
Braz J Med Biol Res. 2019;52(5):e8233. doi: 10.1590/1414-431X20198233. Epub 2019 Apr 25.
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.
生物质烟雾所致慢性阻塞性肺疾病(COPD)已受到特别关注,为非吸烟COPD患者的预防和治疗方法提供了新知识。然而,对生物质烟雾所致COPD的认识仍然有限,且存在一定争议。本研究的目的是比较仅由吸烟引起的COPD与仅由环境或职业暴露引起的COPD。在这项横断面研究中,从门诊招募COPD患者并分为两组:不吸烟但暴露于生物质烟雾的非吸烟COPD组(n = 16)和未报告有生物质烟雾暴露的吸烟COPD组(n = 15)。受试者接受肺功能测试、胸部高分辨率计算机断层扫描、6分钟步行试验和痰液诱导检查。非吸烟COPD组的生物质烟雾暴露时间为133.3±86小时-年。吸烟COPD组的吸烟量为48.5±27.4包-年。非吸烟者和吸烟者中女性分别占62.5%和66.7%。非吸烟COPD组呼吸困难的患病率更高,动脉血氧分压(PaO2)和动脉血氧饱和度(SaO2%)更低,而肺活量测定结果、肺容积和弥散能力相似。关于炎症生物标志物,在痰液中淋巴细胞单核细胞数量以及白细胞介素(IL)-6和IL-8的痰液浓度方面检测到差异,吸烟组的值更高。肺气肿在吸烟组中更普遍,通过定量分析还显示其相对支气管壁厚度更高,肺密度更低。在严重程度相似的COPD患者中,与吸烟相比,生物质烟雾导致更多的低氧血症。