Schwartz D A, Galvin J R, Merchant R K, Dayton C S, Burmeister L F, Merchant J A, Hunninghake G W
Department of Internal Medicine, University of Iowa, Iowa City.
Am Rev Respir Dis. 1992 Feb;145(2 Pt 1):400-5. doi: 10.1164/ajrccm/145.2_Pt_1.400.
To investigate the influence of cigarette smoking on bronchoalveolar lavage (BAL) cellularity in asbestos-induced lung disease, we compared BAL cells in asbestos-exposed, nondiseased subjects (n = 20) with those with either asbestosis (n = 25) or asbestos-induced pleural fibrosis (n = 28). Patients with asbestosis (ILO greater than or equal to 1/0) had higher concentrations of BAL macrophages (p = 0.04), neutrophils (p = 0.003), and eosinophils (p = 0.01), while patients with asbestos-induced pleural fibrosis (circumscribed plaques and diffuse pleural thickening) had higher concentrations of BAL lymphocytes (p = 0.02). Within our study population, however, cigarette smoking (smoking status or pack-years of smoking) was strongly associated with BAL macrophages, neutrophils, and eosinophils but was not associated with the concentration of BAL lymphocytes. Using multivariate analysis, we found that although asbestosis remained associated with higher concentrations of BAL macrophages, neutrophils, and eosinophils, cigarette smoking had a far greater contribution to the concentrations of BAL macrophages and eosinophils than did asbestosis. Although cigarette smoking accounted for 17 to 18% of the variance of BAL macrophages and eosinophils, asbestosis was associated with approximately 6% of the variance associated with these cells. In contrast, the concentration of BAL neutrophils remained associated with asbestosis and was not influenced by smoking behavior. We conclude that cigarette smoking strongly influences BAL cellularity (macrophages and eosinophils) in our patients with asbestosis but does not appear to affect the type or concentration of BAL cells in patients with asbestos-induced pleural fibrosis.(ABSTRACT TRUNCATED AT 250 WORDS)
为研究吸烟对石棉所致肺部疾病支气管肺泡灌洗(BAL)细胞成分的影响,我们比较了石棉暴露但未患病的受试者(n = 20)、石棉肺患者(n = 25)和石棉所致胸膜纤维化患者(n = 28)的BAL细胞。石棉肺患者(国际劳工组织分级大于或等于1/0)的BAL巨噬细胞(p = 0.04)、中性粒细胞(p = 0.003)和嗜酸性粒细胞浓度较高(p = 0.01),而石棉所致胸膜纤维化患者(局限性斑块和弥漫性胸膜增厚)的BAL淋巴细胞浓度较高(p = 0.02)。然而,在我们的研究人群中,吸烟(吸烟状态或吸烟包年数)与BAL巨噬细胞、中性粒细胞和嗜酸性粒细胞密切相关,但与BAL淋巴细胞浓度无关。通过多变量分析,我们发现,尽管石棉肺仍与较高浓度的BAL巨噬细胞、中性粒细胞和嗜酸性粒细胞有关,但吸烟对BAL巨噬细胞和嗜酸性粒细胞浓度的影响远大于石棉肺。尽管吸烟占BAL巨噬细胞和嗜酸性粒细胞变异的17%至18%,但石棉肺与这些细胞相关变异的约6%有关。相比之下,BAL中性粒细胞浓度仍与石棉肺有关,不受吸烟行为影响。我们得出结论,吸烟对我们石棉肺患者的BAL细胞成分(巨噬细胞和嗜酸性粒细胞)有强烈影响,但似乎不影响石棉所致胸膜纤维化患者BAL细胞的类型或浓度。(摘要截短于250词)