Influence of cigarette smoking on bronchoalveolar lavage cellularity in asbestos-induced lung disease

Our plain-English summary of Influence of cigarette smoking on bronchoalveolar lavage cellularity in asbestos-induced lung disease, by D.A. Schwartz, J.R. Galvin, R.K. Merchant, et al (The American Review of Respiratory Disease, 1992).

The study

• Authors: D.A. Schwartz, J.R. Galvin, R.K. Merchant, C.S. Dayton, L.F. Burmeister, J.A. Merchant, G.W. Hunninghake
• Journal: The American Review of Respiratory Disease
• Published: 1992;145(2 Pt 1):400-5
• Cited by: 20 articles, as counted by NIH iCite
• Read it: PubMed · Publisher
• In J-M's library: Johns-Manville's company medical library held a copy (J-M no. 004143).

Abstract

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)

In plain English

This University of Iowa study examined whether cigarette smoking affects cells recovered by rinsing part of the lung through a bronchoscope (bronchoalveolar lavage, BAL). It included 73 asbestos-exposed male workers referred for evaluation of asbestos-related lung disease. Twenty had normal chest X-rays, 25 had asbestosis, and 28 had asbestos-induced pleural fibrosis (plaques or diffuse thickening) without asbestosis. Fourteen of those with asbestosis also had pleural fibrosis, so 42 had pleural fibrosis in all. Workers with asbestosis had higher concentrations of macrophages, neutrophils and eosinophils. Those with pleural fibrosis had more lymphocytes. Smoking was associated with higher macrophages, neutrophils and eosinophils, but not lymphocytes. In adjusted analyses, asbestosis remained linked to all three cell types, and current smoking to macrophages and eosinophils. Smoking accounted for 17 to 18% of the variation in macrophages and eosinophils. Asbestosis accounted for 6 to 7% of the variation in macrophages, neutrophils and eosinophils. The authors concluded that smoking strongly influences macrophage and eosinophil counts in workers with asbestosis but does not appear to affect BAL cells in pleural fibrosis. The article did not name asbestos fiber types.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Comparison of bronchoalveolar lavage (lung-washing) cell counts among asbestos-exposed workers with normal chest X-rays, asbestosis, or asbestos-induced pleural fibrosis. Univariate tests and multivariate linear regression were used to separate the effects of smoking and asbestosis.
• Who was studied: 73 asbestos-exposed workers, average age 60, all male and all white according to Table 1. They were referred for evaluation of asbestos-related lung disease to a research program at the University of Iowa. The groups were 20 with normal chest X-rays, 28 with pleural fibrosis but no asbestosis, and 25 with asbestosis. Fourteen of the 25 with asbestosis also had pleural fibrosis, so 42 subjects had pleural fibrosis in total. Study dates were not given.
• Exposure: Occupational asbestos exposure for at least 1 year in a high-exposure setting, with at least 20 years since first exposure. The mean exposure duration was 33 years and the mean time since first exposure was 38 years. Fiber types and specific jobs were not stated. The main factor studied was cigarette smoking, measured as never, former or current smoking status and as pack-years.
• Main results:
  • Patients with asbestosis (ILO 1/0 or greater) had higher BAL concentrations of macrophages (p = 0.04), neutrophils (p = 0.003) and eosinophils (p = 0.01).
  • Patients with asbestos-induced pleural fibrosis (circumscribed plaques and diffuse pleural thickening) had higher BAL lymphocyte concentrations (p = 0.02).
  • Of the 42 subjects with pleural fibrosis, 14 had asbestosis. The higher lymphocyte level linked to pleural disease was still present when the analysis was limited to subjects with normal lung tissue on X-ray.
  • Cigarette smoking (smoking status or pack-years) was strongly associated with BAL macrophages, neutrophils and eosinophils, but not with lymphocytes.
  • Current smokers (n = 10) had higher concentrations of macrophages, neutrophils and eosinophils than never smokers (n = 13).
  • Pack-years of smoking correlated with alveolar macrophages (r = 0.29, p = 0.01) and with neutrophils (r = 0.32, p = 0.007).
  • Subjects with asbestosis had heavier smoking histories than those with normal chest X-rays. Mean pack-years were 42.2 (standard deviation 23.4) in the asbestosis group and 28.1 (standard deviation 23.9) in the normal X-ray group.
  • In multivariate analysis, current smokers were more likely to have higher macrophages and eosinophils.
  • In multivariate analysis, BAL neutrophils remained associated with asbestosis and were not influenced by smoking.
  • Smoking accounted for 17 to 18% of the variance in BAL macrophages and eosinophils. Asbestosis accounted for 6 to 7% of the variance in macrophages, neutrophils and eosinophils.
• The authors' conclusion: The authors concluded that cigarette smoking strongly influences BAL cell counts (macrophages and eosinophils) in their patients with asbestosis. They also concluded that smoking does not appear to affect the type or concentration of BAL cells in patients with asbestos-induced pleural fibrosis.
• Limitations the authors state:
  • The authors hypothesized that the lymphocyte increase seen with pleural fibrosis may represent an early, potentially reversible stage of lung inflammation. They stated that further prospective studies are needed to test whether this is valid.

Topics

The National Library of Medicine indexes this study under subjects our site covers: Asbestosis.

Medical terms in this study, explained in our Lexicon: Bronchoalveolar Lavage (BAL), Fibrosis, Macrophage, Diffuse Pleural Thickening, Multivariate Analysis.

Related studies

• Brief inhalation of asbestos compromises superoxide production in cells from bronchoalveolar lavage — J.M. Petruska, J. Marsh, et al. (1990)
• Bronchoalveolar lavage and 99mTc-DTPA clearance as prognostic factors in asbestos workers with and without asbestosis — N. al Jarad, A.R. Gellert, et al. (1993)
• Bronchoalveolar cell differential count and the number of asbestos bodies correlate with survival in patients with asbestosis — E. Keskitalo, L. Varis, et al. (2019)
• Asbestosis: assessment by bronchoalveolar lavage and measurement of pulmonary epithelial permeability — A.R. Gellert, J.A. Langford, et al. (1985)
• Bronchoalveolar lavage cell and lymphocyte phenotype profiles in healthy asbestos-exposed shipyard workers — J.M. Wallace, J.S. Oishi, et al. (1989)
• The clinical utility and reliability of asbestos bodies in bronchoalveolar fluid — D.A. Schwartz, J.R. Galvin, et al. (1991)

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