Association between acute inflammatory cells in lavage fluid and bronchial metaplasia

Our plain-English summary of Association between acute inflammatory cells in lavage fluid and bronchial metaplasia, by W.W. Merrill, M.R. Cullen, D. Carter, et al (Chest, 1992).

The study

• Authors: W.W. Merrill, M.R. Cullen, D. Carter, M.E. Marenberg
• Journal: Chest
• Published: 1992;102(3):688-93
• Cited by: 2 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

In epidemiologic studies, airway disease and parenchymal injury are known morbid outcomes of occupational exposure to asbestos. However, the relationship of inflammatory events considered to be responsible for parenchymal injury to the subsequent development of airway injury is unknown. To assess this we performed bronchoalveolar lavage (BAL) and airway biopsies on a population of subjects with exposure to asbestos in the workplace. As an index of airway injury, we employed histologic metaplasia seen in mucosal biopsy specimens. Lung BAL fluid was analyzed for two potentially relevant protein markers and for inflammatory cells recovered from the lower respiratory tract. We related metaplasia to demographic features of this study population (eg, smoking history and asbestos exposure data) and also to the protein and cellular markers recovered by BAL. We studied 50 workers and detected keratinizing metaplasia in 15 and varying lesser abnormalities in the other 28. Cigarette smoking was not associated with the presence of metaplasia (p less than 0.2). Smoking status was associated with an increase in BAL cells (p less than 0.02); however, neither the percent nor concentration of acute inflammatory cells was significantly increased. Acute inflammatory cells (percent and cells per milliliter of BAL fluid) were significantly increased among the subjects with severe metaplasia compared with other study subjects. This increase was true of both neutrophils and eosinophils and the sum of these two (p less than 0.02). Stratification of subjects by smoking status demonstrated a persistent association of inflammatory cells with metaplasia. By logistic regression analysis, polymorphonuclear leukocytes per milliliter and eosinophils per milliliter were significantly related to the presence of metaplasia in two independent models (odds ratios, 9.9 and 7.6, respectively). Cigarette smoking and other demographic or BAL variables were not significantly associated with metaplasia in these models.

In plain English

This study asked whether lung inflammation was linked to abnormal changes in the large-airway lining (bronchial metaplasia) in asbestos-exposed workers. Volunteers from a Yale occupational medicine program had bronchoscopy with airway biopsies and a lung washing (bronchoalveolar lavage). The article did not report which fiber types these workers encountered. Doses were estimated on a relative scale because virtually none had worked where asbestos was adequately sampled during exposure. Of 50 workers, 46 gave usable biopsies, and 15 showed the most severe change, keratinizing metaplasia. Smoking was not significantly related to metaplasia, although current smokers had more total cells in their washings. Workers with keratinizing metaplasia had more neutrophils and eosinophils, two inflammatory white cells. In statistical models, the odds ratio for metaplasia was 9.91 (range 1.62 to 61) with high neutrophil levels and 7.6 (95 percent CI 1.05 to 55.2) with the highest eosinophil levels. Within smoking groups, the link was significant only among ex-smokers. The authors called their data not definitive but suggestive of a link between inflammation from smoking and asbestos and airway metaplasia.

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: Cross-sectional clinical study: bronchoscopy with bronchoalveolar lavage and random bronchial biopsies in asbestos-exposed workers, comparing lavage findings with biopsy changes
• Who was studied: Volunteer workers with occupational asbestos exposure, recruited from more than 1,000 patients of the Yale Occupational Medicine Program. 50 had bronchoscopy, 46 had assessable biopsies, and 43 were reported in detail.
• Exposure: Past occupational asbestos exposure. The fiber types these workers encountered were not reported. Average and cumulative doses were estimated on a relative scale (Nicholson et al.), with total dose expressed in insulator-years, because virtually none of the subjects had worked where adequate environmental sampling had taken place during the periods of exposure. Cigarette smoking was also assessed.
• Main results:
  • Keratinizing metaplasia, the most severe change, was found in 15 subjects. 4 had full-thickness hyperplasia and 27 had basal cell hyperplasia (out of 46 with assessable biopsies).
  • Smoking (ever versus never; current, ex- or never; or pack-years) was not significantly related to metaplasia (p greater than 0.2 for all comparisons).
  • Current smokers had significantly more total nucleated cells in lavage fluid than the other groups (p less than 0.02, Kruskal-Wallis test). Differences in acute inflammatory cells across smoking groups were not statistically significant (p greater than 0.2).
  • The two protein markers (free secretory component and keratins) in lavage fluid showed no specific relationship to metaplasia.
  • Neutrophils and eosinophils were more commonly seen in lavage cells of subjects with keratinizing metaplasia. Mean neutrophils per ml were 13±18 in 14 subjects with metaplasia versus 3.7±6.0 in 29 without, in the table's units.
  • When subjects were split by smoking status, the difference was statistically significant only for ex-smokers (p less than 0.05, Mann-Whitney U test).
  • In logistic regression controlling for other variables, high neutrophil concentration (above 5 x 10^3 cells per ml) was associated with squamous metaplasia, odds ratio 9.91 (range 1.62 to 61).
  • In a separate model, subjects in the highest eosinophil group showed a weaker association with metaplasia, odds ratio 7.6 (95 percent CI 1.05 to 55.2).
• The authors' conclusion: The authors concluded that their data suggest a link between inflammation, induced by smoking and asbestos, and the development of metaplasia in large airways. They called their data not definitive and said that, if confirmed, bronchoscopic assessment of inflammation might have a role in assessing exposed patients.
• Limitations the authors state:
  • The authors described their data as not definitive.
  • Within smoking subgroups, the association was significant only for the largest subgroup.
  • Asbestos doses were estimates on a relative scale, because virtually none of the subjects had worked where adequate environmental sampling took place during exposure.

Topics

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

Medical terms in this study, explained in our Lexicon: Occupational Exposure, Bronchoalveolar Lavage (BAL), Biopsy, BAL Fluid, Asbestos Exposure, Odds Ratio.

Related studies

• The relationship between large airway inflammation and airway metaplasia — W.W. Merrill, D. Carter, et al. (1991)
• The relationship between large airway and alveolar space inflammation and airway metaplasia — W.W. Merrill, D. Carter, et al. (1992)
• Dietary vitamin A and prevalence of bronchial metaplasia in asbestos-exposed workers — S.T. Mayne, C.A. Redlich, et al. (1998)
• Association between neutrophil concentration in bronchoalveolar lavage fluid and recent losses in diffusing capacity in men formerly exposed to asbestos — M.R. Cullen, W.W. Merrill (1992)
• Detection of lipid peroxidation in lung and in bronchoalveolar lavage cells and fluid — J.M. Petruska, S.H. Wong, et al. (1990)
• Influence of cigarette smoking on bronchoalveolar lavage cellularity in asbestos-induced lung disease — D.A. Schwartz, J.R. Galvin, et al. (1992)

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