The relationship between large airway and alveolar space inflammation and airway metaplasia

Our plain-English summary of The relationship between large airway and alveolar space inflammation and airway metaplasia, by W.W. Merrill, D. Carter, M.R. Cullen (Respiration; International Review of Thoracic Diseases, 1992).

The study

• Authors: W.W. Merrill, D. Carter, M.R. Cullen
• Journal: Respiration; International Review of Thoracic Diseases
• Published: 1992;59 Suppl 1:38-40
• Read it: PubMed · Publisher

Abstract

Bronchoscopy and bronchoalveolar lavage (BAL) yield important information about the lower respiratory tract of subjects who have been exposed to asbestos. Evidence of metaplasia is easily detected with random biopsies in large airways and a relationship with smoking status can be found. A significant finding, however, is that inflammatory cells recovered by late BAL aliquots which presumably reflect alveolar space inflammation are also importantly associated with the presence of metaplasia. Asbestos provides an important stimulus for recruitment of inflammatory cells. These cells release oxidants which can be responsible for direct or indirect mutagenesis. Our data suggest that this inflammatory cell recruitment may be an important additional factor predictive of airway metaplasia and perhaps subsequent carcinogenesis.

In plain English

This short report described asbestos workers who had bronchoscopy, with lung washing (bronchoalveolar lavage) and random large-airway biopsies. It did not state how many workers took part or their asbestos fiber types. Biopsies were graded for metaplasia, a change in the airway lining. Of the subjects, 24 had basal cell hyperplasia, 4 had full thickness hyperplasia and 15 had full thickness hyperplasia with keratinisation. Metaplasia was somewhat more frequent in current smokers than in ex-smokers and never smokers. Asbestos exposure history did not seem related to it. Inflammatory cells in the first lavage portion, taken to reflect large airways, were not related to metaplasia. Inflammatory cells in later portions, taken to reflect the air sacs, rose with each grade of metaplasia (r=0.42, p = 0.004). They were also higher in current smokers than nonsmokers. Within smoking groups, the link reached p<0.06 for current smokers and nonsmokers and was of marginal significance (p<0.1) for ex-smokers. The authors called this a trend and noted the subgroups were small. The authors concluded this inflammatory cell recruitment may be an additional factor predictive of airway metaplasia and perhaps later cancer.

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 using bronchoscopy, bronchoalveolar lavage and airway biopsies. This is a brief report that draws on the authors' other papers.
• Who was studied: Asbestos workers recruited by the authors (Yale University School of Medicine, New Haven). The total number of subjects, the dates and the recruitment site are not stated. Metaplasia was found in 24 + 4 + 15 subjects.
• Exposure: Asbestos exposure was recorded as age at first exposure, average exposure and total exposure. No fiber types or doses are reported. Cigarette smoking was also recorded.
• Main results:
  • Grades of metaplasia in airway biopsies: 24 subjects had basal cell hyperplasia, 4 had full thickness hyperplasia, and 15 had full thickness hyperplasia with keratinisation.
  • Worsening metaplasia seemed related to smoking. It was somewhat more frequent in current smokers than in ex-smokers and never smokers (chi-square 7.1, p less than 0.01).
  • Asbestos exposure history did not seem to be related to the presence of metaplasia on biopsy.
  • Acute inflammatory cells in the first lavage aliquot (large airways) did not relate to metaplasia in airway biopsies.
  • In the later pooled lavage aliquots (alveolar space), subjects with each grade of metaplasia had progressively higher numbers of inflammatory cells (r=0.42, p = 0.004).
  • Current smokers had a higher mean number of acute inflammatory cells than nonsmokers (p<0.03). Ex-smokers were intermediate.
  • Analysed within smoking groups, inflammatory cells in the pooled sample were associated with metaplasia for current smokers and nonsmokers (chi-square 3.6, p<0.06). For ex-smokers the association was of marginal significance (p<0.1). In their summary the authors described this as a trend.
• The authors' conclusion: The authors concluded that recruitment of inflammatory cells to the alveolar space may be an important additional factor predictive of airway metaplasia and perhaps subsequent carcinogenesis. They also suggested a linkage between asbestos and cigarette smoking in the development of lung carcinoma.
• Limitations the authors state:
  • When the data were split by smoking status, each analysis group was small.

Topics

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

Medical terms in this study, explained in our Lexicon: Inflammation, Bronchoscopy, Bronchoalveolar Lavage (BAL), Carcinogenesis.

Related studies

• The relationship between large airway inflammation and airway metaplasia — W.W. Merrill, D. Carter, et al. (1991)
• Association between acute inflammatory cells in lavage fluid and bronchial metaplasia — W.W. Merrill, M.R. Cullen, et al. (1992)
• Airway epithelial NF-kappaB activation modulates asbestos-induced inflammation and mucin production in vivo — A. Haegens, T.F. Barrett, et al. (2007)
• Morphology of small-airway lesions in patients with asbestos exposure — J.L. Wright, A. Churg (1984)
• Severe diffuse small airways abnormalities in long term chrysotile asbestos miners — J.L. Wright, A. Churg (1985)
• Dietary vitamin A and prevalence of bronchial metaplasia in asbestos-exposed workers — S.T. Mayne, C.A. Redlich, et al. (1998)

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