Our plain-English summary of The relationship between large airway inflammation and airway metaplasia, by W.W. Merrill, D. Carter, M.R. Cullen (Chest, 1991).
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The study
- Authors: W.W. Merrill, D. Carter, M.R. Cullen
- Journal: Chest
- Published: 1991;100(1):131-5
- Cited by: 8 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. 004164).
Abstract
To assess the role of acute inflammatory cells in large airways in the pathogenesis of metaplasia, we performed BAL (divided into aliquots) and mucosal biopsies on asbestos workers. They had evidence of asbestos-related lung injury. We found that acute inflammatory cells were significantly increased in the first aliquot. Ex-smokers had a greater percentage of PMN compared with nonsmokers and current smokers. The subjects were subgrouped with respect to biopsy-detected metaplasia. There was no difference between these groups for percentage or total number of PMN in the first aliquot. However, subjects with metaplasia had significant reduction in FEV1/FVC compared with those without. We conclude that there are significant differences in cells between the first and subsequent aliquots. Although inflammatory stimuli may be important in the pathogenesis of metaplasia, PMN present in the first aliquot could not be related to the severity of the metaplastic changes in these workers.
In plain English
This study asked whether inflammation in the large airways was linked to metaplasia (abnormal changes in the cells lining the airways) in asbestos-exposed workers. The authors studied 50 men, averaging 60 years of age, recruited from an occupational medicine clinic because their chest X-rays indicated significant past asbestos exposure. Their exposure came from construction trades and asbestos products manufacturing. Procedures were bronchoscopy with lung washing (lavage) collected in separate portions, plus airway-lining biopsies. Thirty-six men provided enough of both for analysis. The first portion, thought to sample the large airways, held a higher percentage of neutrophils, a type of inflammatory white blood cell, than later portions. Ex-smokers had a higher percentage than never-smokers or current smokers. Metaplasia was more common among current and ex-smokers. Men with metaplasia had a significantly lower FEV1/FVC breathing-test ratio. However, men with metaplasia did not have more neutrophils in the first portion (4.5 percent versus 7.1 percent, not statistically significant). The authors concluded that these cells could not be related to the severity of metaplasia. They wrote that the precise meaning of their findings was unclear.
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: Clinical study in which subjects underwent bronchoscopy with bronchoalveolar lavage (collected in separate portions) and biopsies of the airway lining, examined at one point in time
- Who was studied: 50 men, average age 60 plus or minus 6 years, with occupational asbestos exposure, recruited at a Yale-affiliated occupational medicine clinic from among workers whose abnormal chest radiographs indicated significant prior asbestos exposure. The group included 8 nonsmokers, 13 current smokers and 29 ex-smokers. 36 had both adequate biopsy material and enough cells in the first lavage portion for analysis.
- Exposure: Occupational asbestos exposure in the construction trades and asbestos products manufacturing. Exposure averaged 14.8 insulator-year equivalents (range 2.5 to 36), first exposure at an average age of 25, and mean latency of 35 years. No fiber type is named. Smoking was also studied.
- Main results:
- Of the 50 men, 36 had both adequate biopsy material and enough cells in the first lavage portion for analysis. Two could not be studied because of coughing or presyncope, and two gave inadequate biopsy material.
- The percentage of neutrophils (PMN) was higher in the first lavage portion than in the pooled later portions (p less than 0.0001)
- No association was found between neutrophil percentages in the first portion and in the pooled later portions (r = 0.12)
- In the first portion, ex-smokers had a higher neutrophil percentage (9.6 plus or minus 8 percent) than never-smokers (2.4 plus or minus 2 percent) and current smokers (5 plus or minus 7 percent), p less than 0.03
- Adequate biopsy material was obtained from 46 of the 50 men
- Metaplasia was seen with equal frequency in each ILO chest radiograph category
- Men with metaplasia on biopsy had a significantly lower FEV1/FVC ratio than those with less severe changes (p less than 0.04)
- Metaplasia was more common among current and ex-smokers (chi-square 7.1, p less than 0.05)
- No combination of smoking or asbestos exposure history, alone or together, predicted the biopsy (pathologic) score
- Men with metaplasia (n = 15) had a slightly lower mean neutrophil percentage in the first portion (4.5 percent) than men with less severe lesions (7.1 percent). The difference was not statistically significant (t = 1.13, p greater than 0.1).
- The authors' conclusion: The authors concluded that cells in the first lavage portion differ from those in later portions. They also concluded that, although inflammatory stimuli may be important in causing metaplasia, neutrophils in the first portion could not be related to the severity of metaplastic changes in these workers.
- Limitations the authors state:
- The authors noted that the lack of association might reflect lavaging one lung segment while biopsying a different (opposite-side) segment, though they considered this unlikely
- Sampling error from random biopsies might introduce error
- The authors stated that the precise meaning of their findings was unclear
Topics
Medical terms in this study, explained in our Lexicon: Inflammation, Biopsy, FEV1/FVC Ratio.
Related studies
- The relationship between large airway and alveolar space inflammation and airway metaplasia — W.W. Merrill, D. Carter, et al. (1992)
- 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)
- Dietary vitamin A and prevalence of bronchial metaplasia in asbestos-exposed workers — S.T. Mayne, C.A. Redlich, et al. (1998)
- Peribronchiolar metaplasia: a common histologic lesion in diffuse lung disease and a rare cause of interstitial lung disease: clinicopathologic features of 15 cases — J. Fukuoka, T.J. Franks, et al. (2005)
- Nongynecologic metastases to fallopian tube mucosa: a potential mimic of tubal high-grade serous carcinoma and benign tubal mucinous metaplasia or nonmucinous hyperplasia — J.T. Rabban, P. Vohra, et al. (2015)
Browse more research in Chest, or return to medical research.
Cited on this site
How to cite it
Cite the study
W.W. Merrill, D. Carter, M.R. Cullen. The relationship between large airway inflammation and airway metaplasia. Chest 1991;100(1):131-5. doi:10.1378/chest.100.1.131. PMID: 2060332.
Cite our summary
“The relationship between large airway inflammation and airway metaplasia.” AsbestosClaims.Law Library. https://asbestosclaims.law/library/research/the-relationship-between-large-airway-inflammation-and-airway.
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