Morphology of small-airway lesions in patients with asbestos exposure

Our plain-English summary of Morphology of small-airway lesions in patients with asbestos exposure, by J.L. Wright, A. Churg (Human Pathology, 1984).

The study

• Authors: J.L. Wright, A. Churg
• Journal: Human Pathology
• Published: 1984;15(1):68-74
• Cited by: 67 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. 001666).

Abstract

The morphologic changes in the small airways of 15 patients who had been exposed to asbestos and had abnormalities of the respiratory bronchioles and alveolar ducts were examined and compared with changes in the small airways of a matched group of cigarette smokers. Lesions were evaluated using a visual grading scheme to determine pathologic severity of fibrosis, inflammation, and pigmentation in these airways. The membranous bronchioles of both asbestos-exposed and cigarette exposed patients showed the deposition of fibrous tissue and pigment; the lesions were morphologically identical, although more severe in the asbestos group (67 per cent of airways) than in the smoking group (19 per cent of airways). A distinctive lesion, consisting of fibrosis often accompanied by pigment, was found in 74 per cent of the respiratory bronchioles in the asbestos-exposed patients, compared with 6 per cent of respiratory bronchioles in the smokers. Similar changes were found in 49 per cent of alveolar ducts in the asbestos group and 1 per cent of the ducts in smoking group. Asbestos bodies were found in only 11 of 15 cases. The authors conclude that a distinctive lesion of small airways exists in some asbestos workers and that it can be identified by the finding of marked fibrosis in the walls of respiratory bronchioles and alveolar ducts. Because there is no proof that this lesion actually progresses to interstitial fibrosis (asbestosis), the authors suggest that it be termed "asbestos airways disease."

In plain English

The authors examined lung tissue to look for a distinctive pattern of damage in the small airways of people exposed to asbestos. They selected 15 asbestos-exposed patients whose small airways showed scarring (fibrosis) and pigment, and compared them with cigarette smokers without asbestos exposure, matched by age, sex and smoking history. Seven exposed patients were chrysotile miners; eight had been exposed mainly to amphibole asbestos, most often as shipyard or insulation workers. Thirteen of the 15 smoked. Airways were graded 0 to 3 for fibrosis, inflammation and pigment. Marked fibrosis appeared in 74 per cent of respiratory bronchioles and 49 per cent of alveolar ducts in the asbestos group, against 6 per cent and 1 per cent in the smokers. Marked fibrosis of membranous bronchioles was more common in the asbestos group (67 versus 19 per cent), but those lesions looked like smokers' lesions. Asbestos bodies were seen in 11 of 15 cases. The authors proposed the term "asbestos airways disease", but said whether the lesion is early asbestosis, or specific to asbestos, is open to question.

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: Comparative pathology study of lung tissue sections. Selected asbestos-exposed cases were compared with matched cigarette-smoker controls using a visual grading scheme for small-airway fibrosis, inflammation and pigment.
• Who was studied: 15 asbestos-exposed patients, selected from lung sections of a larger group because their small airways showed fibrotic and pigmented lesions. They were compared with cigarette smokers with no asbestos exposure, matched by age, sex and smoking history; the number of controls is not stated. Mean age in both groups was 64 years; mean pack-years smoked were 42 (asbestos group) and 45 (controls). Most asbestos specimens came from autopsy and all control specimens from surgery. The study was carried out at the University of British Columbia, Vancouver.
• Exposure: Seven patients were chrysotile miners. The other eight had been exposed predominantly to amphibole asbestos, most commonly as shipyard or insulation workers. Cigarette smoking was present in both groups.
• Main results:
  • Respiratory bronchioles with marked fibrosis (grade 2 or 3): 74 per cent in the asbestos group (144 graded), about half also with marked pigmentation, versus 6 per cent in the smoker controls (103 graded).
  • Alveolar ducts with fibrosis: 49 per cent in the asbestos group (175 graded) versus 1 per cent in the controls (104 graded).
  • Membranous bronchioles with marked (grade 2 or 3) fibrosis: 67 per cent in the asbestos group (134 graded).
  • In the smoker controls, similar-looking membranous bronchiole lesions made up 19 per cent of membranous bronchioles (58 graded). The authors said the membranous bronchiole changes are valid only in a statistical sense and should not be used for diagnosis.
  • In every asbestos-exposed patient, severely affected respiratory bronchioles outnumbered normal or mildly affected ones. This was not seen in the cigarette smokers.
  • No differences in the lesions were seen between patients exposed to amphibole asbestos and patients exposed to chrysotile asbestos.
  • Asbestos bodies were found in tissue sections in 11 of the 15 asbestos-exposed cases: in 8 they were associated with abnormal small airways, and in 3 they were found only in lung tissue away from the airways. None were found in 4 cases.
  • No consistent differences in inflammation were found between the two groups.
• The authors' conclusion: The authors concluded that a distinctive small-airway lesion, marked fibrosis of the respiratory bronchioles and alveolar ducts, exists in some asbestos workers. They suggested that, in patients with known asbestos exposure, it be termed "asbestos airways disease."
• Limitations the authors state:
  • 13 of the 15 asbestos-exposed patients smoked, and a possible combined (synergistic) contribution of smoking to the lesions was not examined.
  • There is no proof that the lesion progresses to asbestosis. The authors said this would require longitudinal data, not a static study like this one.
  • The authors said it is open to question whether the changes are an early form of asbestosis, and whether they are specific to asbestos.
  • The authors had seen similar lesions in people exposed to non-asbestos mineral dusts, suggesting the change may be a nonspecific reaction to mineral dust.
  • The authors had also seen cases of asbestosis without these airway changes.
  • For some asbestos cases (referred cases), nothing was known about how the available slides had been selected.
  • In patients with severe emphysema, the authors said the asbestos-related airway lesion could not be identified.

Topics

Medical terms in this study, explained in our Lexicon: Asbestos Exposure, Fibrosis, Inflammation, Deposition, Asbestos Bodies, Interstitial Fibrosis.

Related studies

• Small-airway lesions in patients exposed to nonasbestos mineral dusts — A. Churg, J.L. Wright (1983)
• Severe diffuse small airways abnormalities in long term chrysotile asbestos miners — J.L. Wright, A. Churg (1985)
• Pathologic changes in the small airways of the guinea pig after amosite asbestos exposure — D. Filipenko, J.L. Wright, et al. (1985)
• The relationship between large airway and alveolar space inflammation and airway metaplasia — W.W. Merrill, D. Carter, et al. (1992)
• Bronchiolar and alveolar lesions in the pathogenesis of crocidolite-induced pulmonary fibrosis in mice — D.H. Bowden, I.Y. Adamson (1985)
• Small airways disease and mineral dust exposure. Prevalence, structure, and function — A. Churg, J.L. Wright, et al. (1985)

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