Severe diffuse small airways abnormalities in long term chrysotile asbestos miners

Our plain-English summary of Severe diffuse small airways abnormalities in long term chrysotile asbestos miners, by J.L. Wright, A. Churg (British Journal of Industrial Medicine, 1985).

The study

• Authors: J.L. Wright, A. Churg
• Journal: British Journal of Industrial Medicine
• Published: 1985;42(8):556-9
• Cited by: 24 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text
• In J-M's library: Johns-Manville's company medical library held a copy (J-M no. 000519).

Abstract

To determine the nature and extent of pathological changes in the small airways induced by asbestos, the pathological lesions of fibrosis and pigmentation of the membranous and respiratory bronchioles and alveolar ducts in lungs obtained from necropy from a group of 36 non-asbestotic long term chrysotile miners and 36 age, sex, and smoking matched controls who had no history of exposure to dust were compared. The airways were graded using a standard visual grading system. Appreciably greater airway fibrosis was found for all types of airway in the whole group of miners compared with the controls. Differences for pigmentation were generally similar but less pronounced. It is concluded that long term exposure to mineral dust as an asbestos miner produces severe diffuse pathological changes in the small airways; these findings may relate to the physiological observation of unusual degrees of airflow obstruction in this group of workers.

In plain English

This study compared autopsy lung tissue from long-term chrysotile asbestos miners and millers with tissue from people who had no work exposure to dust. The authors started with 64 consecutive autopsies of miners and millers at a hospital in Thetford Mines, Quebec, from 1981 to 1983. They excluded everyone with microscopic signs of asbestosis, leaving 36 miners. Each miner was matched for age and smoking to a control autopsied at hospitals in Vancouver. The miners averaged 31 years of dust exposure. Fibrosis (scarring) and pigment in three kinds of small airway were graded on a scale from 0 to 3. Miners had significantly more fibrosis in all three airway types. In membranous bronchioles, for example, the mean fibrosis grade was 1.2 in miners and 0.3 in controls. Pigment was significantly greater in two airway types but not in membranous bronchioles. The authors concluded that long-term dust exposure as an asbestos miner produces severe, diffuse small-airway changes. They said it was uncertain whether these changes resulted only from asbestos, because miners are also exposed to other dusts.

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: Autopsy (necropsy) pathology study comparing lung tissue from miners with matched controls
• Who was studied: 36 long-term chrysotile miners and millers without microscopic asbestosis, drawn from 64 consecutive autopsies at Thetford Mines, Quebec, 1981 to 1983. They were compared with 36 controls from Vancouver hospital autopsy services, matched on age (within 10 years) and smoking (within 10 pack-years), with no occupational dust exposure.
• Exposure: Long-term work as chrysotile miners and millers; mean dust exposure 31 years (SD 11)
• Main results:
  • Miners had significantly more fibrosis (p less than 0.001) in all three airway types. Mean fibrosis grades in miners versus controls: membranous bronchioles 1.2 (SD 0.6) versus 0.3 (SD 0.3).
  • Respiratory bronchioles mean fibrosis grade: 1.1 (SD 0.6) in miners versus 0.2 (SD 0.1) in controls.
  • Alveolar ducts mean fibrosis grade: 0.6 (SD 0.5) in miners versus 0 in controls.
  • Respiratory bronchioles and alveolar ducts were significantly more pigmented in miners than controls (p less than 0.001): 0.9 versus 0.5, and 0.4 versus 0.1.
  • Pigmentation of membranous bronchioles did not differ significantly: 0.7 (SD 0.5) in miners versus 0.6 (SD 0.4) in controls.
  • When miners were split by smoking history (less than or more than 35 pack-years), no differences in the amount of airway disease were found.
  • Agreement between the two observers, and on regrading, had a concordance coefficient of 0.94 (p less than 0.001).
• The authors' conclusion: The authors concluded that long-term exposure to mineral dust as an asbestos miner produces severe diffuse pathological changes in the small airways. They suggested these changes may relate to the unusual airflow obstruction reported in such workers.
• Limitations the authors state:
  • The authors said it is uncertain whether the changes result only from asbestos, since miners are exposed to large amounts of other dusts.
  • The finding of no difference between lighter and heavier smokers may reflect only the miners' rather heavy smoking.
  • Miners came from Quebec and controls from British Columbia. The authors raised this as a possible objection and argued against it: Montreal values from another study and Thetford non-miners resembled their controls.
  • Not all lungs were inflated before fixation. The authors tested this on six control cases and found no significant effect on grading.

Topics

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

Medical terms in this study, explained in our Lexicon: Chrysotile, Fibrosis, Obstructive Lung Disease.

Related studies

• Morphology of small-airway lesions in patients with asbestos exposure — J.L. Wright, A. Churg (1984)
• Asbestos exposure, cigarette smoking, and airflow limitation in long-term Canadian chrysotile miners and millers — R. Bégin, R. Boileau, et al. (1987)
• Long-term mortality experience of chrysotile miners and millers in Thetford Mines, Quebec — W.J. Nicholson, I.J. Selikoff, et al. (1979)
• 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)
• Acquisition of Cancer Stem Cell-like Properties in Human Small Airway Epithelial Cells after a Long-term Exposure to Carbon Nanomaterials — C. Kiratipaiboon, T.A. Stueckle, et al. (2019)

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