Small-airway lesions in patients exposed to nonasbestos mineral dusts

Our plain-English summary of Small-airway lesions in patients exposed to nonasbestos mineral dusts, by A. Churg, J.L. Wright (Human Pathology, 1983).

The study

• Authors: A. Churg, J.L. Wright
• Journal: Human Pathology
• Published: 1983;14(8):688-93
• Cited by: 64 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. 001711).

Abstract

Small-airway lesions were identified in histologic sections from the lungs of seven workers with histories of exposure to nonasbestos dusts. The lesions consisted of deposits of fibrous tissue, often accompanied by pigment, in the walls of membranous and respiratory bronchioles and alveolar ducts. Comparison with a matched population of persons with no dust exposure revealed that the changes in the respiratory bronchioles and alveolar ducts were morphologically distinctive and could be used to diagnose the lesions. Structurally, these lesions were very similar to those described in the airways of asbestos workers, although comparison with the authors' previous results indicated that the number of severely affected airways was less in the nonasbestos dust group. Mineralogic analysis indicated that these abnormalities were produced by a variety of different dusts including silica, iron oxide, and aluminum oxide, and that occult asbestos exposure, although possible in three of the cases, was most likely not a primary cause of disease. The authors suggest that this lesion, which they call mineral dust airways disease, is a nonspecific reaction of the small airways to inorganic particulates. The presence of such changes casts considerable doubt on the theory that small-airway abnormalities in asbestos workers are the earliest form of asbestosis.

In plain English

This pathology study reviewed lung tissue from 30 workers exposed to mineral dusts other than asbestos. Seven showed scarring (fibrosis) and pigment in small-airway walls; each was matched by age, sex and smoking history to a person without dust exposure. Five of the seven were miners; the others were a metal tool maker and a foundry worker. In the dust-exposed group, 63 per cent of respiratory bronchioles and 22 per cent of alveolar ducts were graded markedly fibrotic, compared with 13 per cent and 2 per cent in the controls. The particles identified varied by patient. They were mostly silica in the miners, although mica (51 per cent) led in one. They were mostly iron oxide in the tool maker and aluminum oxide in the foundry worker. Four patients had no amosite or crocidolite asbestos fibers; three had 30- to 100-fold increases over background. The authors found the lesions similar to, but apparently less severe than, those in asbestos workers. They suggested that this 'mineral dust airways disease' is a nonspecific reaction to inorganic dusts, and that the interstitial fibrosis of asbestosis may be a completely separate process.

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: Pathology and mineral-analysis study of a small group of cases, each matched to a control with no dust exposure (age, sex and smoking history)
• Who was studied: Lung tissue from 30 patients with a history of nonasbestos dust exposure was reviewed. The 7 who showed airway fibrosis and pigmentation were studied in detail. All were men. The test group had a mean age of 65 and 38 pack-years of smoking; the 7 controls had a mean age of 66 and 42 pack-years. The work was done at the Department of Pathology, University of British Columbia, Vancouver. Study dates are not given.
• Exposure: Nonasbestos mineral dusts, with no reported asbestos contact. Five patients were miners (patients 5 and 7 had known silicosis), patient 1 was a metal tool maker for 34 years, and patient 6 worked 25 years in a foundry.
• Main results:
  • Membranous bronchioles graded markedly fibrotic (grade 2 or 3): 37 per cent in the nonasbestos dust group, compared with 20 per cent in the control group
  • Markedly fibrotic respiratory bronchioles: 63 per cent in the nonasbestos dust group versus 13 per cent in the smoking control group. Markedly fibrotic alveolar ducts: 22 per cent versus 2 per cent.
  • Asbestos fibers per gram of dry lung in the dust-exposed patients: mean chrysotile was 0.7 million and mean contaminant amphiboles (tremolite, actinolite, anthophyllite) 0.9 million. The reference group of 11 blue-collar men without dust exposure had means of 0.8 million and 0.4 million.
  • Commercial amphiboles (amosite and crocidolite): four dust-exposed patients had none; three had 30- to 100-fold increases over the background level of the reference group
  • Nonfibrous particle types (100 to 200 identified per sample site, as a percentage of particles): in three patients with histories of hard-rock mining or drilling, silica made up more than 88 per cent of the particles
  • In the two silicotic patients, silica made up 43 per cent (patient 5) and 58 per cent (patient 7) of particles. In patient 5, mica was the largest component at 51 per cent; patient 7 also had mica 16 per cent and kaolinite 12 per cent.
  • In the metal tool maker, 94 per cent of particles were iron oxide; in the foundry worker, 76 per cent were aluminum oxide
  • The lesions were very similar in structure to those described in asbestos workers. Compared with the authors' own previous study of asbestos workers, the main difference was that the lesions appeared more severe in the asbestos-exposed group.
• The authors' conclusion: The authors suggested that this type of airway disease, in both asbestos-exposed and nonasbestos-exposed workers, may be a nonspecific reaction to inorganic dusts, and that the interstitial fibrosis of asbestosis may be a completely separate process
• Limitations the authors state:
  • The authors did not formally count the nonasbestos mineral particles
  • The authors stated that working out the exact role of asbestos versus nonasbestos dusts will require more cases and more detailed mineral analyses

Topics

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

Medical terms in this study, explained in our Lexicon: Asbestos Exposure.

Related studies

• Small airways disease and mineral dust exposure. Prevalence, structure, and function — A. Churg, J.L. Wright, et al. (1985)
• Morphology of small-airway lesions in patients with asbestos exposure — J.L. Wright, A. Churg (1984)
• Mineral dusts directly induce epithelial and interstitial fibrogenic mediators and matrix components in the airway wall — J. Dai, B. Gilks, et al. (1998)
• Interleukin 1 production and accessory cell function of rat alveolar macrophages exposed to mineral dust particles — Y. Oghiso, Y. Kubota (1987)
• The ability of mineral dusts and fibres to initiate lipid peroxidation. Part I: parameters which determine this ability — M. Gulumian (1999)
• Airway wall remodeling induced by occupational mineral dusts and air pollutant particles — A. Churg, J.L. Wright (2002)

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