Current issues regarding the pathobiology of asbestosis: a chronologic perspective

Our plain-English summary of Current issues regarding the pathobiology of asbestosis: a chronologic perspective, by E. Kagan (Journal of Thoracic Imaging, 1988).

The study

• Author: E. Kagan
• Journal: Journal of Thoracic Imaging
• Published: 1988;3(4):1-9
• Type of article: Review
• Cited by: 7 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. 000916).

Abstract

Asbestosis is a pneumoconiosis that results from the inhalation of asbestos fibers. There is a body of evidence that implicates the alveolar macrophage in the pathogenesis of asbestosis because of its prominence in asbestos-related histologic lesions. Injury to the alveolar epithelium also may contribute to the pathogenesis of asbestosis. Evidence is presented to suggest that pulmonary fibrosis may result from the persistent release of inflammatory mediators (chemoattractants, lysosomal enzymes, toxic oxygen radicals, arachidonic acid metabolites, interleukins, and fibroblast growth factors) at sites of asbestos deposition. Histologic features of asbestosis can be detected within months after the initial contact with asbestos. In contrast, the stigmata of asbestos-related disease usually are not radiologically detectable, even by the most sensitive imaging techniques, until after a latency period of at least a decade, and often considerably longer. There is, therefore, a long diagnostic delay between the time when asbestosis is histologically detectable and when it is radiographically detectable.

In plain English

This 1988 article was a review, not a new study. The author reviewed research, mostly in rats and other animals and some in asbestos workers, on how asbestosis (lung scarring from inhaled asbestos fibers) develops over time. In the animal inhalation studies it described, characteristic lesions appeared where fibers settled as soon as two to three days after first contact. The author's own group reported lung fibrosis in rats within four weeks after exposure to chrysotile or crocidolite ended. In humans, fibrosis had occasionally been seen at autopsy in asbestos mine workers six to 12 months after first contact. The review described activation of scavenger cells (macrophages) and their release of inflammatory substances as possible mechanisms. By contrast, X-ray signs usually did not appear until at least 10 years after first contact. The author concluded that there is a wide delay between when asbestosis can be seen in tissue and when it shows on imaging. The author also noted that little information exists on when tissue changes begin in humans.

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: Narrative review of published research on how asbestosis develops and the timing of its tissue changes, including the author's own earlier animal studies
• Who was studied: No new study population. The review drew on rodent inhalation studies, a sheep model, and studies of asbestos workers and their lung tissue.
• Exposure: Inhaled asbestos fibers of the commercial types, with discussion of chrysotile, crocidolite, amosite and anthophyllite, and of the noncommercial amphiboles tremolite, actinolite and anthophyllite
• Main results:
  • In the experimental (animal) inhalation studies reviewed, characteristic lesions formed at fiber deposition sites as soon as two to three days after initial contact.
  • The author's group detected interstitial lung fibrosis in rats within four weeks after inhalation of chrysotile or crocidolite asbestos ended.
  • In humans, the review stated that histologic evidence of asbestosis had occasionally been noted at autopsy in asbestos mine workers as soon as six to 12 months after first contact, without previous clinical or radiographic evidence of disease.
  • In the author's rat inhalation model, signs of macrophage activation (more Ia antigen-bearing macrophages and raised interleukin 1) appeared as soon as one week after exposure began and persisted for many months after it stopped.
  • In rats, asbestos fibers were still found inside alveolar macrophages as long as 16 months after experimental exposure ended.
  • The review stated that the lung fiber burden in patients with asbestosis is several orders of magnitude greater than in the general population.
  • The author reported more striking immune abnormalities in patients with X-ray signs of parenchymal asbestosis than in those with only pleural plaques.
  • Clinical symptoms and X-ray signs of asbestos exposure usually were not detected until at least 10 years (sometimes 20 to 40 years) after first contact.
• The authors' conclusion: The author concluded that there is a wide delay between when asbestosis is detectable in tissue (within months) and when it is detectable on imaging (usually at least a decade). The author also concluded that radiography remains the main detection method and that more sensitive, relatively noninvasive methods are needed.
• Limitations the authors state:
  • The author noted that little information exists in the literature on when tissue changes of asbestosis first appear in humans.
  • The author noted that the mechanisms by which asbestos causes lung fibrosis have not been completely worked out.

Topics

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

Medical terms in this study, explained in our Lexicon: Pneumoconiosis, Alveolar Macrophage, Epithelium, Pulmonary Fibrosis, Interleukins, Fibroblast, Deposition, Latency.

Related studies

• The Latrobe Valley: perspectives on asbestos issues — V. Hamilton (2008)
• Regarding "absence of radiographic asbestosis and the risk of lung cancer among asbestos-cement workers: extended follow-up of a cohort", by Murray Finkelstein, American Journal of Industrial Medicine 2010 — R.M. Ross (2011)
• Asbestos-related lung cancer and malignant mesothelioma of the pleura: selected current issues — S. Markowitz (2015)
• Current issues in the pathologic and mineralogic diagnosis of asbestos-induced disease — A. Churg (1983)
• Current issues in malignant pleural mesothelioma evaluation and management — J. Ai, J.P. Stevenson (2014)
• The Peritoneum: Health, Disease, and Perspectives regarding Tissue Engineering and Cell Therapies — R.J.F.C. do Amaral, K.D. Arcanjo, et al. (2017)

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