Mechanisms in the pathogenesis of asbestosis and silicosis

Our plain-English summary of Mechanisms in the pathogenesis of asbestosis and silicosis, by B.T. Mossman, A. Churg (American Journal of Respiratory and Critical Care Medicine, 1998).

The study

• Authors: B.T. Mossman, A. Churg
• Journal: American Journal of Respiratory and Critical Care Medicine
• Published: 1998;157(5 Pt 1):1666-80
• Type of article: Review
• Cited by: 662 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

In plain English

This article was a review, not a new study. The authors summarized published research on how asbestosis (lung scarring from asbestos) and silicosis (lung disease from crystalline silica) develop, drawing on human lung fiber-burden studies, animal experiments and laboratory cell studies. They reported that cited studies point to a threshold dose for asbestosis of at least about 25 to 100 fiber/ml/yr. They also reported that, fiber for fiber, amphibole asbestos appeared more fibrogenic than chrysotile. They cited their group's earlier finding that, in Quebec chrysotile miners and millers, mesothelioma and asbestosis occurred at about the same, very high, fiber burden. They described smoking as increasing the attack or progression rate of asbestosis. For silicosis, they reported that coexposure to other dusts reduced disease at the same silica weight. In a cited rodent inhalation model, catalase reduced asbestos-induced inflammation and fibrosis. The authors concluded that the two diseases share several common mechanisms. They stressed that current understanding is limited, since their summary table and diagram would wrongly suggest the two diseases are identical.

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 (State of the Art article) of clinical, pathologic, fiber-burden, animal and in vitro studies
• Who was studied: Published human, animal (rats, mice, sheep, guinea pigs) and cell-culture studies of asbestosis and silicosis, with mechanistic data emphasized from recent years
• Exposure: Asbestos (chrysotile and the amphiboles crocidolite, amosite, anthophyllite, tremolite, actinolite) and crystalline silica (mainly quartz, also cristobalite, tridymite and others)
• Main results:
  • Based on the epidemiologic studies cited, the authors stated there is a threshold dose for asbestosis of, at a minimum, approximately 25 to 100 fiber/ml/yr
  • The cited studies show that smoking increases the attack and/or progression rate of asbestosis, based on radiographic evidence
  • The estimated lung half-life of amphibole fibers is on the order of decades, compared with a few months for chrysotile
  • In shipyard workers and insulators, amosite fiber concentration was about 12 times higher with asbestosis than with mesothelioma (geometric means, Churg and Vedal)
  • In the authors' group's earlier study of Quebec chrysotile miners and millers, mesothelioma and asbestosis occurred at about the same, very high, fiber burden
  • On a fiber-for-fiber basis, amphibole asbestos appeared more fibrogenic than chrysotile
  • In two human cohorts studied by the authors' group, fibrosis grade was inversely correlated with mean fiber length for amosite, and for chrysotile and tremolite
  • For silicosis, retained loads of 1 to 3 g of relatively pure silica (gold miners, foundry workers) produced silicosis. The same weight of silica with coexposure to other dusts (coal or hematite miners) produced very little silicosis
  • Many cytokines and growth factors are induced by these minerals, but it is uncertain which, if any, are essential to fibrosis
  • In a rodent inhalation model of asbestosis, catalase inhibited inflammation and fibrosis
  • Both asbestosis and silicosis are dose-related diseases
  • In humans and experimental animals there is a strong association between asbestosis and increased lung cancer risk
  • Whether lung cancer risk is increased without asbestosis is debated
• The authors' conclusion: The authors concluded that, despite different microscopic appearances, asbestosis and silicosis share several common mechanisms of development (oxidants, chemokines and cytokines from many cell types)
• Limitations the authors state:
  • Current understanding is limited: their table of mediators (Table 5) and hypothetical diagram (Figure 3) would wrongly imply the two diseases are identical
  • Fiber counts vary greatly between laboratories, so absolute numbers cannot be compared across laboratories
  • The link between dust-induced fibrosis and lung cancer was not addressed in the review

Topics

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

Medical terms in this study, explained in our Lexicon: Silicosis.

Related studies

• Current concepts about the pathogenesis of silicosis and asbestosis — R.D. deShazo (1982)
• An overview of the role of mineral solubility in silicosis and asbestosis — G. Erdogdu, V. Hasirci (1998)
• Serum oncoproteins and growth factors in asbestosis and silicosis patients — P.W. Brandt-Rauf, S. Smith, et al. (1992)
• TruCutR needle biopsy in asbestosis and silicosis: correlation of histological changes with radiographic changes and pulmonary function in 41 patients — P. Tukiainen, E. Taskinen, et al. (1978)
• Mixed pneumoconiosis: silicosis, asbestosis, talcosis, and berylliosis — G.J. Mark, C.B. Monroe, et al. (1979)
• Asbestosis and silicosis — G.R. Wagner (1997)

Browse more research in American Journal of Respiratory and Critical Care Medicine, or return to medical research.