Current concepts about the pathogenesis of silicosis and asbestosis

Our plain-English summary of Current concepts about the pathogenesis of silicosis and asbestosis, by R.D. deShazo (The Journal of Allergy and Clinical Immunology, 1982).

The study

• Author: R.D. deShazo
• Journal: The Journal of Allergy and Clinical Immunology
• Published: 1982;70(1):41-9
• Type of article: Review
• Cited by: 58 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. 000667).

Abstract

Silicosis and asbestosis are two forms of fibrotic lung disease resulting from the inhalation of inert materials indigestible by pulmonary alveolar macrophages. Results of studies of the host response to these particulates have not always been consistent. It is clear, however, that after phagocytosis, both cause alveolar macrophage damage, with resultant release of macrophage products, including fibrogenic factors and chemotactic factors for neutrophils. The latter cells also release lysosomal enzymes and free radicals when exposed to silica and asbestos. The net effect of these observations suggests that the combination of tissue damage and fibroblast stimulation results in the pulmonary fibrosis characterizing these diseases. Patients with silicosis and asbestosis have normal or decreased cell-mediated and increased humoral immunity with a high incidence of circulating immune complexes and autoantibodies. Whether these abnormalities are related to the pathogenesis of pulmonary fibrosis or are epiphenomena remains to be determined.

In plain English

This 1982 article is a review, not a new study. The author summarized published laboratory, animal and human research on how inhaled silica and asbestos may lead to silicosis and asbestosis, two scarring (fibrotic) lung diseases. It named chrysotile, crocidolite and amosite as the most important commercial asbestos fibers. Studies it reviewed reported that both dusts damage lung scavenger cells called alveolar macrophages. Those cells then release substances that attract neutrophils, a type of white blood cell, and may stimulate collagen, the material in scar tissue. Asbestos workers and patients with asbestosis were reported to have decreased cell-mediated immunity but increased antibody production, including antinuclear antibodies and rheumatoid factors. Preliminary data from the author's group, which included 29 asbestos workers, suggested that lymphocyte responses might differ by chest X-ray stage. The author proposed a working hypothesis. The author also speculated that reduced T-cell surveillance could offer a mechanism for the increased tumor incidence in asbestos-exposed patients. The author concluded that whether these immune abnormalities cause the fibrosis or are by-products remains to be determined, noting that the data were conflicting and that few studies had separated key mechanisms.

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 in vitro, animal and human studies, with a proposed working hypothesis for each disease
• Who was studied: No new study population; the review covered published laboratory (in vitro) studies, experimental animals (including mice, rats, guinea pigs, rabbits and sheep), and patients and workers with silica or asbestos exposure
• Exposure: Free crystalline silica (quartz, crystobalite, tridymite) and asbestos; chrysotile (white asbestos), crocidolite (blue asbestos) and amosite (brown asbestos) were named as the most important commercial asbestos fibers, with chrysotile the most common in the United States
• Main results:
  • Reviewed studies reported that silica is cytotoxic to both pulmonary alveolar and circulating macrophages in many species, including humans
  • Patients with silicosis were reported to have a polyclonal increase in serum immunoglobulins and an increased incidence of antinuclear antibodies and rheumatoid factors
  • Asbestos workers and patients with asbestosis were reported to have decreased cell-mediated immunity in a number of functional tests, and the same workers were reported to have polyclonal hypergammaglobulinemia with increased antinuclear antibodies and rheumatoid factors
  • Preliminary data from the author's group (lymphocyte responses to the mitogen phytohemagglutinin in 29 asbestos workers compared with normal controls) suggested that lymphocyte responses may relate to disease stage on chest X-ray; workers with only minimal X-ray abnormalities had lower responses than those with none or with easily detectable abnormalities
  • In the author's hypothesis for asbestosis, neutrophils attracted into the lung release lysosomal enzymes and free radicals that damage lung tissue, while asbestos-exposed alveolar macrophages release fibrogenic factors
  • The author speculated that decreased immune surveillance by T-cells, alongside activated antibody responses, could offer a mechanism for the increased incidence of tumors in patients exposed to asbestos
  • The author noted that the increased risk of malignancy seen in asbestosis patients, and the granulomatous response and mycobacterial susceptibility seen in silicosis, are differences that current theories do not explain
• The authors' conclusion: The authors concluded that it remains to be decided which immunologic abnormalities in silicosis and asbestosis are related to the development of pulmonary fibrosis and which are epiphenomena (by-products)
• Limitations the authors state:
  • The author stated that very few studies had distinguished between the incompletely understood mechanisms (more collagen per cell versus more collagen-producing cells) that influence fibrosis
  • The author stated that the data were conflicting and hard to combine into a single hypothesis

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, Alveolar Macrophage, Phagocytosis, Macrophage, Fibrogenic, Fibroblast, Pulmonary Fibrosis.

Related studies

• Mechanisms in the pathogenesis of asbestosis and silicosis — B.T. Mossman, A. Churg (1998)
• Serum oncoproteins and growth factors in asbestosis and silicosis patients — P.W. Brandt-Rauf, S. Smith, et al. (1992)
• An overview of the role of mineral solubility in silicosis and asbestosis — G. Erdogdu, V. Hasirci (1998)
• Asbestosis and silicosis — G.R. Wagner (1997)
• Cancer incidence and mortality among Finnish asbestos sprayers and in asbestosis and silicosis patients — P. Oksa, E. Pukkala, et al. (1997)
• Serum concentrations of Krebs von den Lungen-6, surfactant protein D, and matrix metalloproteinase-2 as diagnostic biomarkers in patients with asbestosis and silicosis: a case-control study — C. Xue, N. Wu, et al. (2017)

Browse more research in The Journal of Allergy and Clinical Immunology, or return to medical research.