Asbestos toxicity: an immunologic perspective

Our plain-English summary of Asbestos toxicity: an immunologic perspective, by G.J. Rosenthal, P. Simeonova, E. Corsini (Reviews on Environmental Health, 1999).

The study

• Authors: G.J. Rosenthal, P. Simeonova, E. Corsini
• Journal: Reviews on Environmental Health
• Published: 1999;14(1):11-20
• Type of article: Review
• Cited by: 20 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Asbestos has long been associated with a number of life threatening pulmonary diseases, including asbestosis and mesothelioma. While the lung is the primary target organ for asbestos toxicity, a number of clinical and experimental studies over the past 30 years have shown that the immune system may also be altered by exposure to asbestos at occupationally relevant concentrations. Whereas early clinical studies generally focused on systemic observations of immune alteration, more recent studies have assessed the immunological changes occurring in the lung, the primary target organ of asbestos. This review will focus on the investigations that examine the influence of asbestos on systemic and local immunity, as well as the role that the immune system may play in asbestos-related disease.

In plain English

This article was a review. It described about 30 years of clinical and experimental studies on how asbestos may affect the immune system. It did not report a new study of its own. The authors described earlier reports that asbestos-exposed people often showed an overactive antibody-producing (B-cell) response, including autoantibodies. In workers with lung abnormalities on X-ray, these autoantibodies were found at reported rates of 3% to 28% for antinuclear antibody and 10% to 38% for rheumatoid factor. They also described a depressed T-cell response and reduced natural killer cell activity in patients with asbestosis. They summarized an earlier mouse experiment using chrysotile. In it, asbestos-treated immunodeficient (SCID) mice had significantly more lung hydroxyproline, a marker of scarring, than asbestos-treated normal mice. The review also covered how lung macrophages release TNF-alpha, and how iron on fibers, including crocidolite, may drive this. The authors concluded that few if any immune cells are spared by asbestos. They speculated that impaired cell-mediated immunity may predispose people to asbestos-induced fibrosis. They noted it remained unclear whether these immune defects come before scarring or result from it.

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 clinical and experimental studies
• Who was studied: Published clinical studies (asbestos-exposed workers and patients) and experimental studies (cell cultures, rodents) from roughly the preceding 30 years
• Exposure: Asbestos in general. The experimental work described used chrysotile and crocidolite.
• Main results:
  • Reviewed studies indicated that asbestos appears to produce an overactive B-cell (antibody) state in chronically exposed people.
  • In asbestos-exposed workers with radiographic lung abnormalities, earlier studies reported autoantibody rates of 3% to 28% for antinuclear antibody and 10% to 38% for rheumatoid factor.
  • Clinical studies reviewed showed a significantly depressed T-cell-mediated immune response in asbestos-exposed individuals.
  • One earlier clinical study found no association between impaired cellular immunity and malignancy in eight out of ten patients with asbestos-associated pleural mesothelioma and without lung fibrosis.
  • In an earlier mouse inhalation study using chrysotile, asbestos-treated immunodeficient SCID mice had a significant increase in total lung hydroxyproline compared with asbestos-treated immunocompetent mice.
  • Clinical studies reviewed showed impaired natural killer cell activity in blood from patients with asbestosis.
  • In earlier experimental work, the iron chelator desferoxamine markedly diminished the ability of asbestos fibers to induce TNF-alpha from alveolar macrophages.
• The authors' conclusion: The authors concluded that few if any immune cells are spared by asbestos. They speculated that impaired cell-mediated immunity may be a predisposing factor in asbestos-induced fibrosis.
• Limitations the authors state:
  • The authors noted it remained unclear whether the reported immune defects precede fibrosis or are a consequence of it.
  • The authors stated that whether natural killer cell deficits precede or follow neoplastic or fibrotic disease, or are independent of it, remained unclear.

Topics

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

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

Related studies

• Selected new developments in asbestos immunotoxicity — G.J. Rosenthal, E. Corsini, et al. (1998)
• Immunologic aspects of pneumoconiosis — R.K. Scheule, A. Holian (1991)
• Immunologic aberrations in asbestos cement workers: dissociation from asbestosis — R.D. deShazo, D.J. Hendrick, et al. (1983)
• Heterogeneity in immunologic functions of rat alveolar macrophages--their accessory cell function and IL-1 production — Y. Oghiso (1987)
• Immunologic investigations in asbestos-exposed workers — R.D. deShazo, C.B. Daul, et al. (1986)
• Analysis of DNA methylation patterns in the tumor immune microenvironment of metastatic melanoma — S. Mitra, M. Lauss, et al. (2020)

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