Asbestosis: clinical spectrum and pathogenic mechanisms

Our plain-English summary of Asbestosis: clinical spectrum and pathogenic mechanisms, by D.W. Kamp, S.A. Weitzman (Proceedings of the Society for Experimental Biology and Medicine, 1997).

The study

• Authors: D.W. Kamp, S.A. Weitzman
• Journal: Proceedings of the Society for Experimental Biology and Medicine
• Published: 1997;214(1):12-26
• Type of article: Review
• Cited by: 34 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Asbestosis is a diffuse pulmonary fibrotic process caused by the inhalation of asbestos fibers. Despite extensive investigations, the precise mechanisms regulating asbestos-induced lung damage are not fully understood. This review summarizes the important clinical manifestations and pathogenic mechanisms of asbestosis. We focus on the relatively new information that has emerged over the last several years. The diagnosis of asbestosis is often easily established by well-characterized criteria. Pulmonary physiologic testing and high-resolution computed tomography can detect clinically occult disease. The finding of asbestos bodies in the bronchoalveolar lavage fluid confirms that an individual has been exposed to asbestos but is of unclear significance in diagnosing asbestosis. Evidence reviewed herein suggests that asbestos pulmonary toxicity is due in part to the physical properties of the fibers, iron-catalyzed reactive oxygen species (ROS), and macrophage-derived cytokines and growth factors. Special emphasis is given to the hypothesis that iron-catalyzed hydroxyl radicals (HO.-) have a pivotal role in causing asbestosis. Definitive proof of this hypothesis is difficult to obtain since HO.- are highly reactive and their deleterious effects to cells may have occurred years prior to disease presentation. Despite these limitations, considerable data firmly support the notion that ROS have an important role in causing asbestos toxicity. Further, the iron content of asbestos or the redoxactive iron associated with or mobilized from the surface of the fibers is important in generating HO.- as well as in activating inflammatory cells. There also appears to be a close association between asbestos-induced ROS production and cellular toxicity and DNA damage. The full expression of asbestos-induced diseases likely involves the contribution of cytokines, growth factors, proteases, and other inflammatory cell products. Many of the mechanisms by which asbestos- and inflammation-induced ROS activate specific genes in pulmonary cells remain to be elucidated.

In plain English

This article was a short review (labelled a "mini review") of published research on asbestosis, the lung scarring caused by inhaling asbestos fibers. It was not a new study of patients or animals. The authors covered how the disease appears clinically and how it may develop, focusing on work from the preceding several years. Citing other studies, the review described a delay of at least 20 to 40 years between first exposure and symptoms. It stated that lung function tests and high-resolution CT scans can find disease not seen on ordinary X-rays. It also stated that asbestos bodies found in lung-wash fluid confirm exposure but are of unclear value for diagnosing asbestosis. It cited evidence that amphibole fibers cause more scarring than chrysotile. The authors concluded that the evidence strongly supports the idea that asbestos lung damage results largely from oxidant and inflammatory stress. They called laboratory and animal data convincing for a role of reactive oxygen molecules. However, they said evidence for iron-driven hydroxyl radicals in living tissue is largely circumstantial, and that definitive proof is hard to obtain.

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 (mini review) of published clinical, laboratory and animal research
• Who was studied: No new subjects were studied. The review covered published studies of asbestos-exposed workers, patients with asbestosis, cell cultures and laboratory animals, focusing on research from the several years before 1997.
• Exposure: Inhaled asbestos fibers of two kinds: serpentine (chrysotile) and amphibole (crocidolite, amosite, tremolite and others). Exposure came from mining and milling, industrial uses, and nonoccupational sources.
• Main results:
  • Citing other studies, the review stated that there is a latency period of at least 20 to 40 years between initial exposure and respiratory symptoms.
  • The review stated that lung function testing or high-resolution CT scans may detect asbestosis that is not clinically apparent.
  • The review concluded that asbestos bodies in bronchoalveolar lavage (lung-wash) fluid confirm asbestos exposure but are of unclear significance for diagnosing asbestosis.
  • The review cited evidence that amphibole fibers are more fibrogenic (cause more scarring) than chrysotile.
  • The authors stated that laboratory (in vitro) and live-animal (in vivo) data argue convincingly that reactive oxygen species play an important role in asbestos toxicity.
  • The review stated that the full expression of asbestos-induced disease likely also involves cytokines, growth factors, proteases and other inflammatory cell products.
• The authors' conclusion: The authors concluded that the balance of evidence strongly supports one hypothesis: asbestos-induced lung toxicity is in large part a result of the oxidant and inflammatory burden on cells and tissues exposed to the fibers.
• Limitations the authors state:
  • The authors stated that evidence for the role of iron-catalyzed hydroxyl radicals in living tissue is largely circumstantial. Their reason was that these molecules are so reactive that only traces of their past activity can be detected.
  • The authors said that definitive proof of the hypothesis that iron-catalyzed hydroxyl radicals have a pivotal role is hard to obtain. One reason they gave was that the damage to cells may have occurred years before disease appears.
  • The authors stated that many of the mechanisms by which reactive oxygen species activate specific genes in lung cells remain unknown.

Topics

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

Medical terms in this study, explained in our Lexicon: Asbestos Bodies, Bronchoalveolar Lavage (BAL), Reactive Oxygen Species (ROS), Macrophage, Cytokine, Hydroxyl Radical, Inflammation.

Related studies

• Indications for distinct pathogenic mechanisms of asbestos and silica through gene expression profiling of the response of lung epithelial cells — T.N. Perkins, P.M. Peeters, et al. (2015)
• Mechanisms of carcinogenesis and clinical features of asbestos-associated cancers — B.T. Mossman, D.W. Kamp, et al. (1996)
• Effects of Chrysotile Exposure in Human Bronchial Epithelial Cells: Insights into the Pathogenic Mechanisms of Asbestos-Related Diseases — G.R. Gulino, M. Polimeni, et al. (2016)
• Giant Pediatric Rhabdoid Meningioma Associated with a Germline BAP1 Pathogenic Variation: A Rare Clinical Case — A.C. Ravanpay, A. Barkley, et al. (2018)
• Localized pleural mesothelioma. The clinical spectrum — L.A. Robinson, R.B. Reilly (1994)
• Spectrum of peritoneal mesothelioma in childhood: clinical and histopathologic features, including DNA cytometry — F.K. Niggli, T.J. Gray, et al. (1994)

Browse return to medical research.