Role of asbestos in etiology of malignant pleural mesothelioma

Our plain-English summary of Role of asbestos in etiology of malignant pleural mesothelioma, by J.J. Godleski (Thoracic Surgery Clinics, 2004).

The study

• Author: J.J. Godleski
• Journal: Thoracic Surgery Clinics
• Published: 2004;14(4):479-87
• Type of article: Review
• Cited by: 11 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

The evidence presented in this article demonstrates that asbestos fibers may be genotoxic to mesothelial cells through their distinctive structure and chemistry and through their interactions with complex cellular response mechanisms. Reactive oxygen and nitrogen species play a key role. Understanding the balance between these complex mechanisms that permit neoplastic transformation and facilitate the proliferation of tumor cells is the focus of current investigation in the development of mesothelial malignancy. In human disease, the persistence of asbestos fibers in the lung and pleural tumor is a critical feature that links the exposure to asbestos with the development of disease.

In plain English

This article was a narrative review, not a new study. It summarized published research on the link between asbestos and malignant pleural mesothelioma. It covered how asbestos fibers are found and counted in lung, pleura and tumor tissue, and how fibers may lead to cancer. The author wrote that all asbestos fiber types, including the amphiboles (such as amosite, crocidolite and tremolite) and chrysotile, have carcinogenic potential, and that there is no known exposure threshold below which there is no risk. The review described an earlier study by Roggli and colleagues of more than 90 United States mesothelioma cases, which identified amosite in 81% of cases and chrysotile in 21%. It also described cell and animal research suggesting that fibers damage DNA both directly and through reactive oxygen and nitrogen species, with the reactive species partly linked to iron at the fiber surface. The author concluded that asbestos fibers may be genotoxic to mesothelial cells, and that the persistence of fibers in the lung and pleural tumor links asbestos exposure with the disease.

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 human tissue, animal and cell studies; no new data
• Who was studied: No study population of its own. The review drew on earlier published studies of people with mesothelioma, on animal experiments and on cell cultures.
• Exposure: Asbestos in general: the amphiboles (actinolite, amosite, anthophyllite, crocidolite, tremolite) and the serpentine fiber chrysotile
• Main results:
  • Citing earlier studies, the author stated that all asbestos fiber types have carcinogenic potential.
  • Citing an earlier paper, the author stated that there is no known threshold of asbestos exposure below which there is no risk of mesothelioma.
  • An earlier study by Roggli et al examined more than 90 United States mesothelioma cases, almost half of them former asbestos insulators or shipyard workers. Lung digestion found amosite in 81% of cases (58% of longer fibers). It found tremolite, actinolite and anthophyllite in 55% of cases (10% of all fiber types), chrysotile in 21% of cases (3% of longer fibers), crocidolite in 16% of cases (3% of longer fibers), and nonasbestos mineral fibers in 71% of cases (25% of longer fibers).
  • Earlier studies cited by the author found excellent agreement between asbestos body counts in routine tissue sections and counts from lung tissue digestion (r = 0.98; P < 0.001). By the author's account, an average of two asbestos bodies on a 4 cm2 iron-stained section equals about 200 asbestos bodies per gram of wet fixed lung tissue.
  • Most fibers detected in lung and mesothelial tissues are short. On that basis, and citing earlier studies, the author wrote that short, thin fibers, not only long fibers, are suggested to contribute to human mesothelioma.
  • According to the cited studies, DNA damage results both from reactive oxygen and nitrogen species and directly from the fibers.
  • Cited laboratory studies showed that exposing mesothelial cells to asbestos fibers in vitro induced DNA damage mediated by reactive oxygen species.
  • Citing earlier studies, the author noted that p53 gene mutations are infrequent in mesothelioma compared with other tumors.
  • Citing earlier studies, the author wrote that other factors such as SV40 suggest possible co-carcinogenic roles but do not lessen the pre-eminence of the association with asbestos.
• The authors' conclusion: The author concluded that asbestos fibers may be genotoxic to mesothelial cells through their structure, their chemistry and their interactions with cell responses, with reactive oxygen and nitrogen species playing a key role. The author also concluded that the persistence of asbestos fibers in the lung and pleural tumor links asbestos exposure with the development of disease.

Topics

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

Medical terms in this study, explained in our Lexicon: Etiology, Pleural Mesothelioma, Mesothelial Cells.

Related studies

• Metsovo lung: pleural calcification and restrictive lung function in northwestern Greece. Environmental exposure to mineral fiber as etiology — S.H. Constantopoulos, J.A. Goudevenos, et al. (1985)
• Etiology of small cell lung carcinoma — W.J. Zeller, D. Schmähl (1985)
• Etiology of pleural effusions: analysis of more than 3,000 consecutive thoracenteses — J.M. Porcel, A. Esquerda, et al. (2014)
• The interactions of tobacco smoking and other agents in cancer etiology — R. Saracci (1987)
• Epidemiology, etiology, and fertility drugs in ovarian epithelial carcinoma: where are we today? — Z. Shoham (1994)
• Etiology of lung cancer: Evidence from epidemiologic studies — K. Zou, P. Sun, et al. (2022)

Browse more research in Thoracic Surgery Clinics, or return to medical research.