Asbestos-induced lung diseases: an update

Our plain-English summary of Asbestos-induced lung diseases: an update, by D.W. Kamp (Translational Research, 2009).

The study

• Author: D.W. Kamp
• Journal: Translational Research
• Published: 2009;153(4):143-52
• Type of article: Review
• Cited by: 165 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

Asbestos causes asbestosis (pulmonary fibrosis caused by asbestos inhalation) and malignancies (bronchogenic carcinoma and mesothelioma) by mechanisms that are not fully elucidated. Despite a dramatic reduction in asbestos use worldwide, asbestos-induced lung diseases remain a substantial health concern primarily because of the vast amounts of fibers that have been mined, processed, and used during the 20th century combined with the long latency period of up to 40 years between exposure and disease presentation. This review summarizes the important new epidemiologic and pathogenic information that has emerged over the past several years. Whereas the development of asbestosis is directly associated with the magnitude and duration of asbestos exposure, the development of a malignant clone of cells can occur in the setting of low-level asbestos exposure. Emphasis is placed on the recent epidemiologic investigations that explore the malignancy risk that occurs from nonoccupational, environmental asbestos exposure. Accumulating studies are shedding light on novel mechanistic pathways by which asbestos damages the lung. Attention is focused on the importance of alveolar epithelial cell (AEC) injury and repair, the role of iron-derived reactive oxygen species (ROS), and apoptosis by the p53- and mitochondria-regulated death pathways. Furthermore, recent evidence underscores crucial roles for specific cellular signaling pathways that regulate the production of cytokines and growth factors. An evolving role for epithelial-mesenchymal transition (EMT) is also reviewed. The translational significance of these studies is evident in providing the molecular basis for developing novel therapeutic strategies for asbestos-related lung diseases and, importantly, other pulmonary diseases, such as interstitial pulmonary fibrosis and lung cancer.

In plain English

This article was a narrative review of epidemiologic and laboratory studies on asbestos-related lung diseases published in the several years before 2009. It reported no new data of its own. All figures below come from studies it cited. One cited study of 4,768 residents of Wittenoom, Western Australia, who never worked in the crocidolite asbestos mines or mills, reported 67 cases of malignant mesothelioma. A radiographic screening of 6668 people in Libby, Montana, found pleural abnormalities in 1186 (17.8%). The review stated that no firm evidence suggests pleural plaques increase the risk of mesothelioma or lung cancer. It also stated that none of the biomarkers studied had proven useful as a screening test for mesothelioma. It described laboratory studies that, in the author's view, implicate the p53 protein in the death of lung cells after asbestos exposure. The author noted that well-designed studies directly assessing cancer risk from low-dose exposure are lacking. The author concluded that a total worldwide asbestos ban is strongly supported.

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 recent epidemiologic and mechanistic (laboratory and animal) studies; no original data
• Who was studied: Published studies on the epidemiology and biological mechanisms of asbestos-induced lung diseases from the several years before 2009; no study population of its own
• Exposure: Asbestos in general, including serpentine fibers (chrysotile) and amphiboles (crocidolite, amosite, tremolite), from occupational and nonoccupational environmental sources
• Main results:
  • Cited study (Reid et al, 2007): 67 cases of malignant mesothelioma among 4,768 residents of Wittenoom, Western Australia, who never worked in the crocidolite asbestos mines or mills that operated between 1943 and 1966
  • Cited radiographic screening of 6668 Libby, Montana residents: 1186 (17.8%) had pleural abnormalities. Prevalence was highest in WR Grace vermiculite mine workers (51%) and lowest in residents reporting neither occupational nor domestic asbestos exposure (6.7%)
  • The review stated that environmental asbestos exposure is associated with an excess of asbestos-induced lung diseases, but about 10 times lower than that seen with occupational exposure
  • The review stated that no firm evidence suggests pleural plaques increase the risk of malignant mesothelioma or lung cancer. In a cited review of 13 studies, 10 were deemed appropriate and none of the 10 showed a direct relationship with lung cancer
  • Cited study (Oksa et al): 11 of 24 patients with progressive asbestosis (46%) developed lung cancer
  • Same cited study: 5 of 54 patients with stable asbestosis (9%) developed lung cancer
  • The review stated that none of the biomarkers studied in asbestos-exposed workers had proven useful as a screening test for malignant mesothelioma, because of false-positive and false-negative tests
  • The author wrote that laboratory data implicate a prominent role for p53 in asbestos-induced alveolar epithelial cell mitochondrial dysfunction and apoptosis (cell death)
• The authors' conclusion: The author concluded that asbestos-related lung diseases remain a significant challenge and that a total worldwide asbestos ban is strongly supported
• Limitations the authors state:
  • The author stated that well-designed epidemiologic studies directly assessing malignancy risk from low-dose asbestos exposure are lacking
  • The author stated it remains unclear whether asbestosis is simply a marker of high-dose exposure or a necessary requirement for attributing a lung cancer to asbestos

Topics

Medical terms in this study, explained in our Lexicon: Pulmonary Fibrosis, Bronchogenic Carcinoma, Mesothelioma, Latency, Asbestos Exposure, Damages, Reactive Oxygen Species (ROS), Apoptosis.

Related studies

• The role of free radicals in asbestos-induced diseases — D.W. Kamp, P. Graceffa, et al. (1992)
• Molecular basis of asbestos-induced lung disease — G. Liu, P. Cheresh, et al. (2013)
• Multiple roles of oxidants in the pathogenesis of asbestos-induced diseases — A. Shukla, M. Gulumian, et al. (2003)
• Evidence supporting a role for active oxygen species in asbestos-induced toxicity and lung disease — B.T. Mossman, J.P. Marsh (1989)
• Relative release of interleukin-1 beta and interleukin-1 receptor antagonist by alveolar macrophages. A study in asbestos-induced lung disease, sarcoidosis, and idiopathic pulmonary fibrosis — J.N. Kline, D.A. Schwartz, et al. (1993)
• Rapid and easy method for monitoring oxidative stress markers in body fluids of patients with asbestos or silica-induced lung diseases — K. Syslová, P. Kacer, et al. (2009)

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