Pathogenetic mechanisms of asbestos and other mineral fibres

Our plain-English summary of Pathogenetic mechanisms of asbestos and other mineral fibres, by R.C. Brown, J.A. Hoskins, K. Miller, et al (Molecular Aspects of Medicine, 1990).

The study

• Authors: R.C. Brown, J.A. Hoskins, K. Miller, B.T. Mossman
• Journal: Molecular Aspects of Medicine
• Published: 1990;11(5):325-49
• Type of article: Review
• Cited by: 12 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Summary of the article

This review described the chemistry and composition of asbestos and other mineral fibres, including man-made mineral fibres (MMMF). It summarised hypotheses from the authors' laboratories and others about how fibres cause disease. The authors discussed fibre respirability and retention, noting that chrysotile is cleared rapidly from the lungs while amphiboles persist for many years. They summarised epidemiological evidence on pulmonary fibrosis (asbestosis), mesothelioma and lung cancer. From the cited studies they concluded that amphiboles, particularly crocidolite, appear to pose more risk than chrysotile, and that asbestos interacts with tobacco smoke in causing lung cancer. They stated that there were no data linking MMMF exposure to increased mesothelioma incidence. They discussed mechanisms separately for each disease. For fibrosis, they covered products released by macrophages. For mesothelioma, they covered the role of long, thin ('Stanton') fibres, chromosome changes, cell transformation and iron-catalysed oxygen free radicals. For lung cancer, they covered promoting or co-carcinogenic effects, including diacylglycerol accumulation. They considered experiments with milled fibres to be strong arguments against a central role for free radicals. They concluded that a common response might lie in the interaction of fibres with cell surfaces, possibly an exaggeration of normal cellular responses. They recommended that future in vitro studies use standardised fibre preparations of known size distributions.

PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

In plain English

This article was a review of how asbestos and other mineral fibres may cause disease. It described the chemistry of chrysotile, the amphiboles, erionite and man-made mineral fibres. Drawing on earlier studies, the authors reported that evidence suggested crocidolite and other amphiboles cause higher mesothelioma incidence than chrysotile. They also reported that Australian crocidolite miners had been shown to have about 5 times the lung cancer risk of Canadian chrysotile miners. In rodents given fibres by implantation or injection into the pleural or peritoneal cavity, the yield of mesothelioma-like tumours was proportional to the number of long, thin fibres. The authors believed a consensus had developed that fibres were not mutagenic in short-term tests used to detect chemical carcinogens. They described milling experiments as perhaps the most telling arguments against a central role for free radicals in fibre pathogenesis. They stated there were no data linking man-made mineral fibres to increased mesothelioma incidence. The authors suggested that many cellular effects of fibres might reflect an exaggerated normal response to solid surfaces. They called for in vitro studies using standardised fibre preparations of known sizes.

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: review (of chemistry, epidemiology, animal and cell-culture studies of mineral fibres, including hypotheses from the authors' own laboratories)
• Who was studied: No study population of its own; the authors reviewed published epidemiological studies of exposed workers and others, along with animal and cell-culture experiments
• Exposure: Chrysotile (serpentine) and amphibole asbestos (crocidolite, anthophyllite, tremolite, actinolite, amosite); other natural fibres (erionite, attapulgite, sepiolite, wollastonite); man-made mineral fibres (glass, rock and slag wools, ceramic fibres) and other synthetic fibres
• Main results:
  • From the reviewed literature, the authors stated that the evidence suggests crocidolite and other amphiboles cause a higher mesothelioma incidence than chrysotile
  • Citing Hobbs et al. (1980), Australian crocidolite miners had about 5 times the lung cancer risk of Canadian chrysotile miners
  • In experiments where fibrous dusts were implanted or injected into the peritoneal or pleural cavities of laboratory rodents, producing tumours similar to human mesothelioma, the only unifying feature found to correlate with tumour production was the number of long, thin fibres
  • The authors stated their belief that a consensus has developed that fibres are not mutagenic in the types of short-term tests used to detect chemical carcinogens, although chromosome aberrations have been reported in some cell types
  • Milling crocidolite reduced carcinogenesis and cytotoxicity but not free radical production or DNA damage. The authors described such experiments as perhaps the most telling arguments against a central role for free radicals in fibre pathogenesis
  • In lung cancer, the interaction of asbestos with tobacco smoke was described as usually more than additive but not always multiplicative
  • The authors stated there were no data linking man-made mineral fibre exposure to increased mesothelioma incidence
  • The highest human mesothelioma incidence was reported in Turkish villages and had been attributed to inhaled erionite fibres
• The authors' conclusion: The authors suggested that many fibre-induced cellular events (free radical generation, release of inflammatory mediators and growth factors, second messenger synthesis) might reflect an exaggeration of the normal cellular response to solid surfaces. They also said future in vitro work should use standardised fibre preparations of known size distributions
• Limitations the authors state:
  • Disease has mostly followed mixed fibre exposures, and asbestos potentiates other agents such as cigarette smoke, which makes it hard to attribute causality to particular fibre types
  • In vitro assay endpoints are not causally related to carcinogenesis and are hard to relate to disease in living organisms
  • There is no accepted animal model of the synergism between asbestos and cigarette smoke

Topics

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

Medical terms in this study, explained in our Lexicon: Chrysotile, Amphibole Group, Pulmonary Fibrosis, Mesothelioma, Lung Cancer, Crocidolite, Fibrosis, Macrophage.

Related studies

• Mesotheliomas in rats following inoculation with acid-leached chrysotile asbestos and other mineral fibres — G. Monchaux, J. Bignon, et al. (1981)
• Mineral fibres, fibrosis, and asbestos bodies in lung tissue from deceased asbestos cement workers — M. Albin, L. Johansson, et al. (1990)
• Fibrogenesis by mineral fibres: an in-vitro study of the roles of the macrophage and fibre length — M. Aalto, A.G. Heppleston (1984)
• Multiple mechanisms for the carcinogenic effects of asbestos and other mineral fibers — J.C. Barrett, P.W. Lamb, et al. (1989)
• Mechanisms of action of poorly soluble particulates in overload-related lung pathology — B.T. Mossman (2000)
• Morphological and chemical mechanisms of elongated mineral particle toxicities — A.E. Aust, P.M. Cook, et al. (2011)

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