New perspectives on basic mechanisms in lung disease. 5. Respirable industrial fibres: mechanisms of pathogenicity

Our plain-English summary of New perspectives on basic mechanisms in lung disease. 5. Respirable industrial fibres: mechanisms of pathogenicity, by K. Donaldson, R.C. Brown, G.M. Brown (Thorax, 1993).

The study

• Authors: K. Donaldson, R.C. Brown, G.M. Brown
• Journal: Thorax
• Published: 1993;48(4):390-5
• Type of article: Review
• Cited by: 48 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Summary of the article

This review, part of a British Association for Lung Research series, addressed the scientific ideas behind research into how respirable industrial fibres cause disease. The fibres covered were asbestos and natural and man-made non-asbestos fibres. The authors noted that asbestos inhalation is associated with asbestosis, lung carcinoma, mesothelioma and small airways disease. They also noted that some non-asbestos fibres caused asbestos-like effects in biological assays, which raised the question of whether all fibres share asbestos's pathogenic potential. They summarised evidence on fibre deposition, length, surface chemistry and durability. In rat studies, a long-fibre amosite sample produced lung tumours in 32.5% of animals after inhalation and mesotheliomas in 88% after intraperitoneal instillation, while a short-fibre sample produced none. Other evidence reviewed included the following: long fibres were cleared less effectively; surface chemistry (erionite, protein coating, iron) may influence activity; and epidemiological studies suggested chrysotile is much less harmful in man than other asbestos forms. The authors also reviewed fibre effects on epithelial cells, macrophages, inflammation and mesothelial cells, and combined exposures with smoking, ozone and other dusts. They noted that standard non-asbestos fibre samples had been lacking and that the UICC asbestos samples contained mostly short fibres. They concluded that the idea that any long, thin, durable fibre may be pathogenic dominates the field, although there is no consensus on definitions of these terms. They suggested that understanding which fibre characteristics control toxicity may allow industry to design safer fibres.

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, part of a British Association for Lung Research series, of research on how breathed-in industrial fibres cause lung disease. It covered asbestos (chrysotile and amphiboles such as crocidolite, amosite and tremolite) and non-asbestos fibres such as erionite, glass wool, rock wool and ceramics, drawing mainly on animal and laboratory cell studies. The authors stated that the review was not comprehensive. They summarised earlier work showing that long fibres were more biologically active, and cleared from the lung less effectively, than short ones. In rat experiments with long and short amosite placed in the abdominal (peritoneal) cavity, 88% of rats given long fibres developed mesotheliomas, against 0% given short fibres. The authors described evidence that a fibre's surface chemistry, how long it lasts in the lung, and combined exposure to other dusts or ozone may also matter. They judged that iron released from fibres was unlikely to be a factor common to all fibre toxicity. The authors concluded that research was guided by the idea that any long, thin, durable fibre may cause disease, but noted there was no agreed definition of these terms.

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 research on how respirable industrial fibres cause disease, mostly animal and in vitro (laboratory cell) studies
• Who was studied: Published studies, mainly in rats, mice and cultured cells, on the mechanisms of diseases caused by respirable industrial fibres
• Exposure: Asbestos (serpentine group: chrysotile; amphibole group: crocidolite, amosite, anthophyllite, tremolite, actinolite) compared with non-asbestos fibres, both natural (e.g. erionite, wollastonite) and man-made (e.g. slag wool, rock wool, glass wool, ceramics)
• Main results:
  • The review cited earlier studies showing that short fibres (below 5 micrometres) had low ability to cause disease, and that this ability increased with fibre length beyond 8 to 10 micrometres
  • In earlier rat experiments summarised from Davis et al and Donaldson et al, 88% of rats given long-fibre amosite by intraperitoneal instillation developed mesotheliomas, compared with 0% of rats given short-fibre amosite
  • Several studies cited in the review found that long fibres were cleared from the deep lung less effectively than short fibres
  • In the animal studies cited, erionite produced a far higher incidence of mesothelioma than any other fibre
  • The authors judged that iron released from fibres was unlikely to be a factor common to all fibre toxicity
  • The authors reported that epidemiological studies of workers exposed to chrysotile asbestos suggested it is much less harmful in humans than other forms of asbestos
  • Cited rat studies found that low-dose ozone slowed the clearance of asbestos from the lung, and that inhaling asbestos together with titanium dioxide or quartz may produce more lung and pleural tumours than asbestos alone
  • Laboratory studies cited reported that mesothelial cells in culture were particularly susceptible to the toxic effects of fibres
  • Nearly all experiments to that date had used standard asbestos samples containing less than 1% of the long, active fibre fraction
• The authors' conclusion: The authors concluded that the study of fibre disease was dominated by the idea that any long, thin, durable fibre may be able to cause disease. In their view, a ban on fibres would be impractical with the knowledge available at the time, and a better understanding of fibre properties might allow industry to design safer fibres.
• Limitations the authors state:
  • The authors stated that the review was not comprehensive
  • The authors noted that soluble fibres can persist for much of a rodent's short lifespan, so animal experiments might give false positive results compared with humans
  • There was no agreed definition of long, thin or durable fibres
  • The lack of standard non-asbestos fibre samples had held back comparisons between asbestos and other fibres

Topics

Medical terms in this study, explained in our Lexicon: Carcinoma, Mesothelioma, Deposition, Amosite, erionite, Chrysotile, Macrophage, Inflammation.

Related studies

• Superoxide anion release by alveolar macrophages exposed to respirable industrial fibres: modifying effect of fibre opsonisation — K. Donaldson, I.M. Hill, et al. (1995)
• Detection of surface free radical activity of respirable industrial fibres using supercoiled phi X174 RF1 plasmid DNA — P.S. Gilmour, P.H. Beswick, et al. (1995)
• Biological activity of respirable industrial fibres treated to mimic residence in the lung — K. Donaldson (1994)
• An introduction to the short-term toxicology of respirable industrial fibres — K. Donaldson, C.L. Tran (2004)
• Man-made mineral fibers and interstitial lung diseases — E. Fireman (2014)
• Short-term inhalation and in vitro tests as predictors of fiber pathogenicity — R.T. Cullen, B.G. Miller, et al. (1997)

Browse more research in Thorax, or return to medical research.