The early effects of chrysotile asbestos dust on the rat lung

Our plain-English summary of The early effects of chrysotile asbestos dust on the rat lung, by P.F. Holt, J. Mills, D.K. Young (The Journal of Pathology and Bacteriology, 1964).

The study

• Authors: P.F. Holt, J. Mills, D.K. Young
• Journal: The Journal of Pathology and Bacteriology
• Published: 1964;87:15-23
• Cited by: 84 articles, as counted by NIH iCite
• Read it: PubMed · Publisher
• In J-M's library: Johns-Manville's company medical library held a copy.

Abstract

Chrysotile dust of small particle size (<3 µm) rapidly produces fibrotic lesions in the lungs when inhaled by rats. It is suggested that asbestos is fibrogenic only when it can be ingested by phagocytes. The rapid fibrosis that can occur some years after asbestos has been inhaled by man may be due to the breakdown into large numbers of small fragments of fibres; these are then phagocytosed. Alternatively the small particles originally inhaled may act slowly and their effect may be enhanced by a superimposed infection.
An apparatus that maintains an atmosphere containing small asbestos fibres at nearly constant concentration is described.

PubMed has no abstract for this study. This is the authors' abstract, copied from the article.

In plain English

In this animal experiment, the authors exposed 24 rats to a cloud of chrysotile asbestos dust for about 100 hours over 30 days. The dust was made from high-purity Rhodesian chrysotile in a hammer-mill dust generator. Air samples held about 5000 particles per ml, and more than 80 per cent of fibres were shorter than 5 microns. One rat killed on day 14 had little visible dust but a few sharply defined inflammatory lesions containing giant cells. A thin collagen capsule and a reticulin net had already formed in them. Five rats killed 39 days after dusting stopped showed patchy organising pneumonia with early fibrosis. Rats followed for up to a year showed widespread fibrosis. No asbestos bodies were found, and very few fibres longer than about 2 microns were seen. A second group of 25 rats, dusted for only 68 hours, developed similar but smaller lesions. Control rats never showed such lesions. The authors concluded that chrysotile particles under 2 microns long can produce peribronchiolar fibrosis in the rat. They noted that the dust concentration was high compared with industry.

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: animal inhalation experiment in rats, with untreated control rats
• Who was studied: Rats in a laboratory at the Department of Chemistry, University of Reading. The first experiment used 24 rats, exposed for approximately 100 hours over 30 days. A second experiment used 25 rats. Many untreated control rats of all ages were also examined. Study dates are not given.
• Exposure: Chrysotile asbestos dust made from a high-purity Rhodesian chrysotile, produced by a hammer-mill dust generator (Dust Generator Mark II)
• Main results:
  • Air samples from the dust chamber held approximately 5000 particles per ml of air. By length, 24 per cent of particles were under 1 micron, 36 per cent 1 to 2, 24 per cent 2 to 5, 10 per cent 5 to 10, 4 per cent 10 to 20, and 2 per cent over 20 microns. The authors state that more than 80 per cent of the fibres were shorter than 5 microns.
  • In the rat killed on the 14th day of inhalation there were a few sharply defined focal inflammatory lesions, mostly in the walls of terminal bronchioles. A delicate collagen capsule and a reticulin net had already formed in them.
  • The most striking feature of these early lesions was multinucleated giant cells.
  • At 14 days no asbestos bodies were found, and no dust was found in lymphoid tissue within the lung or in the tracheal lymph glands.
  • Five rats were killed 39 days after dusting stopped. Their lungs showed little dust but a patchy organising lobular pneumonia with a more diffuse organising interstitial pneumonia and early fibrosis in the alveolar walls.
  • Rats killed at intervals up to a year (a typical lesion is shown at 364 days) had widespread interstitial cell infiltration and fibrosis.
  • At no stage were asbestos bodies identified. Fibres in the lungs were few and never more than 10 microns long.
  • Histological sections showed very few asbestos fibres longer than about 2 microns; most particles were inside phagocytes.
  • In a second experiment, 25 rats were exposed for only 68 hours over 45 days.
  • In the second experiment, the remaining rats were killed after 167 days without further dusting. They had lesions similar to those in the first experiment but smaller and less obvious, rarely with giant cells, and collagen was present.
  • Similar lesions were never found in the control rats.
• The authors' conclusion: The authors concluded that chrysotile particles less than 2 microns in length can produce peribronchiolar fibrosis in the rat.
• Limitations the authors state:
  • The concentration of asbestos particles in the inhaled air was high compared with that encountered in industry.
  • The dust concentration could not be expressed in absolute terms. It was followed with a light-scattering monitor in arbitrary units.

Topics

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

Medical terms in this study, explained in our Lexicon: Chrysotile, Fibrogenic, Fibrosis.

Related studies

• An electron microscopy study of the effect of asbestos dust on the lung — J.M. Davis (1963)
• The ultrastructure of asbestos bodies from guinea-pig lungs — J.M. Davis (1964)
• Evaluation of the deposition, translocation and pathological response of brake dust with and without added chrysotile in comparison to crocidolite asbestos following short-term inhalation: interim results — D.M. Bernstein, R. Rogers, et al. (2014)
• Evaluation of the dose-response and fate in the lung and pleura of chrysotile-containing brake dust compared to chrysotile or crocidolite asbestos in a 28-day quantitative inhalation toxicology study — D.M. Bernstein, B. Toth, et al. (2018)
• A simple dispenser for generating dust clouds from standard reference samples of asbestos — V. Timbrell, A.W. Hyett, et al. (1968)
• Evaluation of the fate and pathological response in the lung and pleura of brake dust alone and in combination with added chrysotile compared to crocidolite asbestos following short-term inhalation exposure — D.M. Bernstein, R.A. Rogers, et al. (2015)

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