Other diseases in animals

Our plain-English summary of Other diseases in animals, by J.M. Davis (The Annals of Occupational Hygiene, 1994).

The study

• Author: J.M. Davis
• Journal: The Annals of Occupational Hygiene
• Published: 1994;38(4):581-7, 420
• Cited by: 4 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Experimental inhalation in a number of studies has demonstrated that chrysotile asbestos can cause pulmonary fibrosis and both benign and malignant pulmonary tumours, two lesions which are associated in that the studies reporting high tumour rates also found high levels of asbestosis. One comparison reported that animals with malignant tumours had approximately twice the amount of fibrosis in the lung parenchyma as those of similar age without tumours. Many studies have examined the pathogenicity of asbestos administered by ingestion and most of these included chrysotile asbestos: the results have been universally negative apart from one study with amosite that contained no control animals and is best discarded. Only one inhalation study has reported an examination of the larynxes of animals: this found no pathological changes. In many studies, tumours other than the lung had been listed, but significant numbers of kidney tumours have never been recorded. Injection studies inducing mesothelioma have indicated that fibre geometry is important with long thin fibres (> 8 microns in length and < 0.25 microns in diameter) being the most carcinogenic. This has been difficult to confirm for inhaled fibres although fibres less than 5 microns in length appear to cause neither fibrosis nor pulmonary tumours. Similar results have been found with amosite for fibres up to 10-15 microns although longer fibres do produce these conditions. It is suggested that to produce pulmonary fibrosis and neoplasia fibres may need to be longer than 20 microns. Chrysotile has been shown in many studies to be removed from lung tissue much more rapidly than amphibole fibres.(ABSTRACT TRUNCATED AT 250 WORDS)

In plain English

This article was a review, read at a 1993 workshop, of animal studies on asbestos diseases other than mesothelioma. The author described earlier studies, mostly in rats, in which inhaled chrysotile caused lung fibrosis (asbestosis) and lung tumours. In one cited comparison, 59 rats without lung tumours averaged 7.3% of lung tissue affected by fibrosis, against 12.5% in 85 rats with tumours. Of over 20 studies examining gastro-intestinal tumours, all but one were negative. The exception, in which 17 of 49 rats fed amosite developed bowel tumours, had no control animals. One study found no fibrosis or tumours in over 200 rat larynxes. Cited studies indicated that short fibres were far less harmful than long ones, and that chrysotile cleared from rat lungs faster than amosite. From amosite experiments in rats, the author suggested that large numbers of fibres probably longer than 20 micrometres are needed to cause lung tissue disease; comparable chrysotile data were lacking. The author concluded that animal studies can at best identify hazards, not accurately predict human risk.

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 published experimental animal studies (a paper read at a workshop), not a new experiment
• Who was studied: Experimental animals in earlier published studies, mainly rats. Mice, guinea pigs, rabbits, cats, gerbils and primates were also discussed.
• Exposure: Mainly chrysotile asbestos (Canadian, Rhodesian, and chrysotile prepared by a wet dispersion process), compared with amosite and crocidolite. Exposure was given by inhalation, by feeding, and by injection into the chest or abdominal cavity, with long- and short-fibre preparations.
• Main results:
  • In a cited comparison (Davis and Cowie, 1990), 59 rats without pulmonary tumours had a mean of 7.3% of lung tissue affected by fibrosis. The figure for 85 rats with pulmonary tumours was 12.5%. The author wrote that whether fibrosis leads directly to tumours is still to be settled.
  • Of over 20 studies examining the occurrence of gastro-intestinal tumours, several involving chrysotile, all but one were negative. In the exception (Ward et al., 1980), 17 out of 49 rats fed amosite developed tumours of the colon or ileum. That study had no control animals. The author wrote that its results cannot be properly evaluated and probably represent an anomaly.
  • In a rat inhalation study using crocidolite, amosite and Rhodesian chrysotile (Davis et al., 1978), the larynx of over 200 animals was examined and no fibrosis or tumours were found.
  • In cited inhalation studies, long-fibre amosite was extremely fibrogenic and carcinogenic, while short-fibre amosite produced neither fibrosis nor tumours. The 'short' chrysotile produced a small amount of fibrosis and some tumours, which was suggested to be due to a small proportion of long fibres in it.
  • From three amosite preparations compared in rats, the author concluded that fibres longer than 8 micrometres are long enough to cause mesotheliomas after injection. The author also concluded that large numbers of fibres probably longer than 20 micrometres are needed to cause disease in the lung tissue. The author noted that exact comparisons of this type are not available for chrysotile.
  • In a cited clearance comparison (Davis, 1989), clearance over 6 months after dusting ended was 14% and 20% for long and short amosite, compared with 50% and 90% for long and short Canadian chrysotile.
  • In a cited rat study using two doses of Rhodesian chrysotile (2 and 10 mg per cubic metre), pulmonary fibrosis was 2.3 times more severe in the high-dose group, against a five-fold difference in dose. All types of lung tumour together increased 1.8-fold, and malignant lung tumours increased four-fold.
  • In cited inhalation studies, rats, mice, guinea pigs and gerbils all developed pulmonary fibrosis, but only rats developed pulmonary tumours.
• The authors' conclusion: The author concluded that animal experiments can at best be used for hazard identification and that accurate prediction of human risk from animal data should be considered impossible. The author also concluded that injection studies are not reliable for indicating likely human hazard.
• Limitations the authors state:
  • The author stated that animals' short lifespan means doses similar to human exposure cannot build up a dangerous lung burden. Very high doses must therefore be used, and harmful effects can be exaggerated.
  • The author stated that exact fibre-length comparisons of the kind made for amosite are not available for chrysotile.

Topics

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

Medical terms in this study, explained in our Lexicon: Chrysotile, Pulmonary Fibrosis, Fibrosis, Parenchyma, Amosite, Mesothelioma, Carcinogenic, Amphibole Group.

Related studies

• Does qualitative examination of Elongated Mineral Particles (EMP) recovered from human and animal lungs provide reliable information on their carcinogenic and other effects? — B.W. Case (2018)
• The relationship between fibrosis and cancer in experimental animals exposed to asbestos and other fibers — J.M. Davis, H.A. Cowie (1990)
• The long term fibrogenic effects of chrysotile and crocidolite asbestos dust injected into the pleural cavity of experimental animals — J.M. Davis (1970)
• The use of animal models for studies on asbestos bioeffects — J.M. Davis (1979)
• A review of carcinogenicity studies of asbestos and non-asbestos tremolite and other amphiboles — J. Addison, E.E. McConnell (2008)
• Environmental exposure to asbestos and other inorganic fibres using animal lung model — E. Fornero, E. Belluso, et al. (2009)

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