An electron microscopy study of the effect of asbestos dust on the lung

Our plain-English summary of An electron microscopy study of the effect of asbestos dust on the lung, by J.M. Davis (British Journal of Experimental Pathology, 1963).

The study

• Author: J.M. Davis
• Journal: British Journal of Experimental Pathology
• Published: 1963;44(4):454-64
• Cited by: 46 articles, as counted by NIH iCite
• Read it: PubMed · Free full text

Abstract

In a series of experiments on the effect of chrysotile asbestos dust on rat and guinea-pig lungs, it was found that pathological changes occurred in 3 successive stages. The first involved the formation of small nodular giant cell lesions usually in the walls of terminal bronchioles. Later a fibrosing interstitial pneumonia was found scattered widely throughout the lung and this was often followed by complete lung consolidation in some areas. It was found that in rats removed from the dust tunnel for some weeks, the consolidation tended to resolve, but no signs of resolution were seen in guinea-pigs during these experiments. Chrysotile dust was seen only in alveolar macrophages, and it would appear that no other cell types are able to phagocytose this material. It was found that giant cells were formed by the aggregation of dust-carrying macrophages, and it was also found that these macrophages can undergo conversion to fibroblasts. The chrysotile dust found in the animal lungs varied in size from fibres 10 μ long and 2 μ in diameter, to individual crystals less than 1 μ long and only about 200A in diameter. After some months in the lung some of the dust showed structural changes that may indicate that it was being dissolved by the body fluids. An aggregation of ferritin material around particles of chrysotile was commonly found, and this may be associated with the formation of asbestos bodies. Most of the capillary walls in the dusted lungs were normal in structure, but in a few cases the blood-air barrier was found to be much thicker than normal. Where this occurred the basement membrane was found to be very uneven in outline, and numerous impocketings were seen in the cytoplasm of both the epithelial and endothelial cells.

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

In plain English

This was an animal experiment. Rats and guinea-pigs breathed chrysotile asbestos dust in a dusting tunnel; their lungs were examined by electron microscope at intervals from 3 days after dusting began. Lung biopsy tissue from one asbestos worker, exposed to chrysotile, crocidolite and amosite over 24 years, was also examined. The number of animals was not stated. Changes in the lung were already present after 3 days. Dust-laden macrophages (scavenger cells) clumped together to form giant cells, and some were converted into fibroblasts, the cells that make scar tissue. In rats, lung consolidation began to clear about 10 weeks after they left the dust. In guinea-pigs no signs of resolution were seen during the experiments, and most older guinea-pigs had pleural adhesions. After about 7 to 8 weeks, some chrysotile fibres showed structural changes. Only two asbestos bodies were found in the animals, but they were plentiful in the human biopsy. Capillary damage was rare except in consolidated areas, where many capillaries were compressed and obliterated. The author concluded that asbestosis appeared to be caused by a combination of mechanical and chemical effects.

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 examined by electron microscopy (with some light microscopy), plus electron-microscope examination of lung biopsy material from one human case of asbestosis
• Who was studied: Rats and guinea-pigs supplied by Dr. P. F. Holt of Reading University (number not stated), killed at intervals from 3 days after the start of dusting; the last rats and guinea-pigs were killed 35 and 31 weeks after the start of dusting. Also one human asbestos worker (lung biopsy).
• Exposure: Animals were exposed to chrysotile dust in a dusting tunnel. Rats stayed 95 days, with the dust apparatus operating on 50 days for 18 hours a day. Guinea-pigs stayed 77 days, with the generator running on 51 days for 18 hours a day. The author stated that the dust concentrations were very high. The human worker had been exposed to a mixture of chrysotile, crocidolite and amosite over 24 years.
• Main results:
  • In animals dusted for only 3 days, widespread ultrastructural changes were already present in the lung. Many alveolar epithelial cells had become rounded and covered with microvilli.
  • Dust-loaded macrophages aggregated to form giant cells. In small giant cells, all the constituent macrophages were converted into fibroblasts.
  • In rats, consolidation began to clear after the animals had been out of the dust for about 10 weeks. No signs of resolution were seen in guinea-pigs during these experiments.
  • Light microscopy showed multiple pleural adhesions in most of the older guinea-pigs. These were not seen in the rats.
  • No changes in the structure of the dust were found in either species for about the first 7 to 8 weeks of dusting. After that, some chrysotile crystals showed 'droplet' structures and unrolling into flattened plaques.
  • Only two asbestos bodies were found in the animal material, one in a guinea-pig and one in a rat. They were plentiful in the human biopsy material.
  • Very little damage to the lung capillaries was found, except where consolidation had occurred. In those areas the lumen of many capillaries were compressed and obliterated. Other structural changes in capillaries were infrequent and widely scattered.
  • In the human biopsy, asbestos dust was found in only three cell types (lung macrophages, giant cells and fibroblasts). The lung contained chrysotile and amphibole dusts; crocidolite and amosite could not be told apart with the electron microscope.
• The authors' conclusion: The author concluded that the findings appeared to suggest that asbestosis is caused by a combination of mechanical and chemical effects. The author also judged that many of the lung changes seen were likely a general response to lung irritation rather than a reaction specific to asbestos dust.
• Limitations the authors state:
  • Human material came from only one case, so the development of the condition could not be described.
  • Because chrysotile dust tore out of thin sections, thicker sections had to be used, with some loss of resolution at high magnifications.
  • The study gave no definite information on how asbestos bodies form.
  • Dust concentrations in the tunnel were very high. The author said this may account for changes more severe than those in earlier animal experiments.

Topics

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

Medical terms in this study, explained in our Lexicon: Chrysotile, Interstitial, Consolidation, Alveolar Macrophage, Macrophage, Fibroblast, Ferritin, Asbestos Bodies.

Related studies

• The ultrastructure of asbestos bodies from guinea-pig lungs — J.M. Davis (1964)
• The ultrastructure of asbestos bodies from human lung — J.M. Davis (1964)
• The early effects of chrysotile asbestos dust on the rat lung — P.F. Holt, J. Mills, et al. (1964)
• Pulmonary mineral dust. A study of ninety patients by electron microscopy, electron microanalysis, and electron microdiffraction — J.P. Berry, P. Henoc, et al. (1976)
• The effects of chrysotile asbestos dust on lung macrophages maintained in organ culture. An electron-microscope study — J.M. Davis (1967)
• Dust particles in lung sections. Some notes on methods of their visualization — P. Gross, E.B. Tolker (1966)

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