The influence of amosite asbestos exposure on lung permeability

Our plain-English summary of The influence of amosite asbestos exposure on lung permeability, by R.F. Dodson, T. Akematsu, M.G. Williams, et al (Environmental Research, 1984).

The study

• Authors: R.F. Dodson, T. Akematsu, M.G. Williams, J.O. Ford, G.A. Hurst
• Journal: Environmental Research
• Published: 1984;35(2):497-506
• Cited by: 3 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

The effect of amosite asbestos on permeability of the blood/air barrier in the lung was studied using an acute animal model. The ultrastructural tracer selected for the study was horseradish peroxidase which was given intravenously in animals that had been exposed intratracheally to asbestos. The acute period of study was either 1/2, 1, 2, 3, or 4 hr, or 1-7 or 14 days postexposure. The barrier in the normal lung was at the level of the alveolar epithelial lining. Leakage of exudate and tracer occurred through the altered barriers following asbestos exposure and the extent of leakage related directly to the degree of alveolitis and the asbestos present in the area. A trend toward recovery of the barrier occurred with the reestablishment of a more normal-appearing epithelial lining during the second week postexposure.

In plain English

This animal experiment tested whether amosite asbestos changes the barrier between blood and air in the lung. Young adult guinea pigs were given 25 mg of ground amosite in saline into the windpipe. Control animals received saline alone or sham operations. After intervals from 30 minutes to 14 days, a tracer (horseradish peroxidase) was injected into a vein, and the lungs were examined by light and electron microscopy. In controls, the cells lining the air sacs blocked the tracer. In exposed animals, inflammation of the air sacs (alveolitis) developed. The lining cells were altered as early as 1 hour, and tracer reached the air sacs as early as 30 minutes after asbestos exposure. Leakage was directly related to the extent of alveolitis and/or damage to the lining cells, and the most reactive areas had the highest asbestos concentrations. Late in the study, most air-sac surfaces looked more normal and permeability was more restricted. The authors concluded that maximum leakage matched maximum tissue response, and stated that a longer study is needed to know whether permeability fully returns to normal.

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 experiment (acute model): asbestos placed into the windpipe, then an intravenous tracer, with lungs examined by light and electron microscopy
• Who was studied: Young adult Hartley-Duncan guinea pigs (about 600 g), examined 30 minutes, 1, 2, 3 or 4 hours, 1 to 7 days, or 14 days after exposure. Controls received saline or sham operations. The article does not state how many animals were used.
• Exposure: A single intratracheal dose of 25 mg of amosite asbestos in 0.5 ml of saline. The commercial-grade amosite was ground and separated so that most fibers were under 10 micrometers long.
• Main results:
  • In control animals, the epithelial barrier formed by the air-sac lining cells (pneumocytes) was impermeable to the tracer
  • In exposed animals, an early alveolitis developed. Macrophages predominated through the first 3 hours, large numbers of neutrophils were present from 3 hours through the first day, and macrophages predominated again from 2 days to the end of the study (14 days).
  • In exposed animals, altered Type I pneumocytes were seen as early as 1 hour after exposure
  • In exposed animals, significant amounts of tracer were found inside the air sacs as early as 30 minutes after the asbestos was given (the earliest interval studied; the tracer itself circulated for 10 minutes before the animals were killed)
  • Leakage of tracer and exudate was directly related to the extent of alveolitis and/or the degree of changes in Type I pneumocytes
  • The most reactive areas were associated with the highest asbestos concentrations
  • Asbestos particles were occasionally found inside Type I and Type II pneumocytes
  • Tracer-carrying vesicles in Type I cells were not obviously more numerous in exposed animals than in controls. The authors took this to mean asbestos had no effect on this minor pathway.
  • In the latest-examined animals, most air-sac surfaces had begun returning to a more normal appearance, and the restored barrier gave a more normal, restricted permeability
• The authors' conclusion: The authors concluded that, over the short duration of the study, the period of maximum leakage through the air/blood barrier corresponded with the period of maximum tissue response to the asbestos
• Limitations the authors state:
  • The authors stated that a longer study interval is needed to know whether permeability fully returns to normal

Topics

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

Medical terms in this study, explained in our Lexicon: Amosite, Asbestos Exposure, Exudate.

Related studies

• Acute lung response to amosite asbestos: a morphological study — R.F. Dodson, M.G. Williams, et al. (1983)
• Chrysotile asbestos and H2O2 increase permeability of alveolar epithelium — S.Y. Gardner, A.R. Brody, et al. (1997)
• Development of asbestos bodies on amosite, chrysotile and crocidolite fibres in guinea-pig lungs — S.K. Botham, P.F. Holt (1971)
• A procedure for the isolation of amosite asbestos and ferruginous bodies from lung tissue and sputum — M.G. Williams, R.F. Dodson, et al. (1982)
• Chrysotile asbestos causes AEC apoptosis via the caspase activation in vitro and in vivo — T. Kido, Y. Morimoto, et al. (2008)
• P53 mediates amosite asbestos-induced alveolar epithelial cell mitochondria-regulated apoptosis — V. Panduri, S. Surapureddi, et al. (2006)

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