Translocation of inhaled dust to the pleura

Our plain-English summary of Translocation of inhaled dust to the pleura, by P.F. Holt (Environmental Research, 1983).

The study

• Author: P.F. Holt
• Journal: Environmental Research
• Published: 1983;31(1):212-20
• Cited by: 15 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Inhaled chrysotile asbestos or carbon dust that reaches the alveoli in guinea pig lungs is ingested by macrophages which move through the parenchyma of the lung toward the pleura. Some macrophages are eliminated from the lung by passing through blood vessel or bronchiolar walls. Those that reach the pleura are mainly aggregated in a few small areas. They may pass through the pleura. The active macrophages stain blue with Perls' reagent due to iron in the lysosomes. Occasionally, a macrophage may disintegrate while passing through the pleura and Perls-positive lysosomes become distributed over an area, presumably in the lymphatics.

In plain English

This was an animal experiment. The author examined microscope sections of the lining of the lung (the pleura) and nearby lung tissue from guinea pigs that had breathed in chrysotile asbestos or carbon dust. The article does not say how many animals were examined. In animals killed up to 3 months after exposure, very few dust-carrying immune cells (macrophages) were found near the pleura. After 6 months a few were seen, and their number increased with time. These cells were mostly gathered in a few small areas. Some were next to the pleura, part of it, on its outer surface, or apparently in lymph channels, although such cells were rarely seen. In a few sections, iron-containing particles from the cells appeared to have spread out, which the author took to mean that macrophages had broken apart while passing through the pleura. The author concluded that this movement did not depend on the type or toxicity of the dust. The author also suggested it was conceivable that material released from such cells might start asbestos-type pleural changes.

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: microscopic (histological) examination of lung and pleural tissue sections
• Who was studied: Guinea pigs, specific-pathogen-free and one batch of conventionally reared animals, that had inhaled chrysotile asbestos or carbon dust; number of animals not stated
• Exposure: Inhaled chrysotile asbestos (24 hours of inhalation in the animals shown in the figures) or carbon dust, which the author described as considered a safe dust (100 hours of inhalation in most figures, 10 hours in one); animals were killed between 142 and 553 days later
• Main results:
  • Very few macrophages were near the pleura in animals killed up to 3 months after inhaling carbon or chrysotile dust. A few were seen after 6 months, and the number then increased with time.
  • The macrophages near the pleura were mainly concentrated in relatively small areas. Even a year or more after inhalation, only a small number of isolated single cells were found in other areas just under the pleura.
  • Macrophages were found adjacent to, part of, or on the outer surface of the pleura. Some appeared to be in the lymph channel.
  • Macrophages that had penetrated the pleura were rarely seen.
  • Most macrophages contained iron-containing particles that stained blue with Perls' reagent. In a few sections, similar particles were seen outside cells, probably in the lymphatics of the pleura. The author interpreted these as coming from macrophages that broke apart while passing through the pleura.
  • In conventionally reared guinea pigs, some lung areas were consolidated. Many Perls-positive asbestos fibers were still seen in these areas 18 months after chrysotile was inhaled.
• The authors' conclusion: The author concluded that macrophages carrying either carbon or chrysotile drift to the pleura, so their movement does not depend on the chemical nature or toxicity of the dust. The author suggested it is conceivable that lysosome contents released by macrophages breaking apart in the pleura might start changes in the pleura characteristic of asbestos.
• Limitations the authors state:
  • The apparent gaps in the pleura near clusters of macrophages may have been an artifact.
  • Many cells that had penetrated the pleura were probably lost during preparation of the tissue sections.

Topics

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

Medical terms in this study, explained in our Lexicon: Translocation, Pleura, Chrysotile, Alveoli, Macrophage, Parenchyma.

Related studies

• Transport of inhaled dust to extrapulmonary sites — P.F. Holt (1981)
• Translocation of asbestos dust through the bronchiolar wall — P.F. Holt (1982)
• 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)
• 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)
• Translocation pathways for inhaled asbestos fibers — G. Miserocchi, G. Sancini, et al. (2008)
• 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)

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