Translocation of asbestos dust through the bronchiolar wall

Our plain-English summary of Translocation of asbestos dust through the bronchiolar wall, by P.F. Holt (Environmental Research, 1982).

The study

• Author: P.F. Holt
• Journal: Environmental Research
• Published: 1982;27(2):255-60
• Cited by: 11 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Inhaled chrysotile asbestos fibers that settle on the epithelium of the larger bronchioles are removed from the lung by cilia. Fibers that reach the pulmonary alveoli may be phagocytized by macrophages which move toward the periphery of the lung by passing through alveolar walls. Some of these cells aggregate in alveoli near larger bronchioles and may then penetrate the bronchiolar wall. They are shed in the bronchiolar lumen, where they are elevated by cilia to the trachea. Elimination of chrysotile from alveoli depends on macrophages; fibers persist if there are insufficient macrophages.

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

In plain English

This was an animal experiment that looked at how inhaled chrysotile asbestos fibers are moved out of the deepest parts of the lung. Eighteen specific pathogen-free guinea pigs breathed air containing Rhodesian chrysotile (about 1000 fibers longer than 1 micrometre per ml) for 24 hours, then lived in normal laboratory air. Animals were killed after 20, 30 and 41 weeks. Thin lung sections were searched under the microscope, and every macrophage (a scavenger cell) was examined. The author saw many asbestos fibers inside cells, most apparently coated. Several macrophages carrying fibers were caught passing through the walls of the air sacs (alveoli). After about 20 weeks, scavenger cells had gathered in air sacs near bronchioles and blood vessels. They appeared to be moving through the bronchiole walls and were shed as a plug into the airway. By then, many air-sac areas away from these sites were almost free of asbestos. The author concluded that removing chrysotile from the air sacs depends on macrophages, and that fibers persist if there are not enough macrophages.

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 with microscopic (histological) examination of lung sections
• Who was studied: 18 specific pathogen-free guinea pigs, killed after 20, 30 and 41 weeks
• Exposure: Rhodesian chrysotile dust at about 1000 fibers longer than 1 micrometre per ml, for 24 hours; the animals were then kept in normal laboratory air
• Main results:
  • There were numerous asbestos fibers inside cells; most appeared coated and some were beaded
  • Several macrophages containing asbestos fibers were seen passing through alveolar walls
  • After about 20 weeks, scavenger cells (phagocytes) had accumulated in alveoli near bronchioles and blood vessels. They appeared to be moving through bronchiolar walls and were shed as a plug into the airway
  • After 20 weeks, many alveolar areas away from larger bronchioles and blood vessels were almost free of asbestos particles and appeared normal
• The authors' conclusion: The author concluded that elimination of chrysotile from the alveoli depends on macrophages, and that fibers persist if there are insufficient macrophages

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, Chrysotile, Epithelium, Alveoli, Macrophage.

Related studies

• Translocation of inhaled dust to the pleura — P.F. Holt (1983)
• Incorporation of tritiated thymidine by epithelial and interstitial cells in bronchiolar-alveolar regions of asbestos-exposed rats — A.R. Brody, L.H. Overby (1989)
• Bronchiolar and alveolar lesions in the pathogenesis of crocidolite-induced pulmonary fibrosis in mice — D.H. Bowden, I.Y. Adamson (1985)
• 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)
• Dust elimination from pulmonary alveoli — P.F. Holt (1980)
• Analysis of asbestos-induced gene expression changes in bronchiolar epithelial cells using laser capture microdissection and quantitative reverse transcriptase-polymerase chain reaction — C.B. Manning, B.T. Mossman, et al. (2006)

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