Asbestos-induced changes in rat lung parenchyma

Our plain-English summary of Asbestos-induced changes in rat lung parenchyma, by N.F. Johnson (Journal of Toxicology and Environmental Health, 1987).

The study

• Author: N.F. Johnson
• Journal: Journal of Toxicology and Environmental Health
• Published: 1987;21(1-2):193-203
• Cited by: 3 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Fischer 344 rats have been exposed to UICC crocidolite by whole-body inhalation procedures for periods of 1 d to 12 mo. Material was obtained from the same location in the left lung, and the numbers of cells in the parenchyma were identified and determined by transmission electron microscopy. An immediate increase (1 d of exposure) was evident in the number of type II cells, suggesting a direct action of the dust on these cells. The number of interstitial and alveolar macrophages showed a significant increase after 3 mo of exposure. The number of alveolar macrophages containing dust particles after a 1-d exposure was 49%, and the corresponding value after 12 mo of exposure was 92%. The longer periods of exposure were associated with an increase in the number of particles per macrophage. Polymorphs appeared in the interstitium at airway bifurcations, prior to their appearance in the alveolar space. These bifurcations were also the initial sites where evidence of cell damage and collagen deposition was seen. In this experiment crocidolite appears to be weakly fibrogenic, and other factors may be needed to produce the marked lesions seen in human asbestosis.

In plain English

This was an animal experiment. Six-week-old Fischer 344 rats breathed UICC crocidolite asbestos dust in a whole-body chamber at 10 mg/m3, 6 hours a day, 5 days a week, for periods from 1 day to 12 months. Groups were small: 3 rats per period up to 28 days, 4 at 3 and 6 months, and 2 at 12 months, plus equal unexposed controls. The author counted lung cells by electron microscopy. Type II cells, which line the air sacs, increased significantly after only 1 day, and the increase grew with longer exposure. Type I cell counts, relative to endothelial cells, showed no apparent change. Air-space and tissue macrophages (scavenger cells) increased significantly after 3 months. About 50% of air-space macrophages held dust after 1 day. By 12 months, 81% held more than 5 particles. Within 3 months, dust-laden macrophages and white cells (PMN) appeared at airway branch points, which also showed collagen deposition. Fibroblasts were infrequent in the distal lung tissue, with no evident increase. The author concluded that the exposure produced only minimal fibrosis (scarring) and that crocidolite may be a weak fibrogenic agent.

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; lung cells counted and examined by transmission electron microscopy, with unexposed controls
• Who was studied: Six-week-old Fischer 344 rats: groups of 3 exposed for 1, 3, 7, 14 and 28 days; groups of 4 for 3 and 6 months; 2 rats for 12 months; an equal number of unexposed controls at each period. The work was done at the MRC Toxicology Unit, Carshalton, UK; the article gives no dates for the experiment.
• Exposure: UICC crocidolite by whole-body inhalation in a Timbrell chamber, 10 mg/m3, 6 h/day, 5 days/week, for 1 day to 12 months
• Main results:
  • Type II alveolar cells in exposed rats showed a significant (p less than 0.05) increase after 1 day of exposure, measured relative to the number of endothelial cells
  • The type II cell increase was seen at all exposure periods and was greater with longer exposure
  • No change in the number of type I alveolar cells was apparent, measured relative to the number of endothelial cells
  • With longer exposures, aberrant (hyperplastic) type II cells lined alveoli
  • Alveolar macrophages increased significantly over control values after 3 months of exposure
  • Interstitial macrophages increased significantly (p less than 0.05) after the 3-month exposure period
  • After 1 day of exposure, about 50% of alveolar macrophages contained dust, most with fewer than 5 particles per cross section
  • By 12 months (2 rats), 81% of alveolar macrophages contained more than 5 particles
  • After 12 months of exposure, about 8% of alveolar macrophages contained no dust particles
  • The number and percentage of PMN (a type of white blood cell) in the air spaces increased after 12 months of exposure
  • Within 3 months, the alveolar duct and terminal bronchiole bifurcations contained dust-laden macrophages and PMN in the interstitium
  • These bifurcations also showed collagen deposition
  • Fibroblasts were infrequently observed in the distal part of the lung parenchyma, and no increase in their incidence was evident after any exposure period
  • Endocrine-cell hyperplasia was seen in one of the two rats exposed for 12 months
  • Crocidolite fibers were not seen within or penetrating the type I cell layer
• The authors' conclusion: The author concluded that inhaled pure crocidolite for up to 12 months produced a chronic lesion with only minimal fibrosis. The author suggested that crocidolite may be a weak fibrogenic agent that needs co-agents or a prior inflammatory response to produce a rapid and severe fibrotic lesion.
• Limitations the authors state:
  • Too few cells were present in the alveolar duct and terminal bronchiole region for a satisfactory numerical analysis, so changes there were described but not counted

Topics

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

Medical terms in this study, explained in our Lexicon: Parenchyma, UICC, Crocidolite, Transmission Electron Microscopy (TEM), Interstitial, Alveolar Macrophage, Macrophage, Polymorphs.

Related studies

• Chrysotile-induced asbestosis: changes in the free cell population, pulmonary surfactant and whole lung tissue of rats — T.D. Tetley, P.M. Hext, et al. (1976)
• Cytokine regulation of lung fibroblast proliferation. Pulmonary and systemic changes in asbestos-induced pulmonary fibrosis — I. Lemaire, H. Beaudoin, et al. (1986)
• Changes in autacoid and neuropeptide contents of lung cells in asbestos-induced pulmonary fibrosis — R. Day, S. Lemaire, et al. (1987)
• Comparative proliferative and histopathologic changes in rat lungs after inhalation of chrysotile or crocidolite asbestos — K.A. BéruBé, T.R. Quinlan, et al. (1996)
• Reaction of rat lungs to inhaled chrysotile asbestos following acute and subchronic exposures — B.E. Barry, K.C. Wong, et al. (1983)
• Multiwalled carbon nanotube-induced pulmonary inflammatory and fibrotic responses and genomic changes following aspiration exposure in mice: A 1-year postexposure study — B.N. Snyder-Talkington, C. Dong, et al. (2016)

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