Interstitial accumulation of inhaled chrysotile asbestos fibers and consequent formation of microcalcifications

Our plain-English summary of Interstitial accumulation of inhaled chrysotile asbestos fibers and consequent formation of microcalcifications, by A.R. Brody, L.H. Hill (The American Journal of Pathology, 1982).

The study

• Authors: A.R. Brody, L.H. Hill
• Journal: The American Journal of Pathology
• Published: 1982;109(1):107-14
• Cited by: 63 articles, as counted by NIH iCite
• Read it: PubMed · Free full text

Abstract

Previous studies have shown that inhaled chrysotile asbestos impacts initially at the bifurcations of alveolar ducts in the lungs of rats. Asbestos fibers are transported through alveolar epithelial cells at these bifurcation regions to the interstitium during the 24-hour period after a 1-hour exposure. To further these studies, white rats were exposed to an aerosol of chrysotile asbestos for 1 hour. Animals were sacrificed, and the lungs were fixed by vascular perfusion immediately after and 1 month after exposure. Blocks of tissue were prepared for light and electron microscopy. We report here, at 1 month after exposure, that numerous asbestos fibers had accumulated within the lung interstitium at alveolar duct bifurcations. Many of these interstitial fibers were found in te center of intracellular microcalcifications. The presence of calcifications was proven by X-ray energy spectrometric analysis of the inclusions in situ. Clear X-ray peaks for calcium and phosphorus were demonstrated. The authors propose that 1 month after a 1-hour exposure to chrysotile asbestos, fiber-induced membrane injury in cells of the lung interstitium leads to formation of microcalcifications. This may represent the presence of early cell injury in the initial pathogenetic sequence of asbestosis.

In plain English

This was an animal experiment in Fischer 344 white rats. In three separate exposures, 4 rats at a time breathed an aerosol of chrysotile asbestos from the Jeffrey Mine in Quebec, Canada, nose only, for 1 hour, while 4 rats breathed room air. The airborne concentration was about 15 mg per cubic meter (respirable mass). One month later the authors examined the lungs with light and electron microscopy, looking at the first branching points of the small air passages called alveolar ducts. In 12 exposed rats, asbestos fibers were found in 11 of 20 such regions, inside fibroblasts and macrophages or lying in the connective tissue between cells. Deposits of phosphorus and calcium (microcalcifications) were seen in 10 of 20 regions from exposed rats. They were mostly inside fibroblast-like cells, and most had asbestos fibers at their center or edge. No calcifications or fibers were seen in 10 regions from 5 sham-exposed rats. The authors proposed that these changes are early steps of lung injury in rats. They said whether the same happens in human lungs is likely to remain speculation.

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 (rats exposed to asbestos compared with rats exposed to room air), with lung tissue studied by light and electron microscopy and X-ray elemental analysis
• Who was studied: White rats (Fischer 344). There were three exposure runs, each with 4 rats exposed to asbestos and 4 exposed to room air. Lung regions from 12 asbestos-exposed rats and 5 sham-exposed rats were examined 1 month after exposure. The study was carried out at the National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina.
• Exposure: A single 1-hour, nose-only exposure to an aerosol of chrysotile asbestos from the Jeffrey Mine, Quebec, Canada. The airborne concentration was about 15 mg per cubic meter (respirable mass); this is the concentration in the air, not a measured amount received by each rat. The article reports that 97% of fibers were less than 20 microns long and 98% were less than 0.6 microns in diameter.
• Main results:
  • Under the light microscope, the first alveolar duct bifurcations in asbestos-exposed rats were prominent compared with sham-exposed rats, 1 month after exposure.
  • Asbestos fibers were found in 11 of the 20 bifurcation regions dissected from 12 asbestos-exposed rats.
  • In exposed rats, the fibers in the lung interstitium were inside fibroblasts and macrophages or lay outside cells in the interstitial connective tissue matrix.
  • Deposits of phosphorus and calcium were seen in 10 of 20 bifurcations studied from asbestos-exposed rats.
  • No calcifications or asbestos fibers were seen in 10 bifurcations from 5 sham-exposed rats.
  • In exposed rats, asbestos fibers were found at the center or edge of most of the deposits.
  • In exposed rats, the calcium and phosphorus deposits were inside cells, mainly fibroblast-like cells.
  • No recognizable iron signal was detected in any of the calcifications analyzed.
• The authors' conclusion: The authors proposed that, in rats, the rapid build-up of asbestos fibers in the lung interstitium and the resulting calcifications inside cells within 1 month of exposure are initial steps of lung injury that occur sooner than previously expected. They suggested this may represent early cell injury in the sequence leading to asbestosis.
• Limitations the authors state:
  • The authors stated that whether the same rapid sequence of events occurs in the human lung is likely to remain speculation.
  • The authors stated that they had no quantitative data on the sizes of the fibers within the calcifications.
  • The authors stated that whether this change is an early event in the onset of progressive interstitial disease was still being studied.
  • The authors stated that it is not clear how the fibers first injure cell membranes.

Mines named here

Asbestos mines this study is about. Each mine's page says who ran it, when it worked, and what it produced.

• Jeffrey mine, Asbestos, Quebec

All asbestos mines

Topics

Medical terms in this study, explained in our Lexicon: Interstitial, Chrysotile.

Related studies

• Reaction of rat lungs to inhaled chrysotile asbestos following acute and subchronic exposures — B.E. Barry, K.C. Wong, et al. (1983)
• Exposure to low levels of ozone results in enhanced pulmonary retention of inhaled asbestos fibers — K.E. Pinkerton, A.R. Brody, et al. (1989)
• Asbestos body formation and iron accumulation in mouse peritoneal granulomas after the introduction of crocidolite asbestos fibers — H.K. Koerten, J. Hazekamp, et al. (1990)
• Fiber localization and its relationship to lung reaction in rats after chronic inhalation of chrysotile asbestos — K.E. Pinkerton, P.C. Pratt, et al. (1984)
• Lung proliferative and clearance responses to inhaled para-aramid RFP in exposed hamsters and rats: comparisons with chrysotile asbestos fibers — D.B. Warheit, S.I. Snajdr, et al. (1997)
• Deposition pattern and clearance pathways of inhaled chrysotile asbestos — A.R. Brody, L.H. Hill (1981)

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