Persistence of long, thin chrysotile asbestos fibers in the lungs of rats

Our plain-English summary of Persistence of long, thin chrysotile asbestos fibers in the lungs of rats, by P.G. Coin, V.L. Roggli, A.R. Brody (Environmental Health Perspectives, 1994).

The study

• Authors: P.G. Coin, V.L. Roggli, A.R. Brody
• Journal: Environmental Health Perspectives
• Published: 1994;102 Suppl 5(Suppl 5):197-9
• Type of article: Review
• Cited by: 29 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

The distribution of inhaled mineral fibers in the lung determines the site and severity of disease caused by the fibers. Some of our recent work has described the fate of inhaled asbestos fibers in rodents. After a brief inhalation exposure, asbestos fibers are deposited primarily at the first alveolar duct bifurcations, and fibrotic lesions are initiated. These sites of deposition occur as close to the visceral pleura as 220 micron. Several studies have suggested that short fibers are cleared from the lung more efficiently than long ones, and our data support this view. Our laboratory has shown that aerosolized chrysotile fibers longer than 16 microns can be deposited in the peripheral lung parenchyma of rats, and the measured clearance rate of these fibers is not significantly different from zero. Chrysotile, but no amphibole, fibers split longitudinally, so that the number of retained chrysotile fibers > or = 16 microns in length increases over time. We have not observed significant changes in chemical composition of chrysotile fibers up to 30 days post-deposition in the rat. Nor have we observed translocation of chrysotile fibers from the "central" regions of the lung toward the subpleural regions. However, 1 month after a single 3-hr exposure to chrysotile asbestos, the longest, most pathogenic fibers persist throughout the lung parenchyma. These retained fibers have the potential to cause disease in both parenchyma and pleura.

In plain English

This was a short review, presented at a 1992 workshop, of the authors' own recent experiments on inhaled chrysotile asbestos in rat lungs. Most of its data came from their earlier study. In rats exposed to chrysotile for 3 hours, fibers longer than 16 micrometers were deposited abundantly within 1 mm of the visceral pleura, the lung's outer lining. New measurements in 11 rats (106 branch points) placed about half of the first alveolar duct bifurcations within 1 mm of the pleura. The closest was 0.22 mm. Long fibers were not cleared at a significant rate up to 30 days, but they split lengthwise. Their number in the left lung rose from 3.1 x 10^5 at day 1 to 5.1 x 10^5 at day 29, while average diameter fell from 0.191 to 0.125 micrometers. Over about 30 days, long fibers lost no significant magnesium. There was no evidence of fibers drifting from central lung regions toward the regions just under the pleura. The authors concluded that extensive translocation may not be necessary for pleural disease. They noted that their follow-up may have been too short to detect slow movement.

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: Review of the authors' own recent animal (rat inhalation) experiments, presented at a workshop. It adds new measurements of the distance from airway branch points to the pleura. Fiber data in Table 1 come from the authors' earlier study (Coin et al., reference 3).
• Who was studied: Rats. Distances from first alveolar duct bifurcations to the pleura were measured in 11 adult rats (106 bifurcations). Fiber counts in Table 1 came from the entire left lung of four or more animals per time point.
• Exposure: Single 3-hour inhalation exposure to an aerosol of chrysotile asbestos. Fibers were followed from 1 to 29 days after exposure. No dose is given in this article.
• Main results:
  • In the earlier study, even the longest fibers classified (16 micrometers or longer) were deposited abundantly in the peripheral lung region within 1 mm of the visceral pleura.
  • About 50% of first alveolar duct bifurcations in 11 rats were within 1 mm of the visceral pleura. The minimum distance measured was 0.22 mm.
  • Long chrysotile fibers (longer than 16 micrometers) were not cleared at a significant rate up to 30 days after deposition, but they split.
  • Number of retained fibers 16 micrometers or longer in the left lung (geometric means) by day after exposure: 3.1 x 10^5 at day 1, 3.2 x 10^5 at day 8, 6.6 x 10^5 at day 15 and 5.1 x 10^5 at day 29. The correlation with time was r = +0.56, p less than 0.02.
  • Average diameter of retained fibers 16 micrometers or longer fell from 0.191 micrometers at day 1 to 0.150, 0.133 and 0.125 micrometers at days 8, 15 and 29. The correlation with time was r = -0.82, a statistically significant trend (p less than 0.01).
  • The mass of retained long fibers decreased slightly and their surface area increased slightly over time. Neither trend was statistically significant (p = 0.50 and p = 0.36).
  • No significant magnesium leaching was found in long chrysotile fibers after 30 days in the rat lung. The Mg/Si ratio was 0.75 plus or minus 0.04 at day 1 and 0.67 plus or minus 0.08 at day 29 (p greater than 0.80, t-test), based on ten fibers from each of four animals.
  • During the roughly 30-day follow-up, there was no evidence of chrysotile fibers drifting from central lung regions toward the peripheral (subpleural) regions, called "pleural drift". The authors allowed that slow translocation to the pleura, not detectable in their study, could occur.
• The authors' conclusion: The authors concluded that the longest chrysotile fibers are deposited near the visceral pleura and are cleared slowly, if at all. These fibers split so that their number increases. Translocation toward the subpleural regions did not occur in their model. They concluded that extensive and rapid translocation may not be necessary for asbestos-related pleural disease.
• Limitations the authors state:
  • The follow-up (about 30 days) may have been too short to detect a slow translocation process.
  • The study could not distinguish movement of fibers from central to peripheral regions from slower clearance in the peripheral region.
  • The leaching analysis had an 80% chance of detecting a decrease in Mg/Si of 1.3% per day.
  • The chemical analysis was restricted to fibers 16 micrometers or longer. The authors suggest this may explain why their results differed from another study that found leaching.

Topics

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

Medical terms in this study, explained in our Lexicon: Chrysotile, Mineral Fiber, Deposition, Visceral Pleura, Parenchyma, Amphibole Group, Translocation, Pleura.

Related studies

• Changes in numbers and dimensions of chrysotile asbestos fibers in lungs of rats following short-term exposure — V.L. Roggli, A.R. Brody (1984)
• Oxidative effects of lungs in Wistar rats caused by long-term exposure to four kinds of China representative chrysotile — Y. Cui, Y. Zha, et al. (2019)
• Increased lung cancer mortality among chrysotile asbestos textile workers is more strongly associated with exposure to long thin fibres — D. Loomis, J.M. Dement, et al. (2012)
• Sumas Mountain chrysotile induces greater lung fibrosis in Fischer344 rats than Libby amphibole, El Dorado tremolite, and Ontario ferroactinolite — J.M. Cyphert, A. Nyska, et al. (2012)
• The importance of fiber biopersistence and lung dose in determining the chronic inhalation effects of X607, RCF1, and chrysotile asbestos in rats — T.W. Hesterberg, G.A. Hart, et al. (1998)
• 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)

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