Effects of asbestos on the random migration of rabbit alveolar macrophages

Our plain-English summary of Effects of asbestos on the random migration of rabbit alveolar macrophages, by Q.N. Myrvik, E.A. Knox, M. Gordon, et al (Environmental Health Perspectives, 1985).

The study

• Authors: Q.N. Myrvik, E.A. Knox, M. Gordon, P.S. Shirley
• Journal: Environmental Health Perspectives
• Published: 1985;60:387-93
• Cited by: 4 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

The toxicity of sized and characterized chrysotile, crocidolite, and amosite preparations obtained from Dr. K. R. Spurny have been evaluated using alveolar macrophage (AM) migration inhibition assays and viability tests. These results have been compared with asbestos samples obtained from the National Institute of Environmental Health Sciences (NIEHS). These latter samples are designated chrysotile A (RT), crocidolite (RT), and amosite (RT). In addition, filter-isolated preparations of chrysotile A (RT) that consisted mainly of large nonphagocytosable fibers were also tested. Chrysotile (Spurny) and sonicated chrysotile A (RT) produced 50% migration inhibition at about 115 micrograms/mL. Spurny crocidolite produced 50% migration inhibition at about 340 micrograms/mL, whereas RT crocidolite produced 50% migration inhibition at about 230 micrograms/mL. RT amosite caused 50% migration inhibition at about 180 micrograms/mL, whereas Spurny amosite was inactive up to 500 micrograms/mL. The large nonphagocytosable chrysotile A (RT) fibers produced 50% migration inhibition at about 66 micrograms/mL. This indicates that fibers can be toxic for AM through extracellular membrane contact. In general the results from the viability studies paralleled the migration inhibition observations. None of the asbestos preparations induced a burst in the hexose monophosphate shunt of BCG-immune AM at 1 mg/mL. BCG-immune AM were more susceptible to cell death than normal AM when incubated with chrysotile A (RT), amosite (RT) and zymosan. Migration inhibition induced by asbestos fibers probably reflects toxicity of the asbestos preparations and could play an important role in blocking normal alveolar clearance of inhaled particles.

In plain English

This was a laboratory study. The authors exposed alveolar macrophages (lung scavenger cells) from New Zealand White rabbits to chrysotile, crocidolite and amosite asbestos from two sources: sized samples from Dr. K. R. Spurny, and samples from the National Institute of Environmental Health Sciences, labelled RT. They measured the dose that cut the cells' migration in half, and cell survival after 24 hours. Sonicated chrysotile A (RT) halved migration at 110 ± 23 micrograms per mL (cells from 15 rabbits). Spurny chrysotile did so at 117 ± 25 (ultrafine) and 124 ± 13 (fine). RT amosite needed 183 ± 26 and RT crocidolite 231 ± 27. Spurny amosite produced no detectable migration inhibition at 500. Long chrysotile fibers, too large to be engulfed, needed only 66 ± 10. At 250 micrograms per mL, chrysotile A (RT) lowered survival of normal cells from 98% to 63%. In cells from rabbits sensitized with BCG, it lowered survival from 87% to 40%. The authors concluded that chrysotile was the most toxic asbestos type tested. They also concluded that migration inhibition could reduce clearance of inhaled fibers. They noted that the serum in their cultures probably dampened toxicity.

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: Laboratory (in vitro) experiment on alveolar macrophages taken from rabbits, using migration inhibition assays, cell viability (trypan blue) tests and hexose monophosphate shunt activity measurements
• Who was studied: Alveolar macrophages from New Zealand White rabbits of either sex weighing 1.4 to 2.0 kg. Cells came from normal rabbits and from rabbits sensitized 21 days earlier with heat-killed BCG (BCG-immune). The chrysotile A (RT) migration tests used cells from 15 animals.
• Exposure: Chrysotile, amosite and crocidolite in ultrafine and fine sized preparations from Dr. K. R. Spurny. Chrysotile A (UICC), amosite and crocidolite from NIEHS (RT), mostly sonicated. Non-sonicated and filter-isolated large chrysotile A (RT) fibers. Spurny glass fibers and actinolite. Zymosan was used as a control. Doses were in micrograms per mL, up to 500 for migration, 250 for 24-hour viability, and 1 mg/mL for shunt activity.
• Main results:
  • Sonicated chrysotile A (RT) produced 50% migration inhibition of normal rabbit alveolar macrophages at 110 ± 23 micrograms per mL, calculated from 15 animals.
  • Spurny chrysotile produced 50% migration inhibition at about 117 ± 25 micrograms per mL (ultrafine) and 124 ± 13 micrograms per mL (fine). The authors described this as essentially equivalent to chrysotile A (RT).
  • RT amosite needed 183 ± 26 micrograms per mL for 50% migration inhibition. Spurny amosite needed more than 500 micrograms per mL and produced no detectable migration inhibition at 500 micrograms per mL.
  • RT crocidolite needed 231 ± 27 micrograms per mL for 50% migration inhibition. Spurny ultrafine crocidolite needed 335 ± 92 micrograms per mL.
  • Spurny actinolite produced 50% migration inhibition at 343 ± 71 micrograms per mL. Spurny glass fibers produced no detectable migration inhibition at 500 micrograms per mL.
  • Filter-isolated chrysotile A (RT), in which 90% of fibers exceeded 50 micrometres in length, produced 50% migration inhibition at 66 ± 10 micrograms per mL. Sedimented non-sonicated chrysotile needed 88 ± 4 micrograms per mL.
  • Chrysotile A (RT) needed 143 micrograms per mL for 50% migration inhibition with fresh rabbit serum and 123 micrograms per mL with heat-inactivated serum. The authors took this to mean complement was not involved.
  • None of the asbestos preparations at 1 mg/mL produced a detectable burst in the hexose monophosphate shunt of BCG-immune macrophages. Zymosan at 1 mg/mL produced about a 3 to 4-fold burst.
  • Normal macrophages, 24 hours at 250 micrograms per mL: chrysotile A (RT) reduced viability from 98% (controls) to 63%, amosite (RT) to 91%, and crocidolite (Spurny) to 73%.
  • BCG-immune macrophages, 24 hours at 250 micrograms per mL: chrysotile A (RT) reduced viability from 87% (controls) to 40%, and amosite (RT) to 70%. Crocidolite (Spurny) reduced it to 78%, a drop the authors called not significant. Zymosan reduced viability of BCG-immune cells to 74% and caused no detectable loss in normal cells.
• The authors' conclusion: The authors concluded that chrysotile was the most toxic asbestos type compared with amosite and crocidolite, in both the migration and viability tests. They concluded that fibers too large to be engulfed were more potent at inhibiting migration, suggesting surface contact can inhibit migration. They also concluded that migration inhibition could reduce clearance of inhaled fibers from the alveoli.
• Limitations the authors state:
  • The cultures used 10% serum, which the authors said probably dampened toxicity compared with studies that did not use serum.
  • The reasons for the large difference in activity between RT amosite and Spurny amosite were not known. The authors raised leaching of milled fibers as a possible explanation.
  • Concentrations above 500 micrograms per mL were not tested because of complications from the mass of fibers.
  • The mechanism of the increased toxicity of chrysotile A for BCG-immune macrophages was not known.

Topics

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

Medical terms in this study, explained in our Lexicon: Alveolar Macrophage, Chrysotile, Crocidolite, Amosite.

Related studies

• Leaching of chrysotile asbestos in human lungs. Correlation with in vitro studies using rabbit alveolar macrophages — M.C. Jaurand, J. Bignon, et al. (1977)
• Phagocytosis of asbestos fibers by human pulmonary alveolar macrophages — T. McLemore, M. Corson, et al. (1979)
• Role of alveolar macrophages in asbestosis: modulation of neutrophil migration to the lung after acute asbestos exposure — C.I. Schoenberger, G.W. Hunninghake, et al. (1982)
• Differences between particulate and peptide stimuli on activation of oxidant production in alveolar macrophages — G.E. Hatch, A. Spock, et al. (1980)
• In vitro reactivity of alveolar macrophages and red blood cells with asbestos fibres treated with oxalic acid, sulfur dioxide and benzo-3,4-pyrene — M.C. Jaurand, L. Magne, et al. (1981)
• Relative effects of asbestos and wollastonite on alveolar macrophages — W.H. Pailes, D.J. Judy, et al. (1984)

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