The prevention of asbestos-induced hemolysis

Our plain-English summary of The prevention of asbestos-induced hemolysis, by R. Desai, P. Hext, R. Richards (Life Sciences, 1975).

The study

• Authors: R. Desai, P. Hext, R. Richards
• Journal: Life Sciences
• Published: 1975;16(12):1931-8
• Cited by: 56 articles, as counted by NIH iCite
• Read it: PubMed · Publisher
• In J-M's library: Johns-Manville's company medical library held a copy (J-M no. 002320).

Abstract

The hemolytic potency of different types of asbestos dusts and silica (min-u-sil) is described. Dust induced hemolysis can be prevented to varying degrees by protection with erythrocyte membranes, tissue culture medium (containing 20% serum) and by pulmonary surfactant. It is suggested that the binding of relatively non-soluble serum or surfactant materials to asbestos dusts (particularly chrysotile) is important to prevent hemolysis. The relevance of the present study to the initiation of cellular damage by inhaled asbestos is discussed.

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

In plain English

This was a laboratory study, at University College, Cardiff, of how asbestos dusts break open (hemolyse) red blood cells. It used rabbit red blood cells in test tubes, not people or live animals. The authors tested UICC standard reference samples of chrysotile, amosite, crocidolite and anthophyllite. They also tested brucite, silica, 20% and 80% magnesium-depleted chrysotile, chrysotile from individual Canadian mines, and titanium dioxide as a control dust. Chrysotile A, brucite and anthophyllite caused maximum measured hemolysis at 20 to 40 mg dust per sample. Higher amounts gave slightly lower readings, which the authors judged likely due to the dusts binding or precipitating hemoglobin, since microscopy showed lysis was practically complete. Amosite and crocidolite did not cause total hemolysis. Coating the dusts beforehand with red cell membranes, serum-containing culture medium, or lung surfactant reduced hemolysis to varying degrees. Surfactant gave complete protection for every dust except 20% magnesium-depleted chrysotile. The authors suggested that tightly bound, relatively non-soluble serum or surfactant materials on asbestos, particularly chrysotile, are important in preventing hemolysis. They noted that red blood cell membranes differ structurally from lung cell membranes.

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 red blood cells exposed to dusts
• Who was studied: Red blood cells (erythrocytes) from Dutch rabbits, studied in the laboratory at the Department of Biochemistry, University College, Cardiff, Wales; published 1975. No human subjects.
• Exposure: UICC standard reference asbestos dusts (chrysotile A, amosite, crocidolite, anthophyllite), Canadian chrysotile B samples from individual mines, chrysotile with 20% and 80% of its magnesium removed, brucite, silica (min-u-sil) and titanium dioxide as a control dust; amounts of up to 200 mg dust per sample
• Main results:
  • Chrysotile A, brucite and anthophyllite caused maximum measured hemolysis at 20 to 40 mg dust per sample. Higher amounts gave a slight decrease in measured hemolysis.
  • For these dusts, light microscopy showed red cell lysis was practically complete. The authors considered the apparent reduction at higher doses likely due to the dusts binding and/or precipitating hemoglobin.
  • Amosite and crocidolite did not cause total hemolysis; many red cells remained intact.
  • Chrysotile and brucite removed considerable amounts of hemoglobin from solution.
  • At 10 mg of dust, chrysotile and the magnesium-depleted chrysotiles caused extensive hemolysis within 10 minutes; the percentage printed is unreadable in the scan. Hemolysis by the other dusts increased gradually with time.
  • Among the Canadian chrysotile mine samples, those from Mines H and F were the least easily dispersed and the least hemolytic at low concentrations.
  • Coating the dusts first with red cell membranes almost totally prevented hemolysis for all dusts except brucite, chrysotile A and the magnesium-depleted chrysotiles.
  • Fetal bovine serum protected against chrysotile and the magnesium-depleted chrysotiles more than red cell membrane preparations did.
  • Coating with pulmonary surfactant completely prevented hemolysis for all dusts except 20% magnesium-depleted chrysotile.
  • Washing the surfactant-coated dusts with distilled water did not change the protection.
• The authors' conclusion: The authors concluded that tightly bound, non-soluble coating materials, particularly lipid complexes, are more protective against hemolysis. They suggested that, with the possible exception of chrysotile, asbestos dusts would be unlikely to damage lung cell membranes to any great extent in the body, because they would be coated with biological materials, particularly pulmonary surfactant.
• Limitations the authors state:
  • Red blood cells have structurally different membranes from the lung cells that asbestos may target, such as alveolar macrophages, epithelial cells and fibroblasts.

Topics

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

Related studies

• Interrelationship between hemolysis and lipid peroxidation of human erythrocytes induced by silicic acid and silicate dusts — S.V. Singh, Q. Rahman (1987)
• Hemolysis by asbestos — J.S. Harington, K. Miller, et al. (1971)
• Asbestos hemolysis — R.J. Schnitzer, F.L. Pundsack (1970)
• Hemolysis by chrysotile asbestos fibers. I. Influence of the sialic acid content in human, rat, and sheep red blood cell membranes — J.P. Pelé, R. Calvert (1983)
• Dusts causing pneumoconiosis generate .OH and produce hemolysis by acting as Fenton catalysts — T.P. Kennedy, R. Dodson, et al. (1989)
• Surface charge and hemolytic activity of asbestos — W.G. Light, E.T. Wei (1977)

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