Some biochemical effects of asbestos on macrophages

Our plain-English summary of Some biochemical effects of asbestos on macrophages, by K. Miller, J.S. Harington (British Journal of Experimental Pathology, 1972).

The study

• Authors: K. Miller, J.S. Harington
• Journal: British Journal of Experimental Pathology
• Published: 1972;53(4):397-405
• Cited by: 69 articles, as counted by NIH iCite
• Read it: PubMed · Free full text

Abstract

The in vitro effects of chrysotile, crocidolite and amosite asbestos, and silica and rutile dust, on hamster peritoneal macrophages were assessed by estimating the release of acid phosphatase into the culture medium and by changes in the composition of phospholipids in the cells. Chrysotile was as toxic as silica, while crocidolite, amosite and the control dust, rutile were inert. The toxicity of chrysotile and silica is evidently due to the surface interaction of the dusts with phagosomal membranes, leading to the release of lytic enzymes from the damaged phagosomes into the cytoplasm. Considerable amounts of acid phosphatase were released into the medium 28 hours after the phagocytosis of both dusts, whereas very little was found when crocidolite, amosite and rutile were used. Further evidence of cytopathic effects was seen by changes in lipid components of cells which had ingested silica and chrysotile. A decrease in total lipid content and an increase in lysolecithin apparently indicate specific, secondary and toxic effects following the release of lysosomal enzymes.

In plain English

This was a laboratory study of cells, not people. The authors grew macrophages (scavenger cells) taken from the abdominal cavity of young adult male golden hamsters. They exposed them for one hour to one of five dusts at 300 micrograms per million cells: UICC chrysotile, amosite or crocidolite asbestos, an amorphous silica, or rutile (titanium dioxide). After 16 hours, chrysotile- and silica-treated cells showed marked damage, which was not seen with the other dusts or in untreated cells. Between 4 and 28 hours, cell numbers fell by 71% with chrysotile and 68% with silica. The falls were 5% to 8% for amosite, crocidolite and rutile, and 18% for untreated cells. Chrysotile and silica cultures released the enzyme acid phosphatase, peaking at 28 hours. Amosite and crocidolite released very little. Chrysotile and silica also produced a 10-fold rise in the fat lysolecithin. The authors concluded that chrysotile was as toxic as silica to these cells, while crocidolite, amosite and rutile were inert. They wrote that chrysotile probably acts directly on the membranes holding swallowed particles. They said the enzyme release needed confirmation by other methods.

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: In vitro laboratory experiment on cultured animal cells (hamster peritoneal macrophages)
• Who was studied: Peritoneal (abdominal cavity) macrophages from young adult male golden hamsters, studied at the Cancer Research Unit, Johannesburg, South Africa. Cells were pooled for each experiment, and at least 75% of the collected cells were macrophages. The phospholipid experiments used cells from 60 and from 40 male hamsters. Dates of the work are not stated; the paper was received for publication in February 1972.
• Exposure: Standard finely ground UICC chrysotile, amosite and crocidolite asbestos. Comparison dusts were rutile (titanium dioxide) and alkali-etched Fransil silica (an amorphous form). The dose was 300 micrograms of dust per million cells, with cells allowed to take up the dust for 1 hour.
• Main results:
  • After 16 hours, chrysotile- and silica-treated macrophages showed marked degenerative changes (vacuolation, rounding, destruction). These changes were not seen with rutile, crocidolite or amosite, or in untreated control cells.
  • Per cent decrease in cell number from 4 to 28 hours (Table I): silica 68, chrysotile 71, amosite 5, crocidolite 8, rutile 5, untreated control cells 18.
  • Silica- and chrysotile-treated cultures released acid phosphatase into the medium within 16 hours, peaking at 28 hours.
  • Amosite- and crocidolite-treated cultures released very small amounts of acid phosphatase at 28 hours. Control and rutile cultures gave low values (0.07 and 0.14 mmol phosphatase units respectively at 28 hours).
  • In macrophages given chrysotile or silica, lysolecithin increased 10-fold at the expense of lecithin and cephalin. Control cells and rutile-treated cells were unaffected.
• The authors' conclusion: The authors concluded that chrysotile was as toxic as silica to these macrophages, while crocidolite, amosite and the control dust rutile were inert. They wrote that the acid phosphatase release strongly indicated that some forms of chrysotile act directly on the phagosomal membrane, causing cell death. They suggested this was probably through magnesium ions.
• Limitations the authors state:
  • The authors stated that the release of lysosomal enzyme seen here requires confirmation by histochemical studies.
  • The authors stated it was not yet possible to judge whether the increase in lysolecithin is a primary or a secondary event.

Topics

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

Related studies

• Cytotoxic effects of some mineral dusts on Syrian hamster peritoneal macrophages — E. Bey, J.S. Harington (1971)
• Effects of chrysotile and acid-treated chrysotile on macrophage cultures — E.G. Beck, P.F. Holt, et al. (1971)
• Immune adherence reactivity of rat alveolar macrophages following inhalation of crocidolite asbestos — K. Miller, E. Kagan (1977)
• In vitro studies on the cytotoxic action of different varieties of asbestos dust on macrophages — J.L. Kaw, S.H. Zaidi (1975)
• Surface morphology and correlated phagocytic capacity of pulmonary macrophages lavaged from the lungs of rats — D.B. Warheit, L.H. Hill, et al. (1984)
• Interactions of asbestos-activated macrophages with an experimental fibrosarcoma — K. Donaldson, J.M. Davis, et al. (1983)

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