Modification of biological surface activity of particles

Our plain-English summary of Modification of biological surface activity of particles, by R.J. Schnitzer (Environmental Health Perspectives, 1974).

The study

• Author: R.J. Schnitzer
• Journal: Environmental Health Perspectives
• Published: 1974;9:261-6
• Cited by: 12 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

The hemolytic activity of fibrous asbestos varieties and of fibrous or granular silica dust can be markedly reduced by adsorption of polymers. Polyanions exert a specific action on asbestos, particularly chrysotile, whereas silica is inactivated by nonionic polymers. A high degree of reduction of the lytic action by comparatively small amounts of the antagonistic polymers can be demonstrated after short exposure to concentrations of 0.1-0.4 mg/ml of appropriate polymers. Inactivation is based on stable adsorption. Repeated washings of inactivated mineral sediments or exposure to elevated temperatures (80-120 degrees C) produced no essential loss of the reduction of lytic potency. In one example, inactivation of chrysotile by sodium alginate, depolymerization by ascorbic acid was also ineffective.

In plain English

This 1974 article reported laboratory experiments only, not studies of people or animals. The author tested whether coating mineral dusts with polymers stopped them from bursting sheep red blood cells (hemolysis). Four asbestos types (chrysotile, amosite, crocidolite, anthophyllite) were exposed to polymer solutions, then washed. Negatively charged polymers (polyanions) such as sodium alginate, carboxymethyl cellulose and chondroitin sulfate reduced chrysotile B hemolysis by about 80 to 85 percent on average. Polyvinylpyrrolidone, a silica antagonist, had no effect on chrysotile but inactivated silica particles more slowly. The coating on chrysotile formed within about 10 minutes and was not removed by washing. Heating chrysotile coated with sodium alginate or carboxymethyl cellulose to 80 or 125 degrees C for one hour did not reverse inactivation, and ascorbic acid did not break down alginate adsorbed on chrysotile. Alginate-treated chrysotile still caused no hemolysis at 2.5 mg/ml after over 2 years' storage. The author concluded that polyanion coating irreversibly inactivated the fibers' hemolytic property. The author noted that results were limited to hemolysis tests and that effects in other cells or animals, and the polymers' toxicity, needed study.

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) experiments using red blood cell hemolysis tests
• Who was studied: No human or animal subjects. Samples of 40-100 mg of asbestos fibers (and silica particles) were tested against sheep red blood cells in the laboratory. No study dates or location are given beyond the author's affiliation (Mount Sinai School of Medicine, New York).
• Exposure: Chrysotile B (UICC), chrysotile Jeffrey, amosite (UICC), crocidolite (UICC) and anthophyllite asbestos fibers, plus fibrous quartz and microfine precipitated silica (Quso G30, G32). These were coated with polymers: sodium alginate, carboxymethyl cellulose, chondroitin sulfate, pyran copolymer NSC 46015, polystyrene sulfate (RS 781) and polyvinylpyrrolidone (PVP).
• Main results:
  • For chrysotile B, average inactivation of hemolysis by adsorbed polymers was 80±4.4% (sodium alginate), 81±3.1% (carboxymethyl cellulose), 85±1.6% (chondroitin sulfate), 85±5.3% (NSC 46015) and 69±4.2% (polystyrene sulfate RS 781).
  • Polyvinylpyrrolidone (PVP), a silica antagonist, did not inactivate chrysotile B hemolysis (0% in Table 2).
  • Small amounts of sodium alginate inactivated larger amounts of chrysotile B. The 50% endpoint ratio of inactivator to fiber was 1/46 to 1/50 (printed '1-46 to 1-50'; Table 1 shows 1/46 and 1/50), regardless of the amount of fiber.
  • Adsorption onto chrysotile B was rapid, with inactivation seen after about 10 minutes of contact.
  • Inactivation of silica particles (Quso G30 and G32) by PVP was slower and required higher polymer concentrations, an inactivator-to-particle ratio of 1/5 to 1/6 for the 10-minute interval.
  • After washing, approximately 70-80% of the inactivating amount of polymer was bound to chrysotile B fibers, and washing did not change the inactivation.
  • Heating for 1 hour did not reverse the inactivation of chrysotile B by sodium alginate or carboxymethyl cellulose (Table 5: 80 and 125 degrees C) or of silica G32 by PVP (Table 6: 100 degrees C).
  • Chrysotile Jeffrey treated with sodium alginate was not hemolytic at 2.5 mg/ml (untreated fibers had a 50% hemolytic concentration of 0.18 mg/ml), and still showed no hemolysis after more than 2 years of storage.
  • Ascorbic acid failed to break down sodium alginate adsorbed on chrysotile fibers; the alginate's protective effect was not affected. Only sodium alginate was tested this way.
• The authors' conclusion: The author concluded that stable adsorption of polyanions on asbestos fibers irreversibly inactivates their hemolytic property, and that nonionic polymers have comparable effects on silica. The author stated that further studies in other cell systems and toxicological work are needed before animal experiments on preventing fibrosis and cancer.
• Limitations the authors state:
  • Results were limited to hemolysis tests, so their significance for preventing asbestos damage in other cell systems or in living animals is difficult to evaluate and still requires experimental proof.
  • The toxicity of the inactivating polymers themselves, including carcinogenesis, needs extensive study.
  • The effect of enzyme breakdown of the adsorbed polymers had not yet been investigated.

Topics

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

Related studies

• Free radical activity associated with the surface of particles: a unifying factor in determining biological activity? — K. Donaldson, P.H. Beswick, et al. (1996)
• Surface charge and hemolytic activity of asbestos — W.G. Light, E.T. Wei (1977)
• Synthetic chrysotile nanocrystals as a reference standard to investigate surface-induced serum albumin structural modifications — P. Sabatino, L. Casella, et al. (2007)
• Ascorbic acid modifies the surface of asbestos: possible implications in the molecular mechanisms of toxicity — G. Martra, M. Tomatis, et al. (2003)
• Free radical generation in the toxicity of inhaled mineral particles: the role of iron speciation at the surface of asbestos and silica — I. Fenoglio, L. Prandi, et al. (2001)
• Asbestos surface provides a niche for oxidative modification — H. Nagai, T. Ishihara, et al. (2011)

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