Role of iron in the reactivity of mineral fibers

Our plain-English summary of Role of iron in the reactivity of mineral fibers, by B. Fubini, L. Mollo (Toxicology Letters, 1995).

The study

• Authors: B. Fubini, L. Mollo
• Journal: Toxicology Letters
• Published: 1995;82-83:951-60
• Type of article: Review
• Cited by: 92 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Any foreign body containing iron may be (or become) highly toxic in vivo. If its solubility in water is poor, surface chemistry governs the reactivity at the solid-liquid interface. Iron toxicity thus increases with the extent of exposed surface. Iron of endogenous origin may also be deposited on the particle surface and be activated under particular circumstances. The chemical processes that implicate surface iron as a primary cause of toxicity are: free radical release, mobilization by chelators, iron-catalyzed reactions. Three kinds of solids are compared: (i) well-known toxic materials, for example asbestos; (ii) non-toxic iron oxides; and (iii) model solids with surface exposed iron prepared for investigations on the reactivity of iron in biological media. The iron content of the solid is not directly related to the biological response: only a small fraction of ions, in a well-defined coordination and redox state, appears involved in the toxicity of the mineral dust.

In plain English

This paper, from the University of Turin, Italy, was mainly a review of how iron in mineral fibers such as asbestos may relate to their toxicity. It drew on published work by others and by the authors' own laboratory. It also presented cell-free laboratory data, with no people or animals, comparing several iron-containing solids: two iron oxides (hematite and magnetite), chrysotile and crocidolite asbestos, two asbestiform minerals from Piedmont ores (balangeroite and carlosturanite), and two model solids made in the laboratory. The authors reported that the amount of free radicals released did not parallel the solids' iron content. The iron oxides were the richest in iron and the most inactive. Fresh grinding increased one type of radical reaction, particularly with asbestos, but not the other type. After 7 days in the iron-binding chemical desferrioxamine, about 50, 130 and 180 nmol of iron per mg of solid were released from chrysotile, crocidolite and nemalite (a fibrous brucite associated with Canadian chrysotile), respectively. The authors concluded that a solid's iron content is not directly related to the biological response.

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 chemistry of iron in mineral fibers, with comparative cell-free laboratory (test-tube) data on iron-containing solids
• Who was studied: No human or animal subjects. The solids studied were the iron oxides hematite and magnetite; chrysotile (UICC B) and crocidolite asbestos; balangeroite and carlosturanite from Piedmont ores (Italy); an iron-exchanged Y zeolite (FeY) and an FeO/MgO solid solution. Iron removal tests used chrysotile (UICC A and B), crocidolite (UICC) and nemalite.
• Exposure: Iron content and specific surface area of each solid, compared with free radical release measured by spin trapping, in aged versus freshly ground samples; also iron removal by chelators such as desferrioxamine
• Main results:
  • Across the solids tested, free radical release did not parallel iron content or surface iron. The iron oxides had the most iron and were the most inactive.
  • For hydroxyl radical release from hydrogen peroxide (mechanism 1), the most active solid (carlosturanite) released only about twice as many radicals as the least active ones (crocidolite and the Fe-zeolite).
  • Fresh grinding increased radical release by hydrogen abstraction (mechanism 3), particularly with asbestos, but not by mechanism 1.
  • The surface of the FeY model zeolite was inactivated by hydrogen peroxide, and its activity was largely restored by glutathione.
  • In desferrioxamine, iron release was immediate from nemalite, while release from the asbestos samples was weak in the first 2 hours. After 7 days, about 50, 130 and 180 nmol of iron per mg of solid had been released from chrysotile, crocidolite and nemalite, respectively.
  • The authors' laboratory found that how well a chelator removes iron also depends on the solid: the most effective chelator for crocidolite was not necessarily the most effective for amosite.
• The authors' conclusion: The authors concluded that the iron content of a solid is not directly related to the biological response, and that only a small fraction of iron ions, in a particular coordination and redox state, appears to be involved in the toxicity of mineral dust.

Mines named here

Asbestos mines this study is about. Each mine's page says who ran it, when it worked, and what it produced.

• Balangero mine, Balangero, about 20 km north of Turin, Piedmont

All asbestos mines

Topics

Medical terms in this study, explained in our Lexicon: Mineral Fiber.

Related studies

• Iron from a geochemical viewpoint. Understanding toxicity/pathogenicity mechanisms in iron-bearing minerals with a special attention to mineral fibers — A.F. Gualtieri, G.B. Andreozzi, et al. (2019)
• Free radical activity of industrial fibers: role of iron in oxidative stress and activation of transcription factors — P.S. Gilmour, D.M. Brown, et al. (1997)
• Free radical generation at the solid/liquid interface in iron containing minerals — B. Fubini, L. Mollo, et al. (1995)
• Potential toxicity of nonregulated asbestiform minerals: balangeroite from the western Alps. Part 2: Oxidant activity of the fibers — F. Turci, M. Tomatis, et al. (2005)
• Soil fungi reduce the iron content and the DNA damaging effects of asbestos fibers — S. Daghino, F. Turci, et al. (2006)
• Iron-loaded synthetic chrysotile: a new model solid for studying the role of iron in asbestos toxicity — E. Gazzano, F. Turci, et al. (2007)

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