An overview of the role of mineral solubility in silicosis and asbestosis

Our plain-English summary of An overview of the role of mineral solubility in silicosis and asbestosis, by G. Erdogdu, V. Hasirci (Environmental Research, 1998).

The study

• Authors: G. Erdogdu, V. Hasirci
• Journal: Environmental Research
• Published: 1998;78(1):38-42
• Type of article: Review
• Cited by: 12 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Asbestosis and silicosis are fibrotic diseases initiated by the inhalation of silica-containing dusts, asbestos and quartz. There are various approaches for explaining the causes of these diseases. At present, our knowledge on the matter indicates that silicic acid dissolved from these minerals, contact between macrophages and minerals, highly reactive and oxidative species formed on the mineral surface, and lysosomal enzymes released upon engulfment of particulate mineral of appropriate size all contribute to various extents to the initiation of fibrosis. Among these mineral solubility seems to have a substantial contribution as a causative factor.

In plain English

This article was a short overview (a review), not a new study. The authors reviewed published work, including their own earlier research, on how inhaled silica-containing dusts (quartz and asbestos) start the lung scarring (fibrosis) of silicosis and asbestosis. They described several proposed mechanisms: contact between dust and the membranes of alveolar macrophages (lung defense cells), reactive and oxidizing chemicals formed on mineral surfaces, release of enzymes from lysosomes after cells engulf particles, and monosilicic acid dissolving from the minerals. The article cited a report that, per 50 mg of asbestos, chrysotile released silicic acid equal to 21.5 micrograms of silicon dioxide, compared with 5.5 for crocidolite, 7.6 for anthophyllite and 14.0 for amosite. The same report found that interaction with EDTA lowered hemolysis (breaking of red blood cells) by chrysotile from 91.35 to 42%. The review also described substances, such as polyvinylpyridine N-oxide (PVNO), studied as possible blockers of quartz toxicity. The authors concluded that asbestosis and silicosis are caused not by the mineral surface alone but also by compounds that dissolve from these minerals. In their view, monosilicic acid deserves significant attention.

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: Narrative review (overview) of published research on the mechanisms of silicosis and asbestosis; no new study was carried out
• Who was studied: No study population. The article reviewed earlier published laboratory, animal (rat and mouse) and cell studies, and the authors' own earlier work, on how silica-containing dusts cause silicosis and asbestosis
• Exposure: Inhaled silica-containing dusts: quartz and silica particles (silicosis) and asbestos (asbestosis). Asbestos is described as serpentine and amphibole groups. The fibers named are chrysotile, crocidolite, anthophyllite and amosite
• Main results:
  • The review listed factors proposed to damage macrophages: a large membrane contact area, attack by monosilicic acid released from the dust surface, attack by radicals and hydrogen peroxide formed on the dust surface, polysilicic acid forming on the membrane, and lysis of lysosomes by engulfed dust particles
  • The review cited a report (no source given) of the silicic acid released per 50 mg of asbestos, expressed as SiO2 (silicon dioxide): chrysotile (printed 'chrysolite') 21.5, crocidolite 5.5, anthophyllite 7.6 and amosite 14.0 micrograms (units printed as 'lg')
  • In that same cited report, interaction with EDTA lowered hemolysis by chrysotile from 91.35 to 42%, which the article describes as a 50% decrease
  • The review cited Dubois et al. (1989): in rats, silica and chrysotile produced a 3- to 4-fold increase in TNF production and a 13- to 32-fold increase in LTB4 production (both are inflammation-related substances)
  • The review cited the authors' earlier work (Hasirci, 1977): monosilicic acid caused red blood cells to clump together (agglutination), and treatment with PVNO prevented this effect
  • The review stated that, for asbestos, the formation of oxidizing agents has been explained by the magnesium and iron ions present in the fiber structure
• The authors' conclusion: The authors concluded that asbestosis and silicosis are caused not by the mineral surface alone but also by compounds that dissolve from the minerals. They singled out monosilicic acid, together with magnesium and iron ions, as a significant step in starting fibrosis

Topics

The National Library of Medicine indexes this study under subjects our site covers: Asbestosis.

Medical terms in this study, explained in our Lexicon: Silicosis, Macrophage, Fibrosis.

Related studies

• Mechanisms in the pathogenesis of asbestosis and silicosis — B.T. Mossman, A. Churg (1998)
• Current concepts about the pathogenesis of silicosis and asbestosis — R.D. deShazo (1982)
• Serum oncoproteins and growth factors in asbestosis and silicosis patients — P.W. Brandt-Rauf, S. Smith, et al. (1992)
• The ability of mineral dusts and fibres to initiate lipid peroxidation. Part I: parameters which determine this ability — M. Gulumian (1999)
• Asbestosis and silicosis — G.R. Wagner (1997)
• Cancer incidence and mortality among Finnish asbestos sprayers and in asbestosis and silicosis patients — P. Oksa, E. Pukkala, et al. (1997)

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