Biological effects of contaminated silicon carbide particles from a workstation in a plant producing abrasives

Our plain-English summary of Biological effects of contaminated silicon carbide particles from a workstation in a plant producing abrasives, by M. Governa, M. Valentino, M. Amati, et al (Toxicology in Vitro, 1997).

The study

• Authors: M. Governa, M. Valentino, M. Amati, I. Visonà, G.C. Botta, G. Marcer, C. Gemignani
• Journal: Toxicology in Vitro
• Published: 1997;11(3):201-7
• Cited by: 4 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

A sample of silicon carbide dust taken in the field from a plant producing abrasives was studied in vitro. The SiC particles (part unmilled and part milled) were able to disturb the structure of erythrocyte membranes and to lead to blood red-cell lysis; they also either interfered with complement and activated the alternate pathway, or interacted with biological media and polymorphonuclear leucocyte membranes, thus eliciting reactive oxygen species production. These in vitro properties were detected both in original large particles and unmilled particles, over 40% of which were of respirable size. The ability of these SiC particles to produce complement activation in vitro lends support to the previous hypothesis, that the radiographic opacities found in two workers employed in the same area of the plant from which the dust tested was taken are due to a reaction by pulmonary interstitial structures to SiC particle inhalation. It is speculated that SiC particles could act like asbestos, the ability of which to activate complement through the alternate pathway is considered to be one of the mechanisms by which the initial asbestotic lesions and subsequent fibrotic inflammatory infiltrates are generated in the lung.

In plain English

This was a laboratory (in vitro) study of one sample of silicon carbide dust. The dust was collected in the screening and storage departments for finished products of a factory making silicon carbide abrasives, where the authors stated no crystalline silica was present. Part of the sample was milled, and no fibres or whiskers were seen. The authors tested equal surface areas of the dust on human red blood cells, serum and white blood cells. They compared it with quartz and UICC chrysotile asbestos, and in one test with UICC crocidolite asbestos. Unmilled silicon carbide burst red blood cells more readily than chrysotile or quartz did; milled silicon carbide did so less readily. Both forms activated complement, an immune defence, through the alternate pathway. The level was about half that of the reference stimulus and significantly lower than with silica or chrysotile. Both forms raised the white cells' output of reactive oxygen above that of untreated cells, but significantly less than chrysotile, crocidolite or quartz did. The authors concluded that this lends support to an earlier hypothesis: that chest X-ray shadows in two workers from the same plant area came from inhaling silicon carbide. They speculated that it could act like asbestos.

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 testing a field-collected dust sample in short-term cell and serum tests, with quartz and asbestos as positive controls
• Who was studied: One sample of silicon carbide dust from the screening and storage departments for finished products at a silicon carbide abrasives factory (country and date of sampling not stated). It was tested on red blood cells, on white blood cells (polymorphonuclear leucocytes) from apparently healthy adults, and on serum pooled from 10 healthy volunteers.
• Exposure: Unmilled and milled silicon carbide particles. Comparison minerals were quartz (crystalline silica), UICC Canadian chrysotile type B and UICC crocidolite. Doses were matched by specific surface area.
• Main results:
  • Particle examination: more than 95% of the unmilled sample was isometric particles 150 to 300 micrometres across. More than 90% of the milled sample was isometric particles under 10 micrometres. No fibres or whiskers were observed.
  • Red blood cell bursting (haemolysis): the surface area needed to burst half the red cells (HC50%, lower means more potent) was 61.31 cm2/ml for unmilled silicon carbide, 274.29 for milled silicon carbide, 97.94 for chrysotile and 146.79 for quartz.
  • Complement activation: unmilled and milled silicon carbide did not differ. Silicon carbide gave about half the activity of the reference stimulus (zymosan-activated plasma), significantly lower than silica or chrysotile.
  • Activity stayed similar in serum treated with EGTA but dropped significantly (P less than 0.01) in serum treated with EDTA. The authors took this as evidence that the alternate complement pathway was involved.
  • Reactive oxygen production by white blood cells, as a percentage of untreated control cells: unmilled silicon carbide 214.1, milled silicon carbide 214.6, chrysotile 261.2, crocidolite 275.1, quartz 1709.8. Silicon carbide was significantly lower than the three control minerals but significantly higher than cells with no particles.
  • The authors summarised the silicon carbide effects as high red-cell bursting, moderate complement activation and limited reactive oxygen production.
• The authors' conclusion: The authors concluded that the complement activation lends support to an earlier hypothesis (Marcer et al., 1992). That hypothesis held that chest X-ray opacities in two workers from the same plant area were due to a lung reaction to inhaled silicon carbide. The authors speculated that the particles could act like asbestos fibres.
• Limitations the authors state:
  • The asbestos reference samples dated from 1968 and had been exposed to air, so their surfaces may have become less reactive. The quartz surface, by contrast, was freshly created.
  • Iron traces on a few silicon carbide particles and in the biological media could have modified the particles' reactivity.

Topics

Medical terms in this study, explained in our Lexicon: Reactive Oxygen Species (ROS), Interstitial.

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• Pulmonary response, in vivo, to silicon carbide whiskers — G.L. Vaughan, S.A. Trently, et al. (1993)
• In vitro activity of silicon carbide whiskers in comparison to other industrial fibers using four cell culture systems — N.F. Johnson, M.D. Hoover, et al. (1992)
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• Toxicity in vitro of some silicon carbides and silicon nitrides: whiskers and powders — I. Svensson, E. Artursson, et al. (1997)

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