Thermal modification of chrysotile asbestos: evidence for decreased cytotoxicity

Our plain-English summary of Thermal modification of chrysotile asbestos: evidence for decreased cytotoxicity, by R. Valentine, M.J. Chang, R.W. Hart, et al (Environmental Health Perspectives, 1983).

The study

• Authors: R. Valentine, M.J. Chang, R.W. Hart, G.L. Finch, G.L. Fisher
• Journal: Environmental Health Perspectives
• Published: 1983;51:357-68
• Cited by: 13 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

Many asbestiform minerals exhibit temperature-dependent thermoluminescence. Since thermoluminescence involves electronic transitions within crystalline materials, the effect of temperature on asbestos cytotoxicity was evaluated. Heat pretreatment of Canadian chrysotile asbestos reduces its cytotoxicity towards cultured human fibroblasts and bovine alveolar macrophages. When monitored 44 hr after the addition of either 200 degrees C or 400 degrees C heat-pretreated asbestos, alveolar macrophage viability was approximately 40% higher than comparable amounts of unheated asbestos. Similarly, asbestos toxicity, expressed as fibroblast growth inhibition, was inversely related to the asbestos pretreatment temperature in the following manner, 70 degrees C greater than 200 degrees C greater than 400 degrees C = unexposed fibroblast controls. Pretreatment of chrysotile asbestos to 400 degrees C reduced its adsorptive capacity for bovine serum albumin by 25%. Furthermore, asbestos heated to 200 degrees C followed by irradiation with 4 MeV X-rays (4500 rads) resulted in reactivation of asbestos cytotoxicity. Scanning electron microscopy indicated that the ratios of free to fiber-associated alveolar macrophages and the fiber fragment size distributions were unaffected by either heat pretreatment or X-ray irradiation. These observations strongly suggest that the surface charge characteristics and electronic state of asbestos fibers may be responsible for its biological activity.

In plain English

This was a laboratory study of cells, not people. The authors tested whether heating Canadian chrysotile asbestos changed its toxicity to cultured cow lung macrophages (UICC standard sample) and human foreskin fibroblasts (NIEHS standard sample). Asbestos was heated to temperatures from 70 to 400°C. Some samples were also acid-washed or X-rayed. Heated (200°C or 400°C) and acid-washed asbestos was less toxic to macrophages than comparison asbestos. The article's opening summary reports macrophage survival about 40% higher at 44 hours with 200°C- or 400°C-heated than with unheated asbestos. In fibroblasts, growth was held back less as the heating temperature rose. At 400°C, growth matched unexposed cultures. Heating to 400°C cut the fibers' binding of albumin, a blood protein, by about 25%. At 0.02, 0.04 and 0.06 mg/mL, macrophage survival after 44 hours was at least 30% higher with 200°C-heated asbestos than with X-rayed or heated-then-X-rayed asbestos. Measured fiber fragment lengths showed no significant differences between treatments. The authors concluded their data were consistent with the fibers' electronic state affecting their toxicity in the laboratory. They noted they tested only one acid-washing period.

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) cell-culture experiment
• Who was studied: Cultured bovine (cow) alveolar macrophages obtained by washing out the lungs of adult steers, and normal human foreskin fibroblasts (line 149); no human subjects
• Exposure: Two standard Canadian chrysotile asbestos samples: UICC 15-5, used in the macrophage experiments, and NIEHS Plastibest-20, used in the fibroblast experiments; both were used in the albumin-binding tests. Samples were heat-pretreated at 70, 100, 200 or 400°C for 3-5 hours. Some were also treated with ultraviolet light, washed in hydrochloric acid, or irradiated with 4 MeV X-rays (about 4500 rads).
• Main results:
  • Macrophages exposed to UICC chrysotile: asbestos heat-pretreated at 200°C or 400°C, and acid-leached asbestos, was significantly less toxic than the ultraviolet-irradiated control asbestos at 44 hours. The article's opening summary reports macrophage viability about 40% higher with 200°C- or 400°C-heated asbestos than with comparable amounts of unheated asbestos. That figure is not given for acid-leached asbestos.
  • Macrophages, 44 hours after exposure: viability was at least 30% greater with asbestos heat-treated at 200°C for 3 hours, at 0.02, 0.04 and 0.06 mg/mL, than with X-ray-irradiated asbestos or heated-then-X-ray-irradiated asbestos.
  • Human fibroblasts exposed to 10 micrograms per mL NIEHS chrysotile for 24 hours: growth inhibition fell as pretreatment temperature rose, ranked 70°C greater than 200°C greater than 400°C, with 400°C equal to unexposed controls. Growth at 70°C and 200°C was significantly lower than in controls.
  • Albumin binding: heating to 100 or 200°C made no significant difference. Both UICC and NIEHS chrysotile heated to 400°C bound about 25% less bovine serum albumin than control samples.
  • Electron microscopy, with 43 to 74 fiber fragments measured per sample: there were no significant differences in count median fragment length between untreated, heated, X-rayed, and heated-plus-X-rayed UICC chrysotile. The authors also reported no differences in fragment widths or length-to-width ratios.
  • The proportion of macrophages attached to long fibers (over 20 micrometers) did not differ significantly between fiber treatments. It rose with dose: 39% of macrophages at the low dose and 74% at the high dose.
• The authors' conclusion: The authors concluded that their data were consistent with the hypothesis that the electronic state of the fibers modifies chrysotile's toxicity to cells in vitro. They suggested that trapped electrons take part in fiber-membrane interactions.
• Limitations the authors state:
  • Only one time period was tested for the acid-leaching treatment.
  • The albumin-binding method may be less sensitive than the cell toxicity tests for detecting changes in fiber surface charge.
  • A preliminary observation, reduced toxicity after soaking in culture medium, was seen only in the low-dose ultraviolet-irradiated group and needs confirmation.

Topics

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

Medical terms in this study, explained in our Lexicon: Chrysotile, Asbestiform, Crystalline, Fibroblast, Alveolar Macrophage, Scanning Electron Microscopy (SEM).

Related studies

• A possible mechanism of chrysotile asbestos toxicity — G.L. Fisher, B.T. Mossman, et al. (1987)
• Biological effects and comparative cytotoxicity of thermal transformed asbestos-containing materials in a human alveolar epithelial cell line — F. Giantomassi, A.F. Gualtieri, et al. (2010)
• Some observations on the in vitro cytotoxicity of chrysotile prepared by the wet dispersion process — I.P. Gormley, R.E. Bolton, et al. (1983)
• Comparative studies on the cytotoxicity of amphibole and serpentine asbestos — J.E. Craighead, B.T. Mossman, et al. (1980)
• Synthetic chrysotile nanocrystals as a reference standard to investigate surface-induced serum albumin structural modifications — P. Sabatino, L. Casella, et al. (2007)
• Chrysotile asbestos stimulates platelet-derived growth factor-AA production by rat lung fibroblasts in vitro: evidence for an autocrine loop — J.A. Lasky, P.G. Coin, et al. (1995)

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