A possible mechanism of chrysotile asbestos toxicity

Our plain-English summary of A possible mechanism of chrysotile asbestos toxicity, by G.L. Fisher, B.T. Mossman, A.R. McFarland, et al (Drug and Chemical Toxicology, 1987).

The study

• Authors: G.L. Fisher, B.T. Mossman, A.R. McFarland, R.W. Hart
• Journal: Drug and Chemical Toxicology
• Published: 1987;10(1-2):109-31
• Cited by: 6 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

In vitro evaluations of heat treated and/or irradiated chrysotile asbestos indicate the importance of electron transfer in determining the biological outcome of asbestos exposure. Regardless of the assay system used, all show the same trends. Namely, heat treatment reduces cytotoxicity while heat treatment in combination with irradiation increases activity over heat treatment alone. Furthermore, studies of BSA and DNA binding consistently indicate a lower molecular adsorption for heated asbestos. BSA and DNA adsorption are similar for untreated, irradiated and heated or irradiated samples. Physical and chemical analyses indicate that the size and elemental composition are unaffected by the treatment processes. X-ray diffraction indicates no change in the crystal structure of chrysotile asbestos. IR spectroscopy suggests that heat treatment affects the external hydroxyl group population while heat treatment and irradiation may repopulate this functional group. A proposed mechanism consistent with the biological and physical characterization is based upon electron transfer from the chrysotile asbestos matrix to biological receptors.

In plain English

This was a set of laboratory experiments, not a study of people. The authors split a Canadian chrysotile asbestos reference sample into four portions: untreated, heated to 400 degrees C for five hours, X-ray irradiated, and heated then irradiated. The treatments did not significantly change fiber length, diameter or the elements measured, and X-ray diffraction showed no change in the chrysotile's diffraction pattern. Heating cut the fibers' thermoluminescence, a light signal the authors link to trapped electrons, by over 80 percent. Irradiation after heating restored it to nearly 60 percent of untreated values. Heated chrysotile bound less protein (BSA), and at 12 hours less DNA, than the other samples. In cow lung macrophages, human foreskin fibroblasts and hamster windpipe cultures, heated chrysotile was less harmful than untreated chrysotile. In the fibroblast and windpipe tests, heated-then-irradiated chrysotile acted much like untreated fibers. The authors concluded that chrysotile loses some of its toxic activity with heating, regains it to varying degrees with irradiation, and proposed electron transfer from the fiber as a possible mechanism.

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: Series of in vitro (laboratory) experiments comparing treated and untreated chrysotile in cell and organ cultures, binding assays, and physical and chemical analyses
• Who was studied: No human subjects. Pooled IUAC (International Union Against Cancer) reference sample of Canadian chrysotile, tested on bovine pulmonary alveolar macrophages from one healthy adult steer, human foreskin fibroblasts (Line 149), and tracheal organ cultures from 6-8 week old Syrian golden hamsters
• Exposure: Chrysotile asbestos that was untreated, heated (400 degrees C for five hours), irradiated with a 4 MeV x-ray beam (approximately 4500 rad, 45 gy), or heated and then irradiated
• Main results:
  • Neither heating nor irradiation significantly affected fiber diameter or length
  • Major and minor elements measured by neutron activation analysis were not affected by the treatments
  • X-ray diffraction showed no change in the basic diffraction patterns of the four samples. A peak from brucite impurities was lost with heating.
  • Thermoluminescence activity fell by over 80 percent in heated samples compared with untreated asbestos. Irradiation after heating returned it to nearly 60 percent of untreated values.
  • Infrared analysis showed a 3 to 1 ratio of hydroxyl absorption peaks in untreated and irradiated samples. The ratio was 2.6 to 1 in the heated sample and 3.5 to 1 in the heated and irradiated sample.
  • At an asbestos to BSA ratio of 10:1, heated asbestos adsorbed an average of 3.2 (as printed) BSA per mg, significantly different from the other treatments (p less than 0.05)
  • At the 10:1 ratio, untreated asbestos had significantly higher BSA adsorption (52.2) than heated and irradiated asbestos (40.7), but was not different from irradiated asbestos (42.2)
  • DNA adsorption did not differ significantly between treatments at 0 or 6 hours after denaturation. At 12 hours, heated asbestos was significantly different from the other treatments.
  • Relative DNA adsorption for heated compared with untreated asbestos was 47 percent and 65 percent at the two concentrations tested
  • In bovine macrophages, viability decreased with dose, but there were no significant differences between 20-hour treatment groups
  • Macrophage phagocytosis was significantly greater (p less than 0.01) across all dose groups for heated asbestos than for the other treatments. The phagocytic index for heated compared with untreated asbestos was 132, 183, 135 and 164 percent at the four concentrations.
  • In human fibroblasts, there were no significant differences at the two lower concentrations. Untreated, irradiated and irradiated-plus-heated asbestos had a similar significant harmful effect, while heated asbestos was less toxic and inhibited growth less (p less than 0.01, averaged over all concentrations).
  • In hamster tracheal cultures, release of the enzyme LDH was elevated about two-fold with untreated asbestos (p less than 0.05)
  • In hamster tracheal cultures, heating chrysotile diminished LDH release (p less than 0.001)
  • In hamster tracheal cultures, irradiation of heated fibers increased LDH release to levels similar to untreated asbestos
• The authors' conclusion: The authors concluded that chrysotile loses some of its cytotoxic and biologic activity with heating, restored to varying degrees by irradiation. They proposed electron transfer from the chrysotile to biological molecules as a possible mechanism of toxicity consistent with their observations.

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, Asbestos Exposure, X-Ray Diffraction (XRD), Crystal Structure, Hydroxyl Group.

Related studies

• Thermal modification of chrysotile asbestos: evidence for decreased cytotoxicity — R. Valentine, M.J. Chang, et al. (1983)
• In vitro models of lung toxicity — G.L. Fisher, M.E. Placke (1987)
• Ascorbic acid modifies the surface of asbestos: possible implications in the molecular mechanisms of toxicity — G. Martra, M. Tomatis, et al. (2003)
• Human mesothelioma cells and asbestos-exposed mesothelial cells are selectively resistant to amosite toxicity: a possible mechanism for tumor promotion by asbestos — E.W. Gabrielson, A. Van der Meeren, et al. (1992)
• Effects of crocidolite and chrysotile asbestos on cellular uptake and metabolism of benzo(a)pyrene in hamster tracheal epithelial cells — B.T. Mossman, A. Eastman, et al. (1983)
• Evaluation of cellular toxicity of TAFMAG, a natural substitute for asbestos from China — H.J. Kim, H.Y. Nam, et al. (2005)

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