Absence of mutagenic activity of three forms of asbestos in liver epithelial cells

Our plain-English summary of Absence of mutagenic activity of three forms of asbestos in liver epithelial cells, by B. Reiss, S. Solomon, C. Tong, et al (Environmental Research, 1982).

The study

• Authors: B. Reiss, S. Solomon, C. Tong, M. Levenstein, S.H. Rosenberg, G.M. Williams
• Journal: Environmental Research
• Published: 1982;27(2):389-97
• Cited by: 39 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

The amosite, crocidolite, and chrysotile forms of UICC asbestos were assayed for their ability to induce gene mutations at the hypoxanthine-guanine phosphoribosyl transferase locus. Using adult rat liver-derived (ARL-6 and ARL-18) cells in culture, no consistent or significant increase occurred in the number of mutants resistant to the purine analog, 6-thioguanine, after exposure to toxic levels of amosite, crocidolite, or chrysotile. These results support the concept that asbestos is an epigenetic carcinogen that does not alter DNA.

PubMed has no abstract for this study. This is the authors' abstract, copied from the article.

In plain English

This was a laboratory study of cells, not of people or animals. The authors tested whether UICC standard reference samples of Canadian chrysotile B, crocidolite and amosite caused gene mutations in cultured adult rat liver cells of the ARL-6 line; chrysotile alone was also tested in a second line, ARL-18. Cells were exposed for 6 days to levels of asbestos the authors described as toxic. Mutations at one gene (HGPRT) were measured by counting cells able to survive the chemical 6-thioguanine. In ARL-6 cells, exposed cultures had more mutants than unexposed cultures in four of seven chrysotile assays, one of four amosite assays and six of ten crocidolite assays. In all but two experiments, however, these increases were very slight and within the range seen in unexposed control cultures. Chrysotile-exposed ARL-18 cells sometimes showed slight increases, far below those caused by benzo[a]pyrene, a chemical used as a positive control. Statistical testing found no significant increase for any of the three fiber types. The authors concluded that their findings are consistent with asbestos being an 'epigenetic' carcinogen that does not alter DNA.

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 cell culture experiment (in vitro gene mutation assay at the HGPRT locus)
• Who was studied: Two cultured cell lines derived from adult rat liver epithelium: ARL-6, used for all three fiber types, and ARL-18, used for chrysotile only. No people or live animals were studied.
• Exposure: UICC standard reference samples of Canadian chrysotile B, crocidolite and amosite, supplied by the U.S. EPA. They were added to the culture medium for 6 days at levels described as toxic. All three were tested in ARL-6 cells, and only chrysotile in ARL-18 cells. Benzo[a]pyrene was used as a positive control in the ARL-18 experiments.
• Main results:
  • In ARL-6 cells, chrysotile-exposed cultures gave more mutants than unexposed cultures in four out of seven assays.
  • In ARL-6 cells, amosite-exposed cultures gave more mutants than unexposed cultures in one out of four assays.
  • In ARL-6 cells, crocidolite-exposed cultures had a higher mutant frequency than unexposed controls in six out of ten assays.
  • The authors did not consider these increases evidence of mutagenicity. In all but two experiments (experiment 1 with chrysotile and experiment 6 with crocidolite), mutant numbers in exposed cultures were very slight. They did not exceed the range seen in control cultures, which was up to 17.3 mutants per million colony-forming cells.
  • In a separate set of experiments in ARL-18 cells, only chrysotile was tested. Chrysotile sometimes slightly increased mutant recovery compared with unexposed cells. The authors stated that the much higher mutant recovery after benzo[a]pyrene (the positive control) showed the asbestos fibers were ineffective as mutagens.
  • A statistical analysis (Mann-Whitney Wilcoxon test) of all experiments in both cell lines found that none of the three fibers significantly increased mutants over control values. For chrysotile, 13 exposed observations were compared with 7 unexposed (P = 0.819). For amosite the comparison was 4 vs 4 (P = 0.282), and for crocidolite 10 vs 7 (P = 0.461).
• The authors' conclusion: The authors concluded that their findings, together with those in the literature, are consistent with the concept that asbestos is not a genotoxic carcinogen able to alter DNA. In their view it is rather an epigenetic carcinogen of the 'solid-state' type.

Topics

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

Medical terms in this study, explained in our Lexicon: Amosite, Crocidolite, Chrysotile, UICC.

Related studies

• Enhancement of benzo[a]pyrene mutagenicity by chrysotile asbestos in rat liver epithelial cells — B. Reiss, C. Tong, et al. (1983)
• Synthesis of poly(ADP-ribose) in asbestos treated rat pleural mesothelial cells in culture — H.Y. Dong, A. Buard, et al. (1995)
• Asbestos fibers are mutagenic after all: new signs of orthodoxy for a paradoxical group of carcinogens — T.M. Fasy (1991)
• Induction of metaphase and anaphase/telophase abnormalities by asbestos fibers in rat pleural mesothelial cells in vitro — M. Yegles, L. Saint-Etienne, et al. (1993)
• Oxygen radical-mediated mutagenic effect of asbestos on human lymphocytes: suppression by oxygen radical scavengers — L.G. Korkina, A.D. Durnev, et al. (1992)
• Cell toxicity, hemolytic action and clastogenic activity of asbestos and its substitutes — K. Koshi, N. Kohyama, et al. (1991)

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