Enhancement of benzo\[a\]pyrene mutagenicity by chrysotile asbestos in rat liver epithelial cells

Our plain-English summary of Enhancement of benzo[a]pyrene mutagenicity by chrysotile asbestos in rat liver epithelial cells, by B. Reiss, C. Tong, S. Telang, et al (Environmental Research, 1983).

The study

• Authors: B. Reiss, C. Tong, S. Telang, G.M. Williams
• Journal: Environmental Research
• Published: 1983;31(1):100-4
• Cited by: 25 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

The co-mutagenicity of chrysotile asbestos and benzo[a]pyrene (B(a)P) was studied in adult rat liver (ARL-18) epithelial cells. Exposure to chrysotile alone did not increase the mutant incidence whereas B(a)P was mutagenic. Simultaneous exposure of the cells to chrysotile and B(a)P resulted in an enhanced mutant recovery compared to exposure to either of these substances alone. However, chrysotile did not enhance the mutagenicity of the carcinogen, N-methyl-N'-nitro-N-nitrosoguanidine.

In plain English

In this laboratory study of rat cells grown in culture, the authors tested whether chrysotile asbestos changes other chemicals' ability to cause gene mutations. They used adult rat liver epithelial cells (ARL-18) that can activate benzo[a]pyrene (B(a)P), which the authors describe as the predominant polycyclic aromatic hydrocarbon in tobacco smoke. For 3 days, cells were exposed to UICC Canadian chrysotile B, to B(a)P, to a chemical called MNNG, or to chrysotile plus one of these. After an 18-day expression period, cells were grown for 2 weeks in a 6-thioguanine medium that selects for mutants, and mutant colonies were counted. Chrysotile at 0.1 mg/ml was toxic to the cells, but chrysotile alone produced no significant increase in mutations. B(a)P alone caused mutations. Chrysotile combined with B(a)P gave more mutant cells than either substance alone. This increase varied between experiments but, the authors wrote, was consistently substantial. Chrysotile combined with MNNG greatly decreased mutations compared with MNNG alone. The authors concluded that chrysotile interacted synergistically with B(a)P but not MNNG, and that this may underlie asbestos's co-carcinogenicity with cigarette smoking.

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: a gene mutation assay at the HGPRT gene, with cells exposed to chrysotile, chemicals, or both for 3 days. The cells then had an 18-day expression period and were reseeded for a 2-week selection in 6-thioguanine-containing medium. The mutant colonies were then fixed, stained and counted.
• Who was studied: Adult rat liver-derived epithelial cells (line ARL-18) grown in culture at the Naylor Dana Institute for Disease Prevention, Valhalla, New York. The journal received the article in March 1982. The table reports three experiments, and each value is the mean of six flasks.
• Exposure: UICC standard reference Canadian chrysotile B, supplied by the U.S. Environmental Protection Agency, at concentrations stated as 10^-3 to 10^-1 mg/ml. It was given for 3 days, alone or together with benzo[a]pyrene or MNNG. The benzo[a]pyrene concentration is unreadable in the text; MNNG was given at 2.5 x 10^-5 M.
• Main results:
  • Chrysotile at 0.1 mg/ml was toxic to the cells and slowed their growth.
  • Chrysotile alone produced no significant increase in mutations.
  • B(a)P alone caused mutations.
  • Cells exposed to chrysotile and B(a)P together yielded more mutants than cells exposed to either substance alone. The size of the increase varied, but the authors described it as consistently substantial.
  • Cells exposed to chrysotile and MNNG together had greatly decreased mutant recovery compared with MNNG alone.
• The authors' conclusion: The authors concluded that chrysotile interacted synergistically with B(a)P but not with MNNG. They wrote that asbestos, although not mutagenic by itself, can act as a co-mutagen with certain polycyclic aromatic hydrocarbon carcinogens. They added that this may also underlie its co-carcinogenicity with cigarette smoking.

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.

Related studies

• 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)
• Absence of mutagenic activity of three forms of asbestos in liver epithelial cells — B. Reiss, S. Solomon, et al. (1982)
• Studies on in vitro chrysotile-pleural mesothelial cell interaction: morphological aspects and metabolism of benzo-3,4-pyrene — M.C. Jaurand, I. Bastie-Sigeac, et al. (1983)
• Coinhibition of viral interferon induction by benzo[a]pyrene and chrysotile asbestos — N. Hahon, J.A. Booth (1986)
• Presentation of benzo(a)pyrene to microsomal enzymes by asbestos fibers in the Salmonella/mammalian microsome mutagenicity test — K. Szyba, A. Lange (1983)
• On the mechanism of cogenotoxic action between ingested amphibole asbestos fibres and benzo[a]pyrene: I. Urinary and serum mutagenicity studies with rats — C. Varga, G. Horváth, et al. (1998)

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