Use of hamster tracheal organ cultures for assessing the cocarcinogenic effects of inorganic particulates on the respiratory epithelium

Our plain-English summary of Use of hamster tracheal organ cultures for assessing the cocarcinogenic effects of inorganic particulates on the respiratory epithelium, by B.T. Mossman, J.E. Craighead (Progress in Experimental Tumor Research, 1979).

The study

• Authors: B.T. Mossman, J.E. Craighead
• Journal: Progress in Experimental Tumor Research
• Published: 1979;24:37-47
• Cited by: 25 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Polycyclic hydrocarbons bound to 'carrier' particulates cause respiratory tract neoplasms when instilled into laboratory animals by the intratracheal route. To elucidate the changes induced by carcinogens and selected inorganic particles in the respiratory epithelium, tracheal organ cultures were prepared from female BIO 15.16 golden Syrian hamsters. Explants were exposed to 3-MC coated onto either ferric oxide (Fe2O3) or crocidolite asbestos. Control tissues were treated with particulates without 3-MC. At intervals, the cultures either were examined morphologically or implanted subcutaneously into syngeneic hamsters. The amounts of 3-MC required to induce tumors with Fe2O3 were greater than with asbestos. Dose-response determinations indicated a degree of precision in these studies unattainable in whole animal models of respiratory carcinogenesis.

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

In plain English

This laboratory study used pieces of windpipe (tracheal explants) from 6- to 8-week-old female BIO 15.16 golden Syrian hamsters, kept in culture. The explants were exposed to the chemical carcinogen 3-methylcholanthrene (3-MC) coated onto either ferric oxide (Fe2O3) particles or crocidolite asbestos. Control explants got the particles without 3-MC. After 24 hours to 4 weeks, tissues were examined under the microscope or implanted under the skin of same-strain hamsters. Both particle types were retained in the lining tissue. Explants given 3-MC-coated particles showed intense overgrowth and abnormal cells but no invasive cancer in culture. After implantation, explants given particles alone produced no tumors. With ferric oxide, 13 of 42 explants given 10 micrograms of 3-MC developed tumors. With asbestos, 8 of 11 given 1.4 micrograms did, as did 1 of 11 given 0.6 micrograms. Of the 22 tumors, 13 were carcinomas and 9 fibrosarcomas. The authors concluded that much smaller amounts of 3-MC were needed when asbestos was used. They called the tumor results preliminary.

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: Animal experiment using tracheal organ cultures (explants), which were examined in culture or implanted subcutaneously into syngeneic hamsters
• Who was studied: Tracheal explants from 6- to 8-week-old female golden Syrian hamsters of the BIO 15.16 strain, implanted into syngeneic weanling female hamsters. Over 100 explants were used in the tumor-induction studies.
• Exposure: 3-methylcholanthrene (3-MC) adsorbed onto ferric oxide (Fe2O3) or crocidolite asbestos (UICC reference sample). Controls received the particulates without 3-MC. Doses were 0, 5 or 10 micrograms of 3-MC per explant on Fe2O3, and 0, 0.6, 0.8 or 1.4 micrograms per explant on asbestos.
• Main results:
  • Particles of both Fe2O3 and asbestos were retained within the mucosa and submucosa, both in culture and after implantation into animals.
  • Explants exposed to 3-MC-coated particulates showed intense hyperplasia and squamous metaplasia, often with dysplasia. No frank neoplastic transformation or invasion was seen in culture.
  • No tumors developed after implantation of explants that received particulates without 3-MC.
  • Fe2O3 groups: 0/24 tumors at 0 micrograms 3-MC per explant, 0/24 at 5 micrograms, and 13/42 at 10 micrograms.
  • Crocidolite asbestos groups: 0/11 tumors at 0 micrograms 3-MC per explant, 1/11 at 0.6 micrograms, 0/11 at 0.8 micrograms, and 8/11 at 1.4 micrograms.
  • Of the 22 tumors in total, 13 were carcinomas and 9 were fibrosarcomas.
  • The length of time explants were kept in culture before implantation did not appear to affect when tumors developed.
  • At higher concentrations of asbestos, the tissues showed cytotoxic changes and necrosis.
• The authors' conclusion: The authors concluded that 3-MC induced tumors with both carriers, but substantially smaller amounts of 3-MC were required when crocidolite asbestos rather than Fe2O3 was the carrier. They also stated that dose-response determinations gave a degree of precision unattainable in whole-animal models.
• Limitations the authors state:
  • The authors described the tumor-induction results as coming from preliminary studies.

Topics

Medical terms in this study, explained in our Lexicon: Epithelium, Neoplasm, Crocidolite, Dose-response relationship, Carcinogenesis.

Related studies

• Carcinoma induction by 3-methylcholanthrene in hamster tracheal tissue implanted in syngeneic animals — J.E. Craighead, B.T. Mossman (1979)
• Interaction of asbestos with metaplastic squamous epithelium developing in organ cultures of hamster trachea — C.D. Woodworth, B.T. Mossman, et al. (1983)
• Asbestos and benzo[a]pyrene act synergistically to induce squamous metaplasia and incorporation of [3H]thymidine in hamster tracheal epithelium — B.T. Mossman, A. Eastman, et al. (1984)
• Effects of cigarette smoke on epithelial uptake of non-asbestos mineral particles in tracheal organ culture — B. Keeling, J. Hobson, et al. (1993)
• Transfection of a manganese-containing superoxide dismutase gene into hamster tracheal epithelial cells ameliorates asbestos-mediated cytotoxicity — B.T. Mossman, P. Surinrut, et al. (1996)
• 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)

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