Inhalation studies with Syrian golden hamsters

Our plain-English summary of Inhalation studies with Syrian golden hamsters, by A.P. Wehner, B.O. Stuart, C.L. Sanders (Progress in Experimental Tumor Research, 1979).

The study

• Authors: A.P. Wehner, B.O. Stuart, C.L. Sanders
• Journal: Progress in Experimental Tumor Research
• Published: 1979;24:177-98
• Cited by: 11 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

The Syrian golden hamster has been used in our laboratory for chronic inhalation studies in which we investigated the biological effects of cigarette smoke, chrysotile asbestos, NiO, CoO, the latter three materials in combination with cigarette smoke, talc baby powder, radon daughters, uranium ore dust, diesel engine exhaust, radon daughters in combination with uranium ore dust, and radon daughters in combination with uranium ore dust and diesel engine exhaust, asbestos cement, fly ash, and plutonium dioxides. Exposure to asbestos (23 µg/l respirable aerosol concentration, 7 h/day, 5 days/week) for 11 months resulted in asbestosis in all animals, in an increased incidence of lung adenomas, indicating an early neoplastic response, and in a shorter life-span. Life-span exposures to NiO (53 µg/l and to CoO (10 flog/l) resulted in pneumoconiosis. Life-span exposure to cigarette smoke (3 x/day, 5 days/week, in Hamburg II smoking machines) decreased body weight and increased the incidence of tumors and epithelial lesions of the larynx. The increased incidences in the smoke-exposed hamsters were not necessarily caused by the smoke exposures, but might be explained by the significantly longer life-span of the smoke-exposed hamsters. Exposure to talc baby powder (8 µg/l up to 150 min/day, 5 days/week, up to 300 days) caused no significant changes. Exposure to 1,200 working levels of radon daughters 6 h/day, 5 days/week for 15 months produced severe epithelial proliferation culminating in pulmonary squamous carcinoma; the same exposure in combination with 15 µg/l uranium ore dust also produced invasive carcinoma. Exposure to 15 µg/l uranium ore dust alone caused pneumoconiosis and epithelial proliferation. Daily (6 h/day, 5 days/week) life-span exposures to diesel engine exhaust (50±2 ppm CO) caused accumulation of soot in alveolar macrophages, with emphysema, fibrosis and cuboidal metaplasia; the same exposure plus radon daughters and uranium ore dust caused acceleration of these effects plus pulmonary squamous metaplasia. Exposure to 238PuO2 and 239PuO2 particles in male and female Syrian golden hamsters produced a significant life-span shortening only in male hamsters with the highest deposition. Radiation pneumonitis and fibrosis and epithelial metaplasia of the lung were increased with increasing radiation dose. Only 3/448 life-span hamsters developed malignant lung tumors, all adenocarcinomas and all at initial alveolar depositions> 160 nCi. It was concluded that the hamster was resistant to lung tumor formation following inhalation of alpha-emitting radionuclides. Results of the inhalation studies with asbestos cement and with fly ash are not yet available.

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

In plain English

Researchers at Battelle Pacific Northwest Laboratories summarized their own hamster inhalation experiments with cigarette smoke, chrysotile asbestos, nickel and cobalt oxides, talc baby powder, uranium mine contaminants and plutonium dioxide. In the asbestos part, groups of 51 male hamsters breathed chrysotile asbestos dust 7 hours a day, 5 days a week, with or without cigarette smoke. All developed asbestosis, and exposure was stopped after 11 months. Of 12 lung adenomas (benign tumors) among 510 hamsters, 10 were in the 102 asbestos-exposed animals; the authors called this an early neoplastic response. They observed neither a cancer-causing effect of asbestos nor a cocarcinogenic effect of cigarette smoke. Laryngeal lesions and malignant tumors were significantly less common with asbestos plus smoke than with smoke alone. The authors suggested this was perhaps because asbestosis shortened life-span. Talc baby powder did not affect body weight, survival or tissue changes compared with sham-exposed controls. The authors suggested this appears due to cosmetic-grade talc lacking asbestos fibers. The authors concluded that their random bred hamsters were unsatisfactory for producing primary lung cancer from inhaled agents, but acceptable for studying emphysema and fibrosis.

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: Overview of the authors' own laboratory animal inhalation experiments (several studies, most published separately)
• Who was studied: Outbred Syrian golden hamsters at Battelle Pacific Northwest Laboratories, Richland, Washington. In the asbestos/smoke cocarcinogenesis studies, each treatment group had 51 male hamsters, about 2 months old at the start (510 hamsters in total, 102 in the two asbestos groups).
• Exposure: Chrysotile asbestos aerosol at a mean respirable concentration of 23 micrograms per liter, 7 hours a day, 5 days a week, alone or together with cigarette smoke (three 10-minute exposures a day). Other groups received nickel oxide, cobalt oxide or diethylnitrosamine. The article also covers separate experiments with talc baby powder, radon daughters, uranium ore dust, diesel exhaust and plutonium dioxide.
• Main results:
  • Asbestos-exposed hamsters: all developed asbestosis. The authors reported an increased incidence of lung adenomas and a shorter life-span after 11 months of exposure.
  • Of 12 lung adenomas found in all 510 hamsters, 10 occurred among the 102 asbestos-exposed animals.
  • The authors observed neither a carcinogenic effect of asbestos nor a cocarcinogenic effect of cigarette smoke in the asbestos groups.
  • Laryngeal lesions and malignant tumors were significantly less common in the asbestos plus smoke group than in the smoke-exposed control group. The authors said this was perhaps because asbestosis shortened life-span.
  • Asbestos plus smoke hamsters lived on average 13.4 months on experiment, compared with 12.5 months for asbestos plus sham smoke (7% longer). This difference was not statistically significant at the p = 0.05 level. The authors stated that asbestosis shortened the life-span of the asbestos plus smoke group.
  • Talc baby powder inhalation had no effect on body weight, survival or type, incidence or degree of tissue changes compared with sham-exposed controls. The authors suggested the reason appears to lie in cosmetic-grade talc not containing asbestos fibers, unlike industrial-grade talc.
  • In the plutonium dioxide studies, 3 of 448 hamsters observed over their life-spans developed malignant lung tumors, all adenocarcinomas.
• The authors' conclusion: The authors concluded that the Syrian golden hamster is an acceptable model for studying emphysema and fibrosis-causing (pneumoconiotic) effects of inhaled materials. For carcinogenesis or cocarcinogenesis studies aimed at producing primary lung cancer from inhaled agents, they said an inbred strain or a different species should be used, because their random bred animals were unsatisfactory for this purpose.
• Limitations the authors state:
  • The shortened life-span caused by asbestosis may explain the lower incidence of laryngeal lesions and malignant tumors in the asbestos plus smoke group.
  • The increased tumor and larynx lesion incidences in smoke-exposed hamsters might be explained by their longer life-span rather than by the smoke itself.
  • The random bred hamsters used were unsatisfactory for studying the development of primary lung cancer in response to inhaled carcinogenic agents.

Topics

The National Library of Medicine indexes this study under subjects our site covers: Talc and vermiculite.

Medical terms in this study, explained in our Lexicon: Chrysotile, Talc, Asbestos-Cement, Pneumoconiosis, Carcinoma, Alveolar Macrophage, Emphysema, Fibrosis.

Related studies

• Investigations on the effects of chronic cigarette-smoke inhalation in Syrian golden hamsters — W. Dontenwill, H.J. Chevalier, et al. (1973)
• Studies on the inhalation toxicology of two fiberglasses and amosite asbestos in the syrian golden hamster. Part I. Results of a subchronic study and dose selection for a chronic study — T.W. Hesterberg, C. Axten, et al. (1999)
• Studies on the inhalation toxicology of two fiberglasses and amosite asbestos in the Syrian golden hamster. Part II. Results of chronic exposure — E.E. McConnell, C. Axten, et al. (1999)
• Chronic effects of dietary exposure to amosite and chrysotile asbestos in Syrian golden hamsters — E.E. McConnell, A.M. Shefner, et al. (1983)
• Chronic inhalation of asbestos and cigarette smoke by hamsters — A.P. Wehner, R.H. Busch, et al. (1975)
• Chronic inhalation study of fiber glass and amosite asbestos in hamsters: twelve-month preliminary results — T.W. Hesterberg, C. Axten, et al. (1997)

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