Investigations on the effects of chronic cigarette-smoke inhalation in Syrian golden hamsters

Our plain-English summary of Investigations on the effects of chronic cigarette-smoke inhalation in Syrian golden hamsters, by W. Dontenwill, H.J. Chevalier, H.P. Harke, et al (Journal of the National Cancer Institute, 1973).

The study

• Authors: W. Dontenwill, H.J. Chevalier, H.P. Harke, U. Lafrenz, G. Reckzeh, B. Schneider
• Journal: Journal of the National Cancer Institute
• Published: 1973;51(6):1781-832
• Cited by: 127 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

In plain English

This long-term experiment used 4440 male and female Syrian golden hamsters; 3610 were used for their entire lifespans and 830 were exposed for no longer than 52 weeks. Groups received machine-generated smoke from reference or modified cigarettes 5 days a week, the vapor phase of smoke, fresh air only, no treatment, or the carcinogens DMBA or DENA. Two groups received one intratracheal dose of Blue Cape asbestos from a factory exhaust air filter, alone (group 13) or followed by smoke (group 12). The most severe changes were in the larynx. Smoke-exposed animals had many severe epithelial alterations (stages 3 to 5) and early invasive carcinomas (stage 6). Among 960 untreated and air-exposed controls, one animal showed a stage 2 change. Smoke shortened survival compared with untreated controls and raised red-cell counts and hemoglobin. Asbestos-treated lungs showed prominent pigment-free macrophages. The asbestos-alone group had no laryngeal changes of stages 2 to 6. In the larynx, smoke plus asbestos gave almost the same result as smoke alone. The authors judged the asbestos dose too low and concluded the combined results could not be evaluated.

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: Long-term cigarette-smoke inhalation experiment in hamsters. 3610 animals were used for their entire lifespans, and 830 were exposed for no longer than 52 weeks. Some groups received additional carcinogens or asbestos.
• Who was studied: 4440 male and female Syrian golden hamsters from Zucca's Hamstery, Vineland, N.J., aged 8 weeks at the start. Most groups, including asbestos groups 12 and 13, had 80 females and 80 males. 3610 animals were used for their entire lifespans. Not all groups were exposed to smoke: there were untreated controls (groups K and 3) and a fresh-air placebo group (group 8).
• Exposure: Smoke of 30 cigarettes once, twice or three times a day, 5 days a week, from reference and modified cigarettes. Two groups received Blue Cape asbestos from a factory exhaust air filter. Fiber length was graded by sieve to 50-60 micrometres. The dose was 0.05 ml of a 1% suspension given into the windpipe: alone (group 13) or followed by smoke of 30 reference cigarettes twice a day (group 12). Other groups received DMBA (into the windpipe) or DENA (by injection).
• Main results:
  • Among the 960 untreated and air-exposed control animals, there were no laryngeal changes or only slight stage 1 changes, with one stage 2 change. Smoke-exposed animals had many severe laryngeal alterations (stages 3 to 5) and early invasive carcinomas (stage 6).
  • Smoke-exposed hamsters had significantly shorter survival than untreated controls. In males, survival shortened more as the dose increased.
  • In animals exposed to smoke for up to 46 weeks, hemoglobin and red-cell counts increased. White-cell counts did not change.
  • Animals exposed to the vapor phase of smoke only (group 7) had no laryngeal changes of stages 2 to 6. The authors assumed the carcinogenic factors were mainly in the particulate phase.
  • At the same number of cigarettes, the greatest reduction in laryngeal response came from cigarettes with acetate or cellulose filters, reconstituted tobacco sheets with or without sodium nitrate, and 'black' cigarettes.
  • Stage 5 and 6 laryngeal changes were more frequent in group 1 (DMBA plus smoke) than in groups 2 (DMBA alone) and 5 (smoke alone) added together. The authors read this as a more-than-additive effect.
  • Pigment-free macrophages were prominent in the lungs of asbestos-treated animals (groups 12 and 13). Asbestos particles and ferrous pigment deposits were also frequent.
  • The asbestos-alone group (group 13) showed no laryngeal changes of stages 2 to 6.
  • In the larynx, smoke plus asbestos (group 12) produced similar results to the same smoke dose without asbestos (group 5). The group 12 animals entered the experiment about 6 months later.
  • Measurements did not show a distinct increase in pulmonary emphysema in animals exposed to smoke for a long time at high doses.
• The authors' conclusion: The authors concluded that the results of the combined asbestos and smoke experiments could not be evaluated because the amount of asbestos applied was too small.
• Limitations the authors state:
  • The authors stated the asbestos dose was too low, as shown by the minor lung changes in the asbestos-alone group.
  • The authors stated that the effective smoke dose on the hamster larynx was many times greater than the dose per surface area in the human respiratory tract, so exact comparison with human smoking is not possible.
  • Handling in the smoking unit itself shortened survival: fresh-air placebo animals lived less long than untreated controls.

Related studies

• Inhalation studies with Syrian golden hamsters — A.P. Wehner, B.O. Stuart, et al. (1979)
• 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)
• 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)
• Chronic inhalation of asbestos and cigarette smoke by hamsters — A.P. Wehner, R.H. Busch, et al. (1975)
• Chronic effects of dietary exposure to amosite and chrysotile asbestos in Syrian golden hamsters — E.E. McConnell, A.M. Shefner, et al. (1983)
• Aryl hydrocarbon hydroxylase induction in mitogen-stimulated lymphocytes by benzanthracene or cigarette tars adsorbed to asbestos fibers — T.L. McLemore, W.T. Jenkins, et al. (1979)

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