Animals and tobacco smoke
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Methods
The first recorded attempts to artificially induce animal tumors through the application of tobacco products occurred in 1911.[1] A 2004 series of monographs released by the International Agency for Research on Cancer, a part of the World Health Organisation, summarized research from the 1960s onwards about the carcinogenicity of tobacco on various laboratory animals.[1]
As set out in the IARC monographs, the carcinogenicity of cigarette smoke is determined in two ways. The first is through the application of cigarette-smoke condensates to skin. Cigarette-smoke condensates are collected by passing smoke through cold traps and recovering the retained material. The cigarettes are usually machine-smoked and the material is washed from the traps using a volatile substance such as acetone, which is then removed. Many of the procedures for collecting this cigarette-smoke-condensate have not yet been standardized across laboratories, including how the condensate is stored, in what numbers and fashion the cigarettes are smoked, and the type of solvent used. Once the condensate is collected, it is painted onto the skin of the animal test subjects, which are then examined at set intervals to assess the growth of tumors.
The second method, as described by the IARC monographs, used to measure the carcinogenicity of cigarette smoke to animals is by exposing them to mainstream cigarette smoke. The IARC monographs define mainstream cigarette smoke as that which is emitted by the mouth end of the cigarette and therefore the smoke that human smokers would be exposed to most. The IARC monographs describe the methods and equipment that scientists have developed to make more effective and standardize the deliverance of mainstream cigarette smoke. These devices vary between whole-body and nose-only exposure, but typically involve machine smoked cigarette smoke being pumped into a small chamber that contains the animal test subjects. A variety of factors differentiate the experience of a human smoker from these animal test subjects'. Human smokers inhale smoke voluntarily and therefore do so more deeply than do animal test subjects which typically adopt short, shallow breaths when exposed to smoke. The animal test subjects, primarily rodents and dogs, also have significantly morphologically different upper respiratory system from humans. Despite these variables, the doses of smoke administered to these animals can be determined by examining tissue and blood samples. Dogs, which cannot be exposed to cigarette smoke via inhalation chambers as easily as can small rodents, require different methods of cigarette smoke exposure. These methods include thracheostomy, in which smoke is pumped through a tube directly into a hole cut in the dog's throat, or through a mask fitted to the dog's face.[1]
Results
The IARC monographs concluded that the application of cigarette-smoke condensates onto the skin of mice induces tumors, of both benign and malignant variety. Although the carcinogenicity of tobacco smoke was first established in humans, various types of animals have also been exposed to tobacco smoke inhalation in attempts to yield further experimental proof and control for various experimental factors, including types of tobacco and levels of exposure, which would be considered unethical in human studies. The IARC monographs, referencing studies which used various methods of smoke inhalation, concluded that a significantly greater number of pulmonary tumors occurred among mice exposed to smoke than those in the control groups. Since the 1960s, the animal most used in testing the carcinogenicity of tobacco smoke has been the Syrian Golden Hamster due to its resistance to pulmonary infections and the infrequency with which it spontaneously develops pulmonary tumors.[1] According to the IARC monographs these studies have proven, and repeatedly confirmed, the carcinogenicity of tobacco smoke for hamsters.
Some studies referenced in the IARC monographs found that certain, but not all, groups of rats exposed to mainstream smoke were significantly more likely to develop lung tumors. The IARC monographs also referenced studies involving rabbits and dogs that were much less conclusive. The authors, however, cited various experimental limitations, such as small test or control groups and missing data, that could account for the lack of conclusive results.[1]
Effects of environmental tobacco smoke
Multiple studies have also been conducted to determine the carcinogenicity of environmental tobacco to animals. These studies typically fall under the categories of simulated environmental tobacco, administering condensates of sidestream smoke, or observational studies of cancer among pets.
Simulated environmental tobacco smoke
To study the consequences of passive smoking, scientists expose animals to sidestream smoke, that which emanates from the cigarette's burning cone and through its paper, or a combination of mainstream and sidestream smoke.[1] The IARC monographs conclude that mice with prolonged exposure to simulated second-hand smoke, that is six hours a day, five days a week, for five months with a subsequent four-month interval before dissection, will have significantly higher inicidence and multiplicity of lung tumors than with control groups.
Condensates of sidestream smoke
The IARC monographs concluded that sidestream smoke condensates had a significantly higher carcinogenic effect upon mice than did mainstream smoke condensates.[1]
Observational studies in pets
Second-hand smoke is recognized as a risk factor for cancer in pets.[2] A study conducted by the Tufts University School of Veterinary Medicine and the University of Massachusetts Amherst linked the occurrence of feline oral cancer to exposure to environmental tobacco smoke through an overexpression of the p53 gene.[3] Another study conducted at the same universities concluded that cats living with a smoker were more likely to get feline lymphoma; the risk increased with the duration of exposure to second-hand smoke and the number of smokers in the household.[4] A study by Colorado State University researchers, looking at cases of canine lung cancer, was generally inconclusive, though the authors reported a weak relation for lung cancer in dogs exposed to environmental tobacco smoke. The number of smokers within the home, the number of packs smoked in the home per day, and the amount of time that the dog spent within the home had no effect on the dog's risk for lung cancer.[5]
In 1990, a tobacco-industry researcher in Germany proposed a study of the effects on animals of lifetime exposure to second-hand smoke. The proposed study was blocked by Philip Morris,[6] as described in an internal company report:
PM [Philip Morris] recently succeeded in blocking Adlkofer's plan to conduct lifetime animal inhalation study of sidestream smoke. (... an INBIFO study has shown that in 90-day inhalation test, no non-reversible changes has [sic] been detected. In a lifetime study, the results were almost certain to be less favorable. Based on the analysis, the other members of the German industry agreed that the proposed study should not proceed).[7]
A 2008 study conducted by the Henry Ford Health System found that given information about the harmful effects of passive smoking on their pets, 28.4% of pet owners who smoke would be motivated to quit, 8.7% would ask those who live with them to quit, and 14.2% would stop smoking indoors.[8]
