Anti-Tobacco Experiments On Laboratory Animals
Animal rights activists have been brought on board the anti-smoking gravy train. Railing against the tobacco industry for testing its products on laboratory rodents, the activists turn a blind eye to the absolutely horrible experiments on higher animals such as dogs and cats to prove how bad smoking is.
In the earliest experiments (1950s or early 1960s) the "beagles were strapped side-by-side to a long bench, in a rather unnatural upright position. They were fitted with face masks, which forced them to inhale and exhale smoke from lighted cigarettes. A mechanical device lit a new cigarette and dropped it into the air line as soon as an old one was used up.
Colby writes, "Although the Surgeon General later claimed the smoking machines did not force animals to inhale and exhale deeply, the newsreel footage sure make it look as if the dogs were inhaling and exhaling deeply."
Colby then describes an experiment by government scientist Oscar Auerbach et al which was cited in the Surgeon.General's report of 1971. In this one, the government scientists slit the throats of 78 Beagles and inserted mechanisms in these "tracheotomies" which enabled the dogs to "smoke" through their throats. Supposedly (according to Colby's account) among the dogs who managed to survive for 875 days, there were no deaths among the 8 "non-smoking" dogs, but 24 deaths among the smoking dogs. The deaths among the smoking dogs was from various causes such as "aspiration of food" and lung fibrosis. None of the dogs contracted lung cancer. This experiment was again described in the 1977 S.G.'s report. The 1982 S.G.'s report also described it. Chapter 9, In Defense of Smokers
Not covered by Colby but listed in the Center for Disease Control's Bibliography of Continuing Studies on Smoking and Health, 1984-85 is a study on the effect of tobacco to the circulatory system. In this one, the legs of the dogs were completely severed except for the major arteries. The dogs, still living, were monitored for extended periods while the researchers kept track of the effects of nicotine on the circulatory system. Presumably they were unconscious during these tests.
Ten dogs had their chest cavities opened so that their coronary arteries could be mechanically manipulated to reduce blood flow. The dogs were forced to breathe cigarette smoke, then treated with Ethanol. Ethanol then cigarette smoke, cigarette smoke then Ethanol.1
Alcohol and Smoking
15 dogs were subjected to 30 experiments where Ethanol ingestion was combined with tobacco smoke inhalation. The purpose was to prove that smoking and drinking are bad for the heart.2
For a change, no animals were pierced, cut, strapped down, rendered unconscious, shot up with dangerous substances or forced to breath tobacco smoke through tracheotomies. Instead two veterinary teaching hospitals examined pet dogs in the comfort of their own homes. Exposure levels to secondhand smoke were assessed. Disappointingly, the researchers found no dose response, no statistical significant risk.3
PETA's sly innuendo that animals are at risk from secondhand smoke is preposterous given the results of the tests on animals looking for that non-existent link. Of course lab studies haven't been able to induce lung cancer in dogs exposed to any amount of smoke, including those poor dogs given tracheotomies and having smoke pumped into their lungs.
Finding just the right animal for anti-tobacco experimentation
It's doubtful that the horrifying experiments as described above have increased the knowledge of tobacco smoke yet the cruel research continues. If at first you don't succeed, try, try again. If a particular animal doesn't react as it should, then chose another beast to torture.
"To increase our understanding of biological systems, the first step is to make an observation at the level of organization that we wish to understand. It has yet to be conclusively shown that any laboratory animal has contracted emphysema solely as a result of exposure to cigarette smoke. Available mechanism-of-response studies at the tissue, cellular, or biochemical level of organization are not useful in elucidating the relationship between emphysema and exposure to cigarette smoke without an animal model for the disease. If progress in understanding the etiology of emphysema from cigarette smoking is judged to be important to the scientific and regulatory communities, the highest priority should be given to discovering a suitable animal model." Regul Toxicol Pharmacol 1989 Dec;10(3):264-71 Related Articles, Links, Use of laboratory animal models in investigating emphysema and cigarette smoking in humans. Thomas RD, Vigerstad TJ. National Research Council, Washington, DC 20418.
By hitching up with anti-tobacco, PETA is aligning itself with a group of people whose cruelty to animals during the course of twisted, senseless experiments is repugnant to most people, and certainly to the majority of its supporters. Its willingness to turn a blind eye to the atrocities practiced by anti-tobacco on animals indicate that PETA is more concerned with funding a campaign to denigrate an American industry than to persuade the public to pressure scientists and researchers to stop the needless suffering of laboratory animals.
On a positive note, the association between PETA and anti-tobacco may be a good thing. PETA is becoming increasingly unpopular with the public for its radical and sometimes violent tactics. Anti-tobacco is increasingly viewed in a negative light as well. The violence inspired, such as the beating death of a 13 year-old-boy because he was suspected of supplying cigarettes to kids, the demonization of individuals who question anti-tobacco's motives and tactics as well as the glaringly obvious greed common to all those who work for anti-tobacco is taking its toll. Linking two increasingly unpopular causes can only highlight the negativity each is inflicting on the public.
The report about PETA's new anti-tobacco campaign can be viewed on The New York Time's website. Free registration is required.
Cardiovasc Res 1988 Jan;22(1):73-8 Related Articles, Links
Relative effects of cigarette smoke and ethanol on acute platelet thrombus formation in stenosed canine coronary arteries.
Keller JW, Folts JD.
Department of Medicine, University of Wisconsin Medical School, Madison.
In 10 open chest dogs with mechanically stenosed coronary arteries acute platelet thrombus formation with subsequent embolisation reduced coronary blood flow cyclically by -10.2(3.3) ml.min-2 (as measured with an electromagnetic flow probe). Ventilating the dogs with cigarette smoke increased the flow reduction to -13.5(4.6) ml.min-2. Ethanol 1.0 ml.kg-1 iv completely abolished acute thrombus formation and flow reductions in all 10 dogs. Repeat ventilation with cigarette smoke after ethanol failed to renew flow reductions in nine of the 10 dogs. It is suggested that ethanol effectively inhibits the exacerbating effects of cigarette smoke on acute platelet thrombus formation when both are being used simultaneously.
J Cardiovasc Pharmacol 1998 Jun;31(6):930-6 Related Articles, Links
Combined effects of alcohol and nicotine on cardiovascular performance in a canine model.
Mehta MC, Jain AC, Billie M.
Department of Medicine, West Virginia University School of Medicine, Robert C. Byrd Health Sciences Center, Morgantown 26506-9157, USA.
Alcohol and tobacco consumption are correlated. Smokers consume more alcohol than do nonsmokers, and alcohol consumers smoke more than do teetotalers. The independent effects of alcohol and nicotine on the cardiovascular system are well documented, but combined effects of short-term administration are unknown. This experimental work was designed to study the effects due to short-term administration of alcohol and nicotine on cardiovascular system. In phase I, 30 experiments were performed to study the dose-response curve of both the drugs. In phases II and III, 15 dogs were subjected to 30 experiments. In phase II, ethanol, 400 mg/kg, was given i.v., followed by nicotine 50 microg/kg, i.v., and in phase III, sequence of drug administration was reversed to study the effects on hemodynamics and coronary artery blood flow. The dose-response curve established the i.v. dose of ethanol, 400 mg/kg, and nicotine, 50 microg/kg. Ethanol administration caused a nonsignificant increase in heart rate (HR), mean arterial pressure (MAP), left ventricular systolic pressure (LVS), and left ventricular mechanical work (LVMW), and a decrease in maximal rate of increase of LV pressure per second (dP/dt), stroke volume (SV), and systemic vascular resistance (SVR). Left ventricular end-diastolic pressure (LVEDP), pulmonary artery mean pressure (PAM), right atrial pressure (RAP), pulmonary vascular resistance (PVR), myocardial oxygen consumption (MVO2), and average peak velocity of coronary blood flow (APV) had mild significant increases as compared with controls. Nicotine significantly increased heart rate, mean arterial pressures, LVEDP, and pulmonary artery, pulmonary capillary wedge, and right atrial pressures. Nicotine increased dP/dt (2,062-3,188; p < 0.006) and decreased APV (9 to 8; p < 0.03). Combined ethanol followed by nicotine had synergistic increase in HR, SD, MAP, LVS, LVEDP, pulmonary pressures, CO, SV, dP/dt (2,184 > 5,206; p < 0.005), MVO2, and LVMW. However, the excitatory effects of nicotine were attenuated when ethanol was administered after nicotine (dP/dt, reduced from 2,058 to 1,653; p < 0.04, and APV increased from 10 to 12; p < 0.02). We conclude that ethanol increased APV but had nonsignificant effects on the hemodynamics, whereas nicotine reduced the APV and had significant excitatory responses. In combination (i.v.), ethanol + nicotine produced significant synergistic excitatory effects. On the other hand, the nicotine + ethanol combination increased APV and caused attenuation of the excitatory effects of nicotine in dogs.
Am J Epidemiol 1992 Feb 1;135(3):234-9 Related Articles, Links
Passive smoking and canine lung cancer risk.
Reif JS, Dunn K, Ogilvie GK, Harris CK.
Department of Environmental Health, Colorado State University, Fort Collins 80523.
A case-control study was conducted to determine whether household exposure to environmental tobacco smoke is associated with an increased risk for lung cancer in pet dogs. Lung cancer cases and controls with other forms of cancer were obtained from two veterinary teaching hospitals during 1985-1987. Exposures assessed included the number of smokers in the household, the amount smoked, and the proportion of time spent indoors by the pet. A weak relation was found for exposure to a smoker in the home (odds ratio = 1.6, 95% confidence interval 0.7-3.7), after controlling for confounding in stratified analyses. Strong evidence for a further increase in risk associated with more than one smoker in the home was not found, nor was a significant trend observed for increasing number of packs of cigarettes smoked per day or an exposure index based on number of smokers in each household, packs smoked per day, and the proportion of time the dog spent within the home. However, skull shape appeared to exert effect modification; the risk was restricted to breeds with short and medium length noses (odds ratio = 2.4, 95% confidence interval 0.7-7.8). Despite the inconclusive findings of the current study, epidemiologic studies in pet animals may add to our understanding of environmental tobacco smoke effects in human populations.