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Absurdly, researchers rely on animal data over human data. The animal-model approach is practiced even when the chemical is already known to cause cancer in humans, wasting tax dollars and precious time while people continue to get cancer from that carcinogen. When a chemical is found to cause cancer in humans, scientists run to their labs to duplicate this in animals. Usually, the cause and effect relationship is not observed in the animals, and the researchers conclude that the chemical is safe. This foolish system has kept carcinogenic substances available to humans, providing us with a false sense of security and our continued use of toxic substances.


Human cancer has been linked to asbestos since 1907, yet because animals did not contract cancer from repeated, high exposure to asbestos, it was deemed safe. Not until 1986, when the clinical and epidemiological evidence could no longer be ignored even by those within the asbestos lobby, did the Environmental Protection Agency recommend a ban on asbestos. In the interim, people suffered from cancer and died.


Nowhere is the failure of the animal-model in cancer research more apparent than with smoking. For over fifty years, researchers have been forcing animals to inhale smoke. These experiments cause distress and suffering, but not cancer. Therefore, despite immense clinical and epidemiological evidence proving the carcinogenicity of tobacco, smoking was deemed safe. Millions of smokers happily continued to light up, blissfully ignorant of the death sentence they were inflicting upon themselves.


Bear in mind that drugs affect children differently than adults, men differently than women, and there are even differences from person to person, demonstrating the dangers in applying data from another species altogether.


Even from rats to mice, results are disturbingly disparate. Data from the US National Toxicity Program shows rat and mouse tests for 214 chemicals differed 30% of the time.1 Another study comparing the outcome of mouse and rat studies found that 46% of carcinogens in one species were not carcinogenic in the other.2 If the same chemicals are not carcinogenic in rats and mice nearly half the time, how could we expect either to be an accurate test for human carcinogenicity?


Animal experiments suggested folic acid would help cancer patients. But it made the cancer worse. The industrial chemical benzene did not cause cancer in mice, and was therefore allowed to remain on the market. Unfortunately, it caused leukemia in humans. Once this was known, scientists were still unable to reproduce this effect in mice.


Human and non-human cancers differ greatly. Cancers in animals use blood vessels to keep growing; human cancers seem to grow their own blood vessels. Even when infected with a human cancer, the disease progresses differently in an animal. Differences in physiology, biology, and disease manifestation cause chemicals to have differing reactions between species. Of twenty compounds non-carcinogenic to humans, nineteen of these cause cancer in animals.


Mice are highly susceptible to tumors in certain areas of their bodies, such as their lungs. But a lung tumor from a mouse differs greatly from a lung tumor in a human, even though they occurred in the same region. This, coupled with the high instances of such cancers developing naturally in mice, makes them even less suitable as subjects for the study of human cancers. Conversely, some of the more common human tumors, such as colon cancer, are rare in rodents.


Many of the cancers that spontaneously develop in rodents are rarely seen in humans, and vice-versa.3 As an editorial in the journal 'Science' asked, "Are humans to be regarded as behaving biochemically like huge, obese, inbred cancer-prone rodents?" 4


1. L.B. Lave, et al. Nature 336 (1988) 632-3.

2. F.J. Di Carlo, Drug Metabolism Reviews 15 (1984): 409-13.

3. A. Monro, Regulatory Toxicology and Pharmcology 18 (1993): 115-35.

4. P.H. Abelson, Science 255 (1992): 141.