lung cancer. Nevertheless, some still argued that the association was unwarranted because no-one had produced the disease in laboratory animals.39 In a summary of the evidence, Northrup states that the ‘. . . . inability to induce experimental cancers, except in a handful of cases, during 50 years of trying, casts serious doubt on the validity of the cigarette-lung cancer theory.’40 Health warnings were delayed costing many lives. Yet despite years of further experimentation, it proved ‘difficult or impossible’ to induce lung cancer in animals using the method (inhalation) by which people are exposed to the smoke.41 Indeed, if one rat experiment is to be believed, smoking can reduce the risk of cancer!42
The first reports of an association between asbestos and lung cancer came during the 1930s following examination of people who had died with asbestosis. But attempts to induce cancer in animals repeatedly failed and despite further epidemiological evidence from exposed workers (in 1949 and again in 1955), the carcinogenic action of asbestos was doubted until the 1960s.43 Prior to this, researchers pointed out that ‘. . . a large literature on experimental studies has failed to furnish any definite evidence for induction of malignant tumours in animals exposed to various varieties and preparations of asbestos by inhalation or intratracheal injection.’44
An insight into the thinking of animal researchers is given by studies of the carcinogenic effects of silica. Experiments on rats, mice and hamsters have revealed ‘striking’ differences in the toxic effects of silica on the lung. Rats were the most susceptible with many animals developing cancer. In contrast, hamsters were quite resistant to the chemical.45 Species differences like this would appear to invalidate the use of animals for carcinogenicity studies and stress the importance of epidemiology. Indeed, observational studies of workers with silicosis, a well-known lung disease, have shown that silica is a human carcinogen. However, in reviewing the evidence, the Laboratory of Experimental Pathology at America’s National Cancer Institute claims that ‘animal models of human diseases continue to provide critical and indispensable tools for the detection of carcinogenic effects . . .’ It is argued that the different reactions of rats, mice and hamsters may be used to represent human subjects with different levels of susceptibility to silica.45
Animal tests have also provided contradictory results in studies of diet and cancer. Epidemiological research has repeatedly shown that diets rich in fruit and vegetables can protect against cancer and cardiovascular disease. Not content with this, scientists have tried to find the life-saving ingredient of fruit and vegetables. Animal experiments have suggested that vitamin A and beta carotene may be responsible,46 and a number of human trials have been carried out to test the effects of these supplements. However, in people the supplements have no beneficial effects and may even be harmful, increasing the risk of cancer in some trials.47 There is still no substitute for eating a lot of fruit and vegetables.
It is not only cancer research where animal data has undermined human evidence. Emphasis on animal research rather than human studies delayed a proper understanding of poliomyelitis for over 25 years. Following >>
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