In Gauderman et al. 1997 at pp.208-209 the authors stated:
“The results from these analyses support previous findings that a major gene plays an important role in lung cancer risk. An additional finding not previously observed is that there is no apparent interaction between the putative lung cancer gene and smoking.”
At p.177 the authors wrote:
“[T]he flaws we found in the nicotine research literature are of such magnitude and occur in such a regular fashion that they demand an explanation. A partial list of the methodological shortcomings compiled in this book includes:
I Systematic exclusion of subjects from statistical analyses
Absence of saline control groups for injected drugs
Result-biased selection of number of sessions to test manipulations
Absence of statistical comparisons [...]“
Also, from the same book:
“Thus, nicotine’s role in maintaining the smoking habit bears no similarity to the role played by genuinely addictive drugs such as heroin, barbiturates, alcohol or other drugs to which nicotine is routinely compared.”
In Sommers 1972, Dr Sheldon C Sommers, Chairman of the Scientific Advisory Board to the Council for Tobacco Research, a physician specialising in pathology and Clinical Professor of Pathology at Columbia University College of Physicians and Surgeons and University of Southern California School of Medicine, gave evidence which included this statement, at p.96:
“[S]tatistical mathematics can never prove cause and effect. All they show is a relationship requiring further study, usually experiments in animals, to find out the meaningfulness biologically of this relationship. I really believe that among the active researchers in these fields, there is no great preponderance of feeling that cigarette smoke is carcinogenic.”
In Sommers 1976 Dr Sommers said at p.269:
“Now, as to lung cancer, there is a statistical association between cigarette smoking and lung cancer. But at present the nature of the association or whether it is causal are not known. The test of the original Surgeon General’s report [USSG 1964] deals with the difficulties of assigning causality, but the summary and conclusions brush these aside, and assign a causality not demonstrably evident in the text. It is widely known that a statistical association is not by itself proof of causation. A statistical association may point to experiments that will help to determine whether there is cause involved.”
Another:
In Furst 1982 Dr Arthur Furst, Director Emeritus of the Institute of Chemical Biology at the University of San Francisco, said at p.512:
“For many years, I tried to induce lung cancer in animals with cigarette smoke, with no success, despite the most sophisticated smoking machines available. Not only were my colleagues and I unsuccessful, but so was every other investigator. There have been a very small number of published reports of lung cancers occurring in experimental animals during smoke inhalation experiments. Anyone attempting to interpret these as showing that smoking causes lung cancer must understand that animals, like humans, do spontaneously develop lung cancer even in the absence of any suspected carcinogen.”
In explaining his conclusions as at September 2003, Professor Idle said that it was his judgment that cigarette smoking had not been established as a cause of human lung cancer. Indeed, as explained by him, the cause of cancer was unknown. Moreover, the mechanisms by which lung cancer developed were not known. Researchers had not produced squamous cell lung carcinoma in laboratory animals by inhalation exposure to cigarette smoke. No constituent or group of constituents, as they existed in the complex mixture which was cigarette smoke, had been shown to be a cause of lung cancer in smokers. In view of this, it could not be determined whether or not smoking caused lung cancer.
“The results from these analyses support previous findings that a major gene plays an important role in lung cancer risk. An additional finding not previously observed is that there is no apparent interaction between the putative lung cancer gene and smoking.”
At p.177 the authors wrote:
“[T]he flaws we found in the nicotine research literature are of such magnitude and occur in such a regular fashion that they demand an explanation. A partial list of the methodological shortcomings compiled in this book includes:
I Systematic exclusion of subjects from statistical analyses
Absence of saline control groups for injected drugs
Result-biased selection of number of sessions to test manipulations
Absence of statistical comparisons [...]“
Also, from the same book:
“Thus, nicotine’s role in maintaining the smoking habit bears no similarity to the role played by genuinely addictive drugs such as heroin, barbiturates, alcohol or other drugs to which nicotine is routinely compared.”
In Sommers 1972, Dr Sheldon C Sommers, Chairman of the Scientific Advisory Board to the Council for Tobacco Research, a physician specialising in pathology and Clinical Professor of Pathology at Columbia University College of Physicians and Surgeons and University of Southern California School of Medicine, gave evidence which included this statement, at p.96:
“[S]tatistical mathematics can never prove cause and effect. All they show is a relationship requiring further study, usually experiments in animals, to find out the meaningfulness biologically of this relationship. I really believe that among the active researchers in these fields, there is no great preponderance of feeling that cigarette smoke is carcinogenic.”
In Sommers 1976 Dr Sommers said at p.269:
“Now, as to lung cancer, there is a statistical association between cigarette smoking and lung cancer. But at present the nature of the association or whether it is causal are not known. The test of the original Surgeon General’s report [USSG 1964] deals with the difficulties of assigning causality, but the summary and conclusions brush these aside, and assign a causality not demonstrably evident in the text. It is widely known that a statistical association is not by itself proof of causation. A statistical association may point to experiments that will help to determine whether there is cause involved.”
Another:
In Furst 1982 Dr Arthur Furst, Director Emeritus of the Institute of Chemical Biology at the University of San Francisco, said at p.512:
“For many years, I tried to induce lung cancer in animals with cigarette smoke, with no success, despite the most sophisticated smoking machines available. Not only were my colleagues and I unsuccessful, but so was every other investigator. There have been a very small number of published reports of lung cancers occurring in experimental animals during smoke inhalation experiments. Anyone attempting to interpret these as showing that smoking causes lung cancer must understand that animals, like humans, do spontaneously develop lung cancer even in the absence of any suspected carcinogen.”
In explaining his conclusions as at September 2003, Professor Idle said that it was his judgment that cigarette smoking had not been established as a cause of human lung cancer. Indeed, as explained by him, the cause of cancer was unknown. Moreover, the mechanisms by which lung cancer developed were not known. Researchers had not produced squamous cell lung carcinoma in laboratory animals by inhalation exposure to cigarette smoke. No constituent or group of constituents, as they existed in the complex mixture which was cigarette smoke, had been shown to be a cause of lung cancer in smokers. In view of this, it could not be determined whether or not smoking caused lung cancer.
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