Tobacco Documents Online

). LAW OFFtC£S JACOB & MEIDINGEIR 1270 AVENU£ OF THE AMI[RICAS ROCK£F£LLER C£NTER NEW YORK, N Y. I0020 HK12800~0 IEOWIN J JACOB fRANK I-I M[I) INO[ll TIMOTHY i~i. FINNEGAN November 25, 1974 IZl21765-4J00 m C:ABLI: AOOR($$ KC~hIIJAI' Dr. Robert C. Hockett The Council for Tobacco Research ~ U. S. A., Inc. l!0 East 59th Street New York, New York 10022 Dear Bob: and one copy of your statement relating to the proposed regulation of cigarette smoke components. Would you please sign the original and rezurn it to me; the copy is for your files. Sincerely, Timothy M. Finnegan CI-R 90 CONG 0'1200

HK1280089 STATE[,[ENT OF DR. ROBERT C. HOCKETT I am Robert Casad Hockett, a Ph.D. ~n the fields of orsanic chemistry and biochemistry and Research Direc- tor of The Council for Tobacco Research -- U. S. A., Inc. I received my B.S., M.S. and Ph.D. Degrees from The Ohio State University in 1925, 1928 and 1929, respec- tively. Thereafter, I served at the National Insltutes of Health, U. S. Public Health Service, and as Assistant Pro- fessor and later Associate Professor of Chemistry at the Massachusetts Institute of Technology. I have also served as Scientific Director of the Sugar Research Foundation. In 1954, i Joined the Tobacco Industry Research Committee, which was the predecessor to the present Council for Tobacco Research -- U. S. A., Inc. In 1985, 1969 and 19?2, I had the privilege of presen%in~ to various Committees of Congress reviews of tobecc~ and health research sponsored by the Council. On those occasions my thesis was that no research had estab- lished ~nokln~ as a "major health hazard." Nor had it ever teen shown whether, how, to what extent or in whom c~&arette smoking can contribute to the etiology of any diseas~ that is presently a major cause of illness or early death. L

% HK1280090 In 1972, when the regulation of "tar" and nico- tine levels was being proposed, I stated that I could find no convincing evidence that "tar,"* nicotine or any specific ingredient of cigarette smoke had been shown to play a role in producing any human disease. Consequently, there was no scientific basis upon which to establish maximum ae- eeptab]e levels of "tar" or nicotine. My remarks to Congress in 1972 may be briefly summarized as follows: The 1964 Report to the Surgeon General of the U. S. Public Health Service concluded with respect to nicotine: "The rapidity of degradation to non-toxlc me- tabolites, the results from chronic studies on animals, and the low mortality ratios of pipe and cigar smokers when compared with non-smokers indicate that the chronic toxicity of nicotine in quantities absorbed from smoking and other methods of tobacco use is very low and probably does not represent a significant health problem." Since 1964, no data have been published which would require a change in that position. On the contrary, studies have confirmed the conclusion %hat nicotine in the body *The so-called "tars" are complex mixtures of condenseo smoke ingredients. "Tars" vary in composition with tobscco types and ~rea~ments and with conditions oD combustion, collection and storage. Equal.amounts of two different "tars" can have vastly different biological effects in animal experiments. -2- [:IR 98 COH5 01202

HK1280091 is rapidly converted into other substances of much lower pharmacologlcal activity. It has never been scientifically established that nicotine causes or contributes to atherosclerosis or -- for that matter -- any other cardiovascular disease. Rather it is generally recognized that many factors are involved in determining the rate at which atherosclerosls develops and also in influencing the precipitation of acute disease events. At least twenty such factors have been reported and some are clearly of a genetic nature, while others are environmental. Some factors appear to act directly while others, if valid, must exert their in- fluence indirectly. To date no one has been able to define scientifically the predominant causal factors or how they interact in the production of this disease. In general, human studies on atherosclerosis still frequently appear confusing, inconsistent and contradletoryt Recently it has become possible to design more systematic and betzer controlled animal studies to inves- tigate whet role, if any, nicotine could play in the complex etiology of atherosclerosls. So far, such studies have not established that nicotine can be implicated in tne production of this disease. The pharmacological effects of nicotine have been shown to be verytranslent and some may even be -3- EI R 98 EEIN5 0'1203

HK126008Z beneficial. While many studies have been done in this field, none have established nicotine as contributing to the causation, aggravation or precipitation of any cardio- vascular disease. With regard to tobacco smoke, over the years numerous animal inhalation experiments have been conducted. Nevertheless, all such studies have failed to produce human type lung cancers. One experimental method that produced observable results was the painting of smoke condensates (generally but erroneously called "tars'f) on the skins of mice. Such experiments have been chiefly responsible for the unfounded notion ~hat "tar" is dangerous'to human smckers. My skepticism about the relevance of skin painting studies to humans is based upon the following considerations: I. Relatively enormous doses of "tar" were used in the anlmal skin experiments. 2. Great differences exist between mice and primates, including man, in susceptibility 5o cancer- inducin~ chemicals. 3. There are many important differences between skin and lung tissues, including various cleansing mech- anisms. 4. There are both chemical and ;hysical differ- ences beSween smoke condensate or "tars" an5 whole, fresh, CIR gONG 01204

HK1280093 normal smoke. 5. The role, if any, of viral agents in the skin painting experiments is unknown. As to carbon monoxide, it is a normal constitu- ent of human blood produced by metabolism and can be des- troyed by the body, though slowly. Without any exposure at all to carbon monoxide in the air, the blood contains from 0.2% to 1.0% of earboxyhemoglobin (the combination formed by thls gas with the red blood pigment). This level is equivalent to that produced by constant breathing of air containing seven parts per million of the gas. Long ago it was found that smokers, after smok- ing and inhaling from i0 to 15 cigarettes within a period of two hours, showed a rise in percentage saturation of carboxyhemoglobin from 3.1% to 6.7% (average 4.3%). None of them experienced any symptoms attrlbutable to carbon monoxide, which is to be expected since these levels are far below those considered acceptable in industrial ex- posures. Further, cigarette exposure is generally inter- mittent as compared to the day-long exposure often encountered in industries. As to long term exposure to carbon monoxide, .studies of men chronically exposed (10 to ]8 years) in their work to relatively high carbon monoxide levels show no earlier or more substantial circulatory -5- C:IIR 98 COHG 01205

HKt280094 abnormalities attributable to atherosclerosis than the general population. In short, no one has ever scientifi- cally shown carbon monoxide exposures from ordinary smoking to be hazardous to humans. Since 1972, I have not seen any data which would change my opinion that smoking has not been sclen- tlfically established as a "major health hazard" to humans. Nor h~ve I seen any studies in the medical literature which establish "tar," nicotine or any other constituent of tobacco smoke as disease producing in human smokers. This is especially true with regard to the so-called epl- demiologlca! or statistical studies. I~ is generally conceded that the cause or causes of disease cannot be determined by epldemiological studies alone. Such studies merely point to areas in which laboratory experiments with animals, integrated with human clinical observations, are needed to explain and ~nterpret the real meaning of statistical relationships gleaned from human population studies. Experts in the field have pointed out many un- solved problems relating to the epidemiologlcal approach. Perhaps the most disturbing criticism of existing studies is tha~ in human populations, the smoker and the non-smoLer groups are self-selected %o begin with instead of being assigned at random as'~:ould be the case in any competent In_ -6- CTIR 98 CONG OI201S

HK1280095 animal experiment. At present, we do not know enough about the conscious or unconscious motivations involved in the adoption or maintenance of cigarette smoking to Judge fully the nature and extent of the differences between the smoking and non-smoklng populations. Nor can we determine where these differences are themselves associated with disease predispositions apart from smok- ing. Nevertheless, wherever such differences have been explored at the levels of personality, body build, elee- troencephalography, style of life, vocational interests, or psychological make-up, they have been found to be real. It is important to look for still other differences and especially, in each case, to find out what, if any, relationship the differences themselves or any associated differences in health may have to the practice of smoking. in view of these unresolved problems, it is ob- vious that epldemiological studies have not, and cannot, incriminate specific components of cigarette smoke in the causation of human disease. Neither these epldemi- ologica! studies, nor animal and clinical studies,have identified any ingredient or group of ingredients in smoke as disease producing in humans.. In conclusion, it is my opinion that at the present time there is simply no scientific basls'for -7- CTR 98 COI'I5 01207

q • HKt280098 rezulatlon of levels of various cigarette smoke components. -8- C]R 98 CON6 01208