Tobacco Documents Online

6 4, h , ~W OFFtC~ JACOB & MEDINGER z270 AVENUE OF= THE AMERICAS ROCKEFELLER CENTER NEW YORK, N Y, IOO20 HK1280061 EOWIN ~ ,JACOB rRANR ~ ~IEE) INGCR TIt-4OTHy t-~. FINNIEGAN January 22, 1975 12t2] 765-4t00 CABL( AOOR(.~.5 KONh)AY Dr. Robert C. Hockett The Council for Tobacco Research - U. S. A., Inc. 110 East 59th Street New York, New York 10022 Dear Bob: I am enclosing herewith the original and one copy of your statement relating to the NCAB's proposal to regulate cigarette smoke components, together with a copy of the NCAB's recommendations. I would appreciate your signing the original statement and returning it to me. The copy is for your files. Sincerely, Timothy M. Finnegsn BY MESSENGER P.S. Also attached is a copy of your Curriculum Vitae which we discussed this morning. TNF [:I-R .'38 C0HG 011.90

HK1280062 " STATEMENT OF DR. RCBERT C. HOCKETT I am Robert Casad Hockett, a Ph.D. in the fields of organic chemistry and biochemistry and Research Direc- tor of The Council for Tobacco Research -- U. S. A., Inc. In 1965, 1969 and 1972, I had the privilege of presenting to various Committee~of Congress reviews of tobacco and health research sponsored by the Council. My statements setting forth my background and views are attached. In 1972, when the regulation of "tar" and nico- tine levels was being proposed, I stated that I could find no ccnvincing evidence that "tar,"* nicotine or any specific ingredient as found in cigarette smoke had been shown to play a role in producing any human disease. Consequently, there was no scientific basis upon which to establish max- imum acceptable levels of "tar" or nicotine. My remarks to Congress in 1972 may be briefly sum2.arlzed as follows: The 1964 Report to the Surgeon General of the *The so-called "tars" are complex mixtures of condensed smoke ingredients. "Tars" vary in composition with tobacco types and treatments and with conditions of combustion, collection and storage. Equal amounts of two different "tars" can have vastly different biological effects in animal experiments. [;TR 90 COH5 01191

• t • . HK1280063 U. S. Public Health Service concluded with respect to nicotine: "The rapidity of de~radatlon %0 non-toxic me- tabol~tes, the ~esults from chronic studies on animals, and the low mortality ratios of pipe and cigar smokers when compared with non-smokers indicate that thechronlc toxleisy 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 h~ve been published which would require a change in that position. On the contrary, studies have confirmed the conclusion that nicotine in the body is rapidly converted into other substances of much lower pharmacological activity. It has never been scientifically established that nicotine causes or contributes to atherosclerosls or -- for that matter -- any other cardiovascu]ar disease. Rather it is generally recognized that many factors may be 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. 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 atheroscleresls still frequently -2- IZ]R 98 C01'16 (11192

| HK12800~! appear confusing, inconsistent and contradictory° Recently it has b'ecome possible to design more systematic and better controlled animal studies to inves- tigate what role, if any, nicotine could play in the complex etiology of atherosclerosis. So far, such studies have not established that nicotine can be implicated in the production of this disease. The pharmacological effects of nicotine in humans have been shown to be very transient and some may even be beneficial. While many studies have been done in this field, none have established nicotine as contributing to the causation, aggravation or precipitation of any cardiovascular disease. With regard to tobacco s~oke, over the years numerous animal inhalation experiments have been conducted. Nevertheless, all such studies have failed to produce the type of lung cancer that in humans has been statistically associated with smoking. One experimental method that produced observable results was the painting of smoke condensates (generally but erroneously called "tars") on the skins of mice. My skepticism about the relevance of such experiments to humans is based upon the following considerations: i. Relatively enormous doses of 'ttar" were used in the animal skin experiments. -3- CTR 98 COHG 01193

HK1280065 i 2. Great differences exist between mice and primates, including man, in susceptibility to cancer- induclng chemicals. 3. There are many important differences between skin and lung tissues, including various cleansing mech- anisms. 4. There are both chemical and physical differ- 'ences between smoke condensate~or "tars" and whole, fresh, 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 constltu- 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 carboxyhemoglobln (the combination formed by this gas with the red blood pigment). This level is equivalent to that produced by constant breathing of air cgntaining seven parts per million of the gas. Long ago it was found that smokers, after smok- ing and inhaling from 10 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 attributable to carbon monoxide, which is to be expected since these levels are -4- L'.IR 98 COI'16 01194

HK1280066 far below thbse considered acceptable in industrial ex- posures. Further, cigarette exposure is generally inter- mlttent as compared to the day-long exposure often encountered in industries. As to long term exposure to carbon monoxide, studies of men ehornlcally exposed (i0 to 18 years) in their work to relatively high carbon monoxide levels show no earlier or more substantial circulatory ab- normalities attributable to atherosclerosls 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 iq72: I have follo\qed the pertinent scien- tific literature but have not seen any data which would change my opinion that smoking has not been scientifically established as a "major health hazard" to humans. Nor have 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 epldeml- clog!ca! or statistical studies. It Is Kenerally conceded that the cause or causes of disease cannot be determined by epldemlologlcal studies alone. Such studies merely point to areas In whlcb laboratory experiments with animals, integrated with human clinical observations, are needed to explain and -5- [ITD qR I"iqi',l~ n11qq

I HK1280067 interpret the real ~eaning of statistical relationships gleaned from human population studies. Experts in the field have pointed out many un- solved problems relating to the epldemlologieal approach. Perhaps the most disturbing criticism of existing studies is that in human populations, the smoker and the non-smoker groups are self-selected to begin with instead of being assigned at random as would be the ease in any competent 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-smoking populations. Nor can we deter- mine where these differences are themselves associated with disease predispositions apart from smoking. Neverthe- less, wherever such differences have been explored at the levels of personality, body build, electroencephalography, style of llfe, 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 smokingJ In v~ew of these unresolved problems, it is ob- vious that epidemiologlcal studies have not, and cannot, -6- [IR 98 COM6 01196

HK12800U8 incriminate specific components of cigarette smoke in the causation of human disease. Neither these epldemi- ological studies, nor animal and clinical studies, have identified any ingredient or group of ingredients as found in smoke as disease producing in humans. In conclusion, it is my opinion that at the present time there is simply no scientific basis for regulation of levels of various cigarette smoke compon- ents. -7- ClR 9B CON5 01i97