Product Design
Smoking and Health Issues
Abstract
Overviews the smoking and health controversy. Discusses the scientific debate on smoking and health, reviews the concept of addiction, discusses Environmental Tobacco Smoke and restates the tobacco industry's stance on the smoking and health controversy.
Fields
- Hypothesis
- Women TargetingCigarettes designed to target women
- Health effects
Design changes which have measurably altered health effects of cigarette smoke, both for smokers and nonsmokers.- Perceptions of ETS
Design changes to reduce perception of environmental tobacco smoke among smokers and nonsmokers in response to public concerns about the dangers of ETS.- Toxicity and consumer intake
Development of scientifically valid procedures for measuring biological activity and neurological effects of nicotine and smoke constituents. - Health effects
- Keyword
- Carcinogenic (Cancer-causing)
- Cardiovascular system (Heart)
- Cotinine
- Lung cancer
- Smoking and Health Controversy
- Cardiovascular system (Heart)
- Smoke Constituent
- Benzo(a)pyrene
- Beta naphthylamine
- Carbon monoxide
- Hydrogen cyanide (HCN)
- Nicotine
- Nitric oxides
- Nitrosamines (N-nitrosamines)
- Total particulate matter
- Beta naphthylamine
- Design Component
- Reconstituted tobacco
- Expanded tobacco (Puffed tobacco, ET)
- Named Organization
- A.D. Little, Inc. (Performed biological research & testing for Liggett & Myers)Performed biological research and testing for Liggett on XA (Palladium) cigarette
- American Cancer Society
- American Heart Association (Voluntary health organization that focuses on cardiac health)
Voluntary health organization that focuses on cardiac health and stroke. AHA occasionally teams with tobacco retailers to engage in promotions/fund-raisers (see http://www.smokefree.net/doc-alert/messages/247136.html and http://www.rawbw.com/~jpk/stand/Pictures.html).- Barnes Hospital
- British Medical Association
- Brown & Williamson Tobacco Corporation (B&W)
Subsidiary of BAT U.S., located in Louisville, KY.- Columbia University
- Committee for Research on Tobacco and Health
- *Council for Tobacco Research-- U.S.A. Inc. CTR (Formerly Tobacco Industry Research Committee (TIRC))
Created and funded by the tobacco industry to award grants to study of the link between smoking and disease. Part of a four decade effort to cast doubt on the links between smoking and disease.- Creighton University
- Fox Chase Cancer Center
- Harvard University Medical School
- Health Education Council
- Hereditary Cancer Institute
- Industrial Technical Committee
- International Journal of Epidemiology
- Journal of Immunology
- Journal of Medical Sciences
- Journal of the American Medical Assocation JAMA
- Liggett & Myers Inc. (Pioneer in the generic cigarette business)
Cigarette manufacturer; Pioneer in the generic cigarette business; L&M is the manufacturer of Chesterfield, Decade, Dorado, Duke of Durham in 1958, Eagle, Eve, L&M, Lark, Pyramid and Stride cigarettes- Mayo Clinic (Located in Rochester, Minnesota)
Has a nicotine dependence center; runs the smoking cessation program at the Mayo Clinic- Michigan Cancer Foundation
- Microbiological Associates (Research lab in Bethesda, MD)
Research lab in Bethesda, MD. CTR contracted with this lab to do the world's largest inhalation study, involving more than 10,000 mice in 1973-1982.- Mount Sinai Medical School
- National Cancer Institute NCI
Division of Cancer Prevention and Control, National Cancer Institute located in Rockville, MD- National Institute on Drug Abuse (An addiction research center in Baltimore, MD)
An addiction research center located in Baltimore, MD- National Institutes of Health
- New Scientist
- New Zealand Medical Journal
- *Scientific Advisory Board (SAB) (Only use SAB with name of specific org.)
- Surgeon General of the United States Public Health Service (U.S. Federal government public health advocate)
The U.S. Surgeon General's office has found since 1964 that tobacco use causes disease in humans.- Tobacco Industry Research Committee (TIRC) (Renamed Council for Tobacco Research-USA (CTR))
Organized in 1954 as the Tobacco Industry Research Committee (TIRC), and renamed the Council for Tobacco Research-USA (CTR) in 1964.- Tobacco Working Group TWG (Federally funded project to create a safer cigarette)
A federally supported project launched by the National Cancer Institute, with the purpose of developing a less hazardous cigarette.- U.S. Air Pollution Control Association
- *United States Public Health Service (use United States Public Health Service)
- University of California Los Angeles (UCLA)
- University of Chicago
- University of Geneva
- University of Manitoba
- University of Minnesota
- University of Newcastle
- University of Reading (England)
- University of San Francisco Institute of Chemical Biology
- University of Southern California Medical Center
- University of Wisconsin
- W Alton Jones Cell Science Center
- Washington University in St. Louis
- Yale Medical School
- American Cancer Society
- Subject
- Addiction
- Cancer (Health Effects)
- Cardiovascular Effects (Health Effects)
- Effects—Smoking Behavior (Effects)
- health effects
- secondhand smoke/health effects
- Smoke Nicotine (Measures)
- Tar (Measures)
- Test/Animal Subject (Testing)
- Test/Smoke Condensate (Testing)
- Test/Smoke Constituents (Testing)
- Test/Toxicity (Testing)
- Cancer (Health Effects)
Document Images
SMOKING AND HEALTH ISSUES
AUGUST 21, 1989
CONFIDENTIAL ATTORNE¥-CLIENTMEMORANDUM
CONTAINING OPINION AND IMPRESSIONS
OF RETAINED COUNSEL
TABLF. OF CONTENTS
INTRODUCTION .........................
1
THE SCIENTIFIC DEBATE ON SMOKING AND HEALTH .........
5
SMOKING AND' ADDICTION .....................
60
THE NONSMOKER: ENVIRONMENTAL TOBACCO SMOKE ..........
76
PRIOR TOBACCO INDUSTRY POSITIONS ON SMOKING ANDHEALTH
9¸0
CONFIDENTIAL
10125996
- i -
INTRODUCTION
The controversy over the claimed health effects of smoking
is as old as the practice of smoking itself. There is no publ~ic
health topic that has received as intense and prolonged scrutiny
by the Congress, various federal agencies, the medical profession,
and the press as has the issue of smoking and health. Smokers and
non-smokers alike have been inundated with information about the
health risks associated with smoking. The Surgeon General's Office,
for example, in addition to releasing its well-known annual report
dealing with health issues associated with. tobacco use, has for
the last several years been pursuing a highly publicized campaign
directed toward school-age children to achieve a "smoke free
society" by the year 2000. Every pack of cigarettes sold in this
country for the last 23. years has borne a Congressionally-mandated
warning label. For the last 17 years, this same warning has
appeared on all cigarette advertising.
Yet the scientific evidence that smoking cigarettes (and
other forms of tobacco use)~ causes cancer, heart disease, and other
chronic illnesses is not so one-sided as is often claimed.
Reputable independent scientists over the years have questioned
the validity of the various charges made against smoking. Brown &
Williamson. and the other major cigarette manufacturers have
consistently maintained, with. considerable support, that it has
CONF ]DENT IAL
not been proven that smoking causes any chronic disease. The
industry's position is often misunderstood to be that smoking has
been proved not to cause any disease. This is not the industry's
position. The ~ndustry believes that the question, is still
unanswered.
This is not to say that Congress has acted inappropriately
in continuing its scrutiny of the "public health" aspects o~
smoking. The "standard of proof" in a public health sense is quite
different -- and rightly so-- than that required by science, or
that mandated in. a courtroom. Particularly where the question is
whether the public has sufficient information about a particular
product, the government may decide to act before the scientific
"case" regarding the product is complete.
Many products carry with them claimed health risks--
butter, eggs, red meat, and milk are familiar examples. Many other
products carry known health risks -- automobiles, knives, and
whiskey are again familiar examples. The public awareness as to
the claimed risks of these products is much less than that with
regard to cigarettes. Moreover, with the possible exception, of
alcohol, no product other than cigarettes has been subj~ected to as
vehement and concerted an effort to restrict or deny its
availability to the adult consuming public. Thus, the use of
~ONF |'DENT |AL
- 2 -
cigarettes in light of this awareness (and in the face of this
effort) is uniquely a ma£ter of personal and informed choice.
Brown & Williamson and other cigarette manufacturers
market their product for adults precisely because the question of
whether to smoke is one based on an informed personal choice. The
industry recognizes that the consumer has a great deal of negative
information through which he or she must sort in making the decision
to smoke. Because this topic has been so thoroughly and publicly
canvassed,. Brown & Williamson does not agree with those opponents
of smoking who wish to place greater restrictions on the
availability of cigarettes -- those who wish to make the adult
consumer's choice for the consumer, in the mistaken belief that
only the choice not to smoke can be "right" for any individual,
no matter how well informed he or she may be.
The road down which some anti-smoking advocates wish to
take American society is dangerous. Once the government begins to
ban "life-style choices," it is impossible to predict where it
will end. Who will draw the line dividing those products and
activities that are "healthful," and thus "permissible," from those
that are claimed to be "unhealthful," and thus "forbidden?'" More
fundamentally, what will happen to the quality of life for members
of such a society, under the heavy hand of such extraordinarily
intrusive government action?
CONFIDENT IAL
The following material outlines some potential topics for
discussion should Brown & Williamson. determine to pursue a program
of legislative contacts. This program would be designed to. provide
governmental decision-makers with an understandingand appreciation.
of Brown & Wi~liamson's position on smoking and health. At the
same time, Brown & Williamson would acknowledge its understanding
of positions Congress has taken.
CONF ];DENT IAL
- 4 -
THE SCIENTIFIC DEBATE ON SMOKING AND HEALTH
CONFIDENTIAL
- 5 -
Although it is assumed by many people, and often asserted
by anti-smoking advocates, that the scientific community has long:
been unanimous in concluding that smoking "causes" various diseases,
the fact is that respected scientists have stated that the question
of whether cigarette smoking causes disease remains unanswered.
The passage of time has not diminished the flaws in the case for
causation; many of the reasons for skepticism that were cited by
scientists in. the 1950s and 1960s are sti~l valid concerns in the
1980s.
At the same time, Brown. & Williamson and the other
companies in the industry have behaved responsibly in funding
substantial research efforts by independent scientists into the
wide-ranging issues of "smoking and: health." Those efforts -- as
described below -- have not always resulted in findings favorable
to the industry. Much of that research -- favorable and unfavorable
-- has nonetheless been published.
CONFIDENT IAI.
- 6 -
THE NATURE OF THE SCIENTIFIC EVIDENCE ON SMOKING
AND HEALTH.
A. Lunq Cancer
i. Epidemioloqical Data
The most important scientific part of the industry's
critics' case is the various epidemiological studies associating
cigarette smoking with certain chronic diseases.1 A number
independent scientists, however, have expressed concern about the
interpretation of such epidemiological data. These scientists
have been unimpressed by the numbers of such studies,, because of
concern about the underlying validity of the evidence.
For example, in the early ~980s, Dr. Laurence Kupper, in
criticizing many of these studies said:
i. These studies have two primary methods of approach:
retrospective and prospective. A retrospective study selects
a group of lung cancer patients, then tries to backtrack in
time to determine smoking histories. A prospective study
identifies a specific group, determines their smoking habits,
and then observes the disease patterns that develop. Both
types of studies then arrange the raw data into various
categories, and run statistical tests to determine if one
group (smokers) differs from another (nonsmokers) with respect
to a particular disease. These studies have generally shown
that smokers are more likely to get lung cancer than non-
smokers. Approximately 90% of lung cancer cases are smokers;
less than 5% of smokers, however, get lung: cancer.
CONF ],DEN] ],AL
- 7 -
The main. prospective (i,.e., follow-up) studies
concerning smoking and its relationship to
mortality and morbidity from certain diseases
(as discussed in the latest Surgeon. Genera~
reports) d~o not address the issue of causality.
The claim that the conclusions reached are
'impressively uniform and consistent' does not
mean that a causal relationship has been
established, but only that approximately the
same observed associations keep appearing. I_~n
fact, the biases inherent in these studies
preclude the riqht to claim that causality has
been demonstrated. Actually, one could arque
that the same associations keep appearinq
because the same biases are present in each
study.
The fact that so: many studies have produced a
positive association between smoking and lung
cancer has led many people to make the false
conclusion that 'quantity means quality.' The
truth of the matter is that repeatability (!i.e.,
the ability to produce the same estimated
association) does not imply accuracy (i.e., the
ability to produce a valid estimate of the
true association). In this regard, one study
free from all bias and producing a valid
measure of the true smoking-lung cancer
association is worth more than a thousand biased
studies, all of which provide the same
distorted estimate of the true association.. (I)
And, a recent editorial in the International Journal of Epidemioloqy
suggested the following:
CONFIDENT ]AL
We trust that the global differences in cancer
incidence will finally be explained by the
interplay between the environment and our genes.
Thereby, it is certain that molecular biologists
will have to face the challenge to help explain
these variations in. incidence. A question
remains whether cancer epidemiology, and maybe
epidemiology in general, will have to fall to
the same leve~ of academic disrepute as miasma
- 8 -
theory, to facilitate this scientific process
of integration . The way out for
epidem~ology would be to explicitly recogn,ize
the challenge, anddirect research to programmes
that focus specifically on the envi, ronment-
gene interaction. (2')
Specific criticisms of using epidemiological studies to
"prove" causation, include the following points:
First, epidemiological studies can show a statistical
association between factors, but they cannot demonstrate a causal
relationship. Even the 196.4 Surgeon General's Report conceded
this: "Statistical methods cannot establish proof of a causal
relationship in an association." (p. 20) This is self-evident
because "cancer is a biologic, not a statistical problem." (3)
Second, in epidemiological studies smokers, ex-smokers
and nonsmokers are not randomly assigned to their study groups.
Instead, they make their own decisions about smokingi,~ and they,
therefore, constitute "self-selected" samples. Such self-selection
Can introduce considerable bias into an ep~demiological study.
Third, many of the large-scale prospective studies
examining the relationship between smoking and disease do not
adequately account for the potential effects of other factors that
can affect the results. These factors include general l~ifestyle,
CONFIDENT IAL
-- 9 --
alcohol consumption, occupational and envi.ronmental exposures,2
genetics,~ aging and the immune processes. As one statistician has
commented:
In general it is ironic that while studies of
environmental or occupational health effects
are constrained to take population smoking
habits into account, studies on smoking effects
seldom bother to search for a report on
occupational exposures. (4)
Fourth, if smoking causes lung cancer, it would be
reasonable to expect more of the disease in countries where more
cigarettes are smoked per capita. That does not always happen.
For example, Austria, Belgium, and Finland report higher lung cancer
rates but considerably lower per capita tobacco consumption than
the United States, Canada, and Australia. (5)
Fifth, if cigarette smoking does cause cancer, then the
earlier a person starts to smoke and the more he smokes, the sooner
he would be expected to get lung cancer. Yet nonsmokers and smokers
(whether they smoke a lot or a little) all appear to develop the
disease at approximately the same age. (14) According to one
expert: "that both the age of starting to smoke, and the rate of
smoking, should have no appreciable influence on the average age
Indeed, some environmental exposures that now may be
considered significant -- such as radon gas in the home --
were not recognized as potentially hazardous at the time the
studies were conducted.
CONFIDENT IAL
of onset of lung cancer greatly taxes, if it does not destroy, any
causal hypothesis." (6) Similarly, one major study indicated that
inhalers had a lower lung cancer rate than non-inhalers.
Sixth, the same type of epidemiological information used:
to suggest that lung cancer has increased in. smokers, suggests
that it may also have increased in nonsmokers. In an April 1979
report on this phenomenon, a scientist who believes that smoking
causes lung cancer nonetheless conceded that factors besides
cigarette smoking must have had a "significant effect" on the
mortality rate of lung cancer. (7)
Seventh, if cigarettes do cause lung cancer, one might
reasonably expect that heavy smoking would lead invariably to the
disease. Yet, the studies relied upon by the industry"s critics
show that less than 5% of all smokers ever develop lung cancer.
From the first to the most recent hearings .regarding
smoking and health, Congress has heard scientists and physicians
express their skepticism about the relationship between smoking
and lung cancer. In 1957, Dr. Joseph Berkson, of the Mayo: Clinic,
testified that "there is serious doubt as to the scientific
validity" of the conclusion that smoking causes lung cancer. (8)
In 1964, Dr. Thomas Burford, Chief of Thoracic and Cardiovascular
Surgery at Barnes Hospital in St. Louis, Missouri, said "carefu~l
CONF]DENTIAL
- ii --
study of the literature will reveal that many thoughtful studies
by competent people concur in the opinion that the. cause of lung
cancer, or of cancer in any organ, is unknown. Without needlessly
belaboring the issue, it is obvious that there is a large volume
of good scientific evidence which tends to refute the premise that
cigarette smoking is causally related to cancer of the lung." (9)
Almost 20 years later, in 1983~ Dr. Walter Booker said "Despite
what those in the legislative arena might believe, the cause or
causes of cancer of the lung (and other organs) remain unknown.
Both smokers and nonsmokers contract cancer and other diseases
often associated with cigarette smoking, and we still don't know
why." (110)3
The opinion of these scientists that smoking has not
been proven to cause lung cancer rests not only on certain of the
generic criticisms of the epidemiological "case" described above,
but also on factors specific to that particular disease. For
example, ostensibly parallel increases in the 20th century between
the consumption of cigarettes and the incidence of lung cancer have
been cited as one piece of evidence that smoking causes lung cancer.
Yet, both pathologists and thoracic surgeons have repeatedly
Indeed, the fundamental biological mechanisms of cancer are
still largely a mystery. As an a.rticle ~n the Journal of the
National Cancer Institute recently acknowledged: "Although a
large number of factors have been associated with the
development of malignant neoplasms in humans, the mechanisms
are still largely unknown." (Ii)
CONF )DENT IAL
testified before Congress that the data on lung cancer trends over
time are not dispositive because dramatic improvements in
physicians' ability to diagnose lung cancer caused more lung cancer
to be reported in official health statistics. As Dr. Rosenblatt
said in 1965, "statistics showing a tremendous increase in lung
cancer during the past 30 years are misleading. The increase is
only apparent and is [in part] the result of greater skill in the
detection of the disease." (12)
Similarly, changes in the International Classification
of Diseases in the mid-20th century have inappropriately combined
data for cancers that originated in the lung with cancers that
spread to the lung from another part of the body. Since majlor
internal cancers frequently spread to the lung, these secondary
lung cancers have been included in the statistics on. smoking and
lung cancer. This combination of primary and secondary lung cancers
in some statistics has made it impossible accurately to establish
a statistical relationship between primary lung cancer and any
agent, including cigarette smoking.
In sum., the use of epidemiological data to indict smoking
as a "cause" of disease has many flaws, and neither the industry
nor independent scientists have acted irresponsibly in noting those
problems in the public debate over smoking and health.
CONF ]DENT |AL
o
Animal Studies
Those claiming that cigarette smoking causes lung cancer
also rely upon the experiments by Ernst Wynder and other scientists
who. claim to have produced skin cancers by painting the skin of
certain animals (usually mice)with tobacco '"tar."
For several reasons, such skin-painting: studies are not
directly applicable to the human smoking experience. First, the
mice used in many of the experiments have been specially bred to be
extremely sensitive to any possible carcinogenic activity. They
therefore may react positively to many substances which are not
carcinogenic in humans. Further, in the 1950s, Dr. Jonathan
Hartwell of the National Cancer Institute compiled a list of animal
carcinogen studies which included such common items as fructose
(fruit sugar), glucose (processed sugar), and even lactic acid
(made naturally by the human, body). He found that 481 of the 2,.108
common chemical compounds tested (23%) were "carcinogens'" in such.
animal studies. But, neither Dr. Hartwell nor any other responsible
scientist ever concluded that these many "animal carcinogens" were
therefore human carcinogens.
Second, the substance that is applied to the backs of
mice in such. skin-painting experiments -- condensate created by
solidifying tobacco smoke and m~xing it with a chemical solvent --
CONF ]DENT
is not the same substance as the fresh whole smoke a smoker
inhales. It is for this reason that Brown & Williamson and the
other tobacco companies sponsored animal studies by independent
scientists which more closely resemble the human smoking condition-
- i.e., experiments in which the animals inhale fresh, whole smoke.
Despite numerous animal experiments involving many different
species, reproducible human-type lung cancers have never been found
in the lungs of animals as the result of inhaling fresh whole
tobacco smoke.
Third, the organ involved -- mouse skin -- is obviously
quite different from a human lung. For example, animal skin lacks
the intricate clearance mechanisms of the lungs, such as the mucus
blanket which coats the lining of the major airways of the lung.
Even the summary report of a study sponsored by the United States
government utilizing skin painting techniques conceded that there
is an "uncertain relationship between tumors resulting from mouse
skin painted with condensate and human lung cancer." (13)i Once
again, all scientists recognize the importance of inhalation studies
which could tend to support, or as has been the case, cast doubt
on the skin-painting results.
Finally, the doses applied~ in, mouse skin painting are
massively greater than the amounts of particulate matter which a
smoker would encounter in a normal smoking situati~on. Such.
CONF ]DENT [AL
- 15-
experiments involve applying '"the wrong material, in the wrong
form,~ in the wrong concentration, to the wrong tissue of the wrong
animal." (14) As Dr. Greene. stated at the 1957 hearings, "the
[skin-painting] experiments demonstrated that tobacco tar extracted
by a special technique induces cancer in the skin of CAF mice, and!
nothing more. This point is of little significance to workers in
the fiel, d who have found that under certain conditions a
multiplicity of substances in everyday use will induce cancer in
m~ce of highly susceptible strains."
For these reasons, the industry has properly insisted
that animal inhalation experiments are more relevant to the question
of whether cigarette smoking causes human lung cancer. Over the
years, many researchers -- both supported by industry grants and
completely independent of any industry connection -- have conducted
such experiments where test animals have been forced to take in.
large doses of whole smoke. One study recently concluded by
Microbiological Associates (with funding from the Council for
Tobacco Research) involved thousands of animals, in a lifetime
experiment.
These studies have not found any significant pathological
changes, and none have found credible evidence of cancer
CONF ] DEI~T, IAL
-- 16 --
production.4 As Arthur Furst, the Director Emeritus of the
University of San Francisco's Institute of Chemical Biology, said
"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 every other investigator who. attempted to induce
lung: cancer in animals by inhalation of fresh smoke also fail, ed."
Thus, he said: "I have concluded that no reliable, reproducible
animal studies have shown that the inhalation of cigarette smoke
causes lung cancer."
In sum, the totality of the evidence fails to establish
that smoking is a cause of lung cancer.
B. Cardiovascular Disease
Independent scientists have similarly expressed
skepticism about the alleged causal link between smoking and heart
o
One of the most thoroughly discussed animal studies was the
beagle dog inhalation study conducted by Dr. Auerbach. Dr.
Auerbach claimed to find changes which he labeled as cancerous,
but his study was severely criticized. Dr. Victor Buhler
stated in 1982: "That experiment suffered from. severe design
defects, and the photomicrographs published with the article
would not permit most pathologists to reach the conclusions
stated by the authors."
Significantly, Dr. Auerbach and others were unable toreplicate
his results in later studies.
CONFIDENT I~AL
-- 17 --
disease. They have noted the inconsistent statistical correlations
between smoking and heart disease in various populations; the strong:
genetic influence in heart disease; and the failure of the critics
of smoking to establish a mechanism to explain how tobacco smoke
might cause heart disease. In 1964, Dr. Henry Russek testified
before Congress that "statistical findings linking the tobacco
habit to coronary disease afford no proof of a causal relationship.;"
and that his research had shown that emotional stress was far more
significant than cigarette smoking! in the development of heart
attacks. (15) In 1982, Dr. Carl Seltzer, a Fellow of the American
Heart Association's Council on Epidemiology, similarly said that
the statement "'cigarette smoking is a major cause of heart
disease,', is not scientifically valid." (16)
Anti-smoking advocates blame nicotine for the development
of heart disease. Yet no mechanism by which nicotine, or any other
agent, is involved in heart disease has been demonstrated. Serious
questions about what role, if any, nicotine plays have been raised
as a result of autopsy findings of fatty deposits and other changes
in the arteries of individuals who either have not smoked or could
have smoked only briefly, such as infants, children, and young men
killed in battle. (17) Even the 1983 U.S. Surgeon General's
Report, which focused on cardiovascular disease, concedes that
"the evid~ence for and against a primary role for nicotine in the
development or acceleration of atherosclerosi, s is not conclusive."
CONF [DENT [~AL
(18) That opinion was shared by Dr. H. Schievelbein, a German
researcher who conducted research o:n the relationship between
nicotine and the clogging of arteries. After reviewing the
literature, he and his co-author concluded that "there is n_~o
established evidence which supports the hypothesis that nicotine
has any influence on the development" of those changes. [emphasis
added] (19)
The role of nicotine in the development of heart disease
posited by anti-smoking advocates is further undermined by two
epidemiological studies. In. 1983, a study that dealt with
myocardial infarction (heart attack) reported finding -- contrary
to what the authors expected -- that the nicotine and carbon
monoxide levels of the cigarettes smoked by the study's subj~ects
were not related to the risk of heart attack. (20)
The second study, chaired by Dr. N. Wald, a well-known
British scientist opposed to cigarette smoking,: examined the serum.
(blood) levels of cotinine, a nicotine metabolite, in male
nonsmokers and smokers of cigarettes only, cigars only, and pipes
only. The study determined that the mean cotinine level for pipe
smokers was significantly higher than the levels for cigarette and
cigar smokers. Since studies of pipe smokers generally have not
reported an increased risk of coronary heart disease, the
researchers concluded that "niicotine is unlikely to be the major
CONFIDENT I,AL
cause of the excess coronary heart disease mortality in cigarette
smokers." (21) After re-evaluating their methodology in response
to anti-smoking criticism of their study, the researchers agai, n
concluded, "we can be reasonably confident that exposure to high
systemic concentrations of nicotine is not a cause of the disease."
Although the researchers argued that their data "cannot completely
exonerate" nicotine, they added that the data do "substantially
reduce the weight of evidence suggesting that nicotine is a cause
of coronary heart disease." (22)
Animal studies which purport to establish a causal role
for nicotine in heart disease have been soundly criticized for
their unrealistic and excessive test conditions. An American
researcher who conducted animal studies on this subject has noted:
"There have been some studies that have
exhibited minor or questionable changes with
the use of 6:00 or more cigarettes a day in
man. This is such a large number that I think
man would find it difficult to find the time
to smoke them." (23)
Tn contrast, animal studies using realistic doses of nicotine have
"failed to initiate, exacerbate, or otherwise influence" the process
leading to the clogging of arteries in test animals. (24) In one
such study, which was funde~ by the United States government, mal!e
beagle dogs fed a special diet to induce this process were exposed
for two years to cilgarette Smoke containing low. or high levels of
COMF |DENT |AL
- 20-
nicotine and, in some cases, enriched with CO. According: to the
final report of the research laboratory which conducted the study,
"the results of this study lent no support to the suggestion that
cigarette smoking increases the rate of development" of this
process. (25)
The foregoing authorities demonstrate the validity of
one researcher"s summary: "While many studies have been done in
this field, none [sic] have established nicotine as contributing
to the causation, aggravation or precipitation of any cardiovascular
disease." [emphasis added] (26)
C. Chron,ic Obstructive Lunq Di, sease ~Emphysema)
The failure of experiments to produce emphysema in animals
that have inhaled cigarette smoke casts serious doubt on the
statistical associations beween Chronic Obstructive Lung Disease
(COLD) and smoking, in various epidemiological studies. At the 1982
House hearings, Dr. Domingo Aviado described his efforts over many
years to induce emphysema in laboratory animals exposed to cigarette
smoke. None of the experiments produced emphysema in the animals.
Dr. Aviado therefore questioned "the logic of finding cigarette
smoke the major cause of pulmonary emphysema when primary air
pollutants [such. as sulfer oxides] have been shown to cause
CONF ]DENT,|kL
- 21 -
pulmonary emphysema in experimental animals, and. with the same
models, cigarette smoking has not." (2:7)
The 1984 Surqeon General's Report focused on COLD.~
According to the Report, mortality ratios of heavy smokers to
nonsmokers are as high as 30 in published studies, and 80-90% of
deaths from these, diseases are attributable to smoking. The Report
concluded, however, that only 10-15% of smokers woul~d develop
'"moderate or severe airflow obstruction." The Report al.so conceded:
that "an animal model for the development of emphysema using the
inhalation of cigarette smoke alone has not been convincingly
demonstrated."
As with lung cancer and heart disease, COLD appears to
be "multifactorial." The literature has identified possible genetic
factors associated with COLD,. familial and socio-economic factors,
occupational and environmental exposures, poor nutrition, and~
infection. (28)
II. RISK FACTORS: THE ISSUE AND ANALYSIS
The anti-smoking forces, including the Surgeon General,
claim that tobacco kills 350,000 to 400,000 persons per year. The
claim is now so commonplace that most of the people repeating it
CONF |DENT:IAL
- 22 -
have no idea where it came from or what it really means. In, fact,
the number and the computation, upon which it is based are subject
to serious scientific challenge.
The various calculations of numbers of disease cases or
deaths have nothing to do with laboratory research or the biological
mechanisms underlying the disease processes. These numbers are
based solely on statistical associations obtained from
epidemiological studies. Consequently, when a number of excess
deaths is calculated, for example, deaths from lung cancer
attributed to smoking, this number tells nothing about whether an
individual smoker"s lung cancer "~is due" to smoking or some other
factor, nor does it even tell which smokers in a group of lung
cancer patients "developed" their disease because of smoking.
Underlying the calculation of excess deaths due to. smoking
is the scientifically unjustified interpretation of the reported
statistical association between smoking and disease as a causal
relationship. A comment in a recently published book titled~
Statistical Methods In Cancer Research provides a cautionary note
in regard to the interpretation of excess deaths and attributable
risks:
CONF;]DENT|AL
Unfortunately, the only way to be absolutely
certain that a causal relationship exists is
to intervene actively inthe system, by removing
the disputed factor. In the absence of such
- 23 -
evidence, a more cautious interpretation of
the attributable risk measures would be
terms of the proportion of risk explained by
the given factor, where "explain' is used in
the limited sense of statistical association.
(29)
In the context of smoking, this observation is pertinent because
the claimed causal relationships between cigarette smoking and
certain diseases, as discussed above, have not been scientifically
established.
The calculations of excess deaths due to smoking hawe
been. subject to criticism over the years throughout the world.
The Report of the Advisory Committee to the Surqeon General on
Smokinq and Health (the Terry Report) published in 1964 did not
provide a calculation of a number of excess deaths causally related
to smoking in the population because, as the Report noted,, it
"cannot be accurately estimated." (p. 31) In fact, the Committee,
in preparing the report,~ considered the possibility of performing
such calculations but, according to a doctor who attended their
deliberations, decided not to because "it involves making so many
assumptions that the Committee felt it should not attempt this,
that it might be as misleading as it was informing."
(30)
Subsequent Reports have, however, made these calculations.
In 1969, a distingu.ished physician testifying before a
U.S. congressional committee said "the widely publicized accusa-
CONF ],DENT ]~AL
- 24 -
tions of hundreds of thousands of deaths caused by cigarettes, and
of shortening life expectancy a specific number of minutes per
cigarette smoked, are fanciful extrapolations and not factual data."
(31)
In 1986, a critical essay published in The Journal of
Medical Sciences addressed the claim by the Health Education Council
and the British Medical Association that 77,774 deaths in England
and Wales were caused annually by smoking. These were 77,774 deaths
from heart disease, lung cancer, emphysema and bronchitis among
men and women. After a careful scientific analysis of the
assumptions underlining the calculation, the researcher concluded:
his essay by noting that "the notorious 77,774 deaths per year
have to be consigned to the realm of fantasy
" (32)
In 1988, a New Zealand statistician published in the New~
Zealand Medical Journal criticism of the use of the attributable
risk calculations in regard to that country. He described the
estimates of death per year due to smoking as of "spurious accuracy"
because they are based on disease rates subject to error and the
assumption that statistical association is equivalent to causation.
(33)
An examination of the epidemio~ogical concepts used in
the excess deaths cal, culation will highlight the uncertainties
CONF ]~DENT ]:AL
mentioned above. The attributable risk percentage for smoking is.
calculated by using two numbers -- the smokers' "relative risk" for
a disease and the percentage of smokers in the population:. Both
of these components contribute to the uncertainty in the
attributable risk percentage.
"Relative risk" is a statistical term. It represents
the ratio of the number of deaths in a given population exposed to
a substance over the number of deaths in a population that has not
been exposed to the substance. For example, assume that the death
rate for lung cancer among asbestos workers is 60 per i00,000;
assume also that the lung cancer death rate for non-asbestos workers
is I0 per i00,000. The "mortality ratio" is 6:1. Therefore, the
"relative risk" for lung cancer among asbestos workers is 6. The
1989 U.S. Surqeon General's Report indicates that the nonsmoker
death rate for lung cancer per i00,000 for males is 13.6 and for
females is 11.4. These figures are divided into the smoker death
rates for lung cancer per i00,000 to give relative risk for males
of 11.94 and for females of 4.69.
Relative risks are obtained from. epidemiological studies
based on information regarding smokers'~ death rates and nonsmokers'
death rates.5 Consequently, a~l the biases and variations in. those
The epidemiologica~ studies relied upon most heavily in the
1989 Report are the American Cancer Society's CPS-I (1959-1965)
and CPS-II (1982-~986) studies.
CONF IDENT IAL
- 26 -
calculations are transferred to the attributabl~e ri, sk calculation.
In particular, if the population in an epidemiological study is
not representative of the general population, the relative risks
obtained from the non-representative group can be challenged when
used to calculate attributable r~sk in general.
Moreover,. the measurement of the prevalence of smoking
in the population is frequently difficult to estimate accurately.
A 1987 statistical methods text noted: "It is
difficult to obtain
estimates of attributable risk. Even cohorts such as the
British doctors or US veterans d~ffer sufficiently from the general
population., in terms of economic level for example, to. make
extrapolation in terms of attributable risk hazardous." (34)
The attributable deaths figure -- 390,000 in 1985
according to the 1989 Report -- is derived by projecting the
expected non-smoker death rates for various chronic diseases onto
the 1985 population,, subtracting the "expected" number of deaths
from the actual deaths caused by those diseases, and attributing
the difference to smoking. The breakdown o.f extra deaths in the
1989 ~eport is as follows:
COM F i DENT~! AL
- 27 -
Cancer
Cardiovascular Disease
COLD
Other (e.q., residential fires)!
136,100
142,500
571,000
531,000
388,600
This technique has a number of inherent flaws. First,
it assumes that causation, is fully established for lung cancer, a
variety of other cancers, and heart disease; second, it also assumes
that the ACS samples are not only representative of the entire
United States population, but can be projected forward; and third,
it assumes that smoking is the sole and only cause of "extra" smoker
deaths -- an obvious fallacy which renders the 390,000 number
virtually meaningless.
The 1989 Report listed and discussed various
"uncertainties" in its attributable risk calculations. The list
includes the following points: "errors of classification of
exposure levels (e.g., amount smoked, length of time quit),.
representativeness of populations studied, failure to take into
account confounding variables (e.g., occupational exposures),
potential errors in estimating current or past cigarette use or
non-use, and errors in classification of causes of death." (135).
CONF I:DENT |AL
These sources of uncertainty, however, did not prevent the well-
publicized claims of 390,000 excess deaths.
One disquieting problem with the attributable risk calcu-
lation for smoking arises when another attributable risk calculation
is made for the same group for another exposure (e.g., occupational,
diet). The two attributable, risk percentages can add up to over
i00 percent, causing severe interpretational problems. For example,
a report that in a group 60 percent of the deaths are due to smoking:
and 70 percent of the same deaths are due to an occupational
exposure presents problems. This occurs because an attributable
risk percentage for smoking does not and cannot take into account
any suspect other than smoking for the disease in question. An.
epidemiologist pointed this out in discussing attributable risk as
a fraction instead of a percent: "For any given individual,
however, this estimate is fraught with difficulties. For one, the
attributable fraction can have no unique value; when there is
overlap and interaction with other factors, the estimate can always
be eroded." (36)
When the attributable risk formula was examined from a
statistical perspective in view of its possible adoption by the
U.S. Congress as a method of compensation in radiation and cancer
cases, a statistician concluded that " . it is
inappropriate
CONF ),DEMT IAL
- 29 -
either as a statistical measure of probability of causation or as
a guide to share in causation." (37)
No one denies that cancer and, most particularly, heart
disease are multi-factorial diseases. Nor can anyone deny that
smokers, as a class, are more exposed to many of these "other
factors" than are non-smokers. These factors are "lifestyl:e," the
same k~nds of choices or personality characteristics or
environmental influences that may lead people to smoke.
In 1988, the Public Health Service ("PHS"')I issued a report
seeking an answer to the question "whether smokers have other
unhealthy habits that may . . increase their probability of
succumbing to serious illness, disability and even death.." The
report concluded that "smoking is related to other unhealthy
behaviors." Included in the survey were hours of s~eep (31% of
heavy smokers got less than six hours, compared to 21% of never
smokers); breakfast habits (48% of heavy smokers never eat
breakfast, compared to 18% of never smokers); exercise (65% of
heavy smokers were "sedentary," compared to 55% of never smokers);
and alcohol consumption (22.5% of heavy smokers averaged two drinks
a day, compared to 3.5% of nonsmokers). The big surprise was over-
eating, where it was expected that smoking would have a uniformly
favorable effect. In fact, ~t turned out that male heavy smokers
snack more and are not significantly di~fferent in weight.
CONF, IDENTIAL
The PHS results are more notable for their source than
for their substance. Had the PHS surveyed the existing literature,
it would have found evidence for smoker exposure to a wide variety
of "other" risks: socio-economic factors (blue collar, education,
income); geographical factors (urban versus rural); environmental
factors (water and air pollution); alcohol; coffee; dietary habits
(Vitamin A); drug use; lack of exercise; Type-A personality
(aggressive or ambitious); stressed personality (idepressed or
anxious); situational stress (unemployment and divorce); lack of
preventive health care,, suicide, accidents, violence and overall
risk-taking.
The gross error in the attributable risk studies is that
they are "univariate." They take into account only one health
behavior, whereas there are many associated with smoking that might
influence mortality. One way to demonstrate this error is to take
another health behavior, apply a univariate analysis, and see where
it leads. For instance, a recent preliminary report from the
University of Minnesota finds that heavy coffee drinkers have a
relative risk for lung cancer of about 7 to 1 (compared to 10 to 1
for smokers). If it is assumed that the only important variable
is coffee and that a substantial portion of heavy coffee drinkers
are smokers,~ a calculation can be made that re-attributes a very
large portion of lung cancer deaths from smoking to coffee. The
CONFIDENT IAL
- 31 -
same sort of calculation could be done with. respect to exercise or
stress or Type-A behavior or any of the other factors mentioned
above -- if the data were available.
Of course, the result of each of the univariate analyses
would be wrong. Each would fail to take into account the
"confounding" effects of all the others. A "multivariate" approach
is more appropriate.
In fact, many epidemiological studies include a lot of
the relevant behavioral data. Nonetheless, the Surgeon General
and others have chosen to focus only on smoking. In the Cipo~lone
pretrial discovery, the defendants obtained (for the first time):
the underlying American Cancer Society data (ACS Million Persons
Study) relied upon in the 1989 Surgeon General's Report and many.
other "excess death" calculations. Statistician Irwin Miller put
the data (for women and lung cancer) into a computer and did a
"multivariate" analysis -- ~.e., the computer juggled all the
health-related behaviors simultaneously to see which ones were
related to lung cancer. Dr. Miller'.s conclusion was that a great
portion of Hhe apparent relationship between smoking and. lung cancer
disappeared when other factors were taken, into account. He is
doubtful, given the in.terdependence of all the health behaviors
and the absence of full data, that any clear multi-variate
conclusion can be drawn.
CONF:IDENT |AL
III. THE INDUSTRY RESPONSE
Notwithstanding the indictment by its critics, Brown &
Williamson and the tobacco industry responded in an appropriate
fashion to health issues raised about smoking by funding numerous
independent research efforts. These efforts have involved hundreds
of outside institutions and thousands of independent scientists
who have added markedly to science's understanding of a number of
diseases and any possible link between them and smoking.
Council for Tobacco Research
In 1954, the chief officers of nine tobacco products
manufacturing companies in the United States, and five organizations
of growers of leaf tobacco and operators of tobacco warehouses
formed the Tobacco. Industry Research Committee (TIRC). The purpose
of the TIRC was to investigate the connection between tobacco use
and human health. Although the name, TIRC, was changed in. 1964 to
the Council for Tobacco. Research (CTR), the organization continues
to pursue the goals that were established by its founders in 1954.
Seeking to promote objective, independent research on
smoking and health, the TIRC formed a group of independent
scientists called the Scientific Advisory Board (SAB):. This group
CONF ]DENT:]AL
is composed o.f highly-regarded scientists who come fromwell-known
universities, laboratories, and medical centers throughout the
country. The SAB decides what research will be funded.
CTR has been fortunate in that it has been guided by
independent scientists of the highest reputation. The current
members of the SAB are: Richard J. Bing, M.D., Professor of
Medicine,. University of Southern California School of Medicine;
Roswell K. Boutwell, Ph.D., Professor of Oncology, University of
Wisconsin; Drummond H. Bowden, M.D., Professor and Head of
Pathology, University of Manitoba; Michael J. Brennan, M.D.,
President and Medical Director, Michigan Cancer Foundation; Joseph
D. Feldman, M.D., Editor, Journal of Immunoloqy; Jeffrey R. ~dle,
Ph.D., Professor of Pharmacogenetics, University of Newcastle upon.
Tyne; Leon O. Jacobson, M.D., Professor of the Department of
Medicine, University of Chicago; Manfred L. Karnovsky,: Ph.D.,
Professor of Biological Chemistry, Harvard Medical School; Alfred
G. Knudson, Jr., M.D.,. Ph.D., Fox Chase Cancer Center, Institute
for Cancer Research; Henry T. Lynch, M.D., Professor and Chairman,
Department of Preventive Medicine and Public Health, President,:
Hereditary Cancer Institute, Creighton University Schoo~ of
Medicine; G. Barry Pierce, M.D., American Cancer Society Centennial
Research Professor, University of Colorado Health Sciences Center;
Gordon H. Sato, Ph.D., Director,. W. Alton Jones Cell Science Center;
Sheldon C. Sommers, M.D., C~inical Professor of Pathology, Columbla
CONF I DENT | AL
- 34 -
University; Peter K. Vogt, Ph.D., Chairman, Department
Microbiology, University of Southern California School of Medicine.
When an application reaches CTR, the scientific staff
assigns a subcommittee of the SAB to each application. At the SAB
meeting, each application is discussed. A member of the
subcommittee assigned to the application is asked to present a
critique of the proposal. Other critiques are read and a general
discussion is held regarding the application. A vote is then taken
as to whether to. approve the application. If the application is
approved, each SAB member rates the application, as to. its relevance
to smoking and health.. The Scientific Director must fol~low the
advice of the SAB, giving preference to. those applications given
high ratings.
The administrative work of CTR is carried out by a
permanent scientific and administrative staff located in New York
City. CTR has always had distinguished researchers who have served
as its Scientific Director. The first was Dr. Clarence Cook Little,
a prominent researcher in the field of genetics. Others who have
served in this role are Dr. William U. Gardner, a former Professor
of Anatomy at Yale University School of Medicine, and Dr. Sheldon
C. Sommers, a former Professor of Pathology at Columbia University
College of Physicians andSurgeons. The present Scientific Director
is James F. Glenn,~ M.D., former Dean of the Mount Sinai School~ of
CONFIDENTIAL "~
- 35 -
Medicine. The Scientific Director of CTR is responsible for
administering funds for medical and laboratory research. The funds
are appropriated by CTR only upon the recommendation~ of the SAB.
The Industry Technical Committee (ITC), composed of the
research directors of the member companies, acts as an advisory
panel for the Scientific Director and the SAB. They provide
technical information from industry sources about cigarettes and
tobacco. A representative of the ITC may attend SAB meetings,
but has no vote on, research grants.
The overall administration of CTR has been
the
responsibility of the Board of Directors, whose members
are
designated executives of the companies that belong to CTR.
The
Board of Directors is responsible for administrative decisions such
as determining the budget, voting on the bylaws and selecting office
space. The directors, however, have no control over the research
decisions of the SAB.
CTR does not operate its own research facility. Rather,~
research support has been achieved primarily through a program, of
grants-in-aid, supplemented by contracts with institutions and
laboratories. As of the end of 1988, grants and contracts have
been approved totalling more than $136,.000,000. Grants have been
awarded to 1,053 independent scientists in some 30Omedical schools,
CONF ]DENT
- 36 -
hospitals and research institutions. Much of this research was
jointly funded by non-tobacco interests such as the U.S. Public
Health Service, the National Institutes of Health, and the National
Cancer Institute.
CTR grantees have made significant contributions to
scientific research. They have presented their findings at
scientific and medical society meetings too numerous to list.
They are free to publish any of these research results as long as
the research meets the criteria of peer reviewed journals. In
fact, CTR grantees have published over 3000 papers and articles,
some of which have been cited by critics of the industry such as the
Surgeon General.
Since the beginning, CTR has supported research that
would identify and define factors that may be involved in the
causation of certain chronic diseases associated with cigarette
smoking. Approved research has covered a wide range of human
diseases, including many types of cancer, respiratory and
cardiovascular diseases. CTR also approved investigation into
other medical,~ chemical, biochemical and pharmacological areas. In
addition, CTR has sponsored the study and development of basic
laboratory and research, techniques and has underwritten reviews of
research literature in specific areas.
CONF:IDENT,%AL
- 37 -
Research funded by CTR has added much to the present
knowledge about cigarette smoking and health. For example, the
research has: (i) tested the hypothesis that cigarette smoke acts
as a direct contact carcinogen; (2) identified smoke components
that may affect cilia; (3) investigated whether smoking or nicotine
causes cardiovascular disease; (4) attempted to produce pulmonary
squamous cell carcinoma in animal inhalation studies.6 These
studies and other published research demonstrate CTR'~s commitment
to examining the relationship between cigarette smoking and disease
causation.
~Dstitutional Research
Brown & Williamson has demonstrated its interest in
smoking and health issues by supporting research efforts at
prestigious institutions with nonrestrictive funding. Most notably,
three separate multi-million dollar projects have been sponsored
at three universities: Harvard University, the University of
California at Los Angeles, and Washington University.
6o
Microbiological Associates, for example, conducted a CTR-funded
nine-year study, costing some $12 million dollars, in which
over i0,000 mice inhaled the smoke of approximately 800,000
cigarettes. Inhalation of the smoke did not produce any
squamous cell lung cancers. Furthermore, mice in which, cancers
were chemically induced! did not get significantly increased
lung cancers when later exposed to long-term cigarette smoke
inhalation. Experiments were performed using high tar/low
nicotine cigarettes and high tar/high nicotine cigarettes.
CONF |D£1~T
- 38 -
A unique and important aspect of this industry grant
research is the flexibility in the utilization of the funds. This
flexibility has made it possible to provide funding for the
initiation of research programs which are then supported by grants
from the National Institutes of Health and other agencies as well
as providing certain items of core equipment that are shared by the
investigators.
Harvard
In September 1972, Harvard Medical School was awarded a
broad-based institutiona~ grant by Brown & Williamson and other
tobacco companies to launch a five-year investigation into pulmonary
and cardiovascular diseases. In 1977, the grant was renewed for
an additional three-year period.
The project was under the direction of Dr. Gary Huber,
Assistant Professor of Medicine and Director of the Respiratory
Diseases Clinic at Boston City Hospital's Channing Laboratory.
At the time the project was launched, Dr. Huber was already
directing a well-established research program for the study of host
defenses in the lung. With the aid of the grant~ Dr. Huber was
able to expand his program to include studies on the relationship
between tobacco smoke and health, on differences in, host
CONF ]DENT IAL
- 39 -
susceptibility to disease,, and the effect of other environmental
influences, such as air pollutants, on the lung.
Dr. Huber's research proj, ect was designed to contain
four phases. First, he intended to redirect his existing program.
toward the study of possible biological effects of cigarette smoke
on the lung with the, objective of determining what role,~ if any,
cigarette smoking might play in. the development of pu,lmonary
disease. Second, he sought to expand existingi resources to incl~ude
more comprehensive studies in the areas of biochemistry, pathology
and epidemiology. Third, Dr. Huber p~anned to develop resources
for the study of potential relationships between cigarette smoke
and lung cancer. Fourth, he intended to study possible
relationships between cigarette smoke and cardiovascular diseases.
During the eight-year period in which the industry
sponsored the project, Dr. Huber and his co-workers published
approximately 90 articles on their work. The Harvard grant also
made it possible for Dr. Huber and his group to obtain government
funding for other smoking-relating projects. With funds received!
from the Nationa~ Cancer Institute and the National Institutes of
Health, he was able to develop a method of monitoring respiration
and smoke inhalation patterns of human smokers.
CONF %IDENT IAL
-- 40 --
Unfortunately, Dr. Huber was unable to complete the
project because of difficulties with the animal inhalation facility
used by his group. In 1977, the animal facility was closed on the
advice of Harvard veterinarians. A large number of the animals
had developed infections. Although Dr. Huber spent many months
attempting to find other facilities and the sponsoring companies
were making plans for long-term support, a practical solution could
not be found. Consequently, Dr. Huber finished pending research.,.
and the program was terminated in June 1980..
UCLA
The commitment of the cigarette companies to broad-based
research is also demonstrated by their support of a biomedical
research project from 1974 to 1982 at the UCLA School of Medicine.
The UCLA project, under the direction of Dr. Martin J. Cline, Chief
of the School of Medicine's Division of Medical Ontology and
Hematology, facilitated the expansion of the Division and
supplemental ongoing research in three major areas, including the
investigation of a possible relationship between tobacco usage and
disease, particularly lung cancer, as well as exploration of methods
for early cancer detection and therapeutic techniques involving
immunotherapy and chemotherapy.
-41 -
The project researchers determined that the ability to
define alveolar macrophage function could aid in, the analysis of
environmental factors and diseases that might influence macrophage
function. They could not identify any significant abnormalities
or adverse effects of smoking on the performance of human alveolar
macrophages.
The UCLA researchers collaborated with others in an.
attempt to determine whether activation of cancer genes is important
in: causation of tumors. Preliminary data suggested that these
genes may be important in the initiation and maintenance of certain
tumors.
The UCLA project also provided, new information in the
treatment of refractory malignant disease. The researchers in the
project were among the first to develop the concept of freezing
bone marrow for long-term storage in patients with malignant
disease.
As this brief summary suggests, physicians and scientists
involved in the UCLA project were able to address fundamental
problems of human health and disease. Their efforts have resulted
in, the publication of numerous articles in scientific and medi, cal
journals, in which the support of the participating tobacco
companies was acknowledged.
CONFIDENT IAL
Washinqton University
The third of the broad-based institutional grants was
awarded in March 1971, to Washington University in St. Louis for a
basic research program on the immunological properties of cancer.
The project is still being funded today by three tobacco companies.
Initially, the project was conducted under the direction
of Dr. Lauren Ackerman, an international authority on cancer, and
Dr. Paul E. Lacy, head of the University's Department of Pathology
and one of the world's leading experts on cell structure. The
initial purpose of the program was to find and analyze "foreign"
substances or antigens within the cancer cell and to utilize those
antigens for the early detection, treatment and possible prevention
of cancer.
This focus eventually led to immunology studies, on the
role of antibodies in the growth and development of neoplastic
cells; the cellular events involved in antibody production; the
morphologic and biochemical structure of the cell membrane; the
effect of viruses on the genetic information in the cell; and the
effect of physical and chemical carcinogenic agents on the genetic
information in cells.
CONF ]DENT ]AL
- 43 -
The research findings from this program, reported in
more than 300 publications, have made significant contributions
to ongoing work aimed at understanding the basic cause,, development
and treatment of cancer and other diseases. The understanding of
the immune system made possible by this research is relevant not
only to cancer, but it can also be expected to provide insight
into diseases such as lung emphysema, rheumatoid arthritis, lupus
and diabetes.
C. AMA-ERF
The America Medical Association Education and Research
Foundation Project for Research on Tobacco and Health (AMA-ERF)
was funded by six clgarette manufacturers from 1964 through 1972,.
with contributions totaling over $15 million. All administrative,
scientific and policy decisions, screening of grant applications,
and distribution of funds were the responsibility of the AMA-ERF
Board of Directors and the scientific advisory committee appointed
by the board. Other than funding, the project was entirely
independent of the tobacco industry.
In 1963, the AMA House of Delegates adopted a
recommendation from, its Board of Trustees that the AMA-ERF undertake
a comprehensive research program on tobacco and health. The AMA-
ERF was an existing organization within the AMA, primarily
CONF; ! DE NTI] AL
4!4 -
responsible for supporting medical education and
scientific and medical research.
fostering
An AMA announcement indicated that the project would be
financed by a contribution from the AMA and solicited contributions.
Only unrestricted contributions would be accepted. The tobacco
industry wrote the AMA early in 1964, offering to contribute $10
million to the project over a five-year period. The industry was
responding to the Surgeon General's suggestion that more research
was needed. The contributions were made with the understanding
the money would be used only for research on smoking and health.
The AMA-ERF Board of Directors appointed a committee of
distinguished scientists, the Committee for Research on Tobacco
and Health (CRTH), to develop guidelines on research policies and
procedures, to identify significant areas of research, and to screen
applications for research grants. Three of the original five
members .of the CRTH had also served on the Surgeon General's
Advisory Committee that produced the 1964 Report to the Surgeon
General.
Grantees were required to publish their findings in the
medical or scientific journal of their choice so that the
information would become public through the scientific medila.
Grantees were also expected to participate in workshops convened
COMF tDENT:]AL
- 45 -
by the AMA-ERF committee in 19661, 1970 and 1972 for the purposes
of presenting oral reports on their research projects, stimulating
an exchange of ideas, and delineating new areas for investigation.
In 1968, during the AMA's Annual Meeting in San Francisco,
a presentation was made by some of the grantees to report on their
progress. At that time, the AMA-ERF committee indicated that more
research was still needed to clarify many of the issues surrounding
tobacco and health, including
statement become controversial
interpreted as casting doubt
questions of causation. This
because at the time it was
on the Surgeon General's 1964
conclusions. The AMA-ERF committee then. clarified its position in.
a statement pubiished in JAMA two months after the annual meeting,
affirming that research completed under this project in no way
challenged the .conclusions of the 1964 Surgeon General's Report.
In August 1971, seven years after the project had begun,
the tobacco companies and AMA began to consider phasing out the
project. By July 1972, they had agreed to conclude the project by
making no more new grants. The grants then in existence were
allowed to wind down over the next several years. The findings of
the AMA-ERF project were well publicized both in the medical, and
scientific literature and in a final summary report by the AMA-ERF
committee, produced in 19:78 under the title Tobacco and Health,.
The information in the final summary was not new, since the research
COMF ]DENT IAL
- 46 -
results had been published by the grantees in scientific journals
over the previous 14 years. According to the summary, the
foundation had sponsored 219 separate research projects that
resulted in 795 publications and reports. Copies of the report were
provided free of charge to institutional members of the Medical
Library Association. The AMA also sent copies to those who wrote
to request one.
During the life of the AMA-ERF project, anti-smoking
critics became more vocal. The project did not escape these
criticisms, especially those attacking the AMA for associating
itself with the tobacco industry. The project was concluded in
large measure because of the AMA's embarrassment over these attacks.
In sum,, the AMA-ERF project represents a substantial
effort on the part of the tobacco industry to sponsor broad-based
research on smoking and health.
Tobacco Workina Group
The Tobacco Working Group (TWG) was formed in 1968, to.
provide support to the National Cancer Institute's Less Hazardous
Cigarette (LHC) research program. The goal of the LHC research
program initially was, as its name suggests, to identify means of
developing a "less hazardous cigarette;''~ the goal of the TWG was
CONFIDENT IAL
- 47 -
to develop a research program to identify how this product could
be achieved. Thus, the TWG's purpose was to. provide scientific
and technical assistance in designingand developing the experiments
that were being conducted under the LHC program, at the National
Cancer Institute. The LHC program itself was federally funded and
inspired. It lasted approximately Ii years and spent over $32
million dollars on research, on both a grant and a contract basis.
The open and cooperative attitude of the tobacco industry
in investigating smoking and health issues is illustrated by the
participation of company scientists in the TWG and the sharing o£
tobacco industry technical expertise and research results. Company
scientists provided technical advice, reviewed research proposals,
and conducted seminars on topics such as smoke chemistry and
techniques of cigarette manufacturing. This expertise was not
generally available outside the tobacco industry and was, of course,
of particular relevance to the work of the TWG.
The companies also shared technology with the TWG. For
example, A.D. Little's improved smoking machine, developed as a
part of its work for Liggett, was utilized in TWG animal inhalation.
experiments. Moreover, various companies encouraged tobacco
industry suppliers to share new product ideas with the TWG, i.e.,
various new cigarette papers, processes for producing reconstituted~
tobacco sheets, technology concerning expanded tobacco, etc. The
CONF [DENT
- 48 -
suppliers were, of course, dependent upon the tobacco industry for
the potential use of their respective new products. They would not
have shared these concepts for "safer cigarettes" with the TWG if
the cigarette companies had discouraged them.
The work of the TWG began by forming numerous subgroups
to address a number of complex scientific questions central to
smoking and health research: (~) the parameters of ci~garette
manufacturing that influenced smoke constituents; (2) a review of
available bioassay systems; (3) a review of epidemiology; (4.)
smoking machine technology; and (5) the proper method for
generating tars and fresh cigarette smoke for experiments. Then,
TWG designed a series of experiments funded by the National Cancer
Institute and conducted under the auspices of the LHC research
program to identify cigarette characteristics that could be
incorporated into a "less hazardous cigarettes" Eventually, over
150 cigarette variables were tested. The bulk of the work actually
performed focused on investigating the biological activity of
cigarettes with the goal of producing oigarettes with lowered
biological activity. Lowered biological activity was sought by
changing cigarette manufacturing parameters to modify smoke
composition, by use of tobacco substitutes, varying paper porosity,
varying tobacco processing methods, and varying methods in cutting
tobacco. The result was n__Qo significant scientific "breakthroughs"
toward the development of a "less hazardous cigarette."
CONF IDEN%|AL
Following the 1976 elections, the National Cancer
Institute's new leadership determined they should not be funding
what they considered "product development research" for the tobacco
industry in view of the government's position that smoking should
be discouraged. The TWG was formally disbanded in August 1977.
TWG members consulted as individuals on LHC research projects until
the research program ended in 1979. TWG issued four topical~
reports, a fifth report summarizing the skin-painting research,
and separate annual reports, but never issued a final summary report
of all activity. The results of the TWG-LHC experiments pointed out
that regardless of how cigarette design characteristics were
modified, the changes in the tumorigenicity of the smoke condensate
would be marginal, at best.
CO#F ]DENT [AL
END NOTES
(i) I_~d. at 656.
(2)
Vandenbroucke, J., "Is 'The Causes Of Cancer' A Miasma Theory
For The End O:f The Twentieth Century?" 17(4) International
Journal of Epidemioloqy 708, 709 (11988).
(3)
(4)
Berkson, J., "Smoking & Lung: Cancer: Some Observations on Two
Recent Reports," Journal of the American Statistical
Association 53(281):28-38132], March 1958.
Sterling, Cigarette Smoking and Disease, 1976 Hearings before
Senate Subcommittee on Health, p. 456.
(5)
Lee, P. (ed.), "Tobacco Consumption in Various Countries,"
Tobacco Research Council, Research Paper, No. 6 (4th ed.;
Edinburgh: T. and A. Constable, Ltd., 1975).
"'76.' Cancer Facts and Figures, American Cancer Society,"
(New York: The American Cancer Society, 1976).
(6)
Buhler, V., Statement, U.S. Congress, House, Committee on
Interstate and Foreign Commerce, Ciqarette Label:inq and
AdvertisinqD-1969, Hearing, 91st Cong., 1st Sess., April 15-30,
CON£IDENT IAL
and May I, 1969 (Washington:
1969), pp. 769-774.
Government Printing Office,
Burch, P., "Smoking and Cancer," Lancet I- 1316, June 9, 1973.
(17) Burch, "Smoking and Cancer."
(8)
(9)
False and Misleading Advertising, Hearing Before House
Committee on Government Operations, 75; Cigarette Labeling and
Advertising, Hearings Before House Committee on Interstate
and Foreign Commerce, 201-02.
Enstrom, J., Ph.D., "Rising Lung Cancer Mortality Among Non-
Smokers," Journal of the National Cancer Institute 62:4 [755]
(April, 1979).
(i0) Smoking: Prevention Health and Education Act, Hearings Before
Senate Committee on. Labor and Human Resources, 287.
(ii) JNCI, June, 1988.
(12) Cigarette Labeling and Advertising Hearings Before
Committee on Interstate and Foreign Commerce, 248-49.
House
CONF ]DENT IAL
- 52 -
(13) Hockett, R., "Where Do We Go from Here in Tobacco and Health
Research?," Presentation before the Burley and Dark Leaf
Tobacco Export Association, Lexington, Kentucky, October 2,
1967.
(14) Furst 1983 Senate, pp. 465, 467.
(15) NCI Report No.. 5,. "Toward Less Hazardous Cigarettes,'" p. 2
(Sept. 1980).
(16) Seltzer, 1982 House Appendix, p. 757 (emphasis added).
(17) Benditt, E., "The Origin of Atherosclerosis," Sci Amer 236(2):
74-85, February, 1977.
Blumenthal, S., et al., "Risk Factors for Coronary Artery
Disease in Children of Affected Families," Pediatr 87(6, Pt.
2): 1187-1192, 1975.
Newman, W., et al., "Relation of Serum Lipoprotein Levels and
Systolic Blood Pressure to Early Atherosclerosis: The Bogalusa
Heart Study," N Enql J Med 314(3): 138-144, 1986.
CONF ]DENT IAL
- 53 -
Rifkind, B., and C. Lenfant,. "Cholesterol Lowering and the
Reduction of Coronary Heart Disease Risk," JAMA 256(20):
2872-2:873, 1986.
Strong, J., "Coronary Atherosclerosis in Soldiers: A Clue to
the Natural H~story of Atherosclerosis in the Young," JAMA~
256(20): 2863-2866, 1986..
Enos, W., et al.~ "Coronary Disease Among United States
Soldiers Killed in Korea: Preliminary Report," JAMA 152(12):
1090-1093, 1953.
Enos, W., "Pathogenesis of Coronary Disease in American
Soldiers Killed in Korea," JAMA 158(11): 912-914., 1955.
Enos, W., et al.~ "Pathology of Coronary Arteriosclerosis,."
Amer J Cardiol 9(3.): 343-354, 1962.
McNamara, J., et al., "Corona~9 Artery Disease in Combat Casu-
alties in Vietnam," JAMA 216(7): 1185-1187, 1971.
(18) U.S. Public Health Service, Office on Smoking and Health, The
Health Consequences of Smokinq: Cardiovascular Disease. A
Report of the Surgeon General: 1983, Department of Health and
CONFIDENT I:AL
- 54 -
Human Services, Washington, DHHS Publication No.
50204, 1983, p. 50.
(PHS) 84,-
(19). Schievelbein, H. and G. Heinemann, "Nicotine and Athero-
sclerosis," Atherosclerosis VI: Proceedinqs of the Sixth
International Symposium, ed. F. Schettler, et al. (Berlin:
Springer-Verlag, 1983), pp. 899-902.
(20) Kaufman, D., et al., "Nicotine and Carbon Monoxide Content o~
Cigarette Smoke and the Risk of Myocardial Infarction in Young
Men," N Enql J Med 308(8): 409-413, 1983.
(21) Wald, N., et al., "Serum Cotinine Levels in Pipe Smokers:
Evidence Against Nicotine as Cause of Coronary Heart Disease,"
Lancet II(8250): 775-777, 1981.
(22) Wald, N., et al., "Urinary Nicotine Concentrations in Cigarette
and Pipe Smokers," Thorax 39(5): 365-368, 1984..
(23): Fisher, E., Statement, United States House of Representatives
Committee on Energy and Commerce, Subcommittee on Health and
the Environment, Smokinq Prevention Education. Act, Hearings,
98th Congress, First Session, March 9 and 17, 1983 (Washington:
Government Printing Office, 1983), pp. 4.06-423.
CONF |'DENT
(24) I_~d.
(25) Hazleton Laboratories America, Inc., "Final Report --
Inhalation Bioassay of Ciqarette Smoke in Doqs: Effects of
Nicotine and Carbon Monoxide on Atheroqenesis," Project No.
976-904, Contract No. ECI-SHP-75-112, Submitted to the National
Cancer Institute, Division of Cancer Cause and Prevention,
Smoking and Health Program, Washington, D.C., June i0, ~981.
(26) Hockett, Statement, 1976.
(27) 1982 House Appendix, p. 540.
(28) Burrows, B., et al., "The Relationship of Childhood Respiratory
Illness to Adult Obstructive Airway Disease," Am Rev Resp Dis
115: 751-60, 1977.
Fletcher, C., et al.,~ The Natural History of Chronic
~ronchitis and EmDhvsema, Oxford Univ Press, Oxford, 1976,
272 pp.
Lebowitz, M.D., "The Relationship of Soci.o-Environmental
Factors to the Prevalence of Obstructive Lung Diseases and
Other Chronic Conditi.ons," J Chron Dis 30: 599-611, 1977.
CONF]DENTI]AL
Moser, K.M., Bordow, R.A., "Chronic Obstructive Pulmonary
Disease: Definition, Epidemiology, and Pathology," in Manual
of Clinical Problems in Pulmonary Medicine, Bordow, R.A., e__t
al. (eds.), Little, Brown and Company, Boston, 1980.
Openbrier, D.R., et al.~ "Nutritional Status and Lung Function
in Patients with Emphysema and Chronic Bronchitis," Chest 83:
17-22, 1983.
Quanjer, Ph.H., et al., "Maximal Expiratory Flow-Volume Curves
in a Follow-Up Study," Scan J Resp Dis 57: 309-310, 1976.
Salvaggio, J.E., "Overview of Occupational Immunologic Lung
Disease," J Allerqy Clin Immunol 70: 5-10, 1982.
Tager, I., et al., "Studies of the Familiar Aggregation of
Chronic Bronchitis and Obstructive Airways Disease," Int J
Epidemiol 7: 55-62, 1978.
Tisi, G.M., Pulmonary Physioloqy in Clinical Medicine, Second
Edition, Williams & Wilkins, Baltimore/London, 1983.
U.S. Public Health Service, Smokinq and Health: Report of
the Advisory Commilttee to the Surqeon General of the Public
Health Service, DHEW, Pub. No. Ii03,: 1964.
CONF [iDENT |AL
- 57 -
U.S. Public Health Service, Smokinq and Health: A Report of
the Surqeon General, DHEW, Pub. No. (PHS)79-50066, 1979.
U.S. Public ~ealth Service, The Health Consequences of Smoking,
Cardiovascular Disease: A Report of the Surqeon General,
1983, DHHS,. Pub. No. DHH(PHS) 84-50204'.
U.S. Public Health Service, Advance, Report of Final Mortality
Statistics, 1980, Monthly Vital Statistics Report, National
Center for Health Statistics, Vol. 32, No. 4 (Sup.), Aug. ii,
1983.
(29) I N!. Breslow & N. Day, Statistical Methods in Cancer Research,
78 (IARC 1980).
(30) Hundley, J., M.D., Assistant U.S. Surgeon General, U.S.P.H.S.
news conf. i/ii/~4.
(31) Cigarette Labeling and Advertising Hearings Before House
Committee on Interstate and Foreign Commerce (1969), 1256.
(32) Burch, P., M.D., "Can Epidemiology Become A Rigorous Science?"
Journal o~ Medical Sciences 14, 956-951 [!960] (1986).
CON F I DENT
(33!) Mullins, P., Ph.d.~ "The Cost of Cigarette Smoking,"
Zealand Medical Journal 27 July 1988, 491.
New
(34) II N. Breslow & N. Day, Statistical Methods in Cancer Research
21 (IARC 1987).
(35.) "Reducing the Health Consequences of Smoking:
Progress," 122-161 (Surgeon General 1989).
25 Years of
(36)i Susser, M., "Rules of Inference in Epidemiology," Regulatory
Toxicology & Pharmacology, 6:1:16-128 [119] (June 1986).
(37)! Cox, L., "Statistical Issues in the Estimation of Assigned
Shares for Carcinogenesis Liability," Risk Analysis,~ 7"1,
71-80 [72] (April 1987).
CONFIDENTIAL
-- 59 --
SMOKING AND ADDICTION
CONFIiDENT]AL
- 60 -
Tobacco smoking is an activity that has been engaged in
by people from a variety of cultures for hundreds of years. It is
a behavior involving innumerable individual choices, which, are
reflected in each person."s decision of whether, when, where and in
what manner he or she will smoke.
As with many other aspects of personal lifestyle, smoking
appeals to some, but is displeasing to others; some seem to enjoy
smoking only during certain periods of their lives, and eventually
decide tot and do, quit. Among those who dec~de to. smoke, the
activity takes a variety of forms and patterns. Some smokers only
smoke at certain times, or in association with specific activities,
e.q., only in the evenings, following meals, or during an
intellectual activity like reading. Given such idiosyncratic
patterns, it is not surprising that behavioral scientists have had
great difficulty in explaining individual motivations for smoking.
Nevertheless, some researchers with apparent biase~
against smoking seem to pay little attention to the complexities
of smoking behavior. Instead, they focus on a single ingredient
in tobacco smoke, namely nicotine, and say that it is the reason
why people smoke. They observe that some persons smoke frequently
and seem to value the opportunity to smoke and infer that smokers
are "dependent on" c~garettes. Some anti-smokers go so far as to
call smoking a "drug addiction..'" This claim
is clearly
CONF !DENT |AL
- 61 -
inappropriate, but one that often gets media attention when made
by the Surgeon General and others.
Just what is meant by the claim that cigarette smoking
is an "addiction?" A meaningful response to this question must
deal with the term "addiction" as more than merely a term of
convenience used to describe any frequently occurring behavior.
One must put aside, for example, statements by exercise enthusiasts
that they are "addicted" to running, or announcements of parents
that their children are addicted to television. Consider also
that there are books that describe a "love" addiction.. Former
Surgeon General Koop also contributed to the debasement of the
term when he said in 1982 that video games are ":addicting.'" (I)
It is obvious that the word addiction is on the verge of
losing its scientific meaning. Some, in fact, would argue that
the battle has already been lost.
Dr. David M. Warburton, of Reading University, England,
commented in. 1985 on the disturbingly broad usage the term
"addiction" has received:
Thus we can see that addiction in ordinary
usage can refer to work and business, sport
and revels, melancholy and study, Sack and
vice, prayers and virginity. Certainly, it is
a very broad concept which has been applied to
CONF ]DENT XAL
- 62 -
a wide variety of behavioral phenomena.
(P. 285) (2)
Rampant misuse aside, what is meant by the term"addict"
in a technical sense? Generally, there is a consensus that an
addict is a person whose repeated drug use is primarily motivated:
by avoidance or reduction of adverse physical (physiological)
symptoms. In other words, people are, said to be "physically
dependent" on the drug,, because if they do not receive their "fix,"
their bodies will go through an agonizing "withdrawal." Their
behavior is further characterized by ever greater leve~s of drug
intake, as they try to: gain the intoxicating "high" which is so
important in. the addict's life. Yet~ this. is more and more
difficult to do because the addict has developed a "tolerance" to
the drug. Addiction thus leads to the pitiful situation of having
a compelling physical need for a drug, which provides little
pleasure beyond meeting this need.
From a practica! point of view, the addict, when on the
drug, becomes intoxicated and is often unable to function normally.
There is intellectual and social impairment. His "need''~ for the
drug! overrides everything else.
not.
Does the cigarette smoker fit this picture? Of course
CONFIDENTIAl.
- 63 -
Even researchers who are vehemently opposed to smoking
recognize that the scientific evidence for addiction -- for physical
dependence -- to smoking is highly equivocal. But this has not
stopped many of these same researchers from. advocating an
"addiction" label for smoking. Unfortunately, as a result it seems
that the scientific evidence becomes
scientists, along with everyone else,
surrounding the term "addiction."
camouflaged and these
add to the confusion
Some examples of this confusion are instructive. In
1983, Dr. William Pollin, former Director of the National Institute
on Drug Abuse (NIDA):, testified before Congress that tobacco smoking
was "addictive." Yet, almost in the same breath, he also stated:
[e]vidence is not yet conclusive as to whether
or not there is physiologic dependence or what
type of withdrawal syndrome is associated with
cigarette smoking. (Pp. 99-100) (3)
Similarly, much publicity surrounded release of a Public
Health Service Pamphlet purporting to explain, "Why People Smoke
Cigarettes." (4) The pamphlet describes cigarette smoking as
"addictive." Dr. Jack Henningfield of the NIDA, commenting on the
pamphlet,~ is quoted as claiming that "we had filled in all the
gaps in the research" (p. 36) on the issue of addiction in smoking:.
(5) Yet, Henningfield had, only 2 years before, expressed in
CONF | DEN1 IAL
- 64 -
writing that whether physiological diependence is an important factor
in smoking was only "suspected." (P. 212) (6)
The real issue is camouflaged by such blatant statements
that cigarette smoking is an "addiction." Even advocates of th~s
position concede that scientific demonstration of the necessary
element of addiction -- physical dependence -- is "not yet
conclusive" or is only "suspected."
How do advocates of the smoking addiction hypothesis
explain the inconsistency of their positions? They have changed
the "name of the game." They now say that physical dependence is
not a prerequisite for addiction. They emphasize instead some
sort of nebulous, psychological analogue to addiction -- namely,
"dependence."
"Dependence" is an inexact term. It must not be confused
with "physical dependence," which specifies the precise and
objective characteristics of withdrawal and tolerance. The term
"dependence" often seems to be applied merely when some repetitive
behavior is observed which seems to have some importance to a
person, as reflected by indications that the behavior is difficult
to forego. It is a subjective label often referring to vague,
psychological characteristics.
CONF[DENTIAL
- 65 -
An eloquent statement of the near scientific
meaninglessness of the term "dependence" comes from the British
scientist,. Dr. David Warburton, of Reading University:
We all are 'dependent' for our ordinary
happiness, gratification, emotional well-being
and general quality of life on a whole range
of people and objects. We are in this sense
clearly dependent on things like our family and
friends, our job,~ our motor car, our favorite
armchair and the television set. (Pp. 287-
2s8) (7)
The vagueness and broadness of the general notion of
"dependence" can be avoided by focusing on "physical dependence"
as a critical feature of "addiction." When a person is "physically
dependent" on a drug, then abstinence from the drug leads to a
consistent set of physical disturbances, which together constitute
a uniform withdrawal syndrome. As noted above, no such physical
syndrome has been. established: for smoking. Any symptoms
experienced by one who stops smoking are the same as or similar to
those experienced by someone giving up a habit or by someone
dieting. It is probably more difficult for the dieter to give up
certain foods because he or she needs food to survive.
In the absence of solid evidence for withdrawal, an
attempt is sometimes made to keep the physical dependence concept
of addiction alive by claiming '"tolerance" to smoking. "Tolerance"
means that an increasing amount of a substance is needed to achi~eve
the same "high~" or effect on a person.
CONFIDENTIAL
- 66 -
Tolerance claims concerning smoking tend to be highly
anecdotal. For example, it is often pointed out that novice smokers
take a period of time before becoming accustomed to the habit, and
it is ~mplied that this is related to nicotine. However, this is
an obvious misuse of the concept of tolerance. All habits need a
formative period to become established. The concept of "tolerance"
clearly is inapplicable when considering the typical pattern of
smoking, which tends to remain at a fairly constant level throughout
the smoker's life. In addition, there is a category of smokers
who smoke only a few cigarettes a day or only in social situations.
Given the lack of credible evidence for physical
dependence in smoking, it is not surprising that those who advocate
the "addiction" hypothesis rely on indirect arguments. For example,
some have maintained that most smokers would like to quit smoking.
The relevance of this point is questionable for at least two.
reasons. First, even if one accepted that a large percentage of
cigarette smokers say they want to quit, that indicates nothing
about their motivations for continuing. Second, there is evidence
that reports of smokers' desires to quit smoking are highly
unreliable. Even Lynn T. Kozlowski, a scientist well-known for
his anti-tobacco views, commented on this, noting that "answers to
questions on 'wanting to stop' and 'trying to stop' have regu.larly
been. used uncritically. " (P. 699) He "encouraged caution
CON F I!DENT IAl
- 67 --
in what is made of what smokers say about their wish to give up
smoking and their attempts to do so," (p. 699). and advised that
"[b]oth what smokers say about their smoking and: what researchers
make of these statements should be read skeptically." (Pp. 699-
70.0.) (8) The objective observer should have this sort of
skepticism in evaluating such indirect arguments.
Some imply that quitting smoking is a herculean task, at
which only a few succeed. This forms the basis for the c~aim that
the "drug" nicotine has overcome a person's ability to choose
whether or not to smoke. But this is an incredible position. In
fact, as noted by the U. S. Surgeon General,~ over 41 million people
in this country have chosen to quit smoking, and have done so. (9)
The effort involved in quitting smoking is often highly
exaggerated. This is .recognized by even many of the more well-
known opponents of smoking. For example, consider the following:
GONF IDENT IAL
It may also be that, for the general public,
the stories circulating about the agony of
abstinence serve as a self fulfilling prophesy:
smokers expect it to be painful and therefore
it is. Many give up their attempts to break
the habit at the first sign of discomfort,~
anticipating greater pain., which, in reality is
not forthcoming. (P. 34.7). (i0)
[I]t is quite apparent that most smokers can
stop wi.thout formal help. (P. 16)i (ii)
I deplore those who characterize quitting
smoking as a tortured, almost impossible
- 68 -
process.. For many people, it is easy; for
most it is somewhere between, easy and difficult;
and only for a minority is it really difficult.
(P. 25) (12)
Much has been made of the alleged high relapse rates
among quitters. However, studies of such rates have been almost
exclusively based on therapeutic samples -- that is, people who
have had difficulty in. quitting smoking. Those people able to
quit on their own rarely come to the attention of researchers.
However, when dealing with nontherapeutic samples, a different
picture emerges. In the words of one researcher,~ a conclusion to
the effect that cigarette smoking is highly intractable "is a
conclusion based largely on the results of numerous studies of
single therapeutic interventions with populations of self-selected
subjects who had actively sought help." (P. 436) (113)
Dr. Pollin is one of those who states that smokers lose
their ability to choose whether or not to smoke. However, even
his own comments argue otherwise. For example, he points out that
the smoking quit rates for physicians and other health care
professionals are far greater than among other segments of the
population. If loss of personal control to a pharmacological master
explains cigarette smoking, then one would expect uniform quit
rates among: all segments of the population.
CON F ~iDENT ! AL
A similar argument could be made in regard to the social
class gradient for cigarette quitting rates. This was noted in a
1978 New Scientist article, as a challenge to the view that people
smoke for pharmacological reasons:
One of the strongest challenges to the theory
of 'physiological' cigarette dependence is the
simple observation that those who are most
likely to. stop smoking are determined far more
by social class than by individual psychology
or physiology. (P. 148) (14)
Clearly, the social and cultural factors impinging on individuals
have major impacts on their choices of whether to continue or to
quit cigarette smoking.
Thus, there are serious unanswered questions and
inconsistencies in the smoking addiction hypothesis. Despite these
problems, former Surgeon General Koop released a new report on
"Nicotine Addiction" on May 16, 1988. (15) Dr. Koop took a
categorical position regarding cigarettes and addiction. He stated:
This Report shows conclusively that cigarettes
and other forms of tobacco are addicting
the same sense as are drugs such as heroin, and
cocaine. (p. vi).
This "conclusion" was biased by a number of factors,
including: use of the vague term "dependence" which blurs the
distinctions from actual "addiction'"; selective application of
CONE !DENT IAL
- 70 -
data to support his preconceived opinions; and restricting the
review to pharmacological literature which ignores the complex
psychological aspects of smoking. Because of these and other types
of bias, the position of the Surgeon General's Report has been
criticized in the press and by several respected scientists before
a Congressional subcommittee in July, 1988.
What has occurred in recent years is an increasingly
vociferous attack on smoking, and an attempt to label it an
addiction. Lacking scientific demonstration of physical
dependence, these attacks have taken on a distinct emotional and
political tone. Consider, for example, the comments of Dr. Morris
A. Lipton, one of several scientists who performed a review for the
U. S. National Institute on Drug Abuse of the evidence for
"cigarette addiction." He gave the following reason for NIDA's
choice of "addiction" as applicable to cigarette smoking:
It was selected because it's sort of a dirty
word. ~P. 5B) (23)
Obviously, this implies that the label of "addiction" is applied to
smoking for social and political reasons, with little regard for
its scientific meaning.
CONF]DEN;]AL
- "71 -
Cigarette smoking is more accurately classified as a
"habit." As when giving up any habit, a smoker needs the desire
and the motivation to quit. There is nothing in cigarettes which
interferes with a smoker's ability to decide to quit and to carry
out that decision.
COI,/F | DENT ! AL
- 72 -
END NOTES
( 1)~
Mattiace, P., "Surgeon General Says Video Games May Harm
Children," The Associated Press, November 9, 1982, A.M. cycle.
(2)
Warburton, D.M., "Addiction, Dependence and Habitual Substance
Use,." Bulletin of The British Psycholoqical Society 38: 285-
288,~ 1985.
(3)
Pollin, W., Statement for the Record, Smoking Prevention Health
and Education Act of 1983, Hearings before the Committee on
Labor and Human. Resources, United States Senate, May 5 and
12, 1983, pp. 98-103.
(14,)
U. S. Department of Health and Human Services, "Why People
Smoke Cigarettes," U,. S. Government Printing Office, 1983.
(5) Anonymous, "At Last, The Government Calls Smoking an
(6)
Addiction," Medical World News 24(6),, March 28, 1983, pp. 36-
3¸7 .
Henningfield, J. E., Griffiths, R. R. and Jasinski,
'"Human Dependence on Tobacco and Opioids: Common Factors,
'"In: Behavioral Pharmacoloqy of Human Druq Dependence, T.
CONF I!DENT
Thompson and C. H. Johanson (eds.), NIDA Research Monograph
37, July, 1981, pp. 210-234.
(7)
Warburton, D. M., "Addiction, Dependence and Habitual Substance
Use," Bulletin of The British Ps¥choloqical Society 38: 285-
288, 1985.
(8):
Kozlowski, L. T., Herman, C. P. and Frecker, R. C., "What
Researchers Make of What Cigarette Smokers Say: Filtering
Smokers' Hot Air," The Lancet, March 29, 1980, pp. 699-700.
(9)
U. S. Department of Health and Human Services (1988), The
Health Consequences of Smoking: Nicotine Addiction, A Report
of the Surgeon General, Publication No. DHHS (CDC) 88-8406.
U. S. Government Printing Office, Washington, D.C.:
(i0) Pertschuk, M. J., Pomerleau, O. F., Adkins,. D. and Hirsh, C.,
"Smoking Cessation: The Psychological Costs," Addictive
Behaviors 4(4): 345-348, 1979.
(ii) Jaffe, J. H. and Kanzler, M., "Smoking As An Addictive
Disorder," In: Ciqarette Smokinq as a Dependence Process, N.
A. Krasnegor (ed.), NIDA Research Monograph 23,~ January, 1979,
pp. 4-213.
CONF[DENTIAL
- 74 -
(12) Horn, D., "Psychological Analysis of Establishment and
Maintenance of the Smoking Habit," In: Ciqarette Smokinq as
a Dependence Process, N. A. Krasnegor (ed.), NIDA Research
Monograph 23, January, 1979, pp. 24-29.
(13) Schachter, S., "Recidivism and Self-Cure of Smoking and
Obesity," American Psychologist 37(4): 436-4.44., 1982.
(14)i Anonymous, "Addiction or No?" New Scientist, April 20, 1978,
pp. 148-149.
(15)! U. S. Department of Health and Human Services (1988), The
Health Consequences of Smoking: Nicotine Addiction, A Report
of the Surgeon General, Publication No. DMHS (CDC). 88-8406.
U. S. Government Printing Office, Washing, D. C.
(16) Christensen, R., "Cigarettes Addictive, Panel Says," The News
and Observer, Raleigh, N.C., Wednesday, September 3, 1980,
pp.. 1 and 5B.
CONF[DENT]AL
- 75 -
OCR for 2023235876 does not yet exist
Environmental tobacco smoke (ETS), a~so sometimes referred
to as "passive (or involuntary)! smoking", is a shorthand reference
to the presence of diluted side-stream smoke (smoke from the burning
end of the cigarette) and exhaled mainstream smoke in the ambient
air, and, more particularly, to the public controversy over the
effect such smoke has, if any, on non-smokers who are exposed to.
it. Industry critics contend that exposure to ETS both causes
disease in non-smokers and exacerbates existing health conditions
for individuals who suffer from heart and lung disease.
A great deal of public attention has recently been focused
on efforts to curb smoking in the workplace, in restaurants and
other public accommodations, and in airplanes and other forms of
public transportation. There. also has been a good deal of press
attention given to the claim that parents harm their children by
smoking at home. The question of whether ETS exposure is a health
risk for non-smokers is rarely discussed or decided on the basis
of the scientific evidence; rather politics, speculation, and
emotion-laden arguments have replaced open scientific discussion
of ETS' alleged health effects. In a number of instances,
investigators have simply assumed that ETS is. a health risk and
have gone on to attempt to estimate the magnitude of the assumed
risk. Such. reports claim that hundreds or even thousands of non-
smokers die of diseases due to ETS. However, these investigators
COXF |,DENT |AL
fail to acknowledge the serious methodological problems underlying:
their estimates.
At several recent meetings, experts on ETS have reported
the lack of valid scientific data to support such health claims
and the difficulty of interpreting the available scientific data
on the subject. For example, the summary of a report on an
international workshop held at the University of Geneva in March
1983, contains the statement, "an overall evaluation based upon
available scientific data,~ leads to the conclusionthat an increased
lung cancer risk for non-smokers from ETS exposure has not been
established." (I)
Likewise, the organizer of an international symposium on
the medical perspectives of ETS, organized and sponsored by United
States and European private and governmental bodies, and held in,
Vienna, Austria,~ in 1984 notes:
Summarizing all of the results presented here,
I come to the con,clusion that up to now there
is no scientific evidence of a causal
relationship between passive smoking and lung
cancer. In my opinion, all the epidemiological
studies carried out so far lack the appropriate
methods to determine the extent of exposure to
passive smoking. So, I do not think any
epidemiological investigationwi~l be performed
convincingly in the future until the problem
of determining the extent of exposure to passive
smoking has been solved satisfactorily. (12).
CONFIDENTIAl.
A 1983 U.S. Government sponsored review of research on possible
respiratory effects of exposure to ETS concluded:
A review of the data from the studies which
have been carried out or are in progress which
address the effect of passive smoking on the
respiratory system suggests that the effect
varies from negligible to quite small. From
this review, it was not possible to determine
whether there is a specific group which is at
increased risk or what the mechanisms of the
effect (if any) may be. (3)
In 1986, the Surgeon General published a report on ETS
which concluded that ETS is harmful to non-smokers. It specifically
reported that ETS exposure causes lung cancer. Close examination
of this report, however, shows that the conclusion is based on.
studies which even the report acknowledges to have serious
methodological flaws. The report also acknowledges the need for
more accurate data on exposure than simply using a spouse's smoking:
habits.
On the question of the possible effects of ETS exposure
on the adult respiratory function, the report concedes:
CONFIDENTIAL
The physiologic and clinical significance of
the smal~ changes in pulmonary function found
in some studies of adults remains to be
determined. The sma~l magnitude of effect
implies that a previously healthy individual
would not develop chronic lung disease solely
on the basis of involuntary tobacco smoke
exposure in adult life.
With regard to ETS and acute respiratory illness, the
report notes "there are no studies of acute respiratory illness
experienced in adults exposed to environmental cigarette smoke."
The report also acknowledges the lack of data to support claims
that exposure to ETS can induce asthmatic attacks in sensitive
individuals. It notes th, at studies to date used artificial test
settings, unrealistically high levels of smoke, and inadequate
control of psychological facts.
The report concludes that exposure to ETS has not been
shown to contribute to cardiovascular disease or to be hazardous
to patients with pre-existing heart disease:
Further studies on. the relationship between
involuntary smoking and cardiovascular disease
are needed in order to determine whether
involuntary smoking increases the risk of
cardiovascular disease.
The studies cited by industry critics as evidence of
health claims from ETS exposure contain serious methodological
inadequacies. Questions have arisen because in no epidemiological
study to date has the alleged r~sk to non-smokers been assessed by
actual measurements of ETS in the home, in the workplace or in
public. Other problems arise because of the failure to account
and control for the many factors associated with the diseases in
CONFIDENT ]AL
- 80-
question. Such factors commonly overlooked include diet, lifestyle,
heredity, and the wide variety of chemical, physical, and
biological contaminants common to the modern indoor and outdoor
environment. Failure to account and control for these factors
makes interpretation of study results questionable.
British researchers,, for example, examined epidemiological
studies on ETS and lung cancer for possible bias and errors which
could explain the reported increased risk among non-smoking women
married: to smokers. They concluded:
In summary, when a spouse's smoking status is
used to estimate a non-smoker's ETS exposure,,
'a considerable amount of misclassification'
may resu~It. Since selection bias and
confounding must also. be considered, extreme
caution is required in interpretation of these
studies. This is especially so when [the]
literature as a whole contains several studies
reporting no significant association between
ETS exposure and lung cancer, as well as
various inconsistencies, both among and within
studies. (4)
In a paper presented to the U.S. Air Pollution Control
Association meeting in 1986, an American researcher examined the
epidemiological data on ETS and lung cancer and concluded:
The epidemiological data concerning any cause
and effect relationship between ETS and lung
cancer is, at best, equivocal. The most
persistent weakness is the absence of adequate
exposure information. This precludes the
CONFIDENT |AL
- 81 -
evaluation of dose response relationships--
a critical element of the test for causality.
Moreover, the problems of sampling bias and
misclassification complicate interpretation of
studies done to date. (5)
Critics argue that asthmatics and individuals with pre-
existing heart and lung diseases are particularly vulnerable to
various environmental influences, including ETS. Reviews on the
health effects of environmental tobacco smoke exposure, however,
report that the data are limited and conflicting on this subject.
The Surgeon General's 1984 report on chronic obstructive
lung disease contains a chapter on ETS which concludes, among other
points,, that "the limited existing data yield conflicting results
concerning the relationship between passive smoke exposure and
pulmonary function changes in patients with asthma." The report
further explained:
There are very limited data on the effects of
passive smoke exposure in patients with pre-
existing pulmonary disease, and the available
data are conflicting. Clinical studies have
suggested a relationship, between respiratory
symptoms in asthmatics and exposure to parental
cigarette smoke, but methodologic problems
complicate the interpretation of the limited
available data.
CONFIDENTIAL
- 82 -
The 1986 Surgeon General's Report on ETS similarly
acknowledges conflicting data on ETS exposure in children and adults
with asthma. On children it states:
Epidemiologic studies of children have shown
no consistent relationship between the report
of a doctor's diagnosis of asthma and exposure
to involuntary smoking. Although one study
showed an association . . ., others have not.
On the question of whether ETS exposure affects adults with asthma,
the report reviewed three studies on the subject and acknowledged
conflicting results and methodological problems. It states:
Acute exposure in a chamber may not adequately
represent exposure in the general environment..
Biases in observation and [in the] .
selection of subjects and the subject's own
expectations may account for the widely
divergent results. Studies of large numbers
of individualswith measurement of the relevant
physiologic and exposure parameters will be
necessary to adequately address the effects of
environmental tobacco smoke exposure on
asthmatics.
The plausibility of the claim that ETS exacerbates
symptoms in those with existing cardiovascular disease rests on
the observations that ETS contains carbon monoxide and nicotine.
Actual measurements, however, suggest that carbon monoxide and
nicotine in the ambient air do not substantially increase lewels
of these substances in the blood of non-smokers. (6)
CONFIDENT I!AL
- 83 -
The evidence linking parental smoking and children's
health problems is contradictory and weak. There is no agreement
that the reported associations are in fact due to parental smoking
and not to a variety of so-called confounding factors such as socio-
economic status, and the use of gas cookers and heaters. Surveys
and studies on this subject have produced conflicting results.
(7) Some studies report that children whose parents smoke have more
respiratory symptoms and illnesses than those whose parents are
non-smokers. Others report no such effects.
Although some individuals are annoyed by the sight and
smell of tobacco smoke and a few even report experiencing
irritation, the existence of human allergens in tobacco smoke has
not been established. (8) In many cases, the sensitive individual
may be responding to high room temperatures, lack of ventilation,
or even to the mere sight of tobacco smoke. A review of the
scientific literature on. the subject indicates that it must be
questioned what people really mean when they say they are "~allergic"
to tobacco smoke. They may simply not like the sight and smell of
tobacco smoke and interpret this to mean that they are '"allergic'"
to tobacco smoke.
Tobacco smoke is only one of many possible contributors
to indoor air quality. Other suspected factors affecting indoor
CONF [:DENT IAL
air quality include allergens such as dust mites and spores from
fungi, and chemicals such as formaldehyde, ozone, and nitrogen
dioxide. (9). To ban one suspected constituent because it is
visible and commonplace is unjustifiable. Reaction to tobacco
smoke may merely indicate a more general ventilation problem.
The alleged health hazards of ETS exposure in the
workplace have also received considerable attention in the media.
There is very little data on ETS exposures at the workplace;
nonetheless, some reports strongly recommend workplace smoking
restrictions. These recommendations are often implicitly based on
the desire to force smokers to reduce their smoking, rather than
on any sound scientific data.
Scientists who have studied the air quality in office
buildings have concluded that tobacco smoke does not play a major
role in the quality of indoor air. (i0) It has been reported
that neither pollution levels nor complaints about "stale" air are
higher in buildings where smoking is permitted than in buildings
where it is prohibited. (II) Although smoking restrictions that
apply to offices and public places are being considered, none to
date is based on actual air quality studies. When actual
measurements in real life situations are made, the results suggest
that ETS is not a significant factor of indoor air quality, and
that smoking regulations are unnecessary to assure adequate indoor
CONF ]DEN~'IAL
- 85 -
air quality. (12) Current studies suggest that inadequate
ventilation is the most important factor determining indoor air
quality. (13)!
Since the data on ETS are inconclusive, public smoking
laws constitute unnecessary government intervention in matters of
individual behavior. To the extent that scientific debate on ETS
is suppressed and data misused,~ the public may accept coercive or
punitive laws it would not otherwise accept. There is a need for
a balanced discussion on, ETS. Some of the press coverage given to
ETS issues tends to highlight the most alarming or sensational
claims, often without regard to the critical limitations of the
methodologies and data used in the studies. Brown & Williamson
appreciates the desire of some members of the non-smoking public
for "separation" from smokers. The easiest and best response to
this desire is polite courtesy on the part of smoker and non-smoker
alike.
CONFIIOENIIAL
(1)
Rylander, R. et al. (Ed.), ETS--Environmental Tobacco Smoke,
Report from a Workshop on Effects and Exposure Levels, March
15-17, 198.3,. University of Geneva,. Switzerland, published in
European Journal of Respiratory Diseases (1984) Supplementum
No. 133, Vol. 65, page 144..
(2)
Lehnert, G., Chairman, "Round-Table Discussion," Preventive
Medicine (November 1984) 13:6, p. 746.
(3)
U.S. Department of Health and Human Services, Report of Work
Shop on Respiratory Effects of Involuntary Smoke Exposure:
Epidemiologic Studies, May 1-3, 1983, Public Health Service,
National Institute of Health (December 1983).
(4,),
Lee, P.N. et al., "Relationship of Passive Smoking to Risk
of Lung Cancer and Other Smoking Associated Disease," British
Journal of Cancer (1986) 54.:167.
(5)
Balter, N.J. et al., "Causal Relationship Between Environmental
Tobacco Smoke and Lung Cancer in Non-Smokers: A Critical
Review of the Literature," paper presented at the 79th Annual
Meeting of the U.S. Air Pollution Control Association,
Minneapolis, Minnesota, June 22-27, 1986, p. 13.
CONFIDENTIAL
-- 87 --
(6)
Schievelbein, H. & Richter, F., "The Influence of Passive
Smoking on the Cardiovascular System," Preventive Medicine
(November 1984) 13:626.
(7) U.S. Surgeon General, The Health Consequences of Smok~ng--
Chronic Obstructive Lung Disease (1984), pp. 387-389, 392,
401; U.S. Department of Health and Human services,. Report of
Workshop on Respiratory Effects of Involuntary Smoke Exposure:
Epidemiologic Studies,. May 1-3, 1983, Public Health Service,
National Institute of Health (December 1983) p. 3; U.S.
National Research Council, Environmental Tobacco. Smoke--
Measuring Exposures and Assessing Health Effects, prepared by
the NRC Committee on Passive Smokin,g, Board on Environmenta~
Studies and Toxicology (1986), National Academy Press,
Washington, D.C.
(8)i Lehrner, S., et al., "Tobacco Smoke Sensitivity: A Result
Allergy?" Ann. Allerqy 56:1-10, 1986.
(9)
Anderson, I. & Korsgaard, J. "Asthma in the Indoor
Environment--Assessment of the Health Implications of High
Indoor Air Humidity," pp. 79-86; Berglund,~ B., et al. (Eds.).,~
Proceedings of the Third Internationa~ Conference on Indoor
Air Quality and Climate, held in Stockholm, Sweden, August
20-24, 1984.
CONF | DENT
- 88 -
(i0) Sterling, T.D. et al., "Environmental Tobacco Smoke and ~ndoor
Air Quality in Modern Office Work Environments~" Journal of
Occupational Medicine (January 1987), 29:5.7.
(ii) "Statement of Gray Robertson,~ President, ACVA Atlantic, Inc.,"
(December I0, 1987), Statement Accompanying Tobacco Institute
press release.
(12)i Sterling, T.D. et al., ,,Environmental Tobacco Smoke and Indoor
Air Quality in Modern Office Work Environments," Journal of
Occupational Medicine (J~anuary 1987),. 29:61.
(13) ~d.
CONF ]DENT |AL
PRIOR TOBACCO INDUSTRY POSITIONS
ON SMOKING AND HEALTH
CONFIDENTIAL
- 90 -
This section reviews the positions taken by the tobacco
industry on smoking and health issues, both in testimony before
Congress and in publications and programs of The Tobacco Institute.
Not surprisingly, the positions of the industry have changed to
some extent over the years as the scientific studies and debate on
smoking and health have evolved.. This paper merely outlines these
positions and notes some of the specific statements that may be
challenged by industry critics.
In general, the industry has taken a consistent position
that proof is lacking of adverse health effects from smoking,
passive smoking, or any of the constituents found in tobacco smoke.
Industry research expenditures have generally been characterized: as
substantial, more generous than those of other private groups, and
having no restrictions. In addition, the industry has denied any
addictive qualities of smoking. Finally, advertising of cigarettes
has been stated to be merely related to brand preferences, and to
have no effect on recruiting youth, or non-smokers, to smoke.
I. WHETHER SMOKING CAUSES DISEASE
The industry has consistently taken the position, that it
is an "open question" whether there is a causal link between smoking
and various diseases, and that further research is necessary..
This position has been maintained throughout the various
CONF ]DENT ]AL
- 91 -
congressional hearings and industry publications. Industry members
have admitted that statistical associations exist between smoking:
and certain diseases, but they have emphasized that such a
statistical relation does not establish causation. Industry
spokespeople have consistently denied that there is sufficient
proof of a causal link between smoking and lung cancer;
cardiovascular disease (including stroke and high blood pressure);
chronic obstructive lung diseases (including emphysema and
bronchitis)i; cancers of the pancreas, larynx, esophagus, bladder,
and urinary tract; oral and pharyngeal cancer; ulcers (including
peptic ulcers); and overall mortality rates. The industry has
similarly criticized the claim that there are 400,000~ excess deaths
per year due to smoking, characterizing this claim as "sheer
speculation." (i)
There have been similar statements on the effect of
smoking on women, especially during pregnancy. The industry has
acknowledged that "smoking mothers, on the average, have slightly
lighter weight babies." (2) But the industry has denied that
there is proof of a causal link to the following conditions which
have been statistically linked to tobacco use: increased perinatal
mortality, abortion, stillbirth, birth defects, early menopause,
decreased child development, and disease in those using oral
contraceptives.
CONFIDENTIAL
-- 92 --
The industry has likewise stated that there is no
scientific evidence linking passive smoking to any disease.
Statements on passive smoking tend to be stronger than those
regarding primary smoking. (3) The questioning of adverse health
effects includes questioning any effect on children of smoking
parents. (4)
There are also, however, some industry statements which
may raise questions as to adverse health effects, including the
following:
(i) Dr. Little, testifying for the Tobacco Industry
Research Committee ("~TIRC") at 1957 congressional hearings, stated
that any chronic irritation '"is a bad risk in any form of cancer"
and that "inhalation of smoke" is an irritant. Dr. Little also
referred during his testimony to an. article in which he said "it
would seem unwise to fill the lungs repeatedly with the suspension
of fine particles of tobacco products of which smoke consists."
(2) Industry statements have acknowledged that smoking
has a role "in depressing ciliary mobility" but have denied that
this has any proven relation to the development of lung cancer. (5)
(3.) Joseph Cullman., speaking as Chairman of the Executive
Committee of TI at 1969 congressional hearings (April/May hearings),.
CONF|~DENT ~AL
- 93 -
stated that "Caution: Introduction of polluted air into lungs,
including cigarette smoke, is injurious to health" was "a fair
statement,~" but then also said "I don't think people really know"
if smoking is injurious.
(4) Dr. Robert Hockett, in October 5, 1978 testimony,
stated that it is a "plausible possibility" that smoking has "an
effect on small airways," that smoking causes "a certain amount of
irritation," that for a small group of persons who "for genetic
reasonsare highly susceptible to chronic pulmonarydisease" smoking
can be "a grave danger" and that smoking reduces muscle and tissue
production in youth.
(5) In May 1983 congressional testimony Dr. Sheldon
Sommers stated that those with preexisting emphysema should not
smoke and that for them. smoking "is going to cause difficulty."
In addition, the industry has stated that "[.y]oung people
should not smoke." (6)i In October 5, 1978 congressional testimony,
Dr. Robert Hockett similarly stated that nicotine '"and perhaps
other ingredients in smoke reduced somewhat the efficiency of the
production of muscle and other body tissues" in youth, such. that
smoking could cause harm absent adjustments to diet.
CONFIDENTI,AL
There has also been some conflict as to whether smoking
can cause an allergic reaction.. Thus, Science and Smoke (1978),
quotes testimony that "it has not been clearly established that
allergens for man are present in tobacco smoke." A TI newsletter,
however, merely states that "True tobacco allergy
is rare."
(7)i A CTR report, introduced in the 1965 congressional hearings
(April/May hearings), notes research that "certain tobacco effects
• may be due to specific allergic susceptibility of particular
individuals," and an exhibit to testimony fn 1972 by Horace Kornegay
states that "there may be people who have an unusual
hypersensitivity to tobacco smoke.''~
As noted above, the industry has acknowledged that there
is a statistical link between smoking and various diseases, even
if statistics do not prove causation. In some ~nstances, however,
even the statistica~ link of smoking to disease has been d~sputed.
For example in The Ciqarette Controversy: Why More Research is
Needed 9 (Feb. 1984), statistical links to "perinatal problems,
including low birth weight, fetal growth retardation, perinata~
mortality and congenital abnormality" are questioned in light of
recent studies. (8)
Some industry statements also argue that if a causal
relation of cigarettes to disease were ever established, the
industry would take action to modify its product: "If one or more
CONF IDENTI,A1
- 95 -
of these compounds, as found in smoke, can be proved harmful, modern
technology certainly would be applied in efforts to modify the
product accordingly." (19) As Dr. Little stated at the 1957
congressional hearings, "I don't think there is one of them [li.e.,
tobacco executives] that is stupid enough to want to bluff for a
minute" regarding any adverse health effects.
In responding to these criticisms, the industry has noted
that there are a variety of other factors which may be causal agents
for the diseases that have been statistically linked to smoking.
Most emphasis has been placed on the role of heredity and
personality, as well as the role of viruses and of environmental
pollution. One often-cited position is that it is not smoking
that causes disease~ but rather the underlying personality of those
who are most likely to smoke. (I0)
Finally, the industry sometimes noted the potential
benefits of smoking, particularly in the area of stress reduction.
One publication in particular, The Smokinq Controversy: A
Perspective (Dec. 1978), argues for the beneficial effects of
smoking, including the risk that some persons m~ght be subject to
"critical levels of hypertension" if they could not smoke. Dr.
Robert ~ockett, in October 5, 1978 congressional testimony,
similarly notes benefits from smoking in the areas of relieving
anxiety and tension, aidi~ng in. digestion, and reducing the number
CONF ]DE~T ]AI.
of cases of Parkinson's disease and ulcers. The testimony of Dr.
Sheldon Sommers on March 12, 1982 notes beneficial effects of
smoking for those with "severe psychic or psychologic problems."
II. INDUSTRY RESEARCH EFFORTS
The industry's descriptions of its research efforts
usually consist of statements regarding the amount of money spent
on research (either during the prior year or since the establishment
of CTR) and the names of recipients of grant money. Industry
spokespersons also consistently stress that the grantees have
complete freedom, in their research and in the decision whether to
publish the results. The research funding is usually described as
"no-strings-attached," with "complete freedom and autonomy'" g~ven
to the researchers.
The nature of the research is also usually described
only in general terms. Some publications have described tobacco
industry research as directed at "smoking and health," and
congressional testimony has used similar phrases, such as "the
relationship between tobacco use and health." Among the stronger
statements is one (repeated on several occasions by Dr. Sheldon
Sommers) that from 1970 to 1982 $14 million was spent on "whether
cigarette smoking causes lung cancer in animals," and the results
"proved negative." Dr. Sommers also stated in March 1983 testimony
CONF ~,DEII T ~AL
that two-thirds of CTR's research grants were spent on cancer
research. In 1972 testimony, Dr. Sommers, speaking as Chairman of
the Scientific Advisory Board of CTR, noted that grants are awarded
based on, "competitive scientific merit and relevance of the
proposals received to smoking and health problems." Nevertheless,
Dr. Little, in 1957 congressional testimony, stated that grant
money is given out in a "very, very broad" range of ideas "not
confined to the effects of tobacco or any tobacco product." Dr.
Robert Hockett of CTR stated in 1969 testimony (April/May hearings)
that CTR is "concentrating study on the diseases that have been
reported to be associated statistically with tobacco use."
Industry statements have also criticized research by
private organizations active in anti-smoking work, such as the
American Cancer Society. One paper characterizes the research of
these organizations by saying that "there is good reason to suspect
waste and misdirection." (ii) The usual citations are more mild,
however, and merely note that the tobacco industry has spent more
on smoking and health research than any of the other organizations
interested in these issues, such as the American Cancer Society.
II~. INGREDIENTS/CONSTITUENTS OF SMOKE
The industry has stated that no constituent of tobacco.
smoke has been shown to be a cause of cancer in humans as found in
CONFIDENTIAL
- 98 -
smoke. The statements have encompassed the following substances:
"tar," nicotine, carbon monoxide, benzpyrene, nitrosamines and
nitrogen oxides, hydrogen cyanide, and beta naphthylamine. The
industry has repeatedly emphasized the need for "whole smoke"
research.
The precise formulation of this position varies. Most
often, the industry has made the general statement that the
concentrations of these substances in smoke are so minute as to be
inconsequential, and that only sophisticated research tools can
detect some of these constituents. (12) At other times, the focus
in on the absence of any smoke inhalation, studies finding adverse
health effects., or the absence of studies on primates. For nicotine
there have been further statements that not only is nicotine not
harmful, but also that it may have beneficial effects,, including
that it "stimulates the learning process." Nicotine's effect is
often paralleled to that of '"mild exercise." (13)
Statements regarding "tar" focus on arguments that "tar'''
is not actually an ingredient in smoke, and that analysis of it is
not an accurate method of research. Similarly, there is repeated
criticism of skin-painting of "tar" as a method of research, since
such studies "involve the wrong material [that is, the condensate
instead of whole smoke], in the wrong dose, and ~n the wrong form,
applied to the wrong tissue of the wrong animal!." (~4)
CONF | DENT
- 99 -
By contrast, Dr. Little, at the 1957 congressional
hearings, admitted benzpyrene is carcinogenic, although only "[i]f
you get enough of it at the right place." In addition, there is
at least one reference in congressional testimony to the presence
of insecticides and pesticides on cigarettes. Joseph. Cullman,
speaking at 1969 congressional hearings (April/May hearings), stated
that it was unclear "what if anything of these insecticides or
pesticides get through to the products."
Statements regarding the ingredients used in, the
manufacture of cigarettes, as opposed to the natural constituents
of tobacco smoke, are more rare. Beyond broad references to
supplying information to the government, specific ingredients are
not mentioned, and their health effects are not discussed. Instead:,~
there are broad statements that no causal link between disease and
any cigarette ingredient has been proven. The distinction between
ingredients and constituents is often blurred in these statements.
(15)
IV. ADDICTION/WHY PEOPLE SMOKE
There are very few industry statements on the issue of
addiction. To the extent such statements exist, they deny any
addictive effect. (16)
CONFIDENT ]AL
- I0'0 -
More often there are statements regarding why people
smoke, and in particular why young people begin to smoke. In this
regard, the industry position has been that young people begin to
smoke primarily because of peer pressure, and other social
influences, and not as a result of advertising. (17) The industry
explicitly states that it is not aiming its products at youth, and
that smoking is an "adult practice."
ADVERTISING AND PROMOTIONAL ACTIVITY
Industry statements in this area focus on the argument
that the claimed harmful effects from smoking have been. w~dely
stated and are known to more than 90% of the population. (18)
Conversely, Mr. Cullman has stated that reductions in advertising
do not decrease consumption of cigarettes. (19) Finally, the
industry position has been that smoking is an adult habit, and
that advertisements should not be and are not directed toward young
people.
CONF ]'DENT ]AL
END NOTES
(i) See, e.g., The Cigarette: Controversy, Eight Questions and
Answers 26.
(2) The Cigarette Controversy 8 (1974.).
(3) See, e.g., Testimony of Horace Kornegay 633 (1972) (c~a~m
"seems extremely far-fetched").
(4)
Cf. Women and Smoking 7 ("Is it true that smoking mothers can
harm their children by smoking around them? Studies in this
area report conflicting results.'").
(5) See, e.g., Testimony of Dr. Robert Hockett 810
March/April hearings).
( 1965-
(6) Fact or Fancy? 51.
(7) Smokinu and: the Public 5.
(8) See also Testimony of Dr. Sheldon Sommers 1080 (19,69 --
April/May hearings) ("evidence both favoring and opposing'"
statistical links).
CONF I'DENT IAL
- 102 -
(9)
The Ciqarette Consumer Controversy 13 (Jan. 1981). See also
Testimony of Bowman Gray 160 (1964) (if harmful effects were
found "We get awfully fast to work to see what we can do about
it"); Testimony of George Allen 943 (1965 -- March/April
hearings) ("If there is something in tobacco that is causally
related to cancer or any other disease, the tobacco industry
wants to find out what it is").
(i0) See, e.q., Fact of Fancy? 29 ("It may be the smoke__r rather
than the smokinq that should be investigated").
(ii) The, Smokinq Controversy: A Perspective 19 (Dec. 1978).
(12)i Cf. Testimony of Dr. Robert Hockett 105 (1972) (cigarette
smoke is "about 2 or 3 percent carbon monoxide by volume").
(13)i See, e.q., Testimony of Dr. Robert Hockett i~12
April/May hearings) ("effects similar to those
exercise on the work of the heart").
(1969 --
of light
(14)i Testimony of Dr. Robert Hockett 102 (1971).
(15)i See, e.q., Testimony of Bowman Gray 251 (1965 -- March/April
hearings) (i"have not been. able to establish that any particul~ar
CONF IDENT ]AL
- 103 -
ingredient or compound in cigarette smoke is the cause
illness. ")
(16) See, e.q., Testimony of Edward Horrigan 390 (1982 -- March 5,
ii, and 12 hearings) ("absolutely no proof that cigarettes
are addictive"); Testimony of Dr. Robert Hockett 22 (1978 --
October 5 and 61 hearings)("there is an adjustment" to smoking
over time and issue of dependence is "a very tough question")..
(17) See, e.q., Testimon~ of Horace Kornegay 190 (1978 -- February
hearing) ("I do not believe . . that cigarette advertising
induces young people to smoke"); On Tobacco: 21 Questions and
Answers 7 ("complex physiological, cultural and socioeconomic
factors").
(18) See, e.~., Testimony of William Kloepfer 674 (1969-- April/May
hearings) ("Never has any product been so extensively
publicized with an increasing crescendo of inflammatory
insistence that its use is hazardous").
(19) See, e.q., Testimony of Joseph Cullman 114 (1969 -- July
hearings) ("[t]here isn't any evidence around the world that
reduction in advertising or discontinuance of advertising
will materially affect cigarette consumption,).
CON F |:DENT I AI,.
- 104 -
OCR for 2023235905 does not yet exist
