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
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,
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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.
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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
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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)
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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.
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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 --
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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.
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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
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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.
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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."
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