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Re: A Critique of the 1983 Surgeon General's Report

On "The Health Consequences of Smoking -


Cardiovascular Disease"

SUMMARY

The 1983 Surgeon General's Report concludes that

"cigarette smoking is a major cause of coronary heart disease,"

and an important risk factor for other cardiovascular

diseases.* In doing so, the Report, among other things,

overinterprets studies that merely allege an association

between smoking and these diseases. In addition, the Report

almost entirely disregards a large amount of data that is

inconsistent with the smoking causation hypothesis.

For example, findings from worldwide epidemiological

studies including the United States, Great Britain,

Switzerland, Belgium, and Germany do not find an association

between smoking and heart disease. Even some studies that

claim smoking to be a risk factor find it to be so only in the

presence of other risk factors, especially high fat content in

the blood. Further, intervention studies, i.e., studies aimed

at showing that e.g., smoking reduction reduces heart disease,

* About 50% of all adult deaths are attributable to


cardiovascular diseases; this is a larger number than the
deaths attributable to any other disease.

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etc., have found no comparative decrease in these diseases.

Other recent studies have been unable to implicate either

nicotine or carbon monoxide in the association between heart

disease and smoking. Animal experiments involving exposure to

cigarette smoke are similarly negative. One of these negative

studies was a U.S. government study involving 200 dogs. Though

the study was completed in 1981, the results have never been

published. The constitutional hypothesis, i.e., that both

smoking and cardiovascular diseases may be due to common

factors, such as stress, and/or that smoking is a"symptom"'

rather than a cause, is supported by many data.

Introduction and Focus

As other Surgeon General's reports, the 1983 Report is

a political document and from a scientific point of view is

intellectually dishonest, because it does notproperly weigh

all the data and it ignores a great deal of inconsistent

evidence. During the period between the 1979 Surgeon General's

Report, which included a review of cardiovascular diseases, and

the 1983 Report, dedicated solely to cardiovascular diseases, a

great many studies, reviews and other citations have been

published in medical and other scientific journals, which,

include data inconsistent with the causation hypothesis. Of

these, only a limited percentage is mentioned or even cited

among the references in the 1983 Report.

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This critique will discuss a selection of studies that

are either omitted from the 1983 Report or dealt with by the

Report in a biased fashion. These studies show that, contrary

to the conclusion of the 1983 Report, smoking has not been

scientifically established as a cause of cardiovascular

disease, that there are many studies inconsistent with the

causation hypothesis and that there.are many unanswered

questions regarding the cause or causes of cardiovascular

disease. In short, there continue to be many scientific

controversies regarding smoking and cardiovascular diseases.

Epidemiology

There are many epidemiological studies that are

inconsistent with the overall conclusion of the 1983 Report.

Most importantly, the decrease in the United States of


^---------- -- - --------.__^._._.. . -_
age-adjusted death rates from all cardiovascular diseases

started shortly after the end of World War II, during a time of

sharply increasing cigarette consumption and well before the

decline in per capita cigarette consumption. This is shown in

the following graph compiled by the Tobacco Institute from

official U.S. Government sources.

Source: http://industrydocuments.library.ucsf.edu/tobacco/docs/rzdw0083
Per-Capita Cigarette Consumption, 18 Years and Over, and Age-Adjusted
Death Rates for Major Cardiovascular Diseases: United States, 1950-1979
450 4500

/
^

400 4000


Per-Capita
Cigarette
Consumption

350 3500

300 3000

Age-Adjusted Death Rates,


per 100,000 population
250 2500

01 ! 1 1 1 0
Death 1950 1960 1970 1980 Cig arette
Rates Consumption

Sources: U.S. Department of Agriculture, U.S. Public Health Service

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The Tobacco institute, October 1983
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One of the most important studies on cardiovascular

diseases and death rates in general is the so-called "Seven

Countries Study" under the leadership of one of the world's

most renowned epidemiologists - A. Keys of the University of

Minnesota. While the 1983 Surgeon'General's Report does

mention this study, it does so selectively. It omits, for

example, the finding that among the various cohorts in the

study, differences in death rates, including those from

coronary heart disease, were not related to differences in,

among other things, smoking:

"Among 12,763 men aged 0-59, 1512 died in


ten years, 413 from coronary heart disease.
The 60 cohorts differed in all-causes as
well as in coronary death rate. Those
differences were not related to cohort
differences in age, relative weight,
activity, smoking habits, or percentage
calories from total proteins or fats in the
diet but were related to differences in
blood pressure, serum cholesterol, and
percentage calories from saturated fatty
acids ..."(Keys, A. et al., "The Diet
and All-Causes Death Rate nthe Seven
Countries Study" The Lancet II (8237):
58-61, 1981)

In addition, a Belgian study, published in 1981, and

involving some 160 people, found no statistically significant

association between smoking and acute myocardial infarction.

(Chapelle, J.P. et al. "Early Assessment of Risk in*Patients

with Acute Myocardial Infarction." Europ. Heart J. 2(3):

187-96; 1981)

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Further, a Swiss study reports that between 1951-76,

cardiovascular disease mortality dropped 22% in males and 43%

in females. The decline in Swiss men occurred while theie was

no or minimal decrease in their cigarette consumption; the more

dramatic decline in Swiss women occurred at a time when they

smoked more cigarettes, had a higher "cholesterol" consumption,

and other increased risk factors. ..(Guberan, E. "Surprising

Decrease in Cardiovascular Mortality in Switzerland from

1951-76." J. Epidemiol. Comm. Health 33: 114-20; 1979)

In many other countries, such as West Germany, Sweden,

and Great Britain, (a) cardiovascular disease death rates

continue to increase but (b) the % of cigarette smokers in the

population decreased. (See, e.g., (a) 1984 Surgeon General's

Report, Appendix A, Figure 4, p. 338; (b) e.g., John C.

Maxwell, Sr., Maxwell's International Fact Book, 1983).

At the meeting of the American Public Health

Association in Montreal on November 17, 1982 Dr. Ravenholt,

Director World Health Surveys, Centers for Disease Control in

Rockville, MD, gave a widely quoted address alleging that the

1918 flu pandemic "may have greatly increased coronary heart

disease, lung cancer ...":

"Overall, the coronary (ischemic) heart


disease trends shown above are compatible
with a possible late effect of 1918
influenza - with the falling age-adjusted
rates during recent years possibly due to
the die-off of an influenza-damaged
cohort." (Ravenholt, R.T. "Late Effects of
1918 Influenza." Presented at APHA meeting,
Montreal, 1982 (unpublishedj)

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Many scientists who believe smoking to be a

contributory cause to cardiovascular diseases, or at least a

"risk factor", believe that this holds true only in the

presence of other risk factors, most specifically excess of

cholesterol and other fatty substances in the blood. For

example, E. L. Wynder, one of the most prominent anti-smoking

spokesmen, has written:

"... while tobacco smoking has been


established as affecting the risk for
developing cardiovascular episodes, it would
appear to do so only in the presence of
other major risk factors, particularly that
of hyperlipemia."
(Wynder, E.L.. "Forum: Workshop on Carbon
Monoxide and Cardiovascular Disease:
Introduction." Prev. Med. 8: 261-263; 1979)

Many similar statements can be found elsewhere in the

scientific literature. For example, S. Katz and coworker, of,

the State University of New York at Stony Brook, found the

following:

"...in this select group of symptomatic


patients, those whose only risk factor was
cigarette smoking had significantly less
coronary artery disease. When cigarette
smoking was present with either positive
family history or diabetes, more severe
coronary heart disease was found."
(Katz, S., Zeldis, S.M. "The Influence of
Cigarette Smoking on the Severity of
Coronary Artery Disease." Clin. Res. 30:'
672A; 1982)

The causation conclusion reached in the 1983 Surgeon

General's Report is almost entirely based on epidemiological


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data. With respect to epidemiological data generally, J.C.

Bailar of the U.S. National Cancer Institute, has stated:

"A common feature of epidemiologic data is


that they are almost certain to be biased,
of doubtful quality, or incomplete (and
sometimes all three)." (Bailar, J.C. "Cause
and Effect in Epidemiology: What Do We Know
About Hypertriglyceridemia." New Eng. J.
Med. 302: 1417-1418; 1980.)

Intervention Studies

The results of several intervention studies* are also

at odds with the causation hypothesis. One of the largest of

such studies was the Multiple Risk Factor Intervention Trial

(MRFIT), which was recently completed in the United States at a

cost of over $100 million.

The MRFIT study compared two.groups: (1) a "special

intervention" group whose members were heavily counseled by

their physicians to reduce smoking and fat consumption and

encouraged to increase their exercise, etc. (2) a group which

medically received only the "usual care."

There was no significant difference in death rate

between the "special intervention" and the "usual care" groups,

in spite of the fact that there was a much larger reduction in

smoking in the intervention group. In fact, all ri'sk factors

* An intervention study is an attempt to reduce the.incidence


of a particular disease by persuading the participants to
reduce their alleged risk factors,-e.g., smoking", high
cholesterol consumption, etc.

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were reduced more in the intervention group; the reduction in

smoking, however, was significantly greater than the reduction

in other risk factors. The 1983 Surgeon General's Report

ignores this major result of MRFIT and cites only those aspects

of the study, involving subsets of the study population, that

tend to support the theory that reduction in smoking reduces

cardiovascular disease. The report on MRFIT in The Journal of

the American Medical Association more than once cautions

against drawing conclusions from the analysis of these

sub-groups, since such analyses "do not make use of the

randomized control design of a clinical trial." (Multiple Risk

Factor Intervention Trial Research Group, "Multiple Risk Factor

Intervention Trial: Risk Factor Changes and Mortality

Results." J. Am. Med. Assoc. 248: 1465-1477; 1982)*

In a similar study in Great Britain, the intervention

group had a higher cardiovascular rate (although the difference

did not reach statistical significance) than those who did not

reduce their risk factors, including smoking, or reduced those

risk factors less. (Rose, G., Tunstall-Pedoe, H.D., Heller,

R.F. "UK Heart Disease Prevention Project: Incidence and

Mortality Results." LancetI (8333)-: 1062-1066; 1983)

Blood Pressure; Hypertension

As an acute phenomenon, it has long been known that

cigarette smoking significantly -- though transiently --

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increases blood pressure.* On the other hand, there is also a

great deal of data -- some of it even cited in the 1983 Report

-- which show that over an extended time span, i.e.,

chronically, cigarette smokers have significantly lower blood

pressure than non-smokers.

The 1983 Surgeon General's Report also discusses the

effects of hypertension (high blood pressure) and acknowledges

that there has been a decrease in this risk factor and CVD

related thereto since the end of World War I, i.e., since about

1920. The period between 1920 and about 1964 is the period

when per capita cigarette consumption in the United States

steadily and markedly increased. The 1983 Surgeon General's

Report does not explore the hypothesis that this decrease in

high blood pressure-associated cardiovascular disease and this

increase in cigarette consumption are -- at least in part

associated.

Nicotine and Carbon Monoxide

When trying to assess the reasons why smoking

allegedly causes cardiovascular diseases, critics of smoking

try to blame -- nearly always without substantive evidence --

either nicotine or carbon monoxide or both. These speculations

more often than not omit consideration of data which show that,

as regarding at least some physiological parameters relative to

* These acute short-lived rises in blood pressure, however,


have not been shown to be a part of any disease process.

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cardiovascular diseases, nicotine and carbon monoxide seem to

have antagonistic effects. There are, moreover, recent data in

the literature, again published by scientists opposed to

smoking, which suggest a lack of relationship between nicotine

and carbon monoxide and coronary heart disease.

For example, Wald and coworkers have stated:

"Our observations indicatethat nicotine is


unlikely to be a major cause of excess
coronary heart disease mortality in
cigarette smokers."

And further:

"It is not clear which constituent or


constituents of tobacco smoke is the main
cause of the excess risk. Both nicotine and
carbon monoxide (CO) have been suggested but
direct evidence is lacking."
(Wald, N.J. et al., "Serum Cotinine Levels
in Pipe Smokers: Evidence Against Nicotine
as Cause of Coronary Heart Disease", The
Lancet 11(8250): 775-777; 1981)

More recently a paper by several highly prominent

British epidemiologists, though vehemently attacking the

cigarette industry, nevertheless admit that their data

"... provide no evidence that a smoker can


reduce his risk of death by smoking a brand
with a low carbon monoxide yield; he might
even increase it."

The authors conclude:

"We still do not know which components of


cigarette smoke are responsible for its
associated cardiovascular hazard."

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(Borland, C., Chamberlain, A., Higenbottam,
T., Shipley, M., Rose, G. "Carbon Monoxide
Yield of Cigarettes and Its Relation to
Cardiorespiratory Disease", Brit. Med. J.
287: 1583-86; 1983)

Animal Data

Despite many attempts, researchers have been unable to

induce coronary heart disease or other cardiovascular diseases

in animals exposed to cigarette smoke. As a matter of fact, a

U.S. Government study involving cigarette smoke exposures to

more than 200 dogs was completed in 1981. Its conclusions

included the following:

"These results appear to be more indicative


of a possible protective effect for
cigarette smoke and/or carbon monoxide
inhalation than that of atherogenic effect."
(Hazleton Laborotories America, Inc. "Final
Report: Inhalation Bioassay of Cigarette
Smoke in Dogs: Effects of Nicotine and
Carbon Monoxide on Atherogenesis."
Submitted to National Cancer Institute, June
10, 1981 [unpubl.ished])

This study was never published and, of course, is not mentioned

in the 1983 Report. The Tobacco Institute obtained it through

the Freedom of Information Act.

Also with reference to animal experiments, it will be

recalled that some years ago the Danish researchers Astrup and

Hugod claimed, based on experiments with rabbits fed a high

cholesterol diet, that carbon monoxide was causally implicated

in atherosclerosis. (Astrup, P., Kjeldsen, K., Wanstrup, J.)

"Enhancing Influence of Carbon Monoxide on the Development of

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Atheromatosis in Cholesterol-Fed Rabbits." J. Athero. Res. 7:

343-354; 1967) However, when later repeating these

experiments, this time under properly controlled conditions,

these researchers were unable to replicate their earlier

results and thereupon concluded carbon monoxide could not be

implicated. (Hugod, C., Hawkins, L.H., Kjeldsen, K., Thomsen,

H.K., Astrup, P. "Effect of Carbon Monoxide Exposure on Aortic

and Coronary Intimal Morphology in the Rabbit."

Atherosclerosis. 30: 333-342; 1978)

Constitutional Hypothesis

As noted above, the many epidemiological studies

relating to cardiovascular disease are inconsistent and

controversial. Accordingly, a better explanation for the

claimed association between smoking and cardiovascular disease

may be that smoking is a "symptom" rather than a "cause", of

the disease. For example, stress may be what causes both

cardiovascular diseases and especially coronary heart disease

and/or smoking in susceptible individuals.

Support for the constitutional hypothesis can be found

in some of the studies concerning ex-smokers. The thrust of

one such study by G.D. Friedman and coworkers, including C.C.

Seltzer, is that future ex-smokers can be identified and

distinguished from "future" continuing smokers through various

physiological and psychological parameters, not directly

related to smoking. These future ex-smokers more closely

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resemble current non-smokers than current smokers. (Friedman,

G.D., Siegelaub, A.B., Dales, L.G., Seltzer, C.C.

"Characteristics Predictive of Coronary Heart Disease in

Ex Smokers Before They Stopped Smoking: Comparison with

Persistent Smokers and Non Smokers." J. Chron. Dis. 32:

175-190; 1979.) This paper not only supports the

constitutional hypothesis but it also casts doubt on those

studies that claim that.smoking cessation results in a lowering

of cardiovascular death rates.

This study is not included in the 1983 Report. What

the Report does cite is Friedman's later attempt (this time

without.the benefit of the collaboration of Dr. Seltzer) to

"undermine" his own data. (Friedman, G.D. et al. "Mortality in

Cigarette Smokers and Quitters. Effect of Baseline

Differences. New Eng. J. Med. 304: 1407-1410; 1981) His

fallacies, however, were decisively critiqued (Burch, P.R.J.

"Mortality in Cigarette Smokers and Quitters. New Eng. J.

Med. 304: 889-90; 1981); these critiques were never

effectively answered by Friedman.

Another example of the above-mentioned social "copi-ng"

behaviors is related to monotonous work. A series of studies

have recently been published under the leadership of R. Kara*sek

of Columbia University in which he finds that monotbnous work,

such as blue collar assembly line work, is a "risk factor" for

coronary heart disease "roughly of the same order of magnitude

as smoking or serum cholesterol." (e.g., Karasek, R.A. et al.

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"Job, Psychological Factors and Coronary Heart Disease -

Swedish Prospective Findings and U.S. Prevalence Findings Using

a New Occupational Inference Method." Adv. Cardiol. 29:

62-67; 1982)

There are many studies that have shown that the

genetic factor - another aspect of the constitutional

hypothesis - also plays an important role in cardiovascular

diseases. For example, a study by Friedman, who is basically

antagonistic towards smoking, concluded:

"Compared to their nonsmoking counterparts,


cigarette smokers in smoking-discordant
monozygotic (MZ) twins show less increase in
the occurrence of clinical coronary heart
disease (CHD) than do smokers in the general
population [2,8). Although the numbers of
twins studied have been few so far, these
findings have been cited as evidence against
the view that cigarette smoking is a
causative factor in the development of CHD."
(Friedman, G.D. et al. "Characteristics of
Smoking-Discordant Monozygotic Twins" Twin
Research 3: Epidemiological and Clinical
Studies, p. 17-22. Alan R. Liss, NY, 1981)

In summary, the conclusion of the 1983 Surgeon

General's Report that "cigarette smoking is a major cause of

coronary heart disease" and other cardiovascular disease is,

unjustified. There continue to be many scientific

controversies regarding smoking and cardiovascular disease.

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