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QUESTIONING THE RATIONALE FOR THE SMOKING BAN
1) SCIENCE
53,000 Deaths The purpose of the smoking ban states that Environmental Tobacco Smoke (ETS) causes the death of 53,000 Americans each year. Do you know the original source for that number and can you demonstrate that it is scientifically authoritative? Do you know what the impartial and highly respected United States Congressional Research Service wrote about that source (3/23/94)?Congressional Research Service * The Library of Congress *The following 7 excertps are most interesting. The entire report is included below.
1. "The approximately 50,000 number was mentioned in [congressional]
testimony by the AMA...This statement in turn appears to be ultimately
traceable to an article published in 1988 in Environment International:
An Estimate of Adult Mortality in the US from Passive Smoking, A. Judson
Wells. The article used existing epidemiological (statistical)
studies... to estimate [as part of this total] 37,400 deaths from heart
disease.... The editorial in the issue containing the Wells article was
directed at that article [and] indicated that it had received mixed
reviews from referees (two recommending extensive revision and the third
recommending against publication on the grounds that it was too
speculative) but the editors chose to publish the paper [as is] despite
mixed reviews.2. "In the following years there were a series of critiques and rejoinders
related to this paper. The main criticisms related to two points: that
the evidence, particularly with respect to heart disease, was at odds
with information on the physical levels of [actual] exposure, and that
there are a variety of serious problems with epidemiologic studies. The
following discussion elaborates on these issues:(Dear "Colebrook Justice" reader, see the full text below for
discussion of unreliability of studies based on questionnaires, as the
underlying statistical studies here were; the fact that the studies did
not and could not fully control for confounders--other factors that
might be responsible for heart disease]3. "While the [death] estimates from at least some of the epidemiological
studies are significantly larger than the estimates of [actual] physical
exposure, these results are not magnitudes apart. The same cannot be
said , however, for the Wells estimates of deaths from heart disease.4. "Using the same type of linear physical extrapolation [that was used for
the other studies] would result in 700 deaths from coronary disease for
never-smokers... The portion of the Wells' 53,000 estimate from the
studies, even for several years ago, is 37,400, a number enormously
larger....5. "The biological plausibility of passive smoking effects on
cardiovascular disease has been the subject of some discussion ... There
are limited data both to support and refute these hypotheses [based on
the action of carbon monoxide and nicotine as they affect smokers] [but]
exposures from passive smoke are generally thought to be at
concentrations below those at which physiological changes would occur...6. "In sum, this analysis suggests that Wells' estimates are so high
relative to measures of physical exposure that they seem implausible."
C. Stephen Redhead
Analyst of Biomedical Science
Science Policy Research Division
SUBJECT
: Discussion of Source of Claims of 50,000 Deaths from
Passive Smoking
This memorandum is in response to your request for information
on the
possible source of an estimated premature 50,000 deaths from
passive
smoking effects.
This estimate is much larger than the (disputed) estimate of
3,000 premature
deaths from lung cancer due to passive smoking
effects
that was reported in a recent study by the Environmental
Protection
Agency (hereafter EPA Report). [1] The 3,000 estimate is
the only
one mentioned in a recent article on the cause of death in
the United
States [2] and lung cancer is the only passive smoking
illness
that is officially recognized by a government agency.
(1
above) The approximately 50.000 number was mentioned
in testimony by
the American
Medical Association[3] which states that passive
smoking
may kill as many as 53,000 Americans annually. This
statement
in turn appears to be ultimately traceable to an article
published
in 1988 in Environmental International. [4] This article
used existing
epidemiological studies (statistical studies of
incidence
of disease among human populations) to estimate these
deaths
which included, under one set of calculations, 37,000 lung
cancer
deaths, 12,800 deaths from other cancers, and 37,400 deaths
from heart
disease. (Wells actually reported estimate ranging from
38,000
to 53,000, with a preferred estimate of 46,000)
Each issue of Environment International contains an editorial;
the one
in the issue containing the Wells article was directed at
that article.
The editorial indicated that the study received mixed
reviews
from reference (two recommended publication after revision
and the
third recommended against publication on the grounds that
it was
to speculative), but the editors chose to publish the paper
despite
mixed reviews.
(2 above) In the following three years there were
a series of critiques
and rejoinders
related to this paper. [5] The main criticisms
related
to two points; that the evidence, particularly with respect
to heart
disease, was at odds with information on physical levels
of exposure,
and that there are of a variety of serious problems
with epidemiological
studies. The original article and
correspondence
are enclosed. [6] The following discussion elaborates
on those
issues.
Generally, there are two ways that one might try to estimate
the number
of premature deaths, if any, from passive smoking. One
could rely
on estimates of physical absorption of the components of
smoke and
then use those estimates to extrapolate based on studies
of the
effects of active smoking. These are called dosimetric
approaches.
Secondly, one might try to directly estimate the
effects
of passive smoking by comparing disease rates of
individuals
who are and are not exposed to passive smoke. These
studies
are the epidemiological one. [7] Typically, they compare the
rates of
disease in nonsmoking women married to husbands who smoke
and husbands
who do not smoke. Obviously, one might be interested
in the
extent to which the estimates derived from these two
approaches
are similar, or are different.
Consider the lung cancer studies first. Even though these
premature
deaths are only a small part of the total estimate in the
Wells article,
discussing these estimates will clarify some of the
problems
with the Wells estimate.
The recent EPA study estimated a risk for lung cancer of about
30 percent
from passive smoking based on epidemiological studies.
This is,
according to their analysis of the statistical studies,
nonsmoking
wives of men who smoker have 30 percent more lung cancer
than nonsmoking
wives of men who do not smoke. This risk is, in
turn, only
a tiny fraction of the risk from active smoking
(probably
around 3 percent),[8] and the proportion of
passive-smoking
premature deaths to active smoking premature deaths
estimated
by the EPA is between two and three percent. [9]
A physical extrapolation approach would tend to yield smaller
effects.
According to the EPA report, measures of cotinine in the
urine indicate
that, overall, passive smokers have about 1/2 of one
percent
of the level of active smokers. [10] Since the number of
current
and former smokers are the same as the number of never-
smokers,
the estimated premature deaths annually from passive
smoking
for never smokers would be about 600 using a linear
extrapolation.
[11] This number is considerably less than the EPA's
estimate
of 2000 (the remaining 1000 estimate was for effects of
environmental
tobacco smoke on former smokers who are about half
the number
of never-smokers). There us also a section in the EPA
study that
discusses extrapolations based on the physical exposure
to passive
smoking; these estimates also tend to be smaller that
the epidemiological
estimates and some are very low.
These are potential problems with both methods. The physical
extrapolation
method used above assumes a linear relationship
between
the incidence of a disease and exposure. Based on evidence
from the
pattern for active smoking, however, a linear method may
not be
correct. The evidence, however, tends to suggest that such
an adjustment
would reduce the estimates based on physical
exposure.
There is some evidence that disease rises with square of
the exposure
or even with higher powers in the case of lung
cancer.
[12] If the disease were to rise with the square of
exposure,
then the estimate based on cotinine levels would be only
3 people
rather than 600 people. Of course, it is possible that the
disease
rises less than proportionally with exposure. [13] At the
same time,
it is possible that there is a threshold which is so
small that
individuals are not exposed to experience health damage.
It is also
possible that continue is not the best measure of
exposure;
some exposure measures show larger and some show smaller
effects.
Problems also occur with epidemiological studies. It is always
possible
that relationships found with human population studies are
due to
chance, even in a perfectly designed study, and while there
are statistical
methods that assign probabilities of error, they
are still
probabilities. In addition, the precision of the specific
estimates
is always in question. [14]
There are also some specific problems that have been
identified
with passive smoking studies. First, the measures of
exposure
are based on interviews with subjects or their relatives
and are
subject to considerable error. Secondly, the studies might
be picking
up the effects of active smoking, through
misclassification
of never-smokers as smokers. That is some
individuals
who identify themselves as those who never smoked are
actually
current smokers or former smokers and they may be more
likely
to be married to smokers. Indeed, corrections were made for
this effect
in the EPA report, but it is difficult to know whether
they are
accurate. Finally, these studies do not or cannot fully
control
for "confounders" -- other factors that might be
responsible
for the effect that are simply unrelated with marriage
to a smoker.
For example, smokers tend to be less concerned in
general
about health risks and engage in other behaviors (e.g.
diet, lack
of preventive health care) that might be shared with
their spouses
and that may be the cause of the health effect.
The EPA chose the epidemiological studies as a basis of their
approach,
but they nevertheless relied on the cotinine measures for
several
aspects of their estimates (such as extrapolating from the
effects
on spouses of smokers to the population in general.
(3 above)
While the estimates from at least some of the epidemiology
studies
are significantly larger than the estimates of physical
exposure,
these results are not magnitudes apart. The same cannot
be said,
however, for the Wells estimates of deaths from heart
disease.
(4
above) Using the same type of linear physical extrapolation would
result
in 700 deaths from coronary disease for never smokers, and
perhaps
another 350 for former smoker, with a total of about a
1000. The
portion of the Wells' 53,000 estimated from the
epidemiological
studies, even for several years ago, is 37,000, a
number
that is enormously larger.
This large estimate occurs because the epidemiological studies
show a
very high risk estimate for passive smoking relative to
active
smoking for heart disease and not for lung cancer. For
example,
Wells indicates a 30 percent additional risk for heart
disease
for males and a 20 percent rise for females, as compared to
a 70 percent
risk for smokers. These relative risks are enormous
compared
to both the dosimetric ratios and to the epidemiological
results
for lung cancer. Note that although the risk ratios are not
that different
from lung cancer, the absolute risk estimates are
much larger.
The risk of lung cancer for nonsmokers is very low,
and any
percentage of a small number is still a small number. The
risk for
heart disease is much larger initially, and therefore any
significant
percentage change in the risk is larger, Put another
way, even
the epidemiological studies of lung cancer produced
passive-smoking
related deaths of less than 3 percent of active
smoking
related deaths, while the heart disease studies produced
estimates
that were 26 percent of active smoking related deaths.
(5 above)
The biological plausibility of passive smoking effects on
cardiovascular
disease has been the subject of some discussion.
Both Wells
and Sleenland refer to a 1991 review article by Glantz
and Parmley
that suggested that passive smoking may, in
experimental
studies, promote the formation of plaques in blood
vessels,
increase the tendency of blood platelet cells to aggregate
and form
clots, and reduce the oxygen-carrying capacity of the
blood.
[15] There are limited data to support or refute these
hypotheses.
For example, while some studies of nonsmokers found
that passive
smoking appears to promote platelet aggregation,
parallel
studies of active smokers have not consistently shown any
effect
on platelet function. [16]
Among the chemical components in passive smoke, carbon
monoxides
and nicotine are the most likely to adversely effect
cardiovascular
performance. Carbon monoxide binds tightly to
hemoglobin
and diminishes oxygen transport in the blood stream.
Nicotine
acts in the brain and throughout the body, promoting the
release
of adrenalin and increasing heart rate and blood pressure.
Although
these effects might impair performance, exposures from
passive
smoke are generally thought to be at concentrations below
those at
which physiological changes would occur in healthy
persons.
[17]
The most likely explanation of these large risks from passive
smoking
epidemiological studies for heart disease is the absence of
control
for other factors. [18] There are many important concerns
about health
risks in general. In general, studies do not, and
perhaps
cannot, control for many of those factors. If smokers;
wives share
in these behaviors, the relationships found in the
epidemiological
studies are spurious.
The Wells estimate of passive smoking deaths from cancers
other than
lung cancer is even larger relative to active smoking
deaths
than is the case of heart disease--about 50 percent. Again,
these cancers
are influenced by many other factors and the same
general
criticisms can be made about these epidemiological
estimates
as in the case of heart disease.
(6 above)
In sum, this analysis suggests that the Wells estimates are so
high relative
to measures of physical exposure that they seem
implausible.
It also suggests that the absence of controls or the
inability
to control for other factors may be a major problem in
relying
on epidemiological estimates of the health effects of
passive
smoking.
References:
[1] Environmental
Protection Agency. Respiratory Health Effects
of Passive
Smoking: Lung Cancer and Other Disorders. December
1992.
[2] J.Michael
McGinnis and William F. Fooge. Actual Causes of
Death in
the United States. Journal of the American Medical
Association.
November 10, 1993, pp. 2207-2212.
[3] Statement
of the American Medical Association, Health and
the Environmental
Subcommittee, House Committee on Energy and
Commerce,
Rn Adverse Health Effects of Exposure to Environmental
Tobacco
Smoke, July 21, 1993.
[4] A. Judson
Wells, An Estimate of Adult Mortality in the
United
States from Passive Smoking. Environmental International.
Vol. 14,
No.3 1988, 249-265.
[5] Letters
from Alan W. Katzanstein, Peter M. Lee and Larry
Holcoim
criticizing the Wells results; a clarifying letter from
Takoahi
Hirayima, a rebuttal to Katzanstein and Lee from James L.
Repace
and Alfred H. Lowrey, and a response from Wells were
published
in 1990 (Vol. 16, No. 2, pp 175-190. In 1991, a letter
from Stanton
A. Glantz criticizing Lee was published along with
Lee's reply
(Vol. 17, no. 1, pp. 88-91). Later in 1991, a
response
of Lee to the 1990 letters of Repace and Lowery, and
Wells,
a letter from Muin J. Khoury clarifying a point raised in
Lee's letter,
a joint letter from Glantz and Lee clarifying an
issue raised
earlier in the year, and a response from Repace and
Lowrey,
and Wells to Lee's letter were published (Vol. 17, no. 4,
370-387).
In 1992 (Vol. 18, No. 3, pp. 315-317, 321-325) another
letter
from Lee and response from Wells was published.
[6] A more
recent paper of the same general type as the Wells
paper has
been published on heart disease. See Kyle Sleenland,
Passive
Smoking, and the Risk of Heart Disease, Journal of the
America
Association, Vol. 267, No. 1, January 1, 1992.
[7] Of course,
the original estimates of the effects of active
smoking
on disease are based on epidemiological studies in large
part as
well, but there are some problems that occur in passive
smoking
epidemiological studies that are not as serious in active
smoking
studies.
[8] The
risk of lung cancer in smokers and ex-smokers depends
on intensity,
duration, and in the case of ex-smokers, time
elapsed
since quitting. Passive smoking would involve three
percent
of the risk of active smoking if there is a ten fold
active
smoking risk (i.e. smokers have an additional estimated
risk of
lung cancer that is ten times the disease rate of non-
smokers)
which is typical of current estimates of the risk for
women as
reported in the 1989 Surgeon General's Report (Reducing
the Health
Consequences of Smoking. U.S. Department of Health
and Human
Services, DDHS Publication No. (CDC) 89-8411). In
general
the estimates of deaths from passive smoking, the EPA
actually
used the additional risk (of wives married to smokers as
compared
to wives married to non-smokers) in the U.S. passive
smoking
studies, which was about 20 percent. If studies from all
countries
are considered, the estimated risk from these studies
was 30
percent.
[9] The
estimated attributable deaths from lung cancer due to
active
smoking are 118,000. See C. Stephen Redhead, Mortality
and Economic
Costs Attributable to Smoking and Alcohol Abuse,
Congressional
Research Service Report 93-SPR, April 20, 1993.
[10] EPA Report, pp. 3-43.
[11] To
extrapolate, multiply the percentage of cotinine by
the ratio
of ever smokers to never smokers, and by the number of
deaths
attributable to active smoking.
[12] Surgeon General's Report, p. 44.
[13] The
argument has been made for a relationship in which
passive
smoking can have large effects relative to active smoking
for some
specific events in laboratory settings, which is largely
attributed
to increased sensitivity of some nonsmokers. See
Stanton
Glantz and William Parmley, 1991, pp. 1-12. Circulation
is a publication
of the American Heart Association.
[14] For
a discussion of the methods used by the EPA in
combining
existing studies and the findings of studies published
later,
see Appendix A in Cigarette Taxes to Fund Health Care
Reform,
by Jane G. Gravelle and Dennis Zimmerman, Congressional
Research
Service Report 94-214. March 8, 1994.
[15] Glantz and Parmley (1991).
[16] Samet,
J.M., Environmental Tobacco Smoke, In
Environmental
Toxicants, ed, M. Lippman, New York Van Rostrand
Reinhold,
1992.
[17] U.S.
Department of Health and Human Services, The Health
Consequences
of Involuntary Smoking, 1986, Surgeon General's
Report,
DHHS Publication Number (CDC) 87-8938.
[18] This
position is taken by Gary L. Hubert, Robert E.
Brockie,
and Vijay K. Mahajan in a paper written for the layman;
Passive
Smoking and Your Heart, Consumers Research, vol. 75.,
April 1992,
pp. 13-19, 32. These authors consider the results in
the Wells
and Sleenland studies biologically implausible, and
also note
that six of the nine epidemiological studies show
causes
of heart disease (e.g. that, lack of exercise, lack of
preventive
health cure) that may be engaged in by smokers. That
is, there
is much evidence that smokers tend to be less
relative
risks that are in excess of risks estimated for active
smokers
and that most have very few controls for other factors
that might
effect heart disease.