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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)?
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."
Congressional
Research Service * The Library of Congress *
Washington, DC 20540-7000
March 23, 1994
FROM : Jane G. Gravelle
Senior Specialist in Economic Policy
Office of Senior Specialists
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.
This information
found March 2005 on Tripod.com at
http://colebrookjustice.tripod.com/53000.html
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