Effect of passive smoking on health
BMJ 2003; 326 doi: https://doi.org/10.1136/bmj.326.7398.1048 (Published 15 May 2003) Cite this as: BMJ 2003;326:1048
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Professor George Davey Smith has written to me privately with
emphatic assurance that he has never received money from the tobacco
industry, an assurance I accept. I was therefore wrong to imply that his
editorial was in any way influenced by anything but his own objective
analysis (1). I should have contacted Professor Davey Smith personally
first for confirmation, and for this discourtesy I apologize.
(1) Hirschhorn N. George Davey Smith declaration of no competing
interests. BMJ Rapid Response, 27 May 2003.
Competing interests:
I am a paid consultant to the World Health Organization on tobacco industry documents.
Competing interests: No competing interests
I have just come across the well-considered article by Professor
George Davey Smith, whose most cogent statement (followed by firm
evidence)is, "The review of the evidence linking passive smoking to lung
cancer risk produced by the tobacco industry sponsored working group is of
limited use as a scientific document." (1) Professor Davey Smith's review
of the Enstrom-Kabat article is now all the more puzzling.
(1) Davey Smith G, Phillips AN. Passive smoking and health: should we
believe Philip Morris's "experts"? BMJ 1996;313:929-933.
Competing interests:
I am a paid consultant to the World Health Organization on tobacco industry documents
Competing interests: No competing interests
Professor George Davey Smith wrote the cautious editorial
accompanying the now-famous article by Enstrom and Kabat on passive
smoking (1) (2). While one of the latter authors admitted some link to
the tobacco industry, Professor Davey Smith declared none. However,
George Davey Smith was a grantee from the Council for Tobacco Research (on
cervical cancer and human papillomavirus) in 1993 (3). The connection may
be remote; yet I find puzzling that an epidemiologist of his standing
would declare, in the face of current and overwhelming evidence, that
"controversy still exists."
(1) Enstrom J, Kabat G. Environmental tobacco smoke and tobacco
related mortality in a prospective study of Californians, 1960-98. BMJ
2003;326:1057-61.
(2) Davey Smith G. Effect of passive smoking on health [.] More
information is available, but the controversy still exists. BMJ
2003;326:1048-1049.
(3)"CTR Grant Application Cards (Alphabetical)." 3 June 1993.
www.tobaccodocuments.org. Bates No.: 60135419-60136530, at -5736. Accessed
27 May 2003.
Competing interests:
I am a paid consultant to the World Health Organization on tobacco industry documents
Competing interests: No competing interests
For 50 years, the tobacco industry conspired to "create
the appearance of scientific controversy where there was none" on smoking
and health. "Scientists disagree";
"studies are inconclusive"; "not proven"; "merely statistical" -- the
industry pushed this PR for decades,
long after any real controversy had ended in the
scientific community. The goal for the industry was
"keep doubt alive".
Now the industry is doing the same thing with secondhand
smoke. And you are helping. You are saying there is
controversy. There is not.
Let's be blunt: what controversy? I know of exactly
two scientists outside the tobacco industry and
tobacco industry funding who think secondhand smoke
doesn't cause disease. That's not a "controversy".
Any more than two scientists who believe HIV isn't
the cause of AIDS makes it somehow "controversial"
that HIV causes AIDS.
The overwhelming consensus of
the scientific community is there is sufficient scientific
evidence to conclude that this product causes the same
diseases in its customers and those closest to them.
That is the conclusion of every major review of the
scientific literature, and of virtually every major
scientific, health, and medical organization.
WHO, IARC, EPA, NCI, all agree: the product causes
cancer, heart disease, and lung disease, in its
customers and in bystanders. The scientific
evidence establishes this.
There is no controversy
in the scientific community: secondhand smoke kills.
It's time for you to publish that fact here: there
is no controversy here. There is a poor study which
fails to detect what other studies have.
Or else you must use the same standards and say that
it's "controversial" whether HIV causes AIDS.
Competing interests:
None declared
Competing interests: No competing interests
"Environmental Tobacco Smoke" is, first off, a term coined by the
tobacco industry to minimize the severity of the by-product of smokers.
Score one for the tobacco industry.
My mother lived with a smoker for a few months short of 50 years - a
smoker, my father died of lung cancer months before their golden wedding
anniversary.
Score two for the tobacco industry.
My mother and we live daily with her emphysema - caused by exposure
to tobacco smoke pollution (well, that's if her team of doctors are to be
believed). Other risk factors and the remote possibility she has alpha 1-
antitrypsin type of emphysema were eliminated. She has no history of
exposure to vinyl chloride, no family history of COPD and no other
predisposing factors aside from living with a smoking spouse - something
Enstrom and Kabat claim to be inconsequential - to have resulted in this
devastating condition causing her to suffocate, slowly, to death.
I will tell her of the tobacco-funded conclusions that living with a
smoking spouse (who did not know what the tobacco companies kept secret
about the harm caused by exposure to tobacco smoke pollution) did not
cause her to become semi-invalid, her very life dependent on plastic
tubing attached to a cylinder of oxygen.
I will also advise my mother she is "statistically insignificant" the
next time I find it necessary to call an ambulance to administer requisite
care when she has collapsed, because her tobacco-smoke damaged lungs no
longer breathe for her. Her care and medications cost the government of
British Columbia over $1,000 each month. I can only hope administrators
will be gratified to hear exposure to tobacco smoke pollution is not
responsible for this inconvenient expense.
Despite your cover, your editorial and your article, nobody of
discretion can ever be expected to believe tobacco smoke pollution is
harmless.
Score three for the tobacco industry.
Competing interests:
None declared
Competing interests: No competing interests
Sirs,
Notoriously the impact of environmental tobacco smoke on health remains
under dispute. In my opinion, this issue will last controversial for long
time, untill we shall decide to consider not only EBM, but also, as I
suggest unheeded, SPBM, i.e., “Single Patient Based Medicine”. In fact,
although unfortunately overlooked all around the world, Biophysical
Semeiotics Constitutions do really exists, as I referred in my earlier
Rapid Response http://bmj.com/cgi/eletters/324/7348/0/h#22477, as well as
on my HONCode site 233736,
http://digilander.libero.it/semeioticabiofisica; Biophysical-Semeiotic
Constitutions). Certainly, in individuals whithout Oncological Terrain
(Constitution) cancer will surely not occur, even in lasting presence of
passive tobacco smoke. In a few word, we can now-a-day easily recognize at
the bed-side subjects with particular constitution(s), who can be involved
by defined diseases under environmental tobacco smoke. Therefore,
statements such as “A substantial increased risk of chronic obstructive
pulmonary disease could result from exposure to environmental tobacco
smoke” are valid if we can precisely examine the “single” subject
presenting with well-defined inherited predispositions, evaluated properly
by means of Biophysical Semeiotics. For example, there is convincing
evidene that cigarette smoking is a risk factor for type 2 diabetes.
Cigarette smoking has been consistently associated with a relatively small
byt significantly increased risk of type 2 diabetes in both men (2) and
women (3) in large prospective cohort studies. However, only individuals
with both “diabetic “ and “dyslipidemic” biophysical-semeiotic
constitutions can suffer from diabetes mellitus type 2, as allows me to
state a 46-year-long clinical experience (4, 5).
1) Smith GD. Effect of passive smoking on health BMJ 2003;326:1048-
1049 (17 May)
2) Rimmm EB., Chan J., Stampfer MJ., et al. Prospective study of cigarette
smoking, alcohol use, and the risk of diabetes in men. BMJ 1995; 310 555-
559.
3) Rimmm EB., Manson JE., Stampfer MJ., et al. A prospective study of
cigarette smoking and the risk of diabetes in women. Am.J Public Health
1993; 83:211-214.
4) Stagnaro S., Diet and Risk of Type 2 Diabetes. N Engl J Med. 2002 Jan
24;346(4):297-298. letter [PubMed –indexed for MEDLINE].
5) Stagnaro S., Stagnaro-Neri M. Valutazione percusso-ascoltatoria del
Diabete Mellito. Aspetti teorici e pratici. Epat. 32, 131, 1986.
Competing interests:
None declared
Competing interests: No competing interests
Earlier longer version of this editorial
We had asked the author to shorten an earlier longer version of this
editorial, which he had submitted to us. We are posting the earlier
version (unedited) as a rapid response.
Rajendra Kale
Editorials editor, BMJ
---
(Competing interests: None declared by the author)
Passive smoking: will we ever know the truth?
George Davey Smith
Department of Social Medicine
Canynge Hall
Whiteladies Road
Bristol
BS8 2PR
In 1928 Schönherr presented a lung cancer case-series from Chemnitz
and discussed the contribution of smoking to the disease[1]. He noted that
none of the small number of cases among women occurred in smokers, but
concluded that these cancers could have been caused by the inhalation of
their husband's smoke. Thus passive smoking was identified as a potential
cause of lung cancer at the same time as active smoking was first formally
studied as a putative cause. While the issue of personal smoking and lung
cancer is now resolved, the impact of environmental tobacco smoke (ETS)
remains highly controversial[2] [3]. Partly this is because of technical
issues related to measurement error, confounding and the identification of
small risks in epidemiological studies, as Enstrom and Kabat discuss in
their paper in this week's BMJ. However it also reflects the large
investment by the tobacco industry in keeping this issue from closure,
through the funding of research, review articles, commentaries and
methodological critiques from "scientists" who, unsurprisingly, generally
seem to reach the conclusion that the evidence regarding any causal effect
of ETS is limited, and that the profits of their paymasters (and thus the
source of their rewards) should not be interfered with.
The study by Enstrom and Kabat has considerable relevance for the debate
on the health effects of passive smoking. Given the small risks associated
with ETS exposure, meta-analysis has played an important role in
demonstrating an apparent adverse effect on lung cancer, coronary heart
disease (CHD) and chronic obstructive pulmonary disease (COPD). The
consistent elevated risks associated with ETS in these meta-analyses are,
however, potentially influenced by publication bias, with small negative
studies being less likely to get published (and thus into the public
domain) than positive studies[4]. A controversial issue in this regard
relates to a tobacco industry funded analysis of the American Cancer
Society's first Cancer Prevention Study (ACS I)[5]. This has not generally
been included in published meta-analyses, although it would contribute by
far the largest number of events - and thus statistical power - to such an
analysis. The main argument advanced by the meta-analysts who have not
included the study in their reviews is that the published ACS I analysis
was not presented in a format that allowed for the combination of
equivalent effect estimates across studies. Enstrom and Kabat have
analysed the California sub-sample of the ACS I, with considerable
additional follow-up, and have presented the data in a format that allows
inclusion in future meta-analyses. They also present data that give a
handle on the degree to which misclassification of ETS exposure may dilute
the association with mortality. They interpret their findings as null,
although, inevitably, statistical uncertainty remains. Indeed they may
over-emphasise the negative nature of their findings. With respect to
chronic obstructive pulmonary disease (COPD) - plausibly related to ETS
exposure - the estimates based on the most accurately classified exposure
groups give relative risks of 1.80 in men and 1.57 in women. These are
said to be non-significant, but combining them - and there is no good
evidence that ETS exposure has a different effect for men and women -
gives a relative risk of 1.65 (95% confidence intervals 1.0-2.73). A
substantial increased risk of COPD could result from ETS exposure.
Despite this, it is certain that this paper will be hailed as
demonstrating that the detrimental effect of passive smoking has been
overstated, and controversy will continue. What are the issues?
Confounding is clearly important, with ETS exposed individuals in many
situations being likely to display adverse profiles in relation to socio-
economic position and health-related behaviors. The ACS I was established
in 1959, when smoking was much less related to such factors than it is
currently within the US, as is evident from Enstrom and Kabat paper. It
could be argued that this is why smaller - if any - ETS-associated risks
are seen in the first compared to the second American Cancer Society study
(ACS II)[6]. In ACS II, with participants recruited in 1982, women exposed
to ETS had less education than those unexposed, as opposed to the lack of
any such gradient in ACS I. Similarly amongst men in the 1982 cohort there
was little education gradient, whilst amongst men in the 1959 cohort the
exposed group had more education than the unexposed group. These figures
reflect a changing social gradient in smoking amongst men and women over
time. Socio-economic confounding in ACS II would lead to over-estimation
of the effect of ETS, whereas there is relatively little confounding in
ACS I, and what confounding there is could lead to under-estimation of the
ETS effects. The findings of the two studies are, in some respects, in
line with this - in ACS II exposure to ETS was associated with increased
risk of coronary heart disease mortality, while this is not seen in ACS I.
Misclassification is a key issue in studies of passive smoking. It is not
being married to a smoker - the indicator of ETS exposure utilized in the
Enstron and Kabat paper - that leads to disease, rather it is the
inhalation of ETS. As an indicator of ETS exposure the smoking status of
spouses is a highly approximate measure. This will lead to the ETS-
associated risk being under-estimated. Conversely misclassification of
confounders can lead to statistical adjustment failing to fully account
for confounding, leaving apparently "independent" elevated risks that are
residually confounded[7]. Methods of statistically correcting for
misclassification in both the exposure of interest and in confounders
exist, but they are highly dependant upon the validity of assessments of
measurement imprecision7 , which renders them a highly unsatisfactory
method for resolving such issues. In the passive smoking field the tobacco
industry has eagerly discussed measurement error that would lead to the
effect of passive smoking being over estimated, and rely on the work of
its consultants in this regard[8], while ignoring misclassification that
would lead to underestimation of the strength of the ETS-disease
association2.
A second approach to evaluating the risks of passive smoking is to assess
the exposure to known carcinogens produced by ETS. Tobacco industry
consultants have repeatedly suggested that levels of such exposures are to
low to be of concern, with even a heavily exposed passive smoker inhaling
much less than the equivalent of one cigarette a day2. However the amount
of exposure to the 4,000+ compounds within cigarette smoke differs between
passive and active smokers, since sidestream and mainstream smoke have
different compositions. Tobacco-specific nitrosamine 4-(methylnitrosamino)
-1-(3-pyridyl)-1-butanone (NNKs) is metabolized and metabolites excreted
in urine, and levels in non-smoking women married to smokers are about 6%
of those of their spouses (and 8 times higher in women not married to
smokers)[9]. Given the strength of relationship between active smoking
and, say, lung cancer, exposure to 6% of the dose that is received by an
active smoker could easily produce the level of risk associated with
passive smoking[10]. However the exact factors in cigarette smoke
responsible for its detrimental health consequences are not fully
understood and thus these forms of calculation are highly approximate.
Given the considerable problems with measurement imprecision, confounding
and the small predicted excess risks associated with passive smoking,
conventional observational epidemiology is somewhat limited in addressing
this issue. Randomised controlled trials of exposure to ETS will clearly
not be carried out, but it may be possible to improve understanding
through a form of natural experiment: "Mendelian Randomisation"[11].
Genetic polymorphisms that are associated with poor detoxification of
tobacco smoke carcinogens have been identified. The distribution of these
polymorphisms in the population will not be related to the same
behavioural in socioeconomic confounders that ETS exposure is currently
associated with. Amongst people unexposed to such carcinogens there is no
reason to believe that the polymorphisms would be related to lung cancer
risk. However amongst the ETS-exposed a decrease in the ability to
detoxify the carcinogens should be related to increased lung cancer risk,
if ETS exposure is responsible for increased lung cancer risk. Indeed one
study suggested that a null (non-functional) variant for one such
detoxification enzyme, GSTM1, was associated with an increased risk of
lung cancer in non-smoking women exposed to ETS, but not in non-exposed
non-smoking women[12]. However a later study failed to confirm this
finding[13], reflecting one limitation of Mendelian Randomisation, which
is that large sample sizes are required to produce robust results. However
this is a promising strategy if we really want to know whether passive
smoking increases the risk of various diseases.
Enstrom and Kabat's study demonstrates yet again the huge elevated risks
for lung cancer, COPD and - to a lesser extent - coronary heart disease,
seen among active smokers. Why, then, is there interest in passive
smoking? It is obvious that smokers have large potential health gains from
quitting. Several commercially sensitive reasons particular to passive
smoking exist. First, legal action against tobacco companies for
compensation with respect to health damaging consequences of active
smoking are opposed on the grounds that smokers should have known of the
risks. The same cannot be said of those involuntarily exposed to other
people's smoke. Second, adverse health consequences of passive smoke
encourage smoking bans in work places and other public spaces, which would
lead to reduced cigarette sales. Both strictures imposed on smoking and
the effectiveness of health promotion may increase if it is shown that
those that have no say in their exposure to tobacco smoke are being made
sick. The financial interests in this regard make it unlikely that the
debate about passive smoking and health will go away.
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2 Davey Smith G, Phillips AN. Passive smoking and health: should we
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Competing interests:
None declared
Competing interests: No competing interests