How acute and reversible are the cardiovascular risks of secondhand smoke?BMJ 2004; 328 doi: https://doi.org/10.1136/bmj.328.7446.980 (Published 22 April 2004) Cite this as: BMJ 2004;328:980
All rapid responses
Tobacco is actually NOT a legal drug: it is NOT legal to poison
people, no matter how slowly you do it. Tobacco products also deprive the
user of his/her right to a product which is not addictive, defective and
lethal, when used as intended.
Ambient tobacco smoke is a witch's brew of carcinogens and poisons
which kills hundreds of thousands of innocent people around the world
every year. There is nothing "minimal" about that!
Competing interests: No competing interests
When Sir Ronald Fisher doubted the causal correlation between tobacco
use and lung cancer, he doubted a twentyfold difference in occurrence
between smokers and non-smokers. That seemed to be the viewpoint of an old
intellectual warrior who hated to see a lifelong friend, his pipe,
scoffed. But the correlation between ischemic heart disease and passive
smoking (or environmental tobacco smoke, ETS) is hundred times smaller :
an increased risk of 25%. Ischemic heart disease is a disease with notable
multifactorial causation, many causes being correlated to psychosocial
factors. The table shows the results of the famous study of Doll et al.,
expressed as excess risks (relative risk minus 1) compared to non-smokers
The excess risk of 25% for lung cancer of ETS is consistent with a
small and proven exposure to tobacco smoke, a well known carcinogen. The
excess risk of ETS for ischemic heart disease is as high as that of former
smokers and of light smokers, exposed 10 to 75 times more. That unlikely
‘non-linear’ model is covered by ‘biological plausible’ mechanisms. The
cited references contain (at best) interesting observations of discrete
biochemical and physiological changes in passive smokers and/or far
fetched hypotheses about the consequences of these changes.
I added the risks of trauma and poisoning in the table. Former
smokers, not exposed to nicotine, carry increased risks of trauma, as they
do for ischemic heart disease after many years of quitting.(2) People who
took up a lethal drug as smoking take up other risky lifestyles. If they
do, their partners do, too – most of the epidemiological evidence is based
on non-smoking partners of smokers. Homo sapiens mates assortatively.(3)
If smokers run increased risks for ischemic heart disease other than
caused by smoking, the assortative model of human mate selection predicts
their mates do. With no exception to the rule : though we are told that
opposites attract, the only characteristic that is not positively
correlated in human mates is gender.(3) The rock bottom theory of
associative mating in Homo sapiens easily explains a small increased
ischemic heart disease risk in partners of smokers.
An environmental hazard increasing total mortality by 1% (as
predicted for passive smoking by simple linear models) is a serious and
preventable hazard that should be reduced. Moreover, tobacco smoke bothers
non-smokers, and harms children and persons with sensitive airways. But
the inflated body counts of passive smoking, based on small numbers and
large hypotheses, misuse epidemiology and mislead the public. It is a sad
sign of the times that we still needed to market a sensible and decent
decision, a smoking ban everywhere where smokers and non-smokers mix, by
another health scare.
1. Doll R, Peto R, Wheatley K, Gray R, Sutherland I. Mortality in
relation to smoking: 40 years' observations on male British doctors. BMJ
2. Lightwood JM, Glantz SA. Short-term economic and health benefits
of smoking cessation: myocardial infarction and stroke. Circulation
3. Gould JL, Grant Gould C. Human mate selection. In: Gould JL, Grant
Gould C, editors. Sexual selection. Mate choice and courtship in nature.
revised edition 1997 ed. New York: Scientific American Library, 1989,
Sorry, I really tried but couldn't discover how to send this as HTML.
As the table is instrumental, I had to invent a new technique: the Clumsy
Excess risk by smoking status.
Between parentheses the tobacco use, expressed as cigarettes per day,
former use and exposure to ETS.
lungcancer * 2293% (25+) * 1386% (15-24) * 650% (1-15) * 314%
(former) * 25% (ETS)
IHD * 79% (25+) * 56% (15-24) * 40% (1-15) * 18% (former) * 25% (ETS)
All trauma * 139% (25+) * 25% (15-24) * 43% (1-15) * 17% (former) *
Luc Bonneux is a non-smoker with to ETS hyperreactive upper airways
Competing interests: No competing interests