Intended for healthcare professionals

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Environmental tobacco smoke and tobacco related mortality in a prospective study of Californians, 1960-98

BMJ 2003; 326 doi: (Published 15 May 2003) Cite this as: BMJ 2003;326:1057

Rapid Response:

More scepticism for your review.

"Environmental tobacco smoke revisited: the reliability of the data
used for risk assessment."

Nilsson R.

Department of Genetic and Cellular Toxicology, Stockholm University,

Several epidemiological studies have found a weak, but consistent
association between lung cancer in nonsmokers and exposure to
environmental tobacco smoke (ETS). In addition, a purported link between
such exposure and coronary heart disease (CHD) has been of major concern.
Although it is biologically plausible that ETS has a contributory role in
the induction of lung cancer in nonsmoking individuals, dose-response
extrapolation-supported by the more solid database for active smokers-
gives an additional risk for lung cancer risk that is more than one order
of magnitude lower than that indicated by major positive epidemiological
studies. The discrepancy between available epidemiological data and
dosimetric estimates seems, to a major part, to reflect certain systematic
biases in the former that are difficult to control by statistical analysis
when dealing with risks of such low magnitudes. These include, most
importantly, misclassification of smoking status, followed by
inappropriate selection of controls, as well as certain confounding
factors mainly related to lifestyle, and possibly also hereditary

A significant part of an association between lung cancer and exposure
to ETS would disappear, if, on the average, 1 patient out of 20 nonsmoking
cases had failed to tell the interviewer that he had, in fact, recently
stopped smoking. In the large International Agency for Research on Cancer
(IARC) multicenter study even lower misclassification rates would abolish
the weak, statistically nonsignificant associations that were found. In
the former study an apparent significant protective effect from exposure
to ETS in childhood with respect to lung cancer later in life was
reported, a most surprising finding. The fact that the mutation spectrum
of the p53 tumor suppressor gene in lung tumors of ETS-exposed nonsmokers
generally differs from that found in tumors of active smokers lends
additional support to the notion that the majority of tumors found in ETS-
exposed nonsmokers have nothing to do with tobacco smoke. The one-sided
preoccupation with ETS as a causative factor of lung cancer in nonsmokers
may seriously hinder the elucidation of the multifactorial etiology of
these tumors. Due to the high prevalence of cardiovascular disease in the
population, even a modest causal association with ETS would, if valid,
constitute a serious public health problem. By pooling data from 20
published studies on ETS and heart disease, some of which reported higher
risks than is known to be caused by active smoking, a statistically
significant association with spousal smoking is obtained. However, in most
of these studies, many of the most common confounding risk factors were
ignored and there appears to be insufficient evidence to support an
association between exposure to ETS and CHD. Further, it seems highly
improbable that exposure to a concentration of tobacco smoke at a level
that is generally much less than 1% of that inhaled by a smoker could
result in an excess risk for CHD that-as has been claimed-is some 30% to
50% of that found in active smokers.

There are certainly valid reasons to limit exposure to ETS as well as
to other air pollutants in places such as offices and homes in order to
improve indoor air quality. This goal can be achieved, however, without
the introduction of an extremist legislation based on a negligible risk of
lung cancer as well as an unsupported and highly hypothetical risk for

PMID: 11726024 [PubMed - indexed for MEDLINE]

Competing interests:
David Atherton. Director

See previous posts.

Competing interests: No competing interests

24 February 2010
Dave C Atherton