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Rapid response to:

Research

Active and passive smoking and development of glucose intolerance among young adults in a prospective cohort: CARDIA study

BMJ 2006; 332 doi: https://doi.org/10.1136/bmj.38779.584028.55 (Published 04 May 2006) Cite this as: BMJ 2006;332:1064

Rapid Response:

Response to Passive Smoking & Diabetes

There are several parts of the paper by Houston et al (BMJ,
doi:10.1136/bmj.38779.584028.55 (April 7 2006) that are inaccurate,
contradictory or complete supposition.

The article cites the fabled cotinine test for use as a measure of
the amount of tobacco smoke that an individual is subject to. This is not
a proven method and is therefore unreliable. It is widely assumed that the
production of cotinine by the human body is a direct indication of the
amount of tobacco smoke ingested. This has not been properly proven beyond
doubt and therefore should never be used within a scientific environment.

The authors then go on to add a hypothesis to the experiment which is
subsequently applied to the null hypothesis and then used as a basis upon
which to conduct the experiment. This is invalid scientific practice. The
hypothesis in question concerns the effect of varying degrees of exposure
to tobacco smoke and their effect on the likelyhood of diabetes. Once one
makes assumptions like this, the whole experiment cannot help but be
conducted with this assumption in mind.

Later on in the paper, under the section on methods, another wild
assumption is made. The inconvenient fact that some subjects' cotinine
levels didn't tally with what was expected at baseline is simply brushed
aside and the subjects are effectively made out to be giving false
information to the scientists. No justification whatsoever is given for
this and it appears that no attempt was made to investigate this matter.
This involved 85 people out of an initial 1390---not a significant number
but it does raise the question of how many other "awkward" problems were
simply swept under the carpet in this manner, during the course of the
experiment.

Moving on the results of the experiment, and specifically table four
which details glucose intolerance by category. Looking particularly at the
incidence precentages, in one case the incidence percentage works out
higher for "never" smokers with passive smoke exposure than it does for
current smokers. It would be reasonable to expect that current smokers are
subject to greater levels of tobacco smoke than non-smokers of whatever
category. The results do not reflect this and there is no attempt at
explaining this within the text. Additionally, the majority of the figures
do not show a deviation of greater than 10% between smoker categories.
Such a deviation is considered the minimum acceptable in order to give
meaning to experimental results. Accordingly, this paper appears to be
inconclusive.

There has been no attempt made to split the "previous smoker" group
into passive smoke and non-passive smoke categories, as has been done with
non-smokers. Therefore any comparison made with this group is unreliable
and should be ignored.

Moving back to table one in the results. Three factors are listed
without justification for their inclusion. These are to do with high
school education, income and health insurance. How these factors affect
the outcome is not made clear in the text.

To summarise, this paper is currently being cited as definitive
evidence that environmental tobacco smoke increases the chance of
contracting diabetes. Due to the reasons above, this paper most certainly
does not prove this to be so. The authors should therefore make it clear
to the world's media that there has been some misunderstanding regarding
the interpretation of this document and also should modify the synopsis at
the end to delete the reference to passive tobacco smoke.

Alastair G. Browne MSc, BEng(Hons)

Competing interests:
None declared

Competing interests: No competing interests

07 April 2006
Alastair G Browne
Civil Servant
Scottish Executive, Saughton House, Edinburgh, EH11 3XD