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I have just read, with mounting incredulity, the paper by Irvine et al on what determines levels of passive smoking in children with asthma.1 These authors have surveyed 501 families with an asthmatic child, recording the smoking habits of the adults in the home and relating these data to exposure of the child to smoke as measured by salivary cotinine levels. They found that exposure is related to total amount smoked by parents, amount smoked in the home by parents, frequency of parental smoking in the same room as the child, smoking by both parents, and contact with smokers other than parents. They conclude that “. . . it is proximity to smoking adults which determines passive exposure of the children”.
What other conclusion could possibly have been envisaged? What hypothesis was being tested? I would say that these “results” are totally predictable to anyone with a smattering of common sense and that this “investigation” has no scientific merit. It is merely a waste of precious research funding when many more useful projects are being turned down for lack of funds.
I note, with even further astonishment, that the same group is now conducting a trial to see whether it is possible to reduce passive smoking by the children by encouraging parents to protect them from smoke, again funded by the Wellcome Trust! I hope the results will not be published in Thorax as I feel the reputation of this journal can only be damaged by association with pseudo science of this sort.
authors’ reply It was with some disappointment that we read the letter from Dr Ashcroft. He claims that the research was pointless because the findings were obvious. Even if this were true, the research would still be needed. How often in the history of medicine have we seen obvious or common sense ideas totally refuted by subsequent research? It is the purpose of research to test our preconceptions.
However, in our case the findings were not obvious. We were surprised and concerned at the number of asthmatic children exposed to high levels of passive smoke. We had expected social factors to be strongly related to the children’s cotinine levels but they were not. We were also surprised at the strength of the effect of age, particularly as we had constructed an argument for the age effect being in the opposite direction to that found. Finally, we were surprised at the strength and consistency with which the proximity factors predicted cotinine levels to the exclusion of all other variables except age.
Dr Ashcroft may be interested to know that his opinions are not shared by the three expert referees who reviewed the paper nor the many colleagues with whom we have discussed our findings. Indeed, the results attracted much interest when presented at the American Thoracic Society and Scottish Thoracic Society earlier this year. Currently we are receiving requests for reprints from scientists throughout the world. We can only wonder what prompted Dr Ashcroft to make his intemperate and unwarranted comments.
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