Cancer and TV towers: association but not causation A more complete knowledge of the causes of childhood leukaemia is essential before progressing from association to causation MJA 1996; 165: 599 Readers may print a single copy for personal use. No further reproduction or distribution of the articles in whole or in part should proceed without the permission of the publisher. For copyright permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au/>". Register to be notified of new articles by e-mail - Current contents list - ©MJA1996 Nothing concentrates public concern more than links -- real or supposed -- between pollution from man-made objects and malignant diseases. This is probably made worse if we do not particularly enjoy the aesthetic appeal of the objects in question, and worse still if we do not understand what the biological effects might be of the pollutants involved. This situation is exemplified by the study by Hocking et al. in this issue of the Journal. They report an excess of leukaemia in people living near the TV towers just north of Sydney, the excesses being mainly in children and in certain time periods. Technically epidemiologists will regard such an observation as an "association" -- that is to say, pretty difficult (if not impossible) to understand in isolation and one which has to be put into context.
Is this association in Sydney the product of one of these quirks of distribution?	How does one interpret the study of Hocking et al.? Such a question is effectively asking: how can an epidemiological study lead to a causal link being established between radiofrequency irradiation and leukaemia in children? Several informative steps are required. Firstly, is this a new observation? The answer is, nearly but not quite. The authors themselves refer to a rather unsatisfactory study from Honolulu, which might show a non-statistically significant leukaemia excess near radio transmitters. 1 In addition, and potentially more interesting, an extensive study in Britain has shown a nearly twofold excess in leukaemia in residents close to one particular TV transmitter complex -- but only in mixed types of leukaemia in adults and not in children. 2 However, when all the other TV and related radio transmitters in Britain were studied this excess was not confirmed, although a decline in leukaemia incidence with distance from the towers was observed.
	It should be noted that the adult leukaemias are very different diseases, in terms of causation, from childhood acute leukaemia, 3 as indeed the different types of adult leukaemias are from each other. 4 As these other studies do not unequivocally support the findings of Hocking et al., we are left with two further lines of enquiry. One is to ask whether there are other explanations for the leukaemia excesses in northern Sydney, and the second is to question what is known of the physical properties of this type of non-ionising irradiation and whether there are any abnormal biological effects consequent on exposure of human tissue. There is not a great deal known of the possible harmful biological effects of radiofrequency non-ionising irradiations and nothing which might suggest that they cause malignant diseases. 5 A great deal more is known of the lower energy electromagnetic fields (50-60 Hz), but here, broadly speaking, no studies have yet suggested a likely biological link with a leukaemogenic process. This unsatisfactory state of affairs fuels public and clinical concerns and has led to a small epidemic of studies on childhood leukaemias aimed at investigating (using case-control methods) all known and hypothesised causes of the condition. These studies, in New Zealand, Canada, the United States, the United Kingdom and Germany, are all coming to fruition over the next few years. Not only do they represent the concern of the public, but also the general lack of knowledge of common risk factors for childhood leukaemias. Thus, other possible explanations for the observation of Hocking et al. are limited at the moment. Nevertheless, a good deal of descriptive epidemiology of childhood leukaemias is available, mainly from the United Kingdom. 6 This throws up some remarkable features of the diseases. Leukaemia is not evenly distributed among the childhood population -- it is roughly twice as common in areas that are either geographically isolated from major conurbations or of greater affluence. 7 Furthermore, childhood leukaemias do occasionally form close case aggregations or clusters. 8 Rare diseases will form striking clusters by chance, but in the case of childhood acute lymphoblastic leukaemia more occur than simply by chance. Where and why is not known, but is under investigation. 9 Is this association in Sydney the product of one of these quirks of distribution? Is there a local case excess in an affluent area, or even an unrecognised cluster of leukaemia? The way forward would certainly include a closer look at the Sydney data for evidence of these phenomena. Area cluster statistics should be used, 10 as well as a more rigorous application of point-source statistics, which, for example, look for decline in rates by distance for a putative point hazard. 11 These possible local studies, together with epidemiological studies from elsewhere, might show similar, and thus supporting, results. There is also the possibility of new biological studies supporting a causal link. However, a more complete knowledge of the causes of childhood leukaemia is essential in order to go down the road from association to causation. In that regard we have taken only the first few steps of a very long journey. Ray A Cartwright Professor of Cancer Epidemiology Leukaemia Research Fund, University of Leeds, Leeds, UK Maskarinec G, Cooper J, Swygert L. 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