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Childhood leukaemia, population mixing, and paternal occupation
  1. L J KINLEN
  1. CRC Cancer Epidemiology Group, Department of Public Health, University of Oxford, The Radcliffe Infirmary, Oxford OX2 6HE, UK
    1. NICOLA T FEAR,
    2. EVE ROMAN
    1. Leukaemia Research Fund, Centre for Clinical Epidemiology, University of Leeds, 30 Hyde Terrace, Leeds, LS2 9LN, UK

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      The possible infective origin of childhood leukaemia has been the subject of much recent attention.1 Fearet al 2 have taken up my suggestion that my necessarily limited examination of childhood leukaemia relative to levels of paternal occupational contact in the general population3 be extended and (as in my study) found no evidence of a general increase in risk when fathers have jobs involving contact with many people. However, in reporting my hypothesis they did not bring out that the principal question considered in my study did not concern the general population, but rather whether there was a relation with paternal occupational contacts “in population-mixing situations associated with an excess of childhood leukaemia”.3 I investigated this question3with data from previous studies that were carried out to test the view that it is a rare response to some unidentified infection, and that situations of unusual urban-rural population mixing would favour excesses by promoting contacts between infected and susceptible people. This occurs when urban groups are mixed with rural groups that are likely to contain a higher proportion of susceptible people—such as in rural new towns or the North Sea oil industry in northern Scotland. Within the excesses associated with such unusual situations, there was a higher proportion of children with fathers in high contact occupations, as noted in certain established infections.3

      Evidence of a relation with occupational levels of contact (although worth checking formally) would not be predicted in data on childhood leukaemia from the whole of England and Wales, dominated as they are by urban areas. In such areas of high population density, even if exposed to population mixing, the prevalence of susceptible people would tend to be lower, and of immune people to be higher, so that the high level of herd immunity would reduce the likelihood of epidemics. It would be unfortunate if infrequent but informative situations were neglected as a result of a misconception that if infection is present, then evidence should be observable generally. In this connection, it may be worth recalling that those who did the classic work on feline leukaemia virus stressed that nothing about the pattern of the usual (sporadic) cases of leukaemia in domestic urban cats suggested infection; only in the special situation of multicat households did the disease show epidemic features.

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      Fear and Roman reply—In our paper published in an earlier issue of Occupational and Environmental Medicine, we examined the role of father's occupational social contact on the development of childhood leukaemia from data covering the whole of England and Wales.1-1 We found no evidence for an association between death during childhood from leukaemia and father's occupational social contact. Kinlen states that because we examined data for the whole of England and Wales rather than for specific “population-mixing situations associated with an excess of childhood leukaemia” 1-2 it is unsurprising that we found no association. However, given the worrying nature of the suggestion that parents may transmit a workplace acquired leukaemogenic agent to their offspring,1-2 we think that our result, showing that, in general, children of men who have high levels of occupational social contact are not at an increased risk of leukaemia, is important. Further, the first study published on this topic, based within an area identified as having an excess of childhood leukaemia, found no evidence that parental occupational social contact—either with adults or with children—influenced the risk of leukaemia in their offspring.1-3

      The suggestion that infections may be involved in the aetiology of childhood leukaemia, particularly acute lymphoblastic leukaemia (ALL), is not new. Kinlen's population mixing hypotheses, and those of Greaves,1-4 are currently the subject of much research. To date, however, no specific agents or mechanisms have been identified.1-4

      References

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