Family size, childhood infections and atopic diseases. The Aberdeen WHEASE Group

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Abstract
BACKGROUND: This study addresses the causes of the increases in childhood asthma and allergic disease. On the basis of an observed inverse relationship between family size and allergic disease or atopy, it has been proposed that a fall in common childhood infections may have been responsible for the rise in asthma. This study was undertaken to investigate the relationships between family size and reported allergic disease and to test the hypothesis that an inverse relationship between the two is a consequence of childhood infections. METHODS: Data had been obtained in a 1964 cross sectional survey of a random sample of Aberdeen schoolchildren aged between 10 and 14 in that year. Records of the presence or absence of asthma, eczema, or hay fever at the time of the survey and a history of measles, pertussis, varicella, rubella, and mumps before and after the age of three years were available for 2111 subjects. RESULTS: The risks of hay fever (odds ratio 0.2, 95% CI 0.1 to 0.8) and eczema (OR 0.3, CI 0.1 to 0.7) were inversely related to having had three or more older siblings, whilst the risk of asthma (OR 0.4, CI 0.1 to 0.9) was inversely related to having had three or more younger siblings. Increasing total numbers of siblings showed a significant trend in protection against both eczema and hay fever. A weak protective effect against asthma was found for measles after the age of three (OR 0.5, CI 0.3 to 0.9) and slight increases in the risk of eczema were associated with having had rubella or pertussis and of asthma with having had varicella. The number of infections before the age of three was associated with a significant trend in the odds ratios towards increased risk of asthma (p = 0.025). There were significant trends in the odds ratios towards greater risk of eczema and hay fever with increasing exposure to rubella, mumps, and varicella. These relations between infection and atopic diseases were independent of the potential confounding factors age, sex, father's social class, and total number of siblings. CONCLUSIONS: These data add to the accumulating evidence that membership of a large sibship confers some protection against atopic disease. This does not appear to be explained by the common childhood infections which show conflicting relationships with atopic disease, in that measles may have some protective effect against asthma but the more infections a child has had, the more likely he or she is to have atopic disease. The explanation of the sibship effect is likely to lie elsewhere and the fall in common childhood infections is unlikely to explain the rise in atopic disease.