PURPOSE OF REVIEW: It has been hypothesized that increased cleanliness, reduced family size, and subsequent decreased microbial exposure could explain the increases in global asthma prevalence. This review considers the recent evidence for and against the 'hygiene hypothesis'. RECENT FINDINGS: Recent evidence does not provide unequivocal support for the hygiene hypothesis: the hygiene hypothesis specifically relates to atopic asthma, but some of the protective effects (e.g. farm exposures) appear to apply to both atopic and nonatopic asthma; asthma prevalence has begun to decline in some western countries, but there is little evidence that they have become less clean; Latin American countries with high infection rates have high asthma prevalence and the hygiene hypothesis relates to early-life exposures, but exposures throughout life may be important. SUMMARY: There is a considerable body of evidence which warrants scepticism about the hygiene hypothesis. However, these anomalies contradict the 'narrow' version of it in which microbial pressure early in life protects against atopic asthma by suppressing T-helper 2 immune responses. It is possible that a more general version of the hygiene hypothesis is still valid, but the aetiologic mechanisms involved are currently unclear.
PURPOSE OF REVIEW: It has been hypothesized that increased cleanliness, reduced family size, and subsequent decreased microbial exposure could explain the increases in global asthma prevalence. This review considers the recent evidence for and against the 'hygiene hypothesis'. RECENT FINDINGS: Recent evidence does not provide unequivocal support for the hygiene hypothesis: the hygiene hypothesis specifically relates to atopic asthma, but some of the protective effects (e.g. farm exposures) appear to apply to both atopic and nonatopic asthma; asthma prevalence has begun to decline in some western countries, but there is little evidence that they have become less clean; Latin American countries with high infection rates have high asthma prevalence and the hygiene hypothesis relates to early-life exposures, but exposures throughout life may be important. SUMMARY: There is a considerable body of evidence which warrants scepticism about the hygiene hypothesis. However, these anomalies contradict the 'narrow' version of it in which microbial pressure early in life protects against atopic asthma by suppressing T-helper 2 immune responses. It is possible that a more general version of the hygiene hypothesis is still valid, but the aetiologic mechanisms involved are currently unclear.
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