PubMed · 11725609
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R E Esch. 2001. Allergens.. https://doi.org/10.1385/criai%3A21%3A2-3%3A89
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What we know: No one gene is a major cause of asthma. Some racial groups are more at risk of asthma than others. Early exposure to domestic animals appears to reduce the chance of developing asthma. Good hygiene may increase the likelihood of asthma. Impaired early airway function predisposes to asthma. What we need to know: How do several minor genetic factors combine to increase the risk of asthma in individuals and in population groups? Does early exposure to allergens promote sensitisation or tolerance? How do viruses precipitate asthma? Can acute asthma be treated by treating viral respiratory infections? Does impaired early airway function predispose to asthma throughout childhood?
What we know: Sensitisation to indoor allergens (house-dust mite, cat) is related to the level of exposure to these allergens in early childhood. The prevalence of asthma in childhood is independent of allergen exposure in early life. Asthma occurs in a substantial number of young children in the absence of allergen sensitisation. Asthma and allergic sensitisation have increased in recent decades, but there is no conclusive evidence that this is due to changes in environmental allergens. What we need to know: Have changes in environmental allergens contributed to the increasing incidence of asthma in recent decades? Is early childhood asthma (or certain subtypes of asthma) an allergen-induced disease? Is it possible to modify asthma by environmental allergen manipulation in early childhood? Is it possible to modulate the immune response to allergens in a favourable direction in early childhood?
What we know: Epidemiological studies have identified a number of factors associated with increased incidence of asthma. These include allergen sensitisation and exposure, reduced exposure to infections and to farm animals in early childhood, and maternal smoking. These factors may represent "true" risk factors for asthma or may be merely associated factors that do not in themselves cause asthma. The "hygiene hypothesis" has been proposed as one mechanism by which infections may protect against asthma. Current recommendations for the primary prevention of asthma include exclusive breastfeeding for the first six months of life, avoidance of maternal smoking during pregnancy and infancy, and reducing the levels of house-dust mite in some environments. What we need to know: What are the mechanisms by which specific risk factors and prevention strategies lead to or protect from asthma? How do genetic and environmental factors interact to increase the risk of asthma?