In developed countries, such as the U.S., 80% of childhood asthmatics are allergic to indoor allergens (National Academy of Sciences 2000). A growing body of evidence suggests that increased exposure to these types of allergens may be relevant to the increased incidence and severity of asthma in children. Asthma manifests as a set of symptoms ranging from mild to severe. However, displays of asthma-like symptoms in infancy may or may not lead to persistent atopic childhood asthma. Furthermore, while the development of childhood asthma is agreed to result from an interplay of genetics and environment, that interplay is poorly understood. What is known is that most childhood asthma results from allergen sensitization in a genetically predisposed individual. Moreover, immunoregulatory mechanisms may be altered at mucosal surfaces in ways that promote a TH2-mediated allergic inflammatory response, and these alterations may be influenced by cofactors such as tobacco smoke and air pollutants (Holgate 1999; Kay 2001), as well as the frequency and type of respiratory infections, and the frequency (perennial or not) and intensity of allergen exposure (National Academy of Sciences 2000). While indoor allergens certainly exacerbate asthma in children, it must be understood that no specific allergens have been definitively linked to the development of asthma following exposure in utero. For the most part, these studies simply have not been done, and the effect of maternal or neonatal exposure to any allergen during the development of the immune system on enhanced susceptibility to asthma must be explored further. What is known of the influence of common indoor allergens associated with asthmagenesis (asthmagens) will now be discussed.
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