Origins of allergic airway disease and dealing with environmental allergens

Children and adolescents should be safe in their schools. Recent coroners’ cases have emphasized that this is not the case at the moment.1 In an editorial in this month's issue of the Journal, The British Society of Allergy and Clinical Immunology (BSACI), Allergy UK and Anaphylaxis Campaign advocate for simple changes that could be put into place.2 This needs a joined-up approach from the BSACI, the patient support groups and governmental agencies, particularly Department for Education and Department of Health and Social Care. The removal of environmental cat allergen ought to improve the control of cat allergen driven asthma. However, to date approves to controlling environmental allergen exposure has been suboptimal.3 Gherasim et al assess the ability of an air cleaner (Intense Pure Air X) to control lung function responses to cat allergen exposure in an environmental exposure chamber (Fig 1).4 This approach provides optimal control on exposure, minimizing variability with the experimental system and promoting sensitivity to detecting the impact of an intervention. Using a randomized, cross-over, and double-blind placebo-controlled approach, they studied 24 participants with mild asthma and cat allergy. Significantly, less participants experienced an early asthmatic response with active than placebo air cleaner (hazard ratio, 0.10; P = .0019). They also had significantly less late-phase reactions (P = .0024). So impressive results but will there be similar benefit in a real life? There are potentially complicated interrelationships between season of birth and respiratory tract infections and the development of childhood asthma and allergic disease.5 Almqvist et al6 have examined the issue within a population-based setting. They used the nationwide Swedish Medical Birth, Patient and Prescribed Drug Registers. They found that children born during autumn and winter were more likely to have asthma or wheeze after 2 years of age (hazard ratio 1.24, 95% confidence interval 1.17, 1.33). This relationship was partly mediated by lower respiratory infections. While season was also associated with allergic rhinoconjunctivitis, it was not mediated by respiratory tract infections. There are very different expressions of respiratory disease in male and females. While asthma is predominately a male disease in early life, equal numbers of male and females are affected from adolescence. Lacerda et al have examined the underlying mechanisms for this using an experimental mouse model of lung allergic inflammation.7 They found sex-linked differences in inflammation and remodelling linked to weigh gain.

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