Asthma and the westernization ‘package’

Ten years ago we knew what caused asthma, and we knew how to prevent it. Asthma was an atopic disease caused by allergen exposure. The fundamental aetiological mechanism was that allergen exposure, particularly in infancy, produced atopic sensitization and continued exposure resulted in asthma through the development of eosinophilic airways inflammation, bronchial hyper-responsiveness and reversible airflow obstruction. Asthma prevalence was increasing around the world because of changes in lifestyle and domestic building design that were increasing allergen exposure. The solution was therefore clear: to prevent asthma we needed to prevent exposure to allergens.1–3 In recent years it has become increasingly evident that this picture is, at best, too simplistic.4 Bronchial responsiveness is a poor surrogate measure of clinical asthma and the current evidence is that it has lower validity than standard symptom questionnaires.5 Less than one half of asthma cases are attributableto atopy and/or eosinophilic airways inflammation,6 and (non-allergic/non-atopic) neutrophilic airways inflammation may account for the other half.7 Furthermore, although there are some clear cases of allergen exposure causing asthma in adults in the occupational environment, overall there is little evidence that allergen exposure is a major primary cause of asthma,8 and even some evidence that allergen exposure early in life may have a protective effect (see below).