Airborne exposures to protein (and some chemical) respiratory sensitizers in the workplace can induce the development of specific IgE—a state known as ‘sensitization’. Further significant exposure may give rise to clinical symptoms, and workers who are both sensitized and symptomatic thus present with occupational rhinitis and/or occupational asthma. Importantly, however, a state of asymptomatic sensitization is widely recognized and indeed may not be uncommon. This occurs in the general population who are exposed to common aero-allergens such as house dust mite, pollens and cat dander. While atopy, defined as a propensity to produce specific IgE to one or more of these allergens, is a risk factor for developing atopic diatheses such as asthma and allergic rhinitis, not everyone with atopy develops disease. In a large survey of Italian men and women, no more than 30% of those who were atopic had any respiratory or nasal symptoms [1]. Similarly, in the 1970s, when enzyme asthma was first recognized in the detergent industry, 40% of the workforce were sensitized, while only 15% had symptoms [2]. The strength of the relationship between symptoms and sensitization may depend on a complex interplay of factors including the nature of the allergen [3].
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