Pharmacologically mediated hypersensitivity responses, such as those elicited with ^-lactam antibiotics, are well recognized. In addition, a number of industrial materials have known or presumed allergic activities in humans and laboratory animals (Table 1). This response can be mediated by T cells as well as antibodies (e.g. IgE) and can result in allergic contact dermatitis or allergic lung disease (asthma). A compound causing both these responses is toluene diisocyanate (TDI), a classic representative of the iso-cyanate compounds used in the production of plastics and resins. TDI, which acts as a hapten, is particularly reactive with amino groups on proteins. Chemical-induced allergic respiratory responses can also be induced by high molecular weight compounds from animal urine and saliva, enzymes in detergent, plant materials as well as therapeutic peptides. Clinical differentiation of allergic responses from nonimmune irritant responses, without detecting specific immune responses, are often difficult, but the former are usually more persistent and severe.

Tests to identify potential respiratory sensitizers are difficult to undertake and, as such, efforts to validate screening models are limited. Although the guinea pig has some significant immunological differences compared to humans (e.g. IgGl versus IgE reagenic antibodies), it has proved a predictable animal model for humans given the limited comparative data available and has been used to test for both low and high molecular weight sensitizers. As with guinea pig skin tests, the method includes both an aerosol sensitization and challenge phase. There is also a need to measure both immediate and delayed-onset responses, although this does not distinguish between nonspecific pulmonary hyperreactivity and specific immune responses. The latter is commonly

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