Occupational asthma (OA) is the most frequently reported occupational respiratory disease in industrialized nations, and numerous low-molecular weight (LMW) chemicals and high molecular weight (HMW) proteins encountered in the workplace
are known or suspected causative agents (1). Classical and novel animal models are being used to investigate exposure determinants, epitope identity, and the role played by the immune system in OA in order to recapitulate disease phenotype and further current understanding of its pathogenesis. Important aspects of exposure determinants that can be addressed and controlled using animal models include (i) relevant routes of exposure including respiratory and/or skin, (ii) exposure dose, (iii) exposure duration and frequency, and (iv) determination of relevant epitopes. In addition, well defined genetics of animal models present unique opportunities for detailed investigations into pathogenic mechanisms by the use of transgenic models and antibody neutralization strategies. The data generated by the use of animal models is instrumental for risk assessment used to refine workplace exposure limits. Numerous guinea pig, rat, and mouse models of OA have been developed to address these issues. It is likely that key molecular and cellular events will be identified by the use of these models, potentially leading to new treatment modalities that may be specific for these classes of asthmogen and will aid in establishing more protective workplace exposure limits.