Occupational asthma is a form of immunotoxicity resulting from an exaggerated immune response to substances encountered in the workplace. Symptoms include reversible airway obstruction, airway hyperresponsiveness, airway remodeling, mucus production and cellular infiltration into the lung, particularly eosinophilia. The asthmatic response is divided into the induction phase, occurring after initial exposure to allergen, followed by the effector phase where a subsequent exposure to the allergen results in the respiratory symptoms. Animal models have been used to investigate the asthmatic response and this review will focus on mechanistic studies of the effector phase. Variables that may impact the effector phase include strain and species of animal, dose of allergen, route of exposure, and developmental stage of the animal. Both trimellitic anhydride (TMA) and ovalbumin are known causes of occupational asthma. Ovalbumin is also a reference protein allergen in immunology, and TMA is used as a prototype of a low molecular weight respiratory allergen. Differences in effector mechanisms for TMA and ovalbumin have been noted in different animal models. Studies in the guinea pig provide the most direct comparisons of effector mechanisms of TMA and ovalbumin, with differences in the role of the complement system and arachidonate metabolites being noted. Besides the guinea pig, the Brown Norway rat, and various mouse strains provide useful asthma models for TMA and ovalbumin. However, studies of effector mechanisms are somewhat lacking in either of these species using TMA as the allergen. Continued studies are indicated to determine if unique effector mechanisms can be identified for the many different causes of occupational asthma.