The respiratory allergen trimellitic anhydride (TMA) has been shown to induce IgE production and immediate ear swelling in mice sensitized to it. We studied whether TMA sensitivity could be used as an animal model for immunological contact urticaria. BALB/C mice were sensitized to TMA by topical applications. Groups of animals were pretreated on the ears with the glucocorticosteroid (GCS) betamethasone-17,21-dipropionate, the antihistamine (AH) diphenhydramine hydrochloride, the non-steroidal anti-inflammatory drug (NSAID) indomethacin or vehicle (VEH). Ears were challenged with TMA and ear thickness was measured at baseline and 1, 2, 4, 8 and 24 h after challenge. Trimellitic anhydride caused a significant biphasic ear swelling response with an early peak at 1-2 h, a plateau at 4 h and a late peak at 24 h. However, there was also an early swelling by TMA in non-sensitized mice, suggesting that non-immunological as well as immunological mechanisms contribute to early swelling by TMA. Glucocorticosteroid suppressed significantly the early and to some extent the late TMA responses, while AH suppressed only early and NSAID only late TMA responses. Ear swelling in TMA-sensitive BALB/C mice may represent a combination of immunological and non-immunological contact urticaria and allergic contact dermatitis. Mice sensitive to TMA may be helpful in defining pharmacological agents affecting contact urticaria and the model is perhaps suitable for identification of some immunologically mediated contact urticants.