Background: Acute exacerbations of asthma are usually triggered by viral infections, which may interact with exposure to allergens. High levels of ambient environmental particulate matter (PM10 i.e. <10 µm median aerodynamic diameter) have also been linked to acute exacerbations of asthma. The mechanism(s) by which non-allergic stimuli such as PM10 trigger exacerbations of allergic asthma are unknown, but may involve injury to airway epithelial cells (AEC). Methods: We assessed the effects of PM10 on AEC with respect to oxidative stress response and expression of relevant cytokines. In BALB/c mice that were sensitised to ovalbumin and then repeatedly challenged with a low (≈3 mg/m3) mass concentration of aerosolised ovalbumin for 4 weeks, we examined the effects of delivering a single dose of Sydney PM10 by intranasal instillation. Asthmatic inflammation was quantified in terms of cellular recruitment and expression of relevant cytokines, both in bronchoalveolar lavage fluid and tissues. Responses were compared to animals administered carbon black as a negative control, or a moderate (≈30 mg/m3) concentration of ovalbumin, as a positive control for an allergen-induced acute exacerbation. Results: Sydney PM10 were associated with various alkanes and polycyclic aromatic hydrocarbons, abundant sulfates and nitrates, and several trace metals. Levels of bacterial endotoxin were very low. Characteristic features of allergic asthmatic inflammation developed in animals which received intranasal particulates, including eosinophil and neutrophil recruitment, similar to that in the acute exacerbation positive control. Ambient particulates induced epithelial injury in vitro, with evidence of an oxidative stress response and production of both pro-inflammatory and Th2-promoting cytokines. Conclusions: This novel experimental model simulates an acute exacerbation of chronic allergic asthma induced by exposure to PM10. Thus it will facilitate investigation of how injury to AEC by particulates drives airway inflammation, and of the role of cross-talk between innate host defences and the adaptive immune response.