COREXIT® EC9500A (CE) was used to disperse crude oil during the 2010 Deepwater Horizon oil spill response. While the environmental impact of CE has been examined, the pulmonary effects of CE are unknown. Here we investigated whether inhaled CE elicits airway inflammation, alters pulmonary function, or affects airway reactivity to methacholine (MCh). Rats were exposed to CE (mean 27 mg/m3, 5 h) and examined 1 and 7 d post-exposure. Under anesthesia, the lung lavage fluid was harvested. Lactate dehydrogenase (LDH) and albumin (A) were measured as indices of lung injury, recovered lung cells were differentiated (macrophages, neutrophils, lymphocytes, and eosinophils) to evaluate inflammation, and oxidant production by macrophages was measured. There were no significant differences in LDH, A, inflammatory cell levels or oxidant production between air- and CE-exposed groups at either time point. Pulmonary function assessed in conscious animals indicated that neither breathing frequency nor specific airway resistance were altered at 1 and 7 d post-exposure. Airway resistance responses to MCh aerosol in anesthetized animals were unaffected at 1 and 7 d post-exposure, while dynamic compliance responses were decreased at 1 d but not at 7 d post-exposure. Our findings suggest that CE inhalation does not initiate lung inflammation, but may transiently increase the difficulty of breathing.