Three months after starting his current job, he developed rhinitis, which improved over the weekends. Nine months after the onset of rhinitis, exposure to colistin caused him to suffer sudden cough, wheeze, and dyspnea. On two occasions, he presented to the ED, and on one of these occasions, he was admitted for 72 h. One month after the second admission, the patient was referred to our department to investigate a possible diagnosis of OA. At this point, he was asymptomatic, and he was not in need of treatment. No abnormality was found during physical examination, chest radiography, or blood testing, and the total serum IgE titer was 33 units/mL. Skin prick tests were positive to Artemisia sp and Alternaria sp. Lung function showed an FVC of 4.69 L (88%), an FEV1 of 4.16 L (97%), and an FEV1/FVC ratio of 88%. The bronchodilator test was negative, and a methacholine concentration of 16 mg/mL was required to produce a 20% decrease in FEV1. The specific inhalation challenge (SIC) to colistin was performed as described for other pharmaceutical agents3 and was positive, illustrating an early response (Fig 1) with the onset of rhinitis symptoms. Given the possibility that this reaction was related to an irritant effect, the same SIC was conducted on a healthy volunteer exposed to the same inhaled concentration of colistin as the patient, with negative results. A dot-blot experiment was negative to colistin. Briefly, 100, 10, 5, and 1 mg/mL solutions of colistin were prepared. Five microliters of each solution were spotted onto nitrocellulose membranes and air dried. After blocking, the membranes were incubated with diluted patient sera (1:2) for 1.5 h. After three washes, the membranes were incubated for 1 h with biotinylated mouse-antihuman IgE. After further washing, the membranes were incubated for 1 h with streptavidin-horseradish peroxidase. All the immunoblots were developed with a hemiluminescent substrate.