Detection of IgE antibodies specific to isonicotinic acid hydrazide and its metabolite by enzyme-linked immunosorbent assay and the mechanism of sensitization by inhalation or ingestion of this compound.

A female hospital pharmacist and a nurse developed occupational asthma due to the inhalation of isonicotinic acid hydrazide (INH) powder. The mechanism of sensitization was examined in this study. Furthermore, IgE antibodies specific to INH and isonicotinic acid (INA), the major metabolite of INH, were examined by means of enzyme-linked immunosorbent assay (ELISA). IgE anti-INH antibody activity was detected by ELISA in sera from 5 out of 8 hospital workers who inhaled INH powder during the handling of INH, and in sera from 10 out of 142 tuberculosis patients receiving oral INH. IgE anti-INA antibody activity was detected in sera from 3 of the 8 hospital workers, and from 7 of the 142 tuberculosis patients. Neither IgE anti-INH nor anti-INA antibody activity was detected in sera from 45 patients with asthma or from 42 healthy volunteers. The specificity of the IgE antibodies and the cross-antigenicity between INH and INA were confirmed by ELISA inhibition studies. Our results indicate that sensitization to INH can occur not only by inhalation but also by oral administration, and that the asthmatic symptoms of the patients were caused by an IgE antibody specific to INH as a hapten.