Quantitation and new antigenic determinant specificity of antibodies induced by inhalation of trimellitic anhydride in man.

Abstract

We have studied the immune response of chemical workers who are exposed to trimellitic anhydride (TMA), a biologically reactive anhydride used in the manufacture of plastics. Serum antibody activity to TMA haptenized human serum albumin (TM-HSA) was measured in workers with three clinically defined respiratory tract syndromes; asthma-rhinitis, a late respiratory systemic syndrome (LRSS), and an irritant syndrome. IgE antibody binding of <sup>125</sup>I TM-HSA was quantitated by polystyrene tube radioimmunoassay and total serum antibody binding of <sup>125</sup>I-TM-HSA by an ammonium sulfate technique. IgE antibody activity ranged from 2 to 55 ng TM-HSA bound per milliliter and was associated with the asthma-rhinitis syndrome. Total serum antibody activity ranged from 0.4 to 56 <i>μ</i>g TM-HSA bound per milliliter and was associated with either the asthma-rhinitis syndrome or LRSS. Antibody specificity for TM-HSA was determined by inhibition studies using sodium trimellitate (NaTM) and a variety of TM substituted carriers. The hapten, NaTM, was an extremely poor inhibitor of IgE or total antibody binding of TM-HSA. The other TMA haptenized carriers were either noninhibitory or had to be added in milligram quantities to effect any inhibition as contrasted with complete inhibition achieved by microgram quantities of TM-HSA. These specificity studies indicate that the inhalation of TMA results in an antibody response with specificity for unique new antigenic determinants (NAD) which arise from the coupling of TMA with autologous respiratory tract proteins.