Background: : The pathogenic mechanisms of toluene diisocyanate (TDI)-induced asthma are not understood clearly.
Methods: : In this review, we summarized recent data to further understand the pathogenic mechanisms through recent approach of molecular genetic studies, and specific antibody responses to cellular mechanisms.
Results: : Genetic polymorphism studies suggested the involvement of oxidant/antioxidant-related genes and neurogenic inflammatory response genes. A high-resolution technique of HLA allele suggested some HLA genetic markers presenting the phenotype of TDI-induced asthma. The new volatile type of TDI-human serum albumin conjugate could improve specific immunoglobulin E and immunoglobulin G bindings in enzyme-linked immunosorbent assay studies for identifying TDI-induced asthma patients. The role of bronchial epithelial cells and cytokeratins derived from epithelial cells could be involved in autoantibody productions, suggesting that an autoimmune mechanism may be involved in airway inflammation. Neutrophil activation and oxidant/antioxidant-related mechanisms were also suggested.
Conclusion: : The pathogenic mechanism of TDI-induced asthma is complicated as various humoral and cellular mechanisms are combined and involved differently on an individual basis. Therefore, additional efforts for further elucidation should follow.