Highly reactive low-molecular compounds diisocyanates represent a significant cause of occupational asthma. Besides formaldehyde and latex, diisocyanates become a significant cause of occupational bronchial asthma (AB) in industrial countries, estimated prevalence of AB caused by diisocyanates is 5–15% of all exposed workers. Diisocyanates (DI) are highly reactive aromatic and aliphatic compounds reacting with compounds rich in hydroxyl groups by polyaddition reaction resulting in polyurethanes. The most commonly used forms of DI are toluendiisocyanate (TDI), methylendiphenyldiisocyanate (MDI), hexamethylendiisocyanate (HDI). They are irreplaceable in furniture-making, motor-car, electronic, clothing and refrigeration industry. Immunopathogenesis of AB caused by DI is studied from many points of view. AB caused by diisocyanates shows some clinical features typical for atopic AB – development of considerable bronchial hyperreactivity to DI in subirritative concentrations, latent period of months to years under continuous exposure, occurence of an early and late phase of bronchial response. At the same time, it differs from atopic AB with some characteristics – absence of eye and nasal allergic symptoms, absence of specific IgE (DI-conjugate) in majority of workers with confirmed AB, frequent occurence of an isolated late phase of bronchial response. Research on bronchial asthma induced by DI is currently focused on several topics: genetic factors which determine susceptibility to the disease, the role of epithelial barrier in sensibilization of organism, identification of DI – protein conjugates in their role of antigens, characteristics of immunological response in AB caused by DI and the role of neurogenic mechanisms in pathogenesis of the disease. Studies concerned with presented topics support the concept that AB caused by diisocyanates is presented by mixed type of the TH1/TH2 response, influx and regulatory role of CD4+ and CD8+ T lymphocytes. The increased frequency of the DQA1*0104 and DQB1*0503 alleles was proved in patients with diagnosed disease compared to exposed individuals without symptoms but confirmed increased frequency of the DQA1* 0101 and DQB1*0501 alleles. Knowledge of the pathogenesis of AB caused by diisocyanates may accelerate the development of diagnostic tests and consequent treatment intervention.

        Key words: occupational bronchial asthma, diisocyanates, immunopathogenesis