For a study, it was determined that in many industrialized nations, diisocyanates were the most prevalent cause of occupational asthma, and numerous pathogenic pathways had been proposed by researchers. Occupational asthma caused airway remodeling if it was not recognized and treated in a timely manner. However, therapy options were restricted due to a lack of knowledge of the underlying pathogenic pathways. Several immunological and non-immunological pathways had been proposed, indicating that occupational asthma might have a more complicated etiology than other kinds of asthma. When exposed to diisocyanates, airway epithelial cells initiated a variety of reactions, including cytokine release, oxidative stress creation, and autoantibody synthesis. Some data suggested that adaptive immune responses were involved. Other processes may be implicated in diisocyanate-induced occupational asthma, according to further data. Oxidative stress was one such possible pathway. In human samples and genetic research, oxidative stress had been found to cause and help in the development of diisocyanate-induced occupational asthma, and several treatment trials had been conducted as a result of this discovery.

A complex interplay of innate and adaptive immunological responses might be responsible for diisocyanate-induced occupational asthma. Through a better understanding of occupational asthma etiology, the insights offered in this study might aid in the development of innovative treatment approaches.

Reference:journals.lww.com/co-allergy/Abstract/2013/04000/Cells_and_mediators_in_diisocyanate_induced.2.aspx