Eosinophil Infiltration in Airways of Mice Exposed to Toluene Diisocyanate

Toluene diisocyanate (TDI) is a chemically reactive low-molecular-weight compound widely used in industries as a polymerizing agent in the production of polyurethanes. TDI has been reported as one of the most important causes of occupational asthma1). Clinical investigations have shown that asthma is an inflammatory disorder of the airways and is referred to as chronic eosiniopilic bronchitis2, 3). Evidence has shown that activation of selected T cells with subsequent eosinophil recruitment and secretion of eosinophil-derived mediators may contribute to both epithelial cell damage and airway hyperresponsiveness4). Our previous study showed that a 5-day exposure to 1.35 ppm TDI vapor resulted in airway inflammatory responses characterized by marked infiltration of eosinophils in central and peripheral airways of an asthmatic mouse model5), but the infiltration of eosinophils in the airways of animals exposed to different concentrations of TDI in different time courses is unknown. To address this problem, in the present study, mice were exposed to three doses of TDI, and the infiltration of eosinophils was determined at three different stages of exposure under each respective concentration.