Airway inflammatory response to diesel exhaust generated at urban cycle running conditions

Diesel exhaust (DE) is an important component in traffic-related air pollution, associated with adverse health effects. DE generated at idling has been demonstrated to induce inflammation in human airways, in terms of inflammatory cell recruitment, enhanced expression of vascular endothelial adhesion molecules, cytokines, mitogen-activated protein kinases, and transcription factors in the bronchial epithelium.

This study aimed to investigate airway inflammatory responses in healthy subjects exposed to DE generated during transient speed and engine load under the urban part of the European Transient Cycle.

Fifteen healthy subjects were exposed to DE at an average particulate matter concentration of 270 µg/m(3) and filtered air for 1 h. Bronchoscopy with endobronchial mucosal biopsy sampling and airway lavage was performed 6 h postexposure.

Compared with filtered air, DE exposure caused an increased expression of the vascular endothelial adhesion molecules P-selectin and vascular cell adhesion molecule-1 (P  =  0.036 and P  =  0.030, respectively) in bronchial mucosal biopsies, together with increased numbers of bronchoalveolar lavage eosinophils (P  =  0.017).

DE generated under urban running conditions increased bronchial adhesion molecule expressions, together with the novel finding of bronchoalveolar eosinophilia, which has not been shown after exposure to DE at idling. Variations in airway inflammatory response to DE generated under diverse running condition may be related to differences in exhaust composition.