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Examination of cytokines and metals in exhaled breath condensate and lung lavage fluids after diesel exhaust exposure
Citation:
MADDEN, M. C., J. Pleil, AND K. Sawyer. Examination of cytokines and metals in exhaled breath condensate and lung lavage fluids after diesel exhaust exposure. Presented at International Association for Breath Research, Dortmund, GERMANY, April 26 - 30, 2009.
Impact/Purpose:
research results
Description:
Epidemiology studies link human exposure to ambient air pollution with the development and exacerbation of cardiopulmonary disease. Diesel exhaust (DE) is a significant source of ambient air pollution, and thus may contribute to adverse pulmonary health effects. Previous human research demonstrates that DE stimulates acute airway inflammation, measured as increased lung neutrophilia after an acute DE exposure. In this study, we evaluate whether DE can stimulate airway inflammation in humans 20 hours after exposure. In addition we evaluate whether repeated non-invasive lung sampling with exhaled breath condensate (EBC), can provide additional information about lung inflammatory responses. Human volunteers were exposed to DE (100μg/m3) and filtered air for 2 hours with intermittent exercise. EBC was collected pre-, immediately post, and 20 hours post DE exposure, followed at 20 hour with bronchoscopy with bronchial (BW) and bronchoalveolar lavage (BAL). BW, BAL, and EBC were analyzed for elemental metals and inflammatory (Th1) and allergy (Th2) related cytokines. Our data demonstrated elevated 20 hour EBC IL-1 β concentrations regardless of DE or filtered air exposure, suggesting a possible latent exercise-induced effect. Other Th1 and Th2 cytokines were relatively undetectable in EBC. EBC calcium concentrations decrease immediately post DE exposure, but not at 20 hours post DE exposure. DE exposure did not influence BAL metal concentrations. DE exposure significantly decreased TH1 cytokine concentrations and elevated TH2 cytokines concentrations in BW fluids 20 hours after DE exposure. Decreased Th1 and increased Th2 cytokines in BW and BAL indicated that DE can shift the pulmonary immune response toward an allergic-type response 20 hours after exposure. [This abstract does not necessarily represent official US EPA policy.]