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DIESEL AND CARBON PARTICLES ENHANCE HOUSE DUST MITE-INDUCED PULMONARY HYPERSENSITIVITY IN BROWN NORWAY RATS
Citation:
Singh, P., M. J. Daniels, D Winsett, J. Richards, K Crissman, AND M. Madden. DIESEL AND CARBON PARTICLES ENHANCE HOUSE DUST MITE-INDUCED PULMONARY HYPERSENSITIVITY IN BROWN NORWAY RATS. Presented at SOT, San Francisco, CA, March 25-29, 2001.
Description:
Diesel and Carbon Particles Enhance House Dust Mite-Induced Pulmonary Hypersensitivity in Brown Norway Rats. P. Singh1, M.J. Daniels2, D. Winsett2, J. Richards2, K. Crissman2, M. Madden2 and M.I. Gilmour2. 1NCSU, Raleigh, NC and 2 USEPA, Research Triangle Park, NC.
Epidemiological studies have shown that ambient air particulate matter (PM) can have significant health effects in exposed populations and especially in asthmatic individuals. Recent studies have also shown 1) that diesel exhaust particles (DEP) exposed to ozone (0.1 ppm for 48 hr) produce increased lung injury and inflammation in rats compared to unexposed DEP and 2) that ultra fine carbon black (UFCB) is more inflammatory than fine carbon black (FCB) in the rat lung. It has been previously demonstrated in this laboratory that Brown Norway (BN) rats exposed to residual oil fly ash (ROFA) have more severe asthmatic responses to house dust mite (HDM) than unexposed rats. The objective of the current study was to use our BN rat model of allergic airway responses to investigate the effects of pre-sensitization exposure to diesel (? pre-exposure to ozone) and carbon particles on airway hypersensitivity and lung injury. Female BN rats were instilled intratracheally (IT) with 100 ug of air-exposed DEP, ozone-exposed DEP, UFCB or FCB on day 0, followed by IT sensitization with 5 ug HDM on days 1 and 3. Rats were challenged IT with 10 ug HDM on day 15 and euthanized 2 and 7 days later. All particles increased the Th2 cytokines IL-4 and IL-13 as well as TNFa in the bronchoalveolar lavage (BAL) fluid and markedly increased antigen induced bronchoconstriction compared to saline controls. All animals had high eosinophil numbers, however a notable increase occurred only in the air-exposed DEP group. Increased lymphocyte function was limited to the ozone-exposed DEP treated rats, and serum IgE levels were only elevated with FCB exposure. This study shows that particle administration prior to allergic sensitization can enhance pulmonary injury and hypersensitivity in the following order of adjuvancy: DEP-air > DEP-ozone > UFCB > FCB. (This abstract does not reflect EPA policy.)