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NASAL RESPONSES OF ASTHMATIC AND NON-ASTHMATIC VOLUNTEERS TO DIESEL EXHAUST PARTICLES
Citation:
MADDEN, M. C., J. KONGERUD, J. E. GALLAGHER, M. HAZUCHA, AND DAVE B. PEDEN. NASAL RESPONSES OF ASTHMATIC AND NON-ASTHMATIC VOLUNTEERS TO DIESEL EXHAUST PARTICLES. Presented at American Thoracic Society Meeting, San Diego, CA, May 19 - 24, 2006.
Description:
Asthma rates have been increasing world-wide, and exposure to diesel exhaust particles (DEP) may be implicated in this increase. Additionally DEP may also play a role in the increased morbidity and mortality associated with ambient airborne PM exposure. Two types of nasal responses have been reported for human subjects nasally instilled with one type of DEP: alterations in cytokines responses and an increase in IgE production. Since DEP composition can vary depending on several factors fuel composition and engine load, the ability of another source of DEP to alter nasal IgE and cytokine production was examined. Nonasthmatic and asthmatic subjects were intranasally instilled with 300 g NIST 1650 DEP per nostril, NIST 1650 DEP previously exposed to ozone (ozDEP; 300 g/nostril), or vehicle. Subjects underwent nasal lavage before DEP exposure, and 4 and 96 hr after exposure. Nasal cell populations and soluble mediators in the
Title: NASAL RESPONSES OF ASTHMATIC AND NON-ASTHMATIC VOLUNTEERS TO DIESEL EXHAUST PARTICLES
M.C. Madden, PhD1, J. Kongerud, MD2, J.E. Gallagher, PhD1, M.J. Hazucha, MD, PhD3 and D.B. Peden, MD3. 1US EPA, Research Triangle Park, NC, United States; 2Lungeavdelingen , Rikshospitalet, University of Oslo, Oslo, Norway and 3Univ N Carolina, Chapel Hill, NC, United States.
Asthma rates have been increasing world-wide, and exposure to diesel exhaust particles (DEP) may be implicated in this increase. Additionally DEP may also play a role in the increased morbidity and mortality associated with ambient airborne PM exposure. Two types of nasal responses have been reported for human subjects nasally instilled with one type of DEP: alterations in cytokines responses and an increase in IgE production. Since DEP composition can vary depending on several factors fuel composition and engine load, the ability of another source of DEP to alter nasal IgE and cytokine production was examined. Nonasthmatic and asthmatic subjects were intranasally instilled with 300 g NIST 1650 DEP per nostril, NIST 1650 DEP previously exposed to ozone (ozDEP; 300 g/nostril), or vehicle. Subjects underwent nasal lavage before DEP exposure, and 4 and 96 hr after exposure. Nasal cell populations and soluble mediators in the nasal lavage fluid were characterized. No alterations in total cell number or cell types were observed at either time post exposure. Concentrations of soluble mediators (including IL-8, IL-6, and GM-CSF) were not altered. IgE concentrations in lavage of asthmatic subjects were not altered by either DEP or ozDEP-exposure, and levels were generally not detectable in nonasthmatic subjects. Nitrogen oxide levels were not altered by either particle exposure. DNA bulky adduct levels in lavage cells recovered from the nonasthmatic subjects were not increased by instillation with either particle. These findings suggest that DEP can be relatively noninflammatory and nontoxic, and that the physicochemical characteristics of DEP need to be considered when assessing the health effects of exposure to diesel exhaust. [This abstract may not represent official EPA policy.]