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pubmed:abstractText |
Asthma rates have been increasing worldwide, and exposure to diesel exhaust particles (DEP) may be implicated in this increase. DEP may also play a role in the increased morbidity and mortality associated with ambient airborne particulate matter (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 immunoglobulin E (IgE) production. Since DEP composition can vary depending on several factors, including fuel composition and engine load, the ability of another DEP particle and ozone-treated DEP to alter nasal IgE and cytokine production was examined. Nonasthmatic and asthmatic subjects were intranasally instilled with 300 microg NIST 1650 DEP per nostril, NIST 1650 DEP previously exposed to ozone (ozDEP; 300 microg/nostril), or vehicle. Subjects underwent nasal lavage before DEP exposure, and 4 and 96 h after exposure. Nasal cell populations and soluble mediators in the nasal lavage fluid were characterized. Total cell number, cell types, cell viability, concentrations of soluble mediators (including interleukin [IL]-8, IL-6, IgE, and granulocyte-macrophage colony-stimulating factor [GM-CSF]) were not altered by either DEP or ozDEP exposure. NO levels were not altered by either particle exposure. 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.
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