Exposure Response Variation among Differing Diesel Particulate Types

Toxicological Sciences 2009 107(2):522-534;
Allergic Lung Disease in Mice Exposed to Chemically Distinct Diesel Samples


Tina Stevens*, Seung-Hyun Cho,, William P. Linak and M. Ian Gilmour,1
* Curriculum in Toxicology, University of North Carolina, Chapel Hill, North Carolina 27599 Air Pollution and Prevention Control Division, National Risk Management Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina 27711 Research Participation Program, Oak Ridge Institute for Science and Education, Oak Ridge, Tennessee 37831 Experimental Toxicology Division, National Health and Environmental Effects Research Laboratory, Research Triangle Park, North Carolina 27711
1 To whom correspondence should be addressed at U.S. Environmental Protection Agency, Research Triangle Park, NC 27711. Fax: (919) 541-0026. E-mail: gilmour.ian@epa.gov

Abstract
Numerous studies have demonstrated that diesel exhaust particles (DEP) potentiate allergic immune responses, however the chemical components associated with this effect, and the underlying mechanisms are not well understood. This study characterized the composition of three chemically distinct DEP samples (N, C, and A-DEP), and compared post-sensitization and post-challenge inflammatory allergic phenotypes in BALB/c mice. Mice were instilled intranasally with saline or 150 µg of N-DEP, A-DEP, or C-DEP with or without 20 µg of ovalbumin (OVA) on days 0 and 13, and were subsequently challenged with 20 µg of OVA on days 23, 26, and 29. Mice were necropsied 18 h post-sensitization and 18 and 48 h post-challenge. N-DEP, A-DEP, and C-DEP contained 1.5, 68.6, and 18.9% extractable organic material (EOM) and 47, 431, and 522 µg of polycyclic aromatic hydrocarbons (PAHs), respectively. The post-challenge results showed that DEP given with OVA induced a gradation of adjuvancy as follows: C-DEP A-DEP > N-DEP. The C- and A-DEP/OVA exposure groups had significant increases in eosinophils, OVA-specific IgG1, and airway hyperresponsiveness. In addition, the C-DEP/OVA exposure increased the T helper 2 (TH2) chemoattractant chemokine, thymus and activation-regulated chemokine and exhibited the most severe perivascular inflammation in the lung, whereas A-DEP/OVA increased interleukin (IL)-5 and IL-10. In contrast, N-DEP/OVA exposure only increased OVA-specific IgG1 post-challenge. Analysis of early signaling showed that C-DEP induced a greater number of TH2 cytokines compared with A-DEP and N-DEP. The results suggest that potentiation of allergic immune responses by DEP is associated with PAH content rather than the total amount of EOM.
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BrooklynDodger(s) comment: The Dodger(s) need(s) to figure out the provenance of these different diesel exhaust types. The article was not available in full text, at least yet. Since extractable organic matter and PAH were confounded, it's not clear why the authors conclude it's PAH.