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Although it has been shown that exposure to diesel exhaust (DE) is linked to the induction or exacerbation of respiratory disorders, the major components responsible have not been fully identified. We examined the effects of airway exposure to nanoparticle-rich DE (NR-DE) or DE without particles on allergic pulmonary inflammation in mice. We also investigated the cellular responses to intratracheal instillation of NR-DE particles (NR-DEP). ICR mice inhaled one of four different mixtures (control air, low-concentration DE, high-concentration DE, and high-concentration DE without particles) for 8 weeks in the presence or absence of repeated intratracheal administration of ovalbumin (OVA). In a separate study, NR-DEP and/or OVA were repeatedly administrated intratracheally to mice. High-concentration NR-DE or DE without particles substantially exacerbated OVA-induced eosinophilic airway inflammation. This exacerbation was concomitant with increases in lung levels of Th2 cytokines such as interleukin (IL)-4, IL-5, and IL-13 and of chemokines such as monocyte chemotactic protein-1. Furthermore, in the presence of allergen, both DE without particles and high-concentration NR-DE strongly enhanced the production and release of myeloperoxidase into the alveolar spaces. Repeated administration of NR-DEP did not substantially affect the allergic asthma. These results strongly suggest that gaseous compounds in NR-DE aggravate murine allergic airway inflammation, mainly via amplification of the Th2 response.

Effects of exposure to nanoparticle-rich or -depleted diesel exhaust on allergic pathophysiology in the murine lung