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Inhalation Toxicology
International Forum for Respiratory Research
Volume 20, 2008 - Issue 13
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Research Article

Effects of Gasoline Engine Emissions on Preexisting Allergic Airway Responses in Mice

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Pages 1145-1155 | Received 01 Jul 2008, Accepted 01 Aug 2008, Published online: 02 Dec 2008
 

Abstract

Gasoline-powered vehicle emissions contribute significantly to ambient air pollution. We hypothesized that exposure to gasoline engine emissions (GEE) may exacerbate preexisting allergic airway responses. Male BALB/c mice were sensitized by injection with ovalbumin (OVA) and then received a 10-min aerosolized OVA challenge. Parallel groups were sham-sensitized with saline. Mice were exposed 6 h/day to air (control, C) or GEE containing particulate matter (PM) at low (L), medium (M), or high (H) concentrations, or to the H level with PM removed by filtration (high-filtered, HF). Immediately after GEE exposure mice received another 10-min aerosol OVA challenge (pre-OVA protocol). In a second (post-OVA) protocol, mice were similarly sensitized but only challenged to OVA before air or GEE exposure. Measurements of airway hyperresponsiveness (AHR), bronchoalveolar lavage (BAL), and blood collection were performed ∼24 h after the last exposure. In both protocols, M, H, and HF GEE exposure significantly decreased BAL neutrophils from nonsensitized mice but had no significant effect on BAL cells from OVA-sensitized mice. In the pre-OVA protocol, GEE exposure increased OVA-specific IgG1 but had no effect on BAL interleukin (IL)-2, IL-4, IL-13, or interferon (IFN)-γ in OVA-sensitized mice. Nonsensitized GEE-exposed mice had increased OVA-specific IgG2a, IgE, and IL-2, but decreased total IgE. In the post-OVA protocol, GEE exposure reduced BAL IL-4, IL-5, and IFN-γ in nonsensitized mice but had no effect on sensitized mice. These results suggest acute exposure to the gas–vapor phase of GEE suppressed inflammatory cells and cytokines from nonsensitized mice but did not substantially exacerbate allergic responses.

This work was supported by the National Environmental Respiratory Center, which was funded by numerous industry, state, and federal sponsors, including the U.S. Environmental Protection Agency, U.S. Department of Energy (Office of Freedom Car and Vehicle Technologies), and U.S. Department of Transportation. This article does not represent the views or policies of any sponsor. The authors also thank Dr. Joe Mauderly for his careful review and edit of this article.

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