You are here:
Effect of Near-Road Particulate Matter on Respiratory Responses and Inflammation in Healthy and Ovalbumin-Allergic Mice
Citation:
Marie, M., J. Mcgee, E. Boykin, M. Daniels, L. Copeland, D. Andrews, J. Richards, Ian Gilmour, AND S. Gavett. Effect of Near-Road Particulate Matter on Respiratory Responses and Inflammation in Healthy and Ovalbumin-Allergic Mice. Presented at Society of Toxicology, Phoenx, AZ, March 23 - 27, 2014.
Impact/Purpose:
This abstract contributes to understanding of PM attributes contributing to exacerbation of allergic asthma, and supports epidemiological research conducted with the NEXUS study.
Description:
The Near-Road Exposures and Effects of Urban Air Pollutant Study (NEXUS) previously examined the association of near-roadway exposures to air pollutants and respiratory outcomes in children with asthma. This toxicological study was designed to complement NEXUS and determine which particulate matter (PM) characteristics may contribute to exacerbation of allergic asthma. Samples of coarse, fine and ultrafine PM were collected upwind and downwind from I-96 in Detroit, MI during Winter 2010/11. Healthy and ovalbumin (OVA)-sensitized female Balb/cJ mice were exposed via oropharyngeal (OP) aspiration to 20 or 100 μg coarse, fine, or ultrafine fractions of upwind or downwind PM 2 hr prior to OP challenge with 20 μg OVA. No samples caused significant changes in immediate responses to OVA challenge as determined by whole body plethysmography (WBP). Two days later, airway responsiveness to methacholine aerosol (assessed by WBP) was not significantly affected by PM exposure in either healthy or allergic mice. In OVA-allergic mice, 100 μg downwind coarse PM caused a greater increase than downwind fine or ultrafine PM in bronchoalveolar lavage (BAL) neutrophils (7x vs. control blank filter extract) and eosinophils (10x) and also caused significant increases in BAL LDH and NAG. Interestingly, 100 μg upwind fine PM produced greater increases in neutrophils (7x vs. control blank filter extract) and eosinophils (4x) than upwind coarse or ultrafine PM. Ultrafine PM did not significantly increase neutrophils or eosinophils in comparison to allergic mice given ultrafine blank filter extract. Further analyses will be conducted to investigate associations between chemical components and phenotypic effects of allergic lung disease. We conclude that coarse PM downwind and fine PM upwind of traffic promote allergic inflammation in OVA-allergic mice. (This abstract does not represent U.S. EPA policy.)