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Effects of Source-Apportioned Coarse Particulate Matter (PM) on Allergic Responses in Mice
McGee, M., J. Mcgee, E. Gibbs-Flournoy, Y. Kim, S. Snow, L. Copeland, J. Richards, R. Jaskot, J. Dye, Ian Gilmour, AND S. Gavett. Effects of Source-Apportioned Coarse Particulate Matter (PM) on Allergic Responses in Mice. Society of Toxicology, Baltimore, MD, March 12 - 16, 2017.
Complex mixtures of local, urban, and regional air pollution sources contribute to adverse health and ecological effects. Recent health studies suggest differences in exposure relationships and health effects for different sources, highlighting the need to understand the relative contribution of these sources. Source-speciated particulate matter was used in this study to determine the specific industrial sources which may contribute to exacerbation of allergic inflammation in a mouse model of allergic asthma.
The Cleveland Multiple Air Pollutant Study (CMAPS) is one of the first comprehensive studies conducted to evaluate particulate matter (PM) over local and regional scales. Cleveland and the nearby Ohio River Valley impart significant regional sources of air pollution including coal combustion and steel production. Size-fractionated PM (coarse, fine and ultrafine) were collected from an urban site (G.T. Craig (GTC)) and a rural site (Chippewa Lake monitor (CLM) located 53 km southwest of Cleveland) from July 2009 to June 2010. Following collection, resulting speciated PM data were apportioned to identify local industrial emission sources for each size fraction and location, indicating these samples were enriched with resident emission sources. This study was designed to determine whether exposure of the CMAPS coarse PM contributes to the exacerbation of allergic asthma. Non-sensitized and house dust mite (HDM)-sensitized female Balb/cJ mice (n= 8/group) were exposed via oropharyngeal (OP) aspiration to 100 g coarse fractions of one of five source apportioned groups representative of distinct time periods of 4-6 weeks (traffic, coal, steel 1, steel 2, or winter PM) and OP challenge with HDM conducted 2 hr following dosing with PM. Two days later, airway responsiveness to methacholine aerosol was assessed in anesthetized ventilated control and HDM mice. The HDM-allergic mice demonstrated increased airway reactivity in comparison to control mice. Bronchoalveolar lavage fluid (BALF) eosinophils in HDM-allergic mice were significantly elevated when compared to non-allergic control mice. Both CLM and GTC Coarse traffic PM significantly increased BALF neutrophils in non-allergic mice in comparison to blank coarse filter and saline controls. These samples also produced significant increases in BALF lactate dehydrogenase (LDH). CLM coal PM exacerbated both BALF LDH and protein levels within non-allergic mice. Further analyses will be conducted to evaluate airway mechanics, pulmonary histological changes and cytokine levels following exposure to the CMAPS coarse PM samples. We conclude that the CMAPS coarse PM attributed to traffic and coal sources causes pulmonary injury and inflammation in healthy non-allergic mice. (This abstract does not represent U.S. EPA policy.)