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Inhalation Toxicology
International Forum for Respiratory Research
Volume 16, 2004 - Issue 10
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Research Article

Pulmonary Retention of Particulate Matter is Associated with Airway Inflammation in Allergic Rats Exposed to Air Pollution in Urban Detroit

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Pages 663-674 | Published online: 19 Oct 2008
 

Abstract

A collaborative research study was conducted in order to improve our understanding of the source-to-receptor pathway for ambient fine particulate matter (aerodynamic diameter ≤ 2.5 μ m; PM2.5) and subsequently to investigate the identity and sources of toxic components in PM2.5 responsible for adverse health effects in allergic humans. This research used a Harvard fine particle concentrator to expose Brown Norway rats, with and without ovalbumin-induced allergic airway disease, to concentrated air particles (CAPs) generated from ambient air in an urban Detroit community where the pediatric asthma rate was three times higher than the national average. Rats were exposed to CAPs during the exposure periods in July (mean = 676 μg/m3) and September (313 μg/m3) of 2000. Twenty-four hours after exposures lung lobes were either lavaged with saline to determine cellularity and protein in bronchoalveolar lavage fluid (BALF), or removed for analysis by inductively coupled plasma–mass spectrometry (ICP-MS) to detect ambient PM2.5-derived trace element retention. PM2.5 trace elements of anthropogenic origin, lanthanum (La), vanadium (V), manganese (Mn), and sulfur (S), were recovered from the lung tissues of CAPs-exposed rats. Recovery of those pulmonary anthropogenic particles was further increased in rats with allergic airways. In addition, eosinophils and protein in BALF were increased only in allergic animals exposed to CAPs. These results demonstrate preferential retention in allergic airways of air particulates derived from identified local combustion sources after a short-term exposure. Our findings suggest that the enhancement of allergic airway responses by exposure to PM2.5 is mediated in part by increased pulmonary deposition and localization of potentially toxic elements in urban air.

This research was supported by the Health Effects Institute, number 99-7. We gratefully acknowledge the field efforts of Jim Barres, Fuyuen Yip, Mary Lynam, and staff members at the UMAQL. We also thank Ellen Snedeker of Maybury Elementary School for support at the study location in Detroit.

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