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ToxSci Advance Access published online on September 14, 2005
Toxicological Sciences, doi:10.1093/toxsci/kfi317
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© The Author 2005. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Received June 1, 2005
Accepted September 4, 2005

Respiratory Toxicology

Low Level Subchronic Exposure to Wood Smoke Exacerbates Inflammatory Responses in Allergic Rats

Yohannes Tesfaigzi 1*, Jacob D. McDonald 1, Matthew D. Reed 1, Shashibhushan P. Singh 1, George DeSanctis 2, Paul R. Eynott 2, Fletcher F. Hahn 1, Matthew J. Campen 1, and Joe L. Mauderly 1

1 Lovelace Respiratory Research Institute, Albuquerque, NM 87108
2 Sanofi/Aventis Pharmaceuticals, Inc., Bridgewater, NJ 08870

* To whom correspondence should be addressed.
Yohannes Tesfaigzi, E-mail: ytesfaig{at}lrri.org


  Abstract

Epidemiological studies have implicated wood smoke as a risk factor for exacerbating asthma. However, comparisons of findings in animal models with those in humans are currently not possible, because detailed clinically relevant measurements of pulmonary function are not available in animal studies. Brown Norway rats were immunized with ovalbumin and exposed to either filtered air or wood smoke at 1 mg particulate matter/m3 for 70 d and challenged with allergen during the last 4 d of exposure. Baseline values for dynamic lung compliance were lower while functional residual capacity was increased in rats exposed to wood smoke compared to rats exposed to filtered air. IFN-{gamma} levels were reduced and IL-4 levels increased in the bronchoalveolar lavage fluid and blood plasma, inflammatory lesions in the lungs were 21% greater, and airway mucous cells/mm basal lamina were non-significantly increased in rats exposed to wood smoke compared to controls. Collectively, these studies suggest that the pulmonary function was affected in rats by exposure to wood smoke and this decline was associated with only minor increases in inflammation of the lung. Therefore, this animal model may be useful to elucidate the mechanisms of the decline in pulmonary function caused by environmental pollutants when asthmatics are exposed to allergen.

Keywords: Particulate matter; pulmonary function; exacerbation; mucous cell metaplasia; inflammation.
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