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ToxSci Advance Access published online on September 18, 2006
Toxicological Sciences, doi:10.1093/toxsci/kfl107
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Published by Oxford University Press 2006.
Received July 6, 2006
Accepted September 10, 2006

Immunotoxiocology

Airway Responses in Brown Norway Rats following Inhalation Sensitization and Challenge with Trimellitic Anhydride

Xing-Dong Zhang MD, PhD 1, Michael E. Andrew PhD 1, Ann F. Hubbs DVM, PhD 1, and Paul D. Siegel PhD 1 *

1 Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, WV 26505, USA

* To whom correspondence should be addressed.
Paul D. Siegel, E-mail: psiegel{at}cdc.gov


  Abstract

Trimellitic anhydride (TMA) is a cause of asthma in man. Dose-dependent TMA-specific IgE, histopathology and airway responses after sensitization by inhalation were examined in the Brown Norway rat. Rats were exposed of 0.04, 0.4., 4 or 40 mg/m3 TMA aerosol for 10 min, once a week, over 10 weeks. All lower exposures were, subsequently, re-challenged to 40 mg/m3 TMA aerosol. All rats received a sham exposure one week prior to the first TMA exposure. Following the sham exposure and weekly after each TMA exposure, TMA specific-IgE and both early- (EAR) and late-phase airway (LAR) responses were measured using enhanced pause (Penh). All rats sensitized by 40 mg/m3 TMA developed specific IgE, EAR and LAR to one or more of the challenges to 40 mg/m3 TMA. Four mg/m3 TMA induced a much lower, but stable, specific IgE response. EAR and LAR was observed only after a 40 mg/m3 TMA re-challenge in this group, but it was much larger than that observed in the 40 mg/m3 TMA sensitized and challenged group. Exposure-dependent histopathological changes noted included eosinophilic granulomatous interstitial pneumonia, perivascular eosinophils, bronchial-associated lymphoid tissue hyperplasia (BALT) and peribronchiolar plasma cell infiltrates.

Keywords: trimellitic anhydride; inhalation; airway response; IgE.
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