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Airway responses in Brown Norway rats following inhalation sensitization and challenge with trimellitic anhydride.
Toxicol Sci. 2006 Dec;94(2):322-9
Publication Type
Zhang Xing-Dong
Andrew Michael E
Hubbs Ann F
Siegel Paul D
Author Affiliation
Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, West Virginia 26505, USA.
Toxicol Sci. 2006 Dec;94(2):322-9
Publication Type
Administration, Inhalation
Airway Resistance - drug effects - physiology
Allergens - immunology - toxicity
Antibodies, Anti-Idiotypic - blood
Bronchi - drug effects - pathology
Bronchial Hyperreactivity - chemically induced - immunology - pathology
Bronchial Provocation Tests
Immunoglobulin E - blood - immunology
Inhalation Exposure
Phthalic Anhydrides - immunology - toxicity
Plethysmography, Whole Body
Rats, Inbred BN
Respiratory Hypersensitivity - chemically induced - immunology - pathology
Specific Pathogen-Free Organisms
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 to 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, rechallenged to 40 mg/m3 TMA aerosol. All rats received a sham exposure 1 week prior to the first TMA exposure. Following the sham exposure and weekly after each TMA exposure, TMA-specific IgE and both early-phase airway response (EAR) and late-phase airway response (LAR) 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. TMA of 4 mg/m3 induced a much lower, but stable, specific IgE response. EAR and LAR were observed only after a 40 mg/m3 TMA rechallenge 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 eosinophil infiltrates, bronchial-associated lymphoid tissue hyperplasia, and peribronchiolar plasma cell infiltrates.
PubMed ID
16982671 View in PubMed
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