A model of immunologic lung injury induced by trimellitic anhydride inhalation: Antibody response

C. Raymond Zeiss, Doris Levitz, Chester L. Leach, Nabil S. Hatoum, Helen V. Ratajczak, Michael J. Chandler, Jean Claude Roger, Paul J. Garvin

Research output: Contribution to journalArticlepeer-review

21 Scopus citations

Abstract

We studied lung injury induced in Sprague-Dawley rats by trimellitic anhydride (TMA) inhalation. Groups of 40 male and 20 female rats were exposed to TMA by inhalation at target concentrations of 0, 10, 30, 100, and 300 μg/m3, 6 hours per day, 5 days per week, for 2 weeks. Rats in each exposure group were sacrificed after 10 exposures or rested for 12 days and either sacrificed or received a 6-hour TMA challenge at their initial exposure levels and sacrificed at 24 hours. At each sacrifice, serum antibody to radiolabeled trimellityl rat serum albumin (RSA-TM) was measured by an ammonium sulfate technique, and lung pathology was determined. After 10 days of exposure, external hemorrhagic lung foci were directly related to the exposure concentration of TMA. Serum antibody binding of RSA-TM correlated with exposure concentration, hemorrhagic lung foci, and lung weight. There was healing of lung lesions 12 days after exposure with a return of lung lesions only 18 hours after the 6-hour inhalation challenge. A correlation between serum antibody to RSA-TM, hemorrhagic foci, and lung weight existed after challenge. This model clarifies two clinical entities observed in exposed workers, the late respiratory systemic and the pulmonary disease-anemia syndromes.

Original languageEnglish
Pages (from-to)59-63
Number of pages5
JournalJournal of Allergy and Clinical Immunology
Volume79
Issue number1
DOIs
StatePublished - Jan 1987
Externally publishedYes

Fingerprint

Dive into the research topics of 'A model of immunologic lung injury induced by trimellitic anhydride inhalation: Antibody response'. Together they form a unique fingerprint.

Cite this