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Acid anhydrides and asthma.

Abstract
We have studied asthma caused by inhaled acid anhydrides as a model of hapten-induced airway hyperresponsiveness. Inhalation tests with the relevant anhydride in sensitised individuals reproducibly provoked a significant increase in non-specific airway responsiveness identifiable 3 h after the test and prior to the development of the late asthmatic reaction. Seven cases of asthma caused by tetrachlorophthalic anhydride (TCPA) had specific IgE in their serum to a TCPA-human serum albumin conjugate. RAST inhibition studies showed the anhydride to be involved in the antibody-combining site. Survey of the factory population where these 7 cases worked allowed investigation of the determinants of the specific IgE response: its presence was associated with intensity of exposure and current cigarette smoking; in addition smoking interacted with atopy to increase the prevalence of specific IgE. During a 5-year period of avoidance of exposure to TCPA specific IgE declined exponentially with a half-life of one year, suggesting continuing IgE secretion. Five years after avoidance of exposure, airway hyperresponsiveness remained increased in several cases.
AuthorsA J Taylor, K M Venables, S R Durham, B J Graneek, M D Topping
JournalInternational archives of allergy and applied immunology (Int Arch Allergy Appl Immunol) Vol. 82 Issue 3-4 Pg. 435-9 ( 1987) ISSN: 0020-5915 [Print] Switzerland
PMID3570506 (Publication Type: Comparative Study, Journal Article)
Chemical References
  • Anhydrides
  • Haptens
  • Immunoglobulin E
  • Histamine
Topics
  • Anhydrides (adverse effects)
  • Asthma (chemically induced, immunology, physiopathology)
  • Bronchial Provocation Tests
  • Bronchial Spasm (chemically induced)
  • Haptens (adverse effects)
  • Histamine
  • Humans
  • Hypersensitivity, Immediate (complications, immunology)
  • Immunoglobulin E (analysis)
  • Occupational Diseases (chemically induced, immunology, physiopathology)
  • Smoking
  • Structure-Activity Relationship

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