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Acid anhydrides and asthma.

A J Taylor, K M Venables, S R Durham

    International Archives of Allergy and Applied Immunology
    |January 1, 1987
    PubMed
    Summary
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    Inhaled acid anhydrides cause asthma by inducing airway hyperresponsiveness. Exposure intensity, smoking, and atopy influence specific IgE responses, which decline slowly after exposure cessation.

    Area of Science:

    • Immunology
    • Occupational Health
    • Respiratory Medicine

    Background:

    • Inhaled acid anhydrides are known occupational sensitizers.
    • Hapten-induced asthma models are crucial for understanding airway hyperresponsiveness.

    Purpose of the Study:

    • To investigate asthma induced by inhaled acid anhydrides as a model of hapten-induced airway hyperresponsiveness.
    • To identify determinants of specific IgE response and its persistence.

    Main Methods:

    • Inhalation tests with acid anhydrides in sensitized individuals.
    • Radioallergosorbent test (RAST) inhibition studies.
    • Population surveys to assess exposure, smoking, and atopy.
    • Longitudinal follow-up of specific IgE levels and airway responsiveness over 5 years.

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    Main Results:

    • Inhalation tests reproducibly increased airway responsiveness 3 hours post-exposure, preceding late asthmatic reactions.
    • Seven cases of tetrachlorophthalic anhydride (TCPA) asthma showed specific IgE to TCPA-human serum albumin conjugate.
    • Specific IgE prevalence was linked to exposure intensity and smoking; smoking interacted with atopy.
    • Specific IgE declined exponentially with a 1-year half-life after TCPA avoidance, suggesting ongoing IgE secretion.
    • Airway hyperresponsiveness remained elevated in several individuals 5 years after exposure cessation.

    Conclusions:

    • Inhaled acid anhydrides induce hapten-specific IgE and airway hyperresponsiveness.
    • Exposure intensity, smoking, and atopy are key determinants of sensitization.
    • Persistence of airway hyperresponsiveness after exposure cessation highlights the long-term impact of anhydride exposure.