Acid anhydrides and asthma.
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.
D000812:Anhydrides / Q000009:adverse effects*; D001249:Asthma / Q000139:chemically induced* / Q000276:immunology / Q000503:physiopathology; D001985:Bronchial Provocation Tests; D001986:Bronchial Spasm / Q000139:chemically induced; D006241:Haptens / Q000009:adverse effects*; D006632:Histamine; D006801:Humans; D006969:Hypersensitivity, Immediate / Q000150:complications / Q000276:immunology; D007073:Immunoglobulin E / Q000032:analysis*; D009784:Occupational Diseases / Q000139:chemically induced* / Q000276:immunology / Q000503:physiopathology; D012907:Smoking; D013329:Structure-Activity Relationship
D000812:Anhydrides; D006241:Haptens; D007073:Immunoglobulin E; D006632:Histamine