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Thorax 1998;53:662-667 doi:10.1136/thx.53.8.662
  • Original article

Individual allergens as risk factors for bronchial responsiveness in young adults

  1. Susan Chinn,
  2. Deborah Jarvis,
  3. Christina Luczynska,
  4. Peter Burney
  1. Department of Public Health Medicine, UMDS Guy’s Campus, London SE1 3QD, UK
  1. Miss S Chinn.
  • Received 22 December 1997
  • Revision requested 2 March 1998
  • Revised 17 April 1998
  • Accepted 22 April 1998

Abstract

BACKGROUND Bronchial responsiveness is known to be related to atopy, but the relative contribution of sensitisation to individual allergens in the UK, or whether serum total IgE is an independent risk factor, is unknown.

METHODS A random sample of 1864 men and women aged 20–44 years, drawn from family health service registers in Cambridge, Ipswich and Norwich, was invited to answer a detailed questionnaire, undergo skin prick tests and methacholine bronchial challenge, and provide a serum sample for measurement of total and specific IgE. The relation of bronchial responsiveness to risk factors was studied in 749 subjects (40.2%) with complete data.

RESULTS Bronchial responsiveness was increased in those sensitised to cat,D pteronyssinus, Timothy grass andCladosporium, but decreased in subjects also positive to birch allergen. Additional skin prick tests added little information. Serum total IgE was not significantly related after adjustment for specific IgE to the five allergens. Increasing titres of specific IgE to D pteronyssinus were associated with increasing bronchial responsiveness. Specific IgE toCladosporium had a prevalence of around 3%, but was associated with greatly increased responsiveness. Decreased baseline lung function was related (p<0.001) to increased responsiveness. There was an interaction between age and smoking status, with lower responsiveness in older non-smokers.

CONCLUSION Atopy is the most important risk factor for bronchial responsiveness in this age group, but effects are not additive across all allergens. Research in reducing exposure to house dust mite should also address the role ofCladosporium sensitisation and exposure to indoor moulds.

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