Pulmonary disease in workers exposed to papain: clinico-physiological and immunological studies
Article first published online: 27 APR 2006
Clinical & Experimental Allergy
Volume 10, Issue 6, pages 721–731, November 1980
How to Cite
NOVEY, H. S., KEENAN, W. J., FAIRSHTER, R. D., WELLS, I. D., WILSON, A. F. and CULVER, B. D. (1980), Pulmonary disease in workers exposed to papain: clinico-physiological and immunological studies. Clinical & Experimental Allergy, 10: 721–731. doi: 10.1111/j.1365-2222.1980.tb02157.x
- Issue published online: 27 APR 2006
- Article first published online: 27 APR 2006
- Received 14 February 1980; accepted for publication 28 March 1980
Of the twenty-three employees at a pharmaceutical plant manufacturing a new product containing papain, twelve had respiratory symptoms of cough, wheezing, dyspnoea, or chest paint. Most were studied with in-depth interviews by a doctor, extensive pulmonary function tests, and imnunoserological tests for IgE and precipitating antibodies specific for papain, as well as total IgE levels and IgE antibodies to common natural allergens.
There were significant correlates (all P values <0.05) between the presence of specific IgE antibodies to papain and decreases of FEV1, FEF75–85, RV, and response to bronchodilators as percentage change from baseline for all spirographic flow rates. Atopic workers developed pulmonary symptoms and antipapain antibodies significantly sooner after papain exposure than did the others.
Duration of exposure had no effect on symptomatology, pulmonary function, or immunological response. However, those judged to have the greatest amount of dust exposure per work-day had significantly more pulmonary symptoms (P < 0.005).
Papain produced lung diseases by acting as an inhalant allergen rather than a proteolytic enzyme, Papain is a potent sensitizer in humans for the production of respiratory disease. The pulmonary reactions, based on physiological data, seem to involve small airways, alveolar, and interstitial lung tissue in an inflammatory rather than destructive manner, and thus resemble bronchitis and interstitial lung disease rather than pulmonary emphysema or typical bronchial asthma.