L Grammer1, M Shaughnessy, B Kenamore. 1. Ernest S. Bazley Asthma and Allergic Diseases Center of the Department of Medicine of Northwestern Memorial Hospital and Northwestern University Medical School, Chicago, IL 60611, USA.
Abstract
OBJECTIVE: To define the utility of serum antibody against trimellitic anhydride (TMA) in predicting which individuals employed, at Amoco Corporation, in the manufacture of TMA have or will develop immunologically mediated respiratory disease, such as asthma, due to exposure to TMA. METHODS: In 1990 we initiated a clinical and immunologic cross-sectional study of 181 subjects exposed to TMA for at least 1 year who had not been diagnosed with an immunologic respiratory disease. We then clinically and immunologically followed 119 of these subjects for the next 5 years to determine whether they would develop an immunologic respiratory disease due to TMA exposure. RESULTS: Of the 16 individuals with IgE against TMA conjugated to human serum albumin (TM-HSA) in 1990, 3 had immediate asthma and another 6 developed asthma during the 5-year follow-up. Of the 165 individuals without IgE against TM-HSA, none had immediate asthma in 1990 and only 1 of 102 individuals followed for 5 years developed asthma. Of the 44 subjects with IgG against TM-HSA, 6 had an immunologic respiratory disease in 1990 and 2 more developed it in the ensuing 5 years. Of the 137 subjects without IgG against TM-HSA, none had an immunologic respiratory disease in 1990 and none of the 80 subjects followed for 5 years developed it. CONCLUSIONS: Development of antibody against TM-HSA, both IgE and IgG, is predictive of subjects who have or will develop immunologically mediated respiratory disease due to TMA exposure. The absence of antibody is a potent negative predictor.
OBJECTIVE: To define the utility of serum antibody against trimellitic anhydride (TMA) in predicting which individuals employed, at Amoco Corporation, in the manufacture of TMA have or will develop immunologically mediated respiratory disease, such as asthma, due to exposure to TMA. METHODS: In 1990 we initiated a clinical and immunologic cross-sectional study of 181 subjects exposed to TMA for at least 1 year who had not been diagnosed with an immunologic respiratory disease. We then clinically and immunologically followed 119 of these subjects for the next 5 years to determine whether they would develop an immunologic respiratory disease due to TMA exposure. RESULTS: Of the 16 individuals with IgE against TMA conjugated to human serum albumin (TM-HSA) in 1990, 3 had immediate asthma and another 6 developed asthma during the 5-year follow-up. Of the 165 individuals without IgE against TM-HSA, none had immediate asthma in 1990 and only 1 of 102 individuals followed for 5 years developed asthma. Of the 44 subjects with IgG against TM-HSA, 6 had an immunologic respiratory disease in 1990 and 2 more developed it in the ensuing 5 years. Of the 137 subjects without IgG against TM-HSA, none had an immunologic respiratory disease in 1990 and none of the 80 subjects followed for 5 years developed it. CONCLUSIONS: Development of antibody against TM-HSA, both IgE and IgG, is predictive of subjects who have or will develop immunologically mediated respiratory disease due to TMA exposure. The absence of antibody is a potent negative predictor.
Authors: Tor B Aasen; P Sherwood Burge; Paul K Henneberger; Vivi Schlünssen; Xaver Baur Journal: J Occup Med Toxicol Date: 2013-06-14 Impact factor: 2.646