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Occupational asthma caused by nickel sulfate
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FAMILIAL C3b/C4b INACTIVATOR DEFECT IN TWO SIBLINGS WITH RECURRENT BACTERIAL INFECTIONS. J. Oleske,M.D., E. GioIi,M.D. , J. Ruiz,M.D., E. Zhu,M.D., A. Minnefor,M.D., T. dela Cruz,M.D., R. Cooper,M.D., Newark, New Jersey and New York New York. A 19 y/o male presented with his second episode of meningococcemia with meningitis. History showed that besides these life threatening infections, he had multiple bouts of otitis media as a child and multiple URI's. At 7 mos. of age he was found to have low gammaglobulin levels and was treated with IM gammaglobulin for 2 years. A 26 y/o sister also was noted to have had recurrent infections. As a child she had multiple severe bouts of otitis media as well as an episode at II y/o of S. pneumonia meningitis. A work up of the family after the last bout of N. meningitis infection in the 19 y/o demonstrated that the father and the 3 y/o son of the 26 y/o sister had low IgG levels and reduced levels of C3b/C4b [nactivator, although the remainder of their compliment profile was normal. Two sisters and the mother had normal immunoglobulin and compliment studies. A 25 y/o brother without history of recurrent infection was not available for testing. Both the 19 y/o patient and his 26 y/o sister had normal immunoglobulin levels but had absent CH50, C3, factor B and C3b/C4b inactivator. This data confirms a defect in C3b/C4b inactivator levels and that factor B and C3 deficiency is due to excessive utilization. Their compliment defect explains their recurrent infection. Both individuals are now under closer medical supervision to prevent future life threatening bacterial infections.
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HYPERSENSITIVITY PNEUMONITIS FROM CONTAMINATED CHILLED WATER HUMIDIFIERS: RELATIONSHIPS OF ANTIGENS FROM DIFFERENT CITIES. J . E . Reed, M. C. Swanson, B.A., and C. E. Reed, M.D., Rochester, MN. Outbreaks of hypersensitivity pneumonitis (HP) occurred in workers in buildings supplied by chilled water humidifiers in three cities: Seaford, DE, Pensacola, FL and Omaha, NE. Crude antigen extracts were prepared from scum growing in the water and coupled to microcrystslline cellulose with cyanogen bromide. IgG antibody was detected with radioiodinated Staphylococcus protein A, and soluble antigen assayed by competitive inhibition. Serum of patients from all three sites reacted with antigen frc~ all three sites, both by immunodiffusion and radioimmunoassay, but had higher titer for autologous antigen. Similarly soluble autologous antigen was more effective than heterologous in inhibiting antibody binding to solid-phase antigen. Serum from normal persons who have never worked in such a building also have antibody detectable By radioimmunoassay and inhibitable by soluble antigens. Soil and outdoor air in Pensacola and Rochester contain antigens that inhibit binding of HP sera to humidifier antigens. These results suggest that the antigens causing humidifier HP are not limited to any one geographical location but may arise from widely distributed soil microorganisms.
OCCUPATIONAL HYPERSENSITIVITY PNEUMONITIS FOLLOWING EXPOSURE TO DIPHENYLMETHANE DIISOCYANATE (MDI). J~L. Malo~ M.D.~ and C.R. Zeiss~ M.D.~ Montreal, Canada, and Chicago, Illinois. A worker who was appointed to the preparation of moulds in a foundry developed dyspnea, cough, fever, and a loss of weight one month after starting to be exposed to MDI at work. When he was first examined in the evening following a day spent at work, his body temperature was 3 7.6 o C, diffused inspiratory crackles were heard, and the leucocyte count was 18 7000/mm 3. One week after he had stopped to work a restrictive breathing defect was documented, together with a reduction in transfer factor and blood oxygen tension, and an increase in lung rigidity. His symptoms and lung function impairment subsided progressively at the assessments done 4 and 8 weeks after he had left work. Specific inhalation challenges with I~DI for 30 and 60 minutes on two consecutive days induced several hours later malaise with an increase in body temperature and leucocyte count, as well as a fall in forced vital capacity and transfer factor. Total antibody activity to a MDl-human serum albumin(HSA)conjugate was detected by ammonium sulfate precipitation which showed 24 ug of MD!-HSA bound per ml(mean of asymptomatic exposed w o r k e r ~ 0 . 6 ug/ml). Specific IgG antibodies to MDI-HSA were demonstrated by the ELISA technique at 0.90 and 0.37 optical density(Oh)with the i: i00 and i: i000 serum dilutions respectively(controls=0.13 and 0 . i 0 0 D respectively ). MDI exposure can thus cause hypersensitivity pneumonitis and induce the production of specific antibodies.
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OCCUPATIONAL ASTHMA CAUSED BY NICKEL SULFATE. A. Cartier, M.D., J.L, Malo~ M.D., M. Doepner, M.D.. E, Nieboer, Ph.D,~ S. Evans, a n d J. DoloVich, MiD. I Montreal and Hamilton, Canada. A 28 y e a r o l d man developed asthma shortly after being exposed to nickel sulfate(NiS04) in a metal-plating factory. Recording of peak expiratory flow rates at work and for a period offwork showed increased variations at work with best values on weekends. Prick skin tests with NiSOh at a l0 mg/ml concentration elicited an immediate reaction. Similar skin tests in 8 nonexposed control subjects were negative. Experimental inhalation challenges with NiS0 h at the same concentration for 1 min produced a bronchial obstruction which was typical of an early asthmatic response with a maximum fall of 34% in FEVI.at i0 min followed by progressive recovery In the first hour after the challenge. A control asthmatic subject with a similar level of bronchial reactivity to histamine did not react to the same inhalation of NiSO 4. This suggests a specific rather than an irritant reaction. The patient bad evidence of IgE antibody to a NiSOh-human serum albumin(HSA)conjugate. NiSO4-HSA RAST values were higher(457 CPM) than every high and low total IgE control sera (means of 3 0 9 ~ 4 SD CPM and 242_+7 SD CPM respectively). HSA RAST values were similar to those of high and low total IgE controls, thus showing that the NiSO 4 component was antigenic. His serum bound 63Ni and this reaction was selectively blocked by non-labeled Ni. These results suggest the development of occupational asthma due to NiSO 4 with the presence of a specific immunologic response.
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FAMILIAL C3b/C4b INACTIVATOR DEFECT IN TWO SIBLINGS WITH RECURRENT BACTERIAL INFECTIONS. J. Oleske,M.D., E. GioIi,M.D. , J. Ruiz,M.D., E. Zhu,M.D., A. Minnefor,M.D., T. dela Cruz,M.D., R. Cooper,M.D., Newark, New Jersey and New York New York. A 19 y/o male presented with his second episode of meningococcemia with meningitis. History showed that besides these life threatening infections, he had multiple bouts of otitis media as a child and multiple URI's. At 7 mos. of age he was found to have low gammaglobulin levels and was treated with IM gammaglobulin for 2 years. A 26 y/o sister also was noted to have had recurrent infections. As a child she had multiple severe bouts of otitis media as well as an episode at II y/o of S. pneumonia meningitis. A work up of the family after the last bout of N. meningitis infection in the 19 y/o demonstrated that the father and the 3 y/o son of the 26 y/o sister had low IgG levels and reduced levels of C3b/C4b [nactivator, although the remainder of their compliment profile was normal. Two sisters and the mother had normal immunoglobulin and compliment studies. A 25 y/o brother without history of recurrent infection was not available for testing. Both the 19 y/o patient and his 26 y/o sister had normal immunoglobulin levels but had absent CH50, C3, factor B and C3b/C4b inactivator. This data confirms a defect in C3b/C4b inactivator levels and that factor B and C3 deficiency is due to excessive utilization. Their compliment defect explains their recurrent infection. Both individuals are now under closer medical supervision to prevent future life threatening bacterial infections.
163
HYPERSENSITIVITY PNEUMONITIS FROM CONTAMINATED CHILLED WATER HUMIDIFIERS: RELATIONSHIPS OF ANTIGENS FROM DIFFERENT CITIES. J . E . Reed, M. C. Swanson, B.A., and C. E. Reed, M.D., Rochester, MN. Outbreaks of hypersensitivity pneumonitis (HP) occurred in workers in buildings supplied by chilled water humidifiers in three cities: Seaford, DE, Pensacola, FL and Omaha, NE. Crude antigen extracts were prepared from scum growing in the water and coupled to microcrystslline cellulose with cyanogen bromide. IgG antibody was detected with radioiodinated Staphylococcus protein A, and soluble antigen assayed by competitive inhibition. Serum of patients from all three sites reacted with antigen frc~ all three sites, both by immunodiffusion and radioimmunoassay, but had higher titer for autologous antigen. Similarly soluble autologous antigen was more effective than heterologous in inhibiting antibody binding to solid-phase antigen. Serum from normal persons who have never worked in such a building also have antibody detectable By radioimmunoassay and inhibitable by soluble antigens. Soil and outdoor air in Pensacola and Rochester contain antigens that inhibit binding of HP sera to humidifier antigens. These results suggest that the antigens causing humidifier HP are not limited to any one geographical location but may arise from widely distributed soil microorganisms.
OCCUPATIONAL HYPERSENSITIVITY PNEUMONITIS FOLLOWING EXPOSURE TO DIPHENYLMETHANE DIISOCYANATE (MDI). J~L. Malo~ M.D.~ and C.R. Zeiss~ M.D.~ Montreal, Canada, and Chicago, Illinois. A worker who was appointed to the preparation of moulds in a foundry developed dyspnea, cough, fever, and a loss of weight one month after starting to be exposed to MDI at work. When he was first examined in the evening following a day spent at work, his body temperature was 3 7.6 o C, diffused inspiratory crackles were heard, and the leucocyte count was 18 7000/mm 3. One week after he had stopped to work a restrictive breathing defect was documented, together with a reduction in transfer factor and blood oxygen tension, and an increase in lung rigidity. His symptoms and lung function impairment subsided progressively at the assessments done 4 and 8 weeks after he had left work. Specific inhalation challenges with I~DI for 30 and 60 minutes on two consecutive days induced several hours later malaise with an increase in body temperature and leucocyte count, as well as a fall in forced vital capacity and transfer factor. Total antibody activity to a MDl-human serum albumin(HSA)conjugate was detected by ammonium sulfate precipitation which showed 24 ug of MD!-HSA bound per ml(mean of asymptomatic exposed w o r k e r ~ 0 . 6 ug/ml). Specific IgG antibodies to MDI-HSA were demonstrated by the ELISA technique at 0.90 and 0.37 optical density(Oh)with the i: i00 and i: i000 serum dilutions respectively(controls=0.13 and 0 . i 0 0 D respectively ). MDI exposure can thus cause hypersensitivity pneumonitis and induce the production of specific antibodies.
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OCCUPATIONAL ASTHMA CAUSED BY NICKEL SULFATE. A. Cartier, M.D., J.L, Malo~ M.D., M. Doepner, M.D.. E, Nieboer, Ph.D,~ S. Evans, a n d J. DoloVich, MiD. I Montreal and Hamilton, Canada. A 28 y e a r o l d man developed asthma shortly after being exposed to nickel sulfate(NiS04) in a metal-plating factory. Recording of peak expiratory flow rates at work and for a period offwork showed increased variations at work with best values on weekends. Prick skin tests with NiSOh at a l0 mg/ml concentration elicited an immediate reaction. Similar skin tests in 8 nonexposed control subjects were negative. Experimental inhalation challenges with NiS0 h at the same concentration for 1 min produced a bronchial obstruction which was typical of an early asthmatic response with a maximum fall of 34% in FEVI.at i0 min followed by progressive recovery In the first hour after the challenge. A control asthmatic subject with a similar level of bronchial reactivity to histamine did not react to the same inhalation of NiSO 4. This suggests a specific rather than an irritant reaction. The patient bad evidence of IgE antibody to a NiSOh-human serum albumin(HSA)conjugate. NiSO4-HSA RAST values were higher(457 CPM) than every high and low total IgE control sera (means of 3 0 9 ~ 4 SD CPM and 242_+7 SD CPM respectively). HSA RAST values were similar to those of high and low total IgE controls, thus showing that the NiSO 4 component was antigenic. His serum bound 63Ni and this reaction was selectively blocked by non-labeled Ni. These results suggest the development of occupational asthma due to NiSO 4 with the presence of a specific immunologic response.
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