Glutaraldehyde: an occupational hazard in the hospital setting

Background: We report a series of 24 health‐care workers with respiratory symptoms suggestive of occupational asthma due to glutaraldehyde exposure. Methods: The history of asthmatic symptoms was investigated with peak expiratory flow rate (PEFR) monitoring, and in eight of the subjects, the specifi...

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Veröffentlicht in:Allergy (Copenhagen) 1999-10, Vol.54 (10), p.1105-1109
Hauptverfasser: Di Stefano, F., Siriruttanapruk, S., McCoach, J., Sherwood Burge, P.
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container_end_page 1109
container_issue 10
container_start_page 1105
container_title Allergy (Copenhagen)
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creator Di Stefano, F.
Siriruttanapruk, S.
McCoach, J.
Sherwood Burge, P.
description Background: We report a series of 24 health‐care workers with respiratory symptoms suggestive of occupational asthma due to glutaraldehyde exposure. Methods: The history of asthmatic symptoms was investigated with peak expiratory flow rate (PEFR) monitoring, and in eight of the subjects, the specific bronchial provocation test (SBPT) was applied as reference standard for diagnosis of occupational asthma. Levels of glutaraldehyde were monitored in the challenge chamber during the SBPT. Work environmental levels of glutaraldehyde were measured from air samples collected at least once during the PEFR monitoring of endoscopy and theatre nurses. Specific IgE antibodies to glutaraldehyde were measured with a series of glutaraldehyde modified proteins. Results: In the eight workers who underwent SBPT, the diagnosis of occupational asthma was confirmed by a positive reaction (late and dual reaction in five and in three subjects, respectively). The mean level of glutaraldehyde observed during the challenge tests was 0.075 mg/m3 (range 0.065–0.084 mg/m3). In 13 out of the 16 remaining workers, the serial PEFR monitoring showed a work‐related effect. In three workers, there was no physiological confirmation of occupational asthma. Levels of glutaraldehyde from the air samples collected in the workplace were as follows: personal short‐term samples (mean 0.208 mg/m3; median 0.14 mg/m3; range 0.06–0.84 mg/m3), personal long‐term samples (mean 0.071 mg/m3; median 0.07 mg/m3; range 0.003–0.28 mg/m3). Measurements of specific IgE antibodies to glutaraldehyde‐modified proteins were positive in seven patients (29.1%) according to a cutoff value of 0.88% RAST binding. The presence of atopy to common environmental allergens and smoking was not associated with specific IgE positivity (P>0.05; Fisher's exact test). Conclusions: Our report indicates the importance of glutaraldehyde as an occupational hazard among exposed health‐care workers. Intervention in the workplace, training of personnel handling this chemical, and accurate health surveillance may reduce the risk of developing occupational asthma due to glutaraldehyde.
doi_str_mv 10.1034/j.1398-9995.1999.00239.x
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Methods: The history of asthmatic symptoms was investigated with peak expiratory flow rate (PEFR) monitoring, and in eight of the subjects, the specific bronchial provocation test (SBPT) was applied as reference standard for diagnosis of occupational asthma. Levels of glutaraldehyde were monitored in the challenge chamber during the SBPT. Work environmental levels of glutaraldehyde were measured from air samples collected at least once during the PEFR monitoring of endoscopy and theatre nurses. Specific IgE antibodies to glutaraldehyde were measured with a series of glutaraldehyde modified proteins. Results: In the eight workers who underwent SBPT, the diagnosis of occupational asthma was confirmed by a positive reaction (late and dual reaction in five and in three subjects, respectively). The mean level of glutaraldehyde observed during the challenge tests was 0.075 mg/m3 (range 0.065–0.084 mg/m3). In 13 out of the 16 remaining workers, the serial PEFR monitoring showed a work‐related effect. In three workers, there was no physiological confirmation of occupational asthma. Levels of glutaraldehyde from the air samples collected in the workplace were as follows: personal short‐term samples (mean 0.208 mg/m3; median 0.14 mg/m3; range 0.06–0.84 mg/m3), personal long‐term samples (mean 0.071 mg/m3; median 0.07 mg/m3; range 0.003–0.28 mg/m3). Measurements of specific IgE antibodies to glutaraldehyde‐modified proteins were positive in seven patients (29.1%) according to a cutoff value of 0.88% RAST binding. The presence of atopy to common environmental allergens and smoking was not associated with specific IgE positivity (P&gt;0.05; Fisher's exact test). Conclusions: Our report indicates the importance of glutaraldehyde as an occupational hazard among exposed health‐care workers. 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Methods: The history of asthmatic symptoms was investigated with peak expiratory flow rate (PEFR) monitoring, and in eight of the subjects, the specific bronchial provocation test (SBPT) was applied as reference standard for diagnosis of occupational asthma. Levels of glutaraldehyde were monitored in the challenge chamber during the SBPT. Work environmental levels of glutaraldehyde were measured from air samples collected at least once during the PEFR monitoring of endoscopy and theatre nurses. Specific IgE antibodies to glutaraldehyde were measured with a series of glutaraldehyde modified proteins. Results: In the eight workers who underwent SBPT, the diagnosis of occupational asthma was confirmed by a positive reaction (late and dual reaction in five and in three subjects, respectively). The mean level of glutaraldehyde observed during the challenge tests was 0.075 mg/m3 (range 0.065–0.084 mg/m3). In 13 out of the 16 remaining workers, the serial PEFR monitoring showed a work‐related effect. In three workers, there was no physiological confirmation of occupational asthma. Levels of glutaraldehyde from the air samples collected in the workplace were as follows: personal short‐term samples (mean 0.208 mg/m3; median 0.14 mg/m3; range 0.06–0.84 mg/m3), personal long‐term samples (mean 0.071 mg/m3; median 0.07 mg/m3; range 0.003–0.28 mg/m3). Measurements of specific IgE antibodies to glutaraldehyde‐modified proteins were positive in seven patients (29.1%) according to a cutoff value of 0.88% RAST binding. The presence of atopy to common environmental allergens and smoking was not associated with specific IgE positivity (P&gt;0.05; Fisher's exact test). Conclusions: Our report indicates the importance of glutaraldehyde as an occupational hazard among exposed health‐care workers. 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Methods: The history of asthmatic symptoms was investigated with peak expiratory flow rate (PEFR) monitoring, and in eight of the subjects, the specific bronchial provocation test (SBPT) was applied as reference standard for diagnosis of occupational asthma. Levels of glutaraldehyde were monitored in the challenge chamber during the SBPT. Work environmental levels of glutaraldehyde were measured from air samples collected at least once during the PEFR monitoring of endoscopy and theatre nurses. Specific IgE antibodies to glutaraldehyde were measured with a series of glutaraldehyde modified proteins. Results: In the eight workers who underwent SBPT, the diagnosis of occupational asthma was confirmed by a positive reaction (late and dual reaction in five and in three subjects, respectively). The mean level of glutaraldehyde observed during the challenge tests was 0.075 mg/m3 (range 0.065–0.084 mg/m3). In 13 out of the 16 remaining workers, the serial PEFR monitoring showed a work‐related effect. In three workers, there was no physiological confirmation of occupational asthma. Levels of glutaraldehyde from the air samples collected in the workplace were as follows: personal short‐term samples (mean 0.208 mg/m3; median 0.14 mg/m3; range 0.06–0.84 mg/m3), personal long‐term samples (mean 0.071 mg/m3; median 0.07 mg/m3; range 0.003–0.28 mg/m3). Measurements of specific IgE antibodies to glutaraldehyde‐modified proteins were positive in seven patients (29.1%) according to a cutoff value of 0.88% RAST binding. The presence of atopy to common environmental allergens and smoking was not associated with specific IgE positivity (P&gt;0.05; Fisher's exact test). Conclusions: Our report indicates the importance of glutaraldehyde as an occupational hazard among exposed health‐care workers. Intervention in the workplace, training of personnel handling this chemical, and accurate health surveillance may reduce the risk of developing occupational asthma due to glutaraldehyde.</abstract><cop>Copenhagen</cop><pub>Munksgaard International Publishers</pub><pmid>10536890</pmid><doi>10.1034/j.1398-9995.1999.00239.x</doi><tpages>5</tpages></addata></record>
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subjects Adult
Air Pollutants, Occupational - adverse effects
Antibodies, Anti-Idiotypic - immunology
Antibody Specificity
Biological and medical sciences
Bronchial Provocation Tests
Chronic obstructive pulmonary disease, asthma
False Positive Reactions
Female
Glutaral - adverse effects
Glutaral - immunology
glutaraldehyde
Humans
Male
Medical sciences
Middle Aged
occupational asthma
Occupational Diseases - chemically induced
Occupational Exposure - adverse effects
Peak Expiratory Flow Rate
Personnel, Hospital
Pneumology
Radioallergosorbent Test
surveillance
title Glutaraldehyde: an occupational hazard in the hospital setting
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