Hypersensitivity reactions and specific antibodies in workers exposed to industrial enzymes at a biotechnology plant.

Thirty-six employees who produced industrial enzymes from selected strains of bacteria and fungi were evaluated by epicutaneous threshold testing and enzyme-linked immunosorbent assays (ELISA) for specific IgE and IgG antibodies. The workers complained of 'asthma- and flu-like' symptoms, which generally lessened away from work. The enzymes evaluated were: alpha-amylase (1,4-alpha-d-glucan glucanohydrolase) from Bacillus licheniformis (alpha ABl), B. subtilis formation 1 (alpha A1Bs) and B. subtilis formation 2 (alpha A2Bs); purified alpha-amylase from B. licheniformis (C alpha ABl) and A. oryzae (C alpha AAo); alkaline protease from B. licheniformis (APBl) and purified alkaline protease (CAPBl); amyloglucosidase (1,4-alpha-d-glucan glucohydrolase) from A. niger (AGAn) and purified amyloglucosidase (CAGAn). Statistically significant increases (P > 0.05) in the proportion of workers having positive skin tests to CAPBl, AGAn and CAGAn were found. Significantly elevated (P > 0.05) mean specific IgE results were observed for C alpha AAo CAGAn and AGAn, and elevated (P > 0.05) mean specific IgGs were observed for C alpha AAo, CAGAn, AGAn, alpha A1Bs, alpha AB1 and alpha A2Bs. These results indicate that occupational exposure to some industrial enzymes can cause immediate-onset cutaneous hypersensitivity reactions, pulmonary function deficits and significantly elevated specific antibody levels. Our results are equivocal as to whether work-related respiratory and cutaneous hypersensitivity reactions are antibody mediated, as there was no statistically significant association between these reactions and specific IgE or IgG levels.

Detection of IgE-mediated respiratory sensitization in workers exposed to hexahydrophthalic anhydride.

Twenty-seven workers with occupational exposure to hexahydrophthalic anhydride (HHPA) from an epoxy resin molding system were studied to evaluate the nature of their reported respiratory complaints. The workers were evaluated by questionnaire, pulmonary function tests, and serologic investigations. The presence of serum-specific IgE and IgG to an HHPA-human serum albumin (HSA) conjugate was measured by use of RAST and ELISA assays. Estimates of exposure to HHPA were made for each worker on the basis of job description and environmental sampling. Seven workers reported symptoms of asthma and rhinitis; four workers had symptoms consistent with occupational asthma. Fourteen of the remaining 20 workers reported nasal or ocular symptoms while they were at work. No worker demonstrated a significant (greater than 20%) pre-to postshift decrement in FEV1. Twelve workers had significant levels of specific IgE to HHPA-HSA; 11 had elevated levels of specific IgG to HHPA-HSA. A group of workers estimated to have higher exposures to HHPA had a significantly higher mean total IgE level (p less than 0.05) and significant titers of HHPA-HSA-specific IgE or IgG, or both (p = 0.048) as compared to a group with lower exposure to the anhydride. All four workers with occupational asthma/rhinitis had significant levels of specific IgE to HHPA-HSA (ranging from 8.7% to 23.4% RAST binding); three workers did not work directly in the HHPA area but were located in nearby sections of the plant with lower exposures to HHPA. Three workers with symptoms of asthma not clearly associated with the workplace did not have significantly elevated specific IgE levels. Another radioimmunoassay with the use of beads coated with mouse monoclonal antihuman IgE was used to quantitate the amount of specific anti-HHPA-HSA binding (range 1.0 ng to 32.6 ng/ml) present in workers' sera. The solid-phase bead radioimmunoassay was inhibited by the homologous HHPA-HSA conjugate but not by HHPA hapten alone in two workers, suggesting that these workers were sensitized to new antigenic determinants. We conclude that HHPA is a potent industrial sensitizer and is capable of inducing IgE-mediated disease. Prospective investigations are required to define the incidence and severity of clinical sensitivity.