D Ghosh1, C Clay1, J A Bernstein1. 1. Division of Immunology/Allergy Section, Department of Internal Medicine, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
Abstract
BACKGROUND: Workplace exposure to trimellitic anhydride (TMA) can elicit TMA-specific IgE (sIgE), which may lead to occupational asthma (OA). An occupational immunosurveillance program (OISP) has been implemented to monitor TMA exposure and immunologic outcomes. The purpose of this study was to determine whether TMA-specific IgG (sIgG) responses can discriminate between TMA-exposed workers with and without sIgE responses. METHODS: Serum TMA-specific antibody (IgG, IgG4, and IgE) levels were estimated longitudinally (years 2006 to 2014) in TMA-exposed workers recruited in low, medium, and high exposure areas. sIgG and sIgE titers plotted against exposure duration were compared between workers with (a) sIgG only and (b) with sIgG who developed sIgE. RESULTS: Among 92 TMA-exposed workers continuously monitored for sIgG and sIgE, 38 developed sIgG; 11 developed a sIgE response 342.38 ± 186.03 days posthire and were removed from exposure. The average detection time of sIgG in removed workers (159 ± 92 days) was significantly shorter than for actively exposed workers with only sIgG (346 ± 187 days). Workers with earlier sIgG responses of higher titer (mean value 42.25 μg/mL) compared to delayed responders with lower sIgG titers (mean value 14.79 μg/mL) more frequently developed sIgE responses. Hierarchical clustering showed the initial magnitude and exposure time required for detectable sIgG production discriminated between workers with only sIgG from workers who subsequently produced sIgE. CONCLUSIONS: This study demonstrates the utility of longitudinally monitoring TMA-specific antibodies in an OISP as exposed workers with early sIgG responses and of higher magnitude are more likely to develop TMA sIgE sensitization.
BACKGROUND: Workplace exposure to trimellitic anhydride (TMA) can elicit TMA-specific IgE (sIgE), which may lead to occupational asthma (OA). An occupational immunosurveillance program (OISP) has been implemented to monitor TMA exposure and immunologic outcomes. The purpose of this study was to determine whether TMA-specific IgG (sIgG) responses can discriminate between TMA-exposed workers with and without sIgE responses. METHODS: Serum TMA-specific antibody (IgG, IgG4, and IgE) levels were estimated longitudinally (years 2006 to 2014) in TMA-exposed workers recruited in low, medium, and high exposure areas. sIgG and sIgE titers plotted against exposure duration were compared between workers with (a) sIgG only and (b) with sIgG who developed sIgE. RESULTS: Among 92 TMA-exposed workers continuously monitored for sIgG and sIgE, 38 developed sIgG; 11 developed a sIgE response 342.38 ± 186.03 days posthire and were removed from exposure. The average detection time of sIgG in removed workers (159 ± 92 days) was significantly shorter than for actively exposed workers with only sIgG (346 ± 187 days). Workers with earlier sIgG responses of higher titer (mean value 42.25 μg/mL) compared to delayed responders with lower sIgG titers (mean value 14.79 μg/mL) more frequently developed sIgE responses. Hierarchical clustering showed the initial magnitude and exposure time required for detectable sIgG production discriminated between workers with only sIgG from workers who subsequently produced sIgE. CONCLUSIONS: This study demonstrates the utility of longitudinally monitoring TMA-specific antibodies in an OISP as exposed workers with early sIgG responses and of higher magnitude are more likely to develop TMA sIgE sensitization.
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