Occupational asthma caused by triglycidyl isocyanurate.

BACKGROUND: Several cases of allergic contact dermatitis, two cases of occupational asthma from over one decade ago and one case of hypersensitivity pneumonitis have been documented in painters who use polyester powder paint containing triglycidyl isocyanurate (TGIC).

METHODS: We report a 28-year-old female who, 4 months after beginning work in a powder-coating factory, developed asthma-like symptoms. In her workplace, aluminium frames were treated with an electrostatic powder paint containing 2.5-10% TGIC.

RESULTS: Serial peak-flow measurements performed during both working and non-working periods demonstrated peak-flow variability of up to 46% on work days. Bronchial methacholine test results also varied between times at work and away from work. PC(20) methacholine was 0.32 mg/ml and fraction of exhaled nitric oxide (FENO) was 18 ppb. A controlled exposure challenge was performed with a placebo yielding no changes in FEV(1) over a 24-hour period. On visit 2, the patient was placed in the chamber and exposed to TGIC (4% in lactose) at a mean concentration of 3.61 mg/m(3) for a total of 15 min. A 20% fall in FEV(1) from baseline was elicited at 10 min, together with cough and wheezing. No late response was demonstrated. Twenty-four hours after the challenge, neither methacholine PC(20) nor FENO levels varied from baseline values. No IgE was detected by ELISA testing and no IgE-binding bands were found by immunoblot analysis of patient and control serum.

CONCLUSIONS: The aforementioned results demonstrate that TGIC inhalation induced immunologic occupational asthma, although no IgE mechanism was evidenced.