Abstract

n June 1997, a 47-year-old mechanic began to repair old painted forest harvesters by metal-inert-gas (MIG) welding. Next autumn, he experienced immediate erythema and edema of the face and later also dyspnea when welding. Peak expiratory flow (PEF) follow-up (twice a day) showed 22% PEF variation during one work day. Slight bronchial hyperreactivity was found. The symptoms diminished during other work but returned when the subject was exposed in welding again.

Our examinations showed normal clinical status. Bronchial hyperreactivity had disappeared. Skin prick tests with common environmental allergens were negative. PEF surveillance pointed strongly to occupational asthma. He had been briefly exposed to the paint fumes for about 10 s, leading to immediate dyspnea, erythema, and edema of the face, and a fall in PEF of 30% (610–430 l/min) and 41% (590–350 l/min). The diurnal PEF variation was <10% during other work days and on days off.

In the material safety data sheets of the two-component paint, only two solvents were given. According to the manufacturer, the hardener contained 65% chlorinated polyester and the paint contained 0.9% alkyd resin. Both phthalic anhydride (PA) and chlorendic anhydride (CA) were identified in the fumes generated from the heated paint.

CA-HSA-conjugate (1%) induced a positive reaction in the skin prick test and also in the open test. Skin prick tests with several common sensitizing acid anhydride-HSA conjugates were positive. Specific IgE antibodies against CA-HSA-conjugate were found (Phadebas RAST®) against all the other sensitizing anhydrides except trimellitic anhydride.

On the basis of these investigations, we diagnosed contact urticaria due to CA and occupational asthma due to the welding fumes of a polyester paint containing PA and CA.

Organic acid anhydrides are used as hardeners of epoxy resins and in the manufacture of alkyd and polyester resins. Several anhydrides have been shown to cause IgE-mediated allergies.

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