AMMONIUM persulfate (APS) is known as a cause of occupational type IV hypersensitivity in hairdressers (1, 2) and as a rare cause of occupational asthma (3, 4). Here we present a hairdresser with both type IV and type I hypersensitivity to APS acquired during work.
A 20-year-old hairdresser was admitted to our department because she had developed rhinitis and asthma during her work at the reception desk of a hairdressers shop. After 1 year of her apprenticeship, she had developed hand eczema, caused by delayed-type hypersensitivity to p-phenylendiamine, p-toluylendiamine, and APS. All three substances are relevant to the work of a hairdresser. As the patient did not want to quit her job, her employer had allowed her to work at the reception desk without direct contact with hair-care products. Two years later, the patient noticed a running nose, coughing, and shortness of breath while leading customers from the reception desk to a seat in the hairdressers shop. Thus, she habitually walked through the shop while other customers were having their hair tinted or bleached. The patient and her family had no history of atopic rhinitis or asthma.
Skin prick testing of a screening series and of indoor allergens revealed no sensitizations. Total IgE was 114 kU/l, a screening for inhalative allergens showed IgE of <0.35 kU/l (CAP class 0), and a screening test for chemical allergens also showed IgE of <0.35 kU/l (CAP class 0). Skin prick testing of a bleaching agent (Blondor Pulver) used in the hairdressers' shop gave a positive reaction (+++). Further investigation revealed that this bleaching agent contained APS and potassium persulfate. Therefore, skin prick testing of a hairdressers' panel used in patch testing was performed, revealing a positive reaction (++) to APS 2.5%. This reaction could be confirmed by negative testing of APS 2.5% in 10 nonatopic and 10 atopic volunteers. No specific IgE (<035 kU/l) to APS could be detected in an external laboratory with a commercially unavailable RAST.
In contrast to type IV sensitizations, which are frequent in hairdressers, type I sensitizations to hair-care products are rare. Besides APS, permanent wave solutions (5), conditioners (6), hair spray (7), and dyes such as henna (8, 9), senna (10), and basic blue 99 (11) have been described as causative.
The mechanism underlying asthma induced by APS is disputed. Asthma due to a type I sensitization, including specific IgE for APS, has been described (12). Besides specific allergy, APS seems to be able to induce bronchial hyperreactivity, at least in a rabbit model (13). In our patient, no specific IgE could be detected, possibly because of the lack of a standardized method for the detection of specific IgE to the hapten APS. Nevertheless, postive skin prick testing, in contrast to negative testing, in a series of volunteers indicates specific sensitization. The good correlation of skin prick testing with APS, history of asthma, and lung function has been shown in a series of industry workers with exposure to APS (14).