Abstract

Patients with airway diseases often experience asthmalike symptoms upon contact with
perfumes. Up to now, they were mainly assumed to be due to the irritative effects of perfumes in patients with preexisting unspecific bronchial hyperreactivity.
A 44-year-old woman worked in a drugstore from 1970 until 1996. Since 1988, she had
noticed dyspnoea while presenting customers with various perfume brands. In 1996, she experienced a severe asthma attack. Because of the respiratory problems, she could no longer work in her profession. Her case history revealed neither previous respiratory disorders nor an atopic disposition. She had smoked 10±15 cigarettes per day for 18 years. Total serum IgE was 65 kU/l and within the normal range. Skin prick tests with 20 common environmental allergens revealed no type I sensitization. The epicutaneous tests with the European standard reagents panel indicated a delayed type-IV reaction to a mixture of odorous substances (HAL,DuÈ sseldorf, Germany). The medical examination did not provide evidence for lung disorders. Lung-function tests showed a moderate and reversible obstructive ventilation pattern (airway resistance Rt=0.52 kP*s/l; FEV%VC 62%; intrathoracic gas volume and residual volume were within
normal ranges).
Workplace-related specific challenges with nine different brands of perfumes as well as with one individual perfume resulted in increased nasal airflow resistance and in
significant bronchial obstruction (Fig. 1).
Cases of airway irritation by perfumes without clinical symptoms or occupational
exposure have been described (1, 2), but the question of whether perfumes alone could cause the development of bronchial asthma has not been answered. There are
contradictory opinions about the pathogenetic role of perfumes. Some authors could not find a correlation between bronchial hyperreactivity, as verified by methacholine, and perfume-related asthma (3, 4), while others (5, 6) reported a clear correlation between the methacholine response and the severity of airway obstruction caused by perfumes. In this otherwise healthy woman, case history and clinical findings suggest obstructive airway disease as a result of occupational exposure to perfumes over a period of 26 years. The long-term exposure to perfumes in the workplace obviously initiated the manifestation of chronic asthma, which
persisted even after the patient avoided further contact. The causative role of perfumes was confirmed by specific challenges when she showed immediate-type asthmatic reactions. However, it should be considered that perfumes are a complex mixture of natural and synthetic substances, including volatile oils, aldehydes, ethanol, and other ingredients, so that an exact identification of the asthma triggering substance(s) cannot be made. Nevertheless, such hypersensitive reactions
are relevant not only to workers' claims of compensation but also to prevention, because an increasing number of air-fresheners used in homes and stores may also contain perfumes, making primary prevention quite difficult.

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