Medline ® Abstracts for References 10,38
of 'Reactive airways dysfunction syndrome and irritant-induced asthma'
Nonsensitizing causes of occupational asthma.
Lemière C, Malo JL, Gautrin D
Med Clin North Am. 1996;80(4):749.
Irritant-induced asthma and RADS are related conditions that need further study focusing on the following questions: (1) Are there differences between the pathologic and functional features that follow single or multiple exposures to an irritant material? (2) What is the time course of the changes? (3) What are the physiologic correlates in terms of onset of airway hyperresponsiveness? (4) What are the risk markers (besides exposure)? (5) Are there means of modulating the reaction by using anti-inflammatory preparations? Developing an animal model of irritant-induced asthma and conducting prospective epidemiologic surveys in high-risk workers may be most effective routes to provide satisfactory answers to these questions. Further examination of the physiopathology of such conditions as byssinosis, grain-dust-induced respiratory disease, and aluminum potroom asthma as well as of the differences from and similarities to OA is also warranted.
Department of Chest Medicine, Sacré-Coeur Hospital, Montreal, Québec, Canada.
Reactive airways dysfunction syndrome due to chlorine: sequential bronchial biopsies and functional assessment.
Lemière C, Malo JL, Boutet M
Eur Respir J. 1997;10(1):241.
Very little information is available on the acute histopathological bronchial alterations caused by reactive airways dysfunction syndrome (RADS). We had the opportunity to carry out sequential bronchial biopsies in a subject with RADS due to chlorine (60 h, 15 days, 2 and 5 months after the acute exposure), and also to assess spirometry and bronchial responsiveness to methacholine. A 36 year old worker in a water-filtration plant (nonsmoker) abruptly inhaled high concentrations of chlorine on September 12, 1994. He experienced immediate nasal and throat burning, retrosternal burning and wheezing, and these symptoms persisted during and after the workshift. Two days later, he complained of retrosternal burning, dyspnoea and wheezing. Inspiratory wheezing was documented. His forced expiratory volume in one second (FEV1) was 66% of predicted and the provocative concentration of methacholine causing a 20% fall in FEV1 (PC20) was slightly abnormal (2.5 mg.mL-1). On the following day, the patient underwent bronchial biopsies, which showed almost complete replacement of the epithelium by a fibrinohaemorhagic exsudate. The subject was prescribed inhaled steroids. Fifteen days after the accident, the PC20 was improved to 6 mg.mL-1. Bronchial biopsies showed considerable epithelial desquamation with an inflammatory exudate and swelling of the subepithelial space. Five weeks after the accident, the PC20 was normal (57 mg.mL-1). Inhaled steroids were stopped. Two months after the accident, the PC20 deteriorated to 4 mg.mL-1. Biopsies then showed regeneration of the epithelium by basal cells and there was still a pronounced inflammatory infiltrate. Inhaled steroids were restarted. Three and five months later, the PC20 was normal (24 mg.mL-1). Bronchial biopsies showed a greatly improved epithelium and reduction of the inflammatory infiltrate. This case report shows that reactive airways dysfunction syndrome can cause acute, marked, though partially reversible, histological abnormalities. Inhaled steroids may modulate changes in bronchial responsiveness in this condition.
Sacré-Coeur Hospital, Montreal, Québec, Canada.