Medline ® Abstracts for References 1,19,40

of 'Reactive airways dysfunction syndrome and irritant-induced asthma'

1
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Reactive airways dysfunction syndrome (RADS). Persistent asthma syndrome after high level irritant exposures.
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Brooks SM, Weiss MA, Bernstein IL
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Chest. 1985;88(3):376.
 
Ten individuals developed an asthma-like illness after a single exposure to high levels of an irritating vapor, fume, or smoke. In most instances, the high level exposure was the result of an accident occurring in the workplace or a situation where there was poor ventilation and limited air exchange in the area. In all cases, symptoms developed within a few hours and often minutes after exposure. We have designated the illness as reactive airway dysfunction syndrome (RADS) because a consistent physiologic accompaniment was airways hyperreactivity. When tested, all subjects showed positive methacholine challenge tests. No documented preexisting respiratory illness was identified nor did subjects relate past respiratory complaints. In two subjects, atopy was documented, but in all others, no evidence of allergy was identified. In the majority of the cases, there was persistence of respiratory symptoms and continuation of airways hyperreactivity for more than one year and often several years after the incident. The incriminated etiologic agent varied, but all shared a common characteristic of being irritant in nature. In two cases, bronchial biopsy specimens were available, and an airways inflammatory response was noted. This investigation suggests acute high level, uncontrolled irritant exposures may cause an asthma-like syndrome in some individuals which is different from typical occupational asthma. It can lead to long-term sequelae and chronic airways disease. Nonimmunologic mechanisms seem operative in the pathogenesis of this syndrome.
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PMID
19
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Outbreak of the reactive airways dysfunction syndrome after a spill of glacial acetic acid.
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Kern DG
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Am Rev Respir Dis. 1991;144(5):1058.
 
The reactive airways dysfunction syndrome (RADS) defines a chronic asthmalike illness with airway hyperresponsiveness that develops within 24 h of a single, brief, highly irritating inhalation exposure. Support for the syndrome has been limited to case reports. A chemical spill, exposing hospital employees to 100% acetic acid, offered an opportunity to more convincingly establish the existence of RADS. All 56 exposed subjects were asked both to complete a questionnaire focusing on their preexposure health status, potential for exposure, and symptom development after the accident, 8 months after the spill, and to undergo methacholine challenge testing to detect airway hyperresponsiveness. An industrial hygienist, blinded to clinical data, estimated each subject's exposure. Preemployment health history forms were reviewed to assess recall bias. The study questionnaire was returned by 51 (91%) subjects; 24 (47%) consented to methacholine challenge, including 7 of the 8 with RADS-consistent symptoms. Diagnostic criteria for RADS were satisfied by none of 7 (0%) subjects with low exposure, 1 of 30 (3.3%) with medium exposure, and 3 of 14 (21.4%) with high exposure (test of trend p value = 0.021). The odds ratio estimate of the relative risk of RADS in subjects with high exposure was 9.8 (95% Cl, 0.902 to 264.6). Neither stratified analysis nor review of the preemployment health history forms revealed evidence of confounding or recall bias, respectively. The reactive airways dysfunction syndrome appears to be a valid clinical entity. Further study of RADS is especially appropriate given increasing evidence that airway inflammation may be etiologically important in all asthma.
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Department of Medicine, Memorial Hospital of Rhode Island, Pawtucket 02860.
PMID
40
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Long-term pathologic consequences of acute irritant-induced asthma.
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Takeda N, Maghni K, Daigle S, L'Archevêque J, Castellanos L, Al-Ramli W, Malo JL, Hamid Q
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J Allergy Clin Immunol. 2009;124(5):975.
 
BACKGROUND: Acute irritant-induced asthma (IrIa) or reactive airways dysfunction syndrome is caused by exposure to a high concentration of an agent. The long-term pathologic consequences of IrIa remain thus far unknown.
OBJECTIVE: The aim of our study was to investigate the chronic airway inflammation and remodeling that occur in association with IrIa.
METHODS: Ten subjects with a history of IrIa (mean interval of 10.9 years, minimum of 4 years, since the inhalational accident) underwent bronchoscopy followed by bronchoalveolar lavage and bronchial biopsies. Immunologic and morphologic data from patients with IrIa were compared with those of patients with mild to moderate asthma as well as healthy controls.
RESULTS: Bronchoalveolar lavage fluid analysis showed increased eosinophil and neutrophil counts in 30% and 60% of subjects with IrIa, respectively. In the supernatant of bronchoalveolar lavage, we found a significant increase in the majority of mediators compared with healthy subjects and a significant increase in eosinophilic cationic protein, IL-8, basic fibroblast growth factor, and matrix metalloproteinase 1 compared with control patients with asthma. Evaluation of basement membrane thickness (subepithelial fibrosis) demonstrated a significant increase in patients with IrIa compared with healthy subjects and subjects with asthma. Basement membrane thickness also significantly correlated with the PC(20) value. The epithelial cell detachment showed an elevated although not significant trend compared with subjects with asthma and control subjects. Immunocytochemical analysis demonstrated increases in the number of eosinophil cationic protein and TGF-beta1-positive cells compared with healthy controls.
CONCLUSION: This study provides evidence of a significant eosinophilic and neutrophilic inflammation as well as remodeling in IrIa many years after an inhalational accident.
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Meakins-Christie Laboratories, McGill University, Montreal, Quebec, Canada.
PMID