Medline ® Abstracts for References 1,19,40

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

1
TI
Reactive airways dysfunction syndrome (RADS). Persistent asthma syndrome after high level irritant exposures.
AU
Brooks SM, Weiss MA, Bernstein IL
SO
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.
AD
PMID
19
TI
Outbreak of the reactive airways dysfunction syndrome after a spill of glacial acetic acid.
AU
Kern DG
SO
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.
AD
Department of Medicine, Memorial Hospital of Rhode Island, Pawtucket 02860.
PMID
40
TI
RADS and RUDS--the toxic induction of asthma and rhinitis.
AU
Meggs WJ
SO
J Toxicol Clin Toxicol. 1994;32(5):487.
 
Inhalation exposures can produce asthma and rhinitis by several mechanisms. Sensitization with the production of IgE specific for a substance can lead to symptoms on reexposure via mast cell degranulation and the release of inflammatory mediators. Some substances, known as environmental adjuvants, enhance the immune response to concomitant exposures with the environmental adjuvant. Respiratory irritants can lead to asthma and rhinitis through interaction with chemical irritant receptors in the airway, leading to release of substance P from sensory nerves and neurogenic inflammation. The reactive airways dysfunction syndrome is a chronic asthma-like syndrome resulting from a single acute exposure to a respiratory irritant, while the reactive upper-airways dysfunction syndrome is chronic rhinitis stemming from an irritant exposure. The dysregulation of neurogenic inflammation by chemical exposures may be an important mechanism in the toxic induction of reactive airways dysfunction syndrome and reactive upper-airways dysfunction syndrome and may play a role in understanding the sick building syndrome and the multiple chemical sensitivity syndrome.
AD
East Carolina University School of Medicine, Greenville, North Carolina.
PMID