UpToDate
Official reprint from UpToDate®
www.uptodate.com ©2017 UpToDate, Inc. and/or its affiliates. All Rights Reserved.

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
Workplace irritant exposures: do they produce true occupational asthma?
AU
Tarlo SM
SO
Ann Allergy Asthma Immunol. 2003;90(5 Suppl 2):19.
 
OBJECTIVE: To describe the features of irritant-induced asthma and discuss the diagnosis in relation to differing workplace irritant exposures and symptomatic responses.
DATA SOURCES: A review of MEDLINE articles on this topic from January 1, 1985, through December 31, 2001 was performed.
STUDY SELECTION: The author selected relevant articles for inclusion in the review.
RESULTS: Many reports indicate that unintentional high-level respiratory irritant exposures can induce the new onset of asthma. Cases that meet strict criteria for a syndrome of irritant-induced asthma, termed reactive airways dysfunction syndrome, can be diagnosed with relative certainty. Several reports of irritant-induced asthma, especially prevalence studies, have relied on historical data or have otherwise modified the reactive airways dysfunction syndrome criteria for diagnosis (eg, expanding the definition to include the symptom onset several days after exposure). Such modifications, or inclusion of cases with incomplete documentation, likely increase diagnostic sensitivity but may reduce the certainty of diagnosis for individual cases. Expanding exposure criteria to moderate or long-term low-level irritant exposures causes difficulty in excluding transient irritant exacerbation of underlying asthma or coincidental onset of asthma during working life. Although recent population studies suggest a greater relative risk of asthma in occupations with expected low-to-moderate respiratory irritant exposures, currently no objective laboratory tests exist to exclude coincidental asthma in such patients.
CONCLUSIONS: Irritant-induced asthma can be produced by high-level unintentional respiratory irritant exposures at work or outside the workplace. Lower levels of exposure to respiratory irritants at work are more common, and additional studies are needed to determine the airway effects of such exposures.
AD
Department of Medicine, University of Toronto, Toronto Western Hospital, Gage Occupational and Environmental Health Unit, Toronto, Ontario, Canada. susan.tarlo@utoronto.ca
PMID
40
TI
Firefighting acutely increases airway responsiveness.
AU
Sherman CB, Barnhart S, Miller MF, Segal MR, Aitken M, Schoene R, Daniell W, Rosenstock L
SO
Am Rev Respir Dis. 1989;140(1):185.
 
The acute effects of the products of combustion and pyrolysis on airway responsiveness among firefighters are poorly documented. To study this relationship, spirometry and methacholine challenge testing (MCT) were performed on 18 active Seattle firefighters before and 5 to 24 h after firefighting. Body plethysmography was used to measure changes in specific airway conductance (SGaw), and results of MCT were analyzed using PD35-SGaw, the cumulative dose causing a 35% decrease in SGaw. Subjects who did not react by the end of the protocol were assigned a value of 640 inhalational units, the largest cumulative dose. Fire exposure was defined as the total time (hours) spent without a self-contained breathing apparatus at the firesite and was categorized as mild (less than 1 h, n = 7), moderate (1 to 2 h, n = 5), or severe (greater than 2 h, n = 6). Mean age of the 18 firefighters was 36.7 +/- 6.7 yr (range, 25 to 51), with a mean of 9.1 +/- 7.9 active years in the trade (range, zero to 22). None was known to be asthmatic. After firefighting, FEV1 % predicted (%pred) and FEF25-75 %pred significantly decreased by means of 3.4 +/- 1.1% and 5.6 +/- 2.6%, respectively. The mean decline in PD35-SGaw after firefighting was 184.5 +/- 53.2 units (p = 0.003). This observed decline in PD35-SGaw could not be explained by decrements in prechallenge SGaw, FEV1, or FVC.(ABSTRACT TRUNCATED AT 250 WORDS)
AD
Department of Medicine, University of Washington, Seattle.
PMID