Chest
ReviewsReactive Airways Dysfunction Syndrome
Section snippets
CLINICAL PRESENTATION
In 1981, Brooks and Lockey4 first used the term reactive airways dysfunction syndrome (RADS) in an abstract that described 13 workers who developed symptomatic and physiologic evidence of bronchoconstriction within hours of a toxic inhalation exposure. In most of these cases, however, symptoms resolved within weeks.
In 1985, Brooks and colleagues1 described ten patients (including six from the earlier abstract4 and two from an earlier publication5) who developed an asthma-like condition that
DIAGNOSIS
The diagnosis of RADS is based on a compatible history and the demonstration of persistent nonspecific bronchial hyperresponsiveness. The latter may be demonstrated by a significant spirometric response to an inhaled bronchodilator or a positive nonspecific bronchoprovocation challenge test.
A case of RADS was defined in the American College of Chest Physicians (ACCP) Consensus Statement on “Assessment of Asthma in the Workplace” as follows: (1) a documented absence of preceding respiratory
BACKGROUND
Case reports documenting a persistent asthma-like illness following a toxic inhalation exposure appeared in the literature prior to 1985. In retrospect, these cases most likely represented examples of RADS. In 1970, Gandevia13 described four workers who developed new-onset asthma after exposure to excessive concentrations of gases and vapors such as hydrogen sulfide, diethylene diamine, fumes from overheated plastics, and smoke and fumes from combustion of a variety of materials. Harkonen et al
EPIDEMIOLOGY
Although the possibility of long-term respiratory problems stemming from a short-term irritant inhalation exposure is well recognized, the actual risk of such an outcome has been difficult to quantify. Blanc and coworkers34 interviewed 323 subjects of a consecutive sample of 693 toxic inhalational exposures that were reported to a poison control center. Only 20% of patients had symptoms that persisted 14 days or more and symptoms rarely lasted more than 2 months. This might suggest that RADS is
Is RADS A REAL CLINICAL ENTITY?
The reality of RADS remains controversial up to the present time. In a recent editorial, Kern and Sherman42 note that the American Thoracic Society,43 the Canadian Thoracic Society,44 and the legal community45 all recognize this disorder. The American College of Chest Physicians has likewise provided recognition of RADS via the consensus statement on “Assessment of Asthma in the Workplace.”8 Nevertheless, not all experts are certain that RADS is a real clinical entity.42 Kennedy46 concluded
Is RADS A FORM OF OCCUPATIONAL ASTHMA?
Because toxic inhalation exposures are most often encountered in the workplace or during the course of employment, RADS is often classified as a form of occupational asthma. Some have argued, however, that RADS is not occupational asthma in the strictest sense. The controversy appears to be predominantly semantic in origin and stems from the lack of a uniformly accepted definition of occupational asthma.51 If occupational asthma is defined narrowly as a syndrome that develops after a variable
PATHOLOGY
Histopathologic studies of patients with RADS are few in number but have the potential to shed light on the pathogenetic mechanisms involved in the development of this syndrome and asthma, in general. In the original report of Brooks et al,5 2 patients underwent transbronchial lung biopsies 9 and 33 months after the inciting incident. Examination showed evidence of airways inflammation with some, but not all, of the changes regarded as characteristic of asthma. Respiratory epithelial injury
MECHANISMS
The pathogenesis of RADS is not clear and to this point it is substantially speculative. Acute symptoms following toxic inhalation exposure are no doubt due to the resulting airway inflammation. What is problematic is how and why the asthmatic state persists in some individuals. The current lack of a satisfactory animal model hampers the testing of hypotheses.
Alberts and Brooks54 have speculated that the onset of RADS may be a “big bang” type of mechanism. The high-level irritant exposure
“IRRITANT-INDUCED ASTHMA” AND “LOW-LEVEL RADS”
Recently, persistent asthmatic conditions have been reported to develop as the result of repeated moderate- or high-level inhalation exposures as opposed to the single massive exposure associated with cases of RADS. These repeated lower-level, though not trivial, exposures do not fit the strict criteria for RADS but may result in asthma via very similar mechanisms. Chan-Yeung and coworkers11 described three pulp mill workers who developed irritant-induced asthma after multiple episodes of
MANAGEMENT
The treatment of the patient with established RADS is no different from that of any other asthmatic. In addition to relieving symptoms with bronchodilators, treatment should be directed at reducing the level of nonspecific bronchial responsiveness. In a recent report, however, Gautrin et al53 found that patients with RADS were significantly less responsive to inhaled β2-adrenergic agents than were patients with conventional asthma. In reviewing their approach to management, Palczynski and
CONCLUSION
RADS is a clinical pathologic entity characterized by exposure to a toxic or irritant chemical, negative history of obstructive symptoms prior to exposure, persistence of obstructive symptoms after exposure, objective evidence of obstructive airways disease and/or nonspecific bronchial hyperresponsiveness, and abnormal bronchial biopsy results.3 It differs from typical occupational asthma because of the absence of a preceding latent period and the onset of the illness after a single exposure.3
REFERENCES (72)
- et al.
Reactive airways dysfunction syndrome (RADS); persistent asthma syndrome after high level irritant exposures
Chest
(1985) - et al.
Severe airways disease due to the inhalation of fumes from cleaning agents
Chest
(1976) Increases in airway responsiveness following acute exposure to respiratory irritants
Chest
(1988)- et al.
Persistent asthma after inhalation of a mixture of sodium hypochlorite and hydrochloric acid
Chest
(1994) - et al.
Airway complications from free-basing cocaine
Chest
(1989) - et al.
Reactive airway dysfunction syndrome in three police officers following a roadside chemical spill
Chest
(1990) - et al.
Persistent respiratory health effects after a metam sodium pesticide spill
Chest
(1994) - et al.
Reactive airways dysfunction after exposure to teargas [letter]
Lancet
(1992) - et al.
Symptoms, lung function, and airway responsiveness following irritant inhalation
Chest
(1993) - et al.
Irritant-induced occupational asthma
Chest
(1989)
The pulmonary sequelae associated with the accidental inhalation of chlorine gas
Chest
What is this thing called RADS?
Chest
Is reactive airways dysfunction syndrome a variant of occupational asthma?
J Allergy Clin Immunol
Advances in occupational asthma
Clin Chest Med
Induction of bronchial hyperresponsiveness following smoke inhalation injury
Br J Dis Chest
Chronic reactive airway disease following acute chlorine gas exposure in an asymptomatic atopic patient
Chest
Pulmonary toxicity following exposure to methylene chloride and its combustion product, phosgene
Chest
Occupational asthma
N Engl J Med
Reactive airways dysfunction syndrome or irritant-induced asthma
Reactive airways disease syndrome (RADS): a newly defined occupational disease [abstract]
Am Rev Respir Dis
Reactive airways dysfunction syndrome
J Occup Med
Toxic gas inhalation
Prevention of occupational asthma
Eur Respir J
Assessment of asthma in the workplace
Chest
Reactive airways syndromes
J Occup Health Safety, Aust NZ
Occupational asthma and related respiratory disorders
Dis Month
Persistent asthma after repeated exposure to high concentrations of gases in pulpmills
Am J Respir Crit Care Med
Aetiologic agents in occupational asthma
Eur Respir J
Occupational asthma
Med J Aust
Long-term effects of exposure to sulfur dioxide
Am Rev Respir Dis
Pulmonary injuries associated with acute sulfur dioxide inhalation
Am Rev Respir Dis
Airway obstruction due to inhalation of ammonia
Mayo Clin Proc
Acute toxic exposure to gases from liquid manure
J Occup Med
Clinical, roentgenologic and physiologic effects of acute chlorine exposure
Arch Environ Health
Pulmonary function measurements in patients with thermal injury and smoke inhalation
Am Rev Respir Dis
Diesel asthma: reactive airways disease following overexposure to locomotive exhaust
J Occup Med
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2016, ChestCitation Excerpt :Persons with RADS may or may not improve,18,20,30 whereas those with occupational COPD typically do not improve.32 Occupational asthma and RADS are usually characterized by BHR—required by most definitions of RADS.31 Although our participants’ BHR was persistent, its prevalence was substantially lower than reported in persons with asthma,33 suggesting that WTC-associated airway disease does not follow the classic trajectory of occupational asthma.
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