Chest
Volume 109, Issue 6, June 1996, Pages 1618-1626
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Reactive Airways Dysfunction Syndrome

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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

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REFERENCES (72)

  • SchwartzDA et al.

    The pulmonary sequelae associated with the accidental inhalation of chlorine gas

    Chest

    (1990)
  • KernDG et al.

    What is this thing called RADS?

    Chest

    (1994)
  • GautrinD et al.

    Is reactive airways dysfunction syndrome a variant of occupational asthma?

    J Allergy Clin Immunol

    (1994)
  • AlbertsWM et al.

    Advances in occupational asthma

    Clin Chest Med

    (1992)
  • StentonSC et al.

    Induction of bronchial hyperresponsiveness following smoke inhalation injury

    Br J Dis Chest

    (1988)
  • MooreBB et al.

    Chronic reactive airway disease following acute chlorine gas exposure in an asymptomatic atopic patient

    Chest

    (1991)
  • SnyderRW et al.

    Pulmonary toxicity following exposure to methylene chloride and its combustion product, phosgene

    Chest

    (1992)
  • Chan-YeungM et al.

    Occupational asthma

    N Engl J Med

    (1995)
  • BrooksSM et al.

    Reactive airways dysfunction syndrome or irritant-induced asthma

  • BrooksSM et al.

    Reactive airways disease syndrome (RADS): a newly defined occupational disease [abstract]

    Am Rev Respir Dis

    (1981)
  • BrooksSM et al.

    Reactive airways dysfunction syndrome

    J Occup Med

    (1985)
  • do PicoGA.

    Toxic gas inhalation

  • VenablesKM.

    Prevention of occupational asthma

    Eur Respir J

    (1994)
  • Chan-YeungM et al.

    Assessment of asthma in the workplace

    Chest

    (1995)
  • BrooksSM.

    Reactive airways syndromes

    J Occup Health Safety, Aust NZ

    (1992)
  • BardanaEJ.

    Occupational asthma and related respiratory disorders

    Dis Month

    (1995)
  • Chan-YeungM et al.

    Persistent asthma after repeated exposure to high concentrations of gases in pulpmills

    Am J Respir Crit Care Med

    (1994)
  • Chan-YeungM et al.

    Aetiologic agents in occupational asthma

    Eur Respir J

    (1994)
  • GandeviaB.

    Occupational asthma

    Med J Aust

    (1970)
  • HarkonenH et al.

    Long-term effects of exposure to sulfur dioxide

    Am Rev Respir Dis

    (1983)
  • CharanNB et al.

    Pulmonary injuries associated with acute sulfur dioxide inhalation

    Am Rev Respir Dis

    (1979)
  • FluryKE et al.

    Airway obstruction due to inhalation of ammonia

    Mayo Clin Proc

    (1983)
  • DonhamKJ et al.

    Acute toxic exposure to gases from liquid manure

    J Occup Med

    (1982)
  • KaufmanJ et al.

    Clinical, roentgenologic and physiologic effects of acute chlorine exposure

    Arch Environ Health

    (1971)
  • WhitenerDR et al.

    Pulmonary function measurements in patients with thermal injury and smoke inhalation

    Am Rev Respir Dis

    (1980)
  • WadeJF et al.

    Diesel asthma: reactive airways disease following overexposure to locomotive exhaust

    J Occup Med

    (1993)
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