Reactive Airway Dysfunction Syndrome


  • Reactive Airway Dysfunction Syndrome: persistent airway reactivity occurring after a single, high-dose exposure to a respiratory irritant
  • Irritant-Induced Asthma: more general term, refers to persistent airway reactivity resulting from single or multiple exposures to non-specific irritant chemical (at concentration high enough to induce airway inflammation or injury)
    • UK SWORD data: Less than 10% of of reported inhalational injuries result in persistent asthma
    • Level of exposure is an important risk factor for irritant-induced asthma (in studies of glacial acetic acid spills, more exposure increased risk of developing asthma)
    • US SENSOR data: Exposure to irritant sensitizers are frequently reported as causes of new-onset asthma
    • Atopy/smoking are risk factors the development of irritant-induced asthma


  • “Reactive Airway Dysfunction Syndrome” was first coined by Brooks in 1985
    Brooks SM, Weiss MA, Bernstein IL. Reactive airways dys- function syndrome (RADS). Persistent asthma syndrome after high-level irritant exposures. Chest 1985;88:376–384]


  • Toxin
    • Acetic Acid Inhalation (see Acetic Acid, [[Acetic Acid]])
    • Ammonia Inhalation (see Ammonia, [[Ammonia]])
    • Chlorine Inhalation (see Chlorine, [[Chlorine]]): most commonly reported agent
    • Chloropicrin Gas Inhalation (see Chloropicrin Gas, [[Chloropicrin Gas]])
    • Chromic Acid Inhalation (see Chromic Acid, [[Chromic Acid]])
    • Diethylaminoethanol (see Diethylaminoethanol, [[Diethylaminoethanol]])
    • Formaldehyde (see Formaldehyde, [[Formaldehyde]])
    • Formic Acid Inhalation (see Formic Acid, [[Formic Acid]])
    • Hydrofluoric Acid Inhalation (see Hydrofluoric Acid, [[Hydrofluoric Acid]])
    • Methyl Isocyanate Inhalation (see Methyl Isocyanate, [[Methyl Isocyanate]])
    • Nitric Acid Inhalation (see Nitric Acid, [[Nitric Acid]])
    • Nitrogen Dioxide Inhalation (see Nitrogen Dioxide, [[Nitrogen Dioxide]]): commonly reported agent
    • Ozone Inhalation (see Ozone, [[Ozone]])
    • Phosgene Gas Inhalation (see Phosgene Gas, [[Phosgene Gas]])
    • Phosphoric Acid
    • Smoke Inhalation (see Smoke Inhalation, [[Smoke Inhalation]])
    • Sodium Azide Inhalation (see Sodium Azide, [[Sodium Azide]]): following automobile airbag deployment
    • Sulfur Dioxide Inhalation (see Sulfur Dioxide, [[Sulfur Dioxide]])
    • Sulfuric Acid Inhalation (see Sulfuric Acid, [[Sulfuric Acid]])
    • Sulfur Mustard Gas Inhalation (see Sulfur Mustard Gas, [[Sulfur Mustard Gas]])
    • Tear Gas Inhalation (see Tear Gas, [[Tear Gas]])
    • Toluene Diisocyanate (see Toluene Diisocyanate, [[Toluene Diisocyanate]]): commonly reported agent
    • Uranium Hexafluoride
    • Zinc Chloride Gas Inhalation (see Zinc Chloride Gas, [[Zinc Chloride Gas]]): smoke bomb exposure


  • Airway biopsies demonstrate subepithelial fibrosis, mucosal and submucosal infiltration by T-cells and eosinophils (similar to asthma)
  • However, T-cell activation and infiltration tends to be less than in classical asthma


Diagnostic Criteria

  • Documented absence of preceding respiratory complaints
  • Onset of symptoms after single specific exposure or incident
    • “Chemical bronchitis” often precedes development of asthma symptoms
  • Exposure was to a gas, smoke, fume, or vapor present in very high concentration and had irritant effects
  • Onset of symptoms occurred within 24 hrs after exposure and persisted for at leads 3 months
  • Symptoms mimicked that of asthma: cough, wheezing, chest tightness, and dyspnea
  • PFT’s with obstruction
  • Positive methacholine challenge
  • Other types of pulmonary disease have been excluded


  • xxxx


  • Reactive airways dysfunction syndrome (RADS). Persistent asthma syndrome after high-level irritant exposures. Chest 1985;88:376–384
  • Which agents cause reactive airways dysfunction syndrome (RADS)? A systematic review. Occupational Medicine 2008;58:205–211