Reactive Airway Dysfunction Syndrome

Definitions

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

Epidemiology

“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]

Etiology

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

Physiology

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

Clinical

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

Treatment

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References

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