Reactive Airways Dysfunction Syndrome (RADS)

Reactive Airways Dysfunction Syndrome (RADS) is an asthma-like illness that starts suddenly after one accidental, very high exposure to an irritating gas, vapor, smoke, or fume (for example, a chlorine spill, a strong bleach–acid mix, or heavy fire smoke). People who were breathing normally before the accident can develop cough, wheeze, chest tightness, and shortness of breath within 24 hours, and these symptoms may last for months or longer. RADS is not allergy-based; it is caused by chemical injury to the breathing tubes (airways) that makes them overly reactive and “twitchy.” Diagnostic criteria and the original description come from Brooks and colleagues, and later professional society statements kept the same core idea: sudden asthma without a latency period, after a single very high irritant exposure. British Thoracic Society+3PubMed+3ScienceDirect+3

Reactive Airways Dysfunction Syndrome (RADS) is a sudden form of asthma that begins within 24 hours of a single, high-level exposure to a strong airway irritant such as chlorine gas, smoke from a fire, ammonia, cleaning or industrial chemicals. People who develop RADS did not have asthma symptoms before the accident. After the exposure, they develop cough, wheeze, chest tightness, and shortness of breath, and their airways stay extra sensitive and twitchy (hyper-responsive) for months or longer. Doctors also call this acute irritant-induced asthma. It is different from usual “allergic asthma” because it does not require months of sensitization to an allergen; it appears quickly after one heavy exposure. American Thoracic Society+3British Thoracic Society+3ScienceDirect+3

RADS is diagnosed by the story of exposure, new asthma-like symptoms within a day, and tests that show airflow obstruction or airway hyper-responsiveness (e.g., spirometry with bronchodilator response or a methacholine challenge). The British Thoracic Society notes Brooks’ classic criteria: no prior asthma, a single high-dose irritant exposure, symptom onset within 24 hours, persistent symptoms for at least 3 months, and objective evidence of variable airflow limitation or hyper-responsiveness. British Thoracic Society

Management of RADS generally follows standard asthma care (reliever inhalers, inhaled corticosteroids, trigger avoidance), plus occupational measures (engineering controls, PPE, removal from exposure). Ongoing assessment of comorbidities (rhinitis, sinus disease, reflux, obesity, anxiety/depression) can improve control. Global Initiative for Asthma – GINA+1

Other names

• Acute irritant-induced asthma (the term many guidelines now prefer; RADS is the classic “acute” form). PubMed+1

• Occupational irritant-induced asthma without latency (when it happens at work). PubMed

• Post-inhalational airway hyper-reactivity (describes the mechanism—very “twitchy” airways after a big exposure). PubMed

Types

1. Classic RADS (acute, single-event) – sudden asthma within 24 hours after one massive irritant exposure; no allergy sensitization period. PubMed+1

2. “Not-so-sudden” irritant-induced asthma – asthma that begins after repeated high or moderate irritant exposures over days to weeks; similar mechanism but not strictly RADS by original criteria. CalDIR

3. Work-exacerbated asthma (WEA) – a person already has asthma, and workplace irritants make it worse (this is not RADS, but it is part of the clinical differential and often discussed together). CalDIR

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Common causes

Below are typical irritants that can cause RADS when someone breathes a very high dose (often in a closed space or during an accident). The mechanism is direct chemical burn/irritation to the airway lining, which then heals with lasting hyper-reactivity.

1. Chlorine gas (e.g., pool chemical release, bleach mixing accident). Chlorine forms acids in the airways, causing acute airway injury; RADS after chlorine leaks and mixing bleach with acids is well described. PMC+1

2. Chloramine gas from mixing bleach with ammonia. A very common home or workplace accident; produces ammonia-like/chlorine-like airway injury. jiaci.org

3. Ammonia (refrigeration plants, cleaners). Strong alkali that penetrates and damages airway tissue. jiaci.org

4. Sulfur dioxide (industrial combustion). Water-soluble gas that irritates upper and lower airways, provoking intense bronchospasm. PubMed

5. Nitrogen oxides (silo gas, welding fumes). Can cause delayed-airway injury and severe reactivity. PubMed

6. Ozone (industrial/printing/UV sources). Powerful oxidant that inflames the airway lining on high exposure. PubMed

7. Hydrochloric acid fumes (acid cleaning, spills). Corrosive acid vapor causes chemical bronchitis and RADS. jiaci.org

8. Sodium hydroxide/alkaline mists (drain cleaners, industrial). Caustic injury similar to acids, but alkaline. jiaci.org

9. Hydrogen sulfide (sewage, oil/gas). High-level exposure can cause intense airway irritation and respiratory failure. PubMed

10. Chlorine dioxide (disinfection). Strong oxidizer used in pulp/paper and water treatment; high exposure irritates airways. PubMed

11. Glutaraldehyde/formaldehyde (disinfectants, labs). Potent airway irritants; high exposures linked with acute asthma-like illness. PubMed

12. Tear gas/pepper spray (riot control). Intense mucosal irritation with cough/wheeze after heavy exposure. PubMed

13. Smoke inhalation from fires (house/industrial). Complex mix of particulates and gases (CO, NOx, SO2) that injure the airway; RADS reported after severe smoke exposure. PubMed

14. Welding fumes (metal oxides, gases). High, unventilated exposure can trigger irritant-induced asthma syndromes. PubMed

15. Diesel exhaust in enclosed spaces. Dense exhaust contains irritant gases/particles; acute massive exposure can precipitate RADS-like illness. PubMed

16. Pesticide fumigants (e.g., sulfuryl fluoride). Acute inhalation causes bronchospasm and airway injury. PubMed

17. Cement/lime dust clouds (alkaline particulate). Massive dust inhalation can burn the airway and lead to persistent reactivity. PubMed

18. Strong cleaning products “mists” in healthcare/hospitality (sprays with bleach, acids, ammonia, quats). Cleaning-related chemicals are a leading source of work-related asthma; very high exposures can cause RADS. PMC+1

19. Oven/grill cleaners and degreasers (alkaline solvents). Aerosolized product in small rooms can injure the airway lining. jiaci.org

20. Mixed unknown chemical releases (factory/lab spills). When the exact agent is unclear, the pattern—sudden symptoms after one big exposure—helps identify RADS. PubMed

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Symptoms

1. Cough (often constant, dry or with little mucus). It starts quickly after the incident and can persist for months.

2. Wheezing (a whistling sound when breathing out) due to narrowed airways.

3. Chest tightness/pressure from airway muscle spasm.

4. Shortness of breath (especially with exertion, fumes, or cold air).

5. Throat burning/irritation right after the exposure, then ongoing tickle or soreness.

6. Eye and nose irritation (burning/tearing/runny nose) during the exposure, often improving later.

7. Voice hoarseness if the larynx was irritated.

8. Sensation of “can’t get air out” (air trapping).

9. Noisy breathing at night; sleep broken by cough/wheeze.

10. Exercise intolerance (reduced capacity because airways tighten sooner).

11. Chest pain with deep breaths from inflamed airways/chest wall strain from prolonged coughing.

12. Mucus production (usually small amounts; can be thick after smoke injury).

13. Frequent “colds” that are actually airway hyper-reactivity episodes triggered by minor irritants.

14. Anxiety about breathing (common after dramatic inhalation incidents).

15. Symptoms worse at the original site/exposures and better away from them.

Guidelines describe the typical sudden onset within 24 hours and persistent hyper-reactive symptoms after a high-dose irritant exposure. PubMed+1

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Diagnostic tests

Important idea: There is no single “RADS test.” Doctors confirm RADS by (1) the history of one massive irritant exposure, (2) asthma-type airway hyper-reactivity on lung tests, and (3) no prior asthma or allergy-sensitization period. They also rule out other diseases. International guidance for asthma testing (spirometry, bronchodilator response, bronchial challenge) supports the objective parts of diagnosis. Global Initiative for Asthma – GINA+1

A) Physical exam (bedside assessment)

1. General observation and vital signs. Doctors look for fast breathing, fast heart rate, or low oxygen right after the exposure. (Helps gauge severity.)

2. Chest auscultation (listening with a stethoscope). Wheezes suggest narrowed airways; a “silent chest” is worrisome if airflow is very low.

3. Upper airway inspection (nose, throat, voice). Irritant injuries often inflame these areas; hoarseness suggests laryngeal irritation.

4. Work/exposure-linked pattern check. Symptoms started within 24 hours of a single high exposure and improve away from the scene—this pattern is central to RADS. PubMed

5. Pulse oximetry (finger oxygen check). Quick, noninvasive check; low values suggest significant impairment.

B) Manual / simple clinic tests (easy, repeatable)

6. Peak expiratory flow (PEF) measurement and diary. A simple handheld device measures how fast air leaves your lungs. Variability or drops with irritants/exertion support asthma-type reactivity. GINA and other guidelines accept serial variability as supportive evidence when spirometry is inconclusive. Global Initiative for Asthma – GINA

7. In-office bronchodilator response with PEF. Record PEF, inhale a quick-relief bronchodilator, then repeat. Improvement suggests reversible airway narrowing. Global Initiative for Asthma – GINA

8. Six-minute walk test (6MWT). Checks exercise tolerance and whether oxygen or symptoms worsen with gentle exertion after injury.

9. Irritant avoidance trial. Time away from the exposure site (home/work) with symptom/PEF tracking helps show exposure-response patterns emphasized in occupational asthma guidance. CalDIR

10. Rescue-medication response tracking. Symptom relief after inhaled bronchodilator fits an asthma-like mechanism.

C) Laboratory and pathological tests

11. Complete blood count (CBC) and inflammatory markers. Often normal, but helpful to exclude infection; classic RADS is not allergic-eosinophilic by definition.

12. Exhaled nitric oxide (FeNO). This measures airway inflammation from type-2 (eosinophilic) pathways. In RADS, FeNO may be normal or only mildly raised, but FeNO can still help confirm asthma in some patients and predict steroid response (per guidelines it’s a supportive test, not a stand-alone diagnosis). Archivos de Bronconeumología+1

13. Induced sputum cell counts. RADS more often shows neutrophilic inflammation after chemical injury, unlike allergic asthma which is often eosinophilic. (Helps with phenotyping.) PubMed

14. Arterial/venous blood gases (ABG/VBG) in severe cases. Check oxygen and carbon dioxide if breathing failure is suspected after a major inhalation.

15. Allergy testing (IgE/skin tests) to rule out sensitizer-induced occupational asthma. In pure RADS, allergy tests are typically negative because there is no latency or sensitization phase. PubMed

D) Electrodiagnostic / functional respiratory tests

16. Spirometry with bronchodilator response (objective cornerstone). Measures FEV₁/FVC before and after a bronchodilator. Reversibility (e.g., ≥12% and ≥200 mL FEV₁ increase) supports asthma. Guidelines recommend objective testing whenever possible. Global Initiative for Asthma – GINA

17. Nonspecific bronchial challenge (e.g., methacholine test). If spirometry is normal but symptoms suggest asthma, methacholine tests airway hyper-reactivity—commonly positive after RADS. Per ERS/ATS technical standards, it should be done in a controlled lab by trained staff. ERS Publications+1

18. Full pulmonary function testing (lung volumes and diffusion). Helps exclude other causes (e.g., restriction) and quantify air trapping or small-airway involvement. GINA and national guidelines encourage objective measures when diagnosing asthma. Global Initiative for Asthma – GINA+1

19. Impulse oscillometry / forced oscillation technique (FOT). Sensitive to small-airway dysfunction and bronchodilator response; useful if spirometry is hard to perform. (Supportive evidence for airway mechanics abnormality.) Global Initiative for Asthma – GINA

20. Cardiopulmonary exercise testing (CPET) with ECG and gas exchange (selected cases). If breathlessness remains unexplained, CPET can separate ventilatory limits from deconditioning and can document exercise-induced bronchoconstriction while the patient is monitored. (Used selectively in specialty labs.) Global Initiative for Asthma – GINA

E) Imaging tests (to exclude other injuries/diseases)

1. Chest X-ray. Usually normal in RADS; helps rule out pneumonia, edema, or structural problems after smoke/chemical inhalation.

2. High-resolution chest CT (HRCT). Used if symptoms are severe or not improving—to check for bronchiolitis, airway wall thickening, or other injury patterns.

3. Sinus CT or laryngoscopy (selected cases). If upper airway injury is suspected (hoarseness, stridor), these tests assess the larynx and sinuses.
   Imaging is supportive and mainly used to exclude other problems rather than to “prove” RADS. Occupational/respiratory society statements emphasize history plus objective lung tests over imaging. British Thoracic Society

Non-pharmacological treatments (therapies & others)

1. Immediate removal from the irritant source
   Description: The first and most effective step after a RADS-triggering incident is simply getting away from the irritant and ensuring it does not happen again. In a workplace, this means stopping the process, ventilating the area, and safely evacuating. For community exposures (e.g., fire), it means leaving the site and seeking fresh air. After the acute event, prevention plans matter most: repair leaks, switch to safer substances, improve ventilation, and post clear warning signs. People with RADS should be moved to low-exposure duties while recovering. Documentation of the exposure, a written safety plan, and training reduce the chance of repeat events. This “remove the hazard first” approach is more effective than relying only on masks or personal habits.
   Purpose: Stop ongoing injury and prevent future episodes.
   Mechanism: Elimination/substitution reduces dose to the airways and lowers inflammation triggers. CDC+1

2. Engineering controls (ventilation and containment)
   Description: Upgrade local exhaust ventilation, closed systems, fume hoods, and negative-pressure rooms to capture irritants at the source. Use automatic shut-offs and leak detection. Maintain and monitor systems with logs.
   Purpose: Reduce irritant levels in the air you breathe.
   Mechanism: Engineering controls physically reduce airborne concentration, making the environment safer without depending on user behavior. CDC+1

3. Administrative controls & training
   Description: Rotate tasks to limit exposure time, enforce safe work procedures, and provide incident drills. Keep Safety Data Sheets accessible; teach early symptom recognition and prompt evacuation.
   Purpose: Lower exposure time and improve rapid response.
   Mechanism: Administrative controls change how work is done to reduce cumulative dose and prevent dangerous peaks. CDC

4. Personal protective equipment (PPE)
   Description: When higher-level controls are not enough, use fit-tested respirators (e.g., half/full-face with appropriate cartridges), protective eyewear, and chemical-resistant gloves. Ensure proper fit testing and replacement schedules.
   Purpose: Protect the airways and eyes from residual irritants.
   Mechanism: Respirators filter or block inhaled irritants, lowering airway exposure. CDC

5. Written asthma action plan
   Description: A simple, personalized plan shows daily controller use, when to take rescue inhalers, and when to seek urgent care. It should list the known irritant and steps to avoid it.
   Purpose: Help patients act early when symptoms rise.
   Mechanism: Action plans improve self-management and reduce severe flare-ups. Global Initiative for Asthma – GINA

6. Breathing retraining (Buteyko/Papworth/yogic breathing)
   Description: Guided breathing can reduce symptoms like over-breathing, chest tightness, and anxiety. Sessions teach slower nasal breathing, diaphragmatic patterns, and relaxation.
   Purpose: Ease symptoms and improve quality of life.
   Mechanism: Alters breathing pattern, reduces dynamic hyperinflation and the sensation of dyspnea. Evidence shows benefit for symptoms/QoL, though lung function changes are small. Cochrane Library+1

7. Pulmonary rehabilitation (PR) with graded exercise
   Description: Supervised PR combines exercise, education, pacing, and breathing skills. It’s helpful for deconditioning or steroid-related weakness.
   Purpose: Improve exercise capacity and confidence.
   Mechanism: Builds peripheral and inspiratory muscle strength; reduces anxiety around exertion. Evidence for asthma-specific outcomes is mixed but promising for symptoms/QoL. PubMed+1

8. HEPA filtration at home/work “clean room”
   Description: Portable HEPA units may reduce particles and some allergens in rooms where you spend most time.
   Purpose: Lower background particle burden that can irritate inflamed airways.
   Mechanism: Mechanical filtration reduces particulate triggers; evidence is mixed and context-dependent. PMC+1

9. Smoking and vaping cessation
   Description: Quitting smoking and avoiding e-cigarette aerosol reduces airway inflammation and improves asthma outcomes. Use counseling and medications if needed.
   Purpose: Reduce symptom burden and flare-ups.
   Mechanism: Removing tobacco toxicants decreases chronic airway injury and restores steroid responsiveness. ERS Publications+1

10. Weight management (if overweight/obese)
    Description: Even 5–10% weight loss can improve asthma control and quality of life. Combine calorie-aware diet with low-impact exercise and sleep support.
    Purpose: Reduce breathlessness and medication needs.
    Mechanism: Lowers systemic inflammation and mechanical load on the lungs. PMC+1

11. Treat comorbid chronic rhinosinusitis
    Description: Nasal steroids, saline rinses, and allergy management can reduce post-nasal drip and cough. In selected cases with severe polyps, ENT evaluation is helpful.
    Purpose: Reduce upper-airway triggers that spill into the lungs.
    Mechanism: Controlling sinonasal inflammation reduces bronchial irritability. Global Initiative for Asthma – GINA

12. Manage reflux (GERD) if present
    Description: Lifestyle steps (smaller meals, head-of-bed elevation, avoiding late-night eating) plus medical therapy as needed.
    Purpose: Reduce micro-aspiration and cough.
    Mechanism: Less acid exposure → fewer reflux-linked bronchospasm episodes. Global Initiative for Asthma – GINA

13. Psychological support / CBT for anxiety & symptom focus
    Description: Sudden breathing problems can be scary. Brief CBT, relaxation, or mindfulness can reduce panic and symptom amplification.
    Purpose: Improve coping and reduce hyperventilation cycles.
    Mechanism: Lowers stress-related autonomic triggers that tighten airways. Cochrane Library

14. Trigger diary & peak-flow monitoring
    Description: Note symptom patterns, exposures, and peak flow readings to spot early declines and relate them to workplace or environmental factors.
    Purpose: Detect worsening early; inform occupational adjustments.
    Mechanism: Objective tracking supports timely therapy changes. Global Initiative for Asthma – GINA

15. Workplace accommodations
    Description: Temporary duty changes, increased breaks, alternative agents, and proximity alarms reduce risk while recovering.
    Purpose: Keep employment while lowering health risk.
    Mechanism: Administrative controls that reduce time at risk. CDC

16. Education on inhaler technique & adherence
    Description: Hands-on teaching to ensure correct device use (MDI with spacer, breath-actuated, DPI).
    Purpose: Maximize benefit from prescribed inhalers.
    Mechanism: Better lung deposition → better control with lower doses. Global Initiative for Asthma – GINA

17. Vaccinations (influenza, pneumococcal as indicated)
    Description: Stay up to date to lower infection-triggered flares.
    Purpose: Prevent exacerbations provoked by respiratory infections.
    Mechanism: Reduces viral/bacterial triggers in vulnerable airways. Global Initiative for Asthma – GINA

18. Emergency preparedness
    Description: Keep reliever inhaler available, know nearest emergency services, and share your action plan with family and supervisors.
    Purpose: Faster treatment during severe episodes.
    Mechanism: Early rescue therapy reduces risk of hospitalization. Global Initiative for Asthma – GINA

19. Allergen and irritant reduction at home
    Description: While RADS is irritant-driven, many patients also react to smoke, sprays, and strong odors; minimize these to reduce day-to-day symptoms.
    Purpose: Lower background airway irritation.
    Mechanism: Less irritant load → calmer airways. Cochrane Complementary Medicine

20. Regular follow-up with lung function testing
    Description: Check spirometry before starting controller therapy, again at 3–6 months, then at least annually.
    Purpose: Track recovery and adjust treatment intensity.
    Mechanism: Objective measures guide step-up/step-down therapy. Global Initiative for Asthma – GINA

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Drug treatments

Important: RADS care usually follows asthma guidelines; some medicines below may be off-label specifically for “RADS,” but are standard for asthma-like airway hyper-responsiveness. Read the official FDA label (linked citations) for dosing, indications, and safety.

1. Albuterol (short-acting β2-agonist, SABA)
   Class & Purpose: Fast “rescue” bronchodilator for quick relief of wheeze and chest tightness.
   Dosage/Time: Inhaled as needed for symptoms; onset in minutes; lasts 3–6 hours (follow label/device instructions).
   Mechanism: Relaxes airway smooth muscle via β2-receptors.
   Side effects: Tremor, palpitations, nervousness. (FDA label example for SABA class in combinations; see maintenance labels noting rescue use alongside controller therapy.) FDAaccessdata

2. Budesonide (inhaled corticosteroid, ICS)
   Purpose: Daily controller to reduce airway inflammation and hyper-responsiveness.
   Dosage/Time: Dose varies by device (nebule/DPI); taken regularly, not for rapid relief.
   Mechanism: Anti-inflammatory; reduces mucosal swelling and mucus.
   Side effects: Oral thrush, hoarseness—rinse mouth after use. FDAaccessdata

3. Beclomethasone (ICS; QVAR RediHaler)
   Purpose: Same as above—daily anti-inflammatory controller.
   Dosage/Time: Twice daily typical; not for acute symptoms.
   Mechanism: Local glucocorticoid action in airways.
   Side effects: Oral candidiasis; dysphonia. FDAaccessdata

4. Mometasone (ICS; Asmanex)
   Purpose: Anti-inflammatory controller.
   Dosage/Time: HFA or Twisthaler forms; regular use is key.
   Mechanism: Reduces airway swelling and reactivity.
   Side effects: Local thrush; rarely systemic steroid effects at high doses. FDAaccessdata+1

5. Fluticasone furoate/vilanterol (ICS/LABA; Breo Ellipta)
   Purpose: Once-daily maintenance for persistent asthma not controlled on ICS alone.
   Dosage/Time: 1 inhalation once daily; use SABA as rescue.
   Mechanism: Anti-inflammatory (ICS) + long bronchodilation (LABA).
   Side effects: Similar to ICS plus LABA effects (e.g., tremor, palpitations); not for acute relief. FDAaccessdata

6. Budesonide/formoterol (ICS/LABA; Symbicort/Symbicort Aerosphere)
   Purpose: Maintenance therapy; certain regimens use as both controller and reliever (per guidelines; follow label where applicable).
   Dosage/Time: Typically 2 inhalations twice daily in labeled use.
   Mechanism: Anti-inflammatory + rapid/long bronchodilation.
   Side effects: As above; not for status asthmaticus. FDAaccessdata+1

7. Tiotropium (LAMA; Spiriva Respimat)
   Purpose: Add-on bronchodilator for asthma not fully controlled on ICS (with/without LABA).
   Dosage/Time: Two inhalations equal one dose; daily.
   Mechanism: Long-acting muscarinic antagonism → airway relaxation.
   Side effects: Dry mouth; avoid spraying in eyes. FDAaccessdata

8. Montelukast (leukotriene receptor antagonist, LTRA)
   Purpose: Nighttime symptoms, exercise-induced bronchospasm, or concomitant allergic rhinitis; boxed warning for serious neuropsychiatric events—use only when benefits outweigh risks.
   Dosage/Time: Once daily in the evening (typical).
   Mechanism: Blocks cysteinyl-leukotriene receptors to reduce bronchoconstriction and inflammation.
   Side effects: Mood/behavior changes, sleep disturbance; FDA advises caution. U.S. Food and Drug Administration+1

9. Prednisone (oral corticosteroid, short course for severe flares)
   Purpose: Short “burst” for significant exacerbations.
   Dosage/Time: Dose and taper individualized; short, time-limited use.
   Mechanism: Systemic anti-inflammatory effect.
   Side effects: Insomnia, hyperglycemia, mood changes, fluid retention; minimize duration. (Use follows asthma standards referenced by GINA.) Global Initiative for Asthma – GINA

10. Fluticasone/salmeterol (ICS/LABA; Advair Diskus/MDI)
    Purpose: Maintenance therapy for persistent asthma.
    Dosage/Time: Twice daily; not for acute relief.
    Mechanism: ICS + LABA synergy to reduce symptoms and flares.
    Side effects: ICS/LABA class effects. FDAaccessdata

11. Ciclesonide (ICS; Alvesco)
    Purpose: Daily controller; pro-drug activated in the lungs.
    Dosage/Time: Once or twice daily per label.
    Mechanism: Local anti-inflammatory activity with potentially lower oropharyngeal deposition.
    Side effects: Similar to other ICS (thrush/hoarseness). (Typical ICS label properties apply.) PMC

12. Levalbuterol (SABA; Xopenex)
    Purpose: Rescue bronchodilator alternative to albuterol.
    Dosage/Time: PRN for symptoms.
    Mechanism: β2-agonist bronchodilation.
    Side effects: Tremor, tachycardia. (SABA class; use per label.) AAFP

13. Ipratropium (short-acting muscarinic antagonist, SAMA)
    Purpose: Adjunct in acute bronchospasm (often in ED settings).
    Dosage/Time: Nebulized or MDI in acute care per protocol.
    Mechanism: Antagonizes muscarinic receptors to relieve bronchospasm.
    Side effects: Dry mouth; bitter taste. (Refer to product labeling.) AAFP

14. Omalizumab (anti-IgE biologic; Xolair)
    Purpose: Add-on for allergic asthma with elevated IgE—RADS often isn’t allergic, so use only when phenotype fits.
    Dosage/Time: Subcutaneous every 2–4 weeks based on weight/IgE.
    Mechanism: Binds IgE to reduce allergic cascade.
    Side effects: Injection reactions; anaphylaxis risk. FDAaccessdata+1

15. Mepolizumab (anti-IL-5; Nucala)
    Purpose: Severe eosinophilic asthma—consider only if eosinophils are high and symptoms persist.
    Dosage/Time: 100 mg SC every 4 weeks (adult asthma; see label).
    Mechanism: Blocks IL-5 → reduces eosinophils.
    Side effects: Headache, injection-site reactions. FDAaccessdata

16. Benralizumab (anti-IL-5 receptor; Fasenra)
    Purpose: Severe eosinophilic asthma (specialist-directed).
    Dosage/Time: SC at 0, 4 weeks, then every 8 weeks.
    Mechanism: IL-5Rα blockade → eosinophil depletion.
    Side effects: Hypersensitivity reactions; not for acute symptoms. FDAaccessdata

17. Reslizumab (anti-IL-5; Cinqair, IV)
    Purpose: Severe eosinophilic asthma; administered IV in clinic.
    Dosage/Time: Weight-based every 4 weeks.
    Mechanism: Neutralizes IL-5 to reduce eosinophilia.
    Side effects: Boxed warning: anaphylaxis (rare). FDAaccessdata+1

18. Dupilumab (anti-IL-4Rα; Dupixent)
    Purpose: Type-2 inflammation asthma (often with high eosinophils or FeNO, or comorbid atopic dermatitis/polyps).
    Dosage/Time: Loading dose then every 2 weeks.
    Mechanism: Blocks IL-4/IL-13 signaling, reducing type-2 airway inflammation.
    Side effects: Injection site reactions; conjunctivitis. FDAaccessdata

19. Tezepelumab (anti-TSLP; Tezspire)
    Purpose: Severe asthma across phenotypes, including non-eosinophilic disease—specialist decision.
    Dosage/Time: 210 mg SC every 4 weeks.
    Mechanism: Blocks TSLP, an upstream alarm cytokine that drives airway inflammation.
    Side effects: Hypersensitivity; avoid live vaccines. FDAaccessdata+1

20. Inhaled reliever with ICS/LABA (where guideline-supported)
    Purpose: Some regimens use low-dose ICS-formoterol as both controller and reliever to cut severe flares; follow local labeling and clinician advice.
    Dosage/Time: As directed by physician.
    Mechanism: Rapid bronchodilation plus immediate micro-dose steroid at each symptom use.
    Side effects: As with ICS/LABA. PMC

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Dietary molecular supplements

Important: Supplements are not a substitute for prescribed therapy. Evidence in asthma is mixed; for RADS (irritant-induced), data are even more limited.

1. Vitamin D
   Description (~150 words): Vitamin D modulates immune pathways. Earlier reviews suggested possible protection against severe attacks; updated Cochrane analyses (2023) found no overall benefit for reducing exacerbations or improving control in typical adults with asthma. In people with very low vitamin D, uncertainty remains, so clinicians may test levels and replete deficiency for general health.
   Dosage: Follow clinician-guided repletion if deficient.
   Function/Mechanism: Immune modulation via vitamin D receptors; uncertain clinical benefit in asthma overall. Cochrane+1

2. Omega-3 fatty acids (EPA/DHA)
   Description: Long-chain omega-3s have anti-inflammatory lipid mediators, but systematic reviews show little consistent benefit for asthma outcomes. A balanced diet with fish may still be healthy.
   Dosage: Food-first approach; supplement only with medical guidance.
   Function/Mechanism: Competes with arachidonic acid pathways; anti-inflammatory mediators (resolvins). Wiley Online Library+1

3. Magnesium (oral)
   Description: IV magnesium helps in severe acute asthma in ED settings; oral magnesium as a daily supplement has inconclusive benefits.
   Dosage: Only with clinician advice; avoid in kidney disease.
   Function/Mechanism: Smooth muscle relaxation and calcium antagonism. Cochrane Library+1

4. N-acetylcysteine (NAC)
   Description: Antioxidant and glutathione precursor; useful in other lung diseases, but not proven helpful for asthma exacerbations and can sometimes irritate airways when nebulized.
   Dosage: If used for another indication, typical oral ranges 600–1200 mg/day, under medical advice.
   Function/Mechanism: Antioxidant replenishment; mucolysis; limited asthma benefit. PMC

5. Probiotics
   Description: For prevention or control of asthma, large reviews show little to no effect; small trials report mixed results. Safe for most, but use caution in immunocompromised people.
   Dosage: Strain-specific; discuss with clinician.
   Function/Mechanism: Gut–lung immune crosstalk; evidence uncertain. Cochrane+1

6. Curcumin (turmeric extract)
   Description: Anti-inflammatory in lab studies; clinical evidence in asthma is limited and not conclusive.
   Dosage: Quality-controlled products only; mind drug interactions.
   Function/Mechanism: Down-regulates NF-κB pathways; uncertain clinical impact. (General evidence base; no strong asthma-specific Cochrane data.) PMC

7. Quercetin
   Description: Flavonoid with antioxidant effects; human asthma data are sparse.
   Dosage: Not standardized for asthma.
   Function/Mechanism: Mast-cell stabilization (theoretical); limited clinical proof. (Evidence in asthma remains preliminary.) PMC

8. Boswellia serrata extracts
   Description: Proposed leukotriene-modulating herb; limited, small studies—use caution due to quality variability.
   Dosage: Not established for asthma.
   Function/Mechanism: 5-lipoxygenase inhibition (theoretical); evidence weak. (Use only with medical guidance.) PMC

9. Bromelain
   Description: Proteolytic enzyme complex from pineapple; anti-inflammatory properties studied, but asthma evidence is minimal.
   Dosage: Variable; watch for bleeding risk with anticoagulants.
   Function/Mechanism: Anti-edema and cytokine modulation; clinical benefit unproven. (Limited human data.) PMC

10. CoQ10
    Description: Antioxidant supporting mitochondrial function; insufficient evidence for asthma control.
    Dosage: Common 100–200 mg/day in other conditions; discuss with a clinician.
    Function/Mechanism: Redox effects; uncertain asthma benefit. (No strong asthma-specific evidence.) PMC

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Immunity-modulating / regenerative drugs

Safety first: There are no FDA-approved “stem-cell drugs” for RADS or asthma. Do not pursue stem-cell infusions outside regulated clinical trials. Instead, in severe asthma phenotypes (which some RADS patients may resemble), specialists may use biologic immunomodulators below. These are add-ons for carefully selected patients—often not first-line for RADS—and they do not replace exposure prevention.

1. Omalizumab (anti-IgE) – for allergic asthma phenotype; reduces exacerbations by neutralizing IgE. Dosed SC every 2–4 weeks per weight/IgE. Key risks: anaphylaxis (rare). FDAaccessdata

2. Mepolizumab (anti-IL-5) – for eosinophilic asthma; SC every 4 weeks; lowers eosinophils and attacks. FDAaccessdata

3. Benralizumab (anti-IL-5Rα) – eosinophil-depleting; SC every 8 weeks after loading; improves control in eosinophilic disease. FDAaccessdata

4. Reslizumab (anti-IL-5, IV) – eosinophilic asthma add-on with boxed anaphylaxis warning; clinic infusion. FDAaccessdata

5. Dupilumab (anti-IL-4Rα) – blocks IL-4/IL-13; useful across type-2 inflammation (often with high eosinophils/FeNO). SC every 2 weeks. FDAaccessdata

6. Tezepelumab (anti-TSLP) – upstream cytokine blocker that works across phenotypes, including non-eosinophilic; SC every 4 weeks. FDAaccessdata

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Procedures / surgeries

Reality check: RADS is not treated by surgery. Very rarely, procedures aimed at severe asthma or comorbid conditions help selected patients. Discuss risks/benefits with specialists.

1. Bronchial thermoplasty (endoscopic, not classic surgery)
   Procedure: Three bronchoscopic sessions use controlled heat to reduce airway smooth muscle.
   Why done: As an add-on for carefully selected adults with severe asthma uncontrolled on maximal therapy.
   Evidence/regulation: FDA-cleared device (Alair). FDAaccessdata

2. Functional endoscopic sinus surgery (FESS) for severe chronic rhinosinusitis/nasal polyps
   Procedure: Endoscopic opening of sinus pathways to improve drainage and polyp removal.
   Why done: To control severe sinonasal disease that worsens lower-airway symptoms; asthma improvements are inconsistent. Archivos de Bronconeumología+1

3. Anti-reflux surgery (e.g., laparoscopic Nissen fundoplication) in proven, severe GERD
   Procedure: Tightens the lower esophageal sphincter to prevent reflux.
   Why done: In selected patients with refractory GERD that appears to trigger asthma symptoms; studies show symptom improvement more than lung function changes. NCBI+1

4. Bariatric surgery (for severe obesity with poor asthma control)
   Procedure: Gastric bypass/sleeve gastrectomy to achieve substantial weight loss.
   Why done: In people with severe obesity where weight reduction improves asthma symptoms, medication needs, and sometimes lung function—data are supportive but heterogeneous. MDPI+1

5. Polypectomy or biologic therapy for nasal polyps (ENT-guided)
   Procedure: Polyp removal or biologic injections per ENT/allergy protocols.
   Why done: Reduce upper-airway inflammatory burden that can aggravate the lower airways. Reuters

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Preventions

1. Avoid the original irritant; ensure workplace elimination/substitution and ventilation upgrades. CDC

2. Keep a written action plan and rescue inhaler available. Global Initiative for Asthma – GINA

3. Don’t smoke or vape; avoid secondhand exposure. ERS Publications

4. Treat rhinitis/sinusitis and GERD if present. Global Initiative for Asthma – GINA

5. Learn breathing techniques; practice during calm periods. Cochrane Library

6. Maintain healthy weight and regular activity. PMC

7. Use PPE correctly when needed; repeat fit-testing. CDC

8. Keep vaccinations current (flu; pneumococcal as indicated). Global Initiative for Asthma – GINA

9. Use HEPA filtering where appropriate; keep good ventilation at home. PMC

10. Schedule regular spirometry and follow-ups. Global Initiative for Asthma – GINA

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When to see doctors

• Immediately / emergency: If you have severe breathlessness, cannot speak full sentences, lips/fingertips turn blue, peak flow is <50% personal best, or rescue inhaler does not help—seek urgent care now. (General asthma emergency guidance per GINA.) Global Initiative for Asthma – GINA

• Soon (appointment): New or worsening symptoms after an irritant exposure; using your rescue inhaler more than 2 days a week; night awakenings; limits in daily activities; or side effects from medicines. You also need review if work conditions still expose you to irritants. (Follow GINA follow-up recommendations.) Global Initiative for Asthma – GINA

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What to eat & what to avoid

1. Balanced diet rich in fruits/vegetables/whole grains; helps weight control and general immunity. (General health advice; weight control helps asthma.) PMC

2. Lean proteins (fish, legumes); oily fish for overall heart health (omega-3 evidence for asthma is mixed). Wiley Online Library

3. Adequate vitamin D through safe sun/foods; supplement only if deficient after testing. Cochrane

4. Limit ultra-processed foods high in salt/sugar (may worsen reflux/weight). PMC

5. Avoid triggers that worsen reflux: late heavy meals, spicy/acidic foods—if you have GERD. NCBI

6. Hydrate well; warm fluids can soothe cough temporarily (supportive). (Symptom comfort; no disease modification.) Global Initiative for Asthma – GINA

7. Limit alcohol if it worsens reflux or sleep. NCBI

8. Caffeine in moderation; excessive intake may aggravate palpitations when using bronchodilators. (Practical safety advice.) Global Initiative for Asthma – GINA

9. Food diary if patterns appear (some people notice sulfites or preservatives worsen symptoms). (Individualized observation.) Global Initiative for Asthma – GINA

10. Focus on sustainable weight loss strategies if needed (diet + activity). Chest Journal

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Frequently Asked Questions

1) Is RADS the same as “reactive airway disease” (RAD)?
No. RADS is a specific, sudden asthma-like illness after a single heavy irritant exposure. “Reactive airway disease” is a vague term sometimes used when asthma is suspected but not confirmed. British Thoracic Society

2) How is RADS diagnosed?
By the exposure history, symptom onset within 24 hours, persistence for months, and objective tests showing variable airflow obstruction or airway hyper-responsiveness. British Thoracic Society

3) Will I have RADS forever?
Some people improve over months; others have persistent sensitivity. Regular follow-up and strict avoidance of the irritant help outcomes. Thorax

4) Do I need the same medicines as asthma patients?
Usually yes—inhaled corticosteroids and reliever bronchodilators are the backbone. Your clinician tailors therapy to your pattern. Global Initiative for Asthma – GINA

5) Are biologics right for RADS?
Only if your disease behaves like severe asthma of a specific phenotype (e.g., eosinophilic). These are specialist decisions. FDAaccessdata

6) Can breathing exercises replace inhalers?
No. They can reduce symptoms and anxiety but do not replace anti-inflammatory therapy when indicated. Cochrane Library

7) Do supplements cure RADS?
No. Evidence for supplements in asthma is limited or mixed; treat deficiencies (e.g., vitamin D) but do not rely on supplements alone. Cochrane

8) What workplace steps protect me?
Follow the hierarchy of controls: elimination, substitution, engineering, administrative, then PPE. This is the safest order. CDC

9) Are HEPA air cleaners useful?
They may help in some contexts but results are mixed—they’re an add-on, not a primary treatment. PMC

10) Why avoid smoking and vaping?
They worsen asthma control and inflame the airways; quitting improves symptoms and lung function. ERS Publications

11) Does weight loss really help?
Yes—modest weight loss can improve control and quality of life in many adults with asthma. Chest Journal

12) Should I wear a mask at work?
Yes if residual exposure exists, but masks are the last line—fix the environment first. CDC

13) Can sinus or reflux surgery fix my lungs?
These surgeries do not treat RADS directly; they may help selected patients with severe comorbid disease. Evidence is mixed. Archivos de Bronconeumología+1

14) Is montelukast safe?
It can help some patients, but the FDA requires a boxed warning about potential serious mental health side effects; discuss risks carefully. U.S. Food and Drug Administration

15) How often should I test my lungs?
Before starting controller therapy, again at 3–6 months, then yearly (or as advised). Global Initiative for Asthma – GINA

Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical  history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.

The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members

Last Updated: November 07, 2025.

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