Occupational asthma

Overview

•Most common occupational lung disease in the UK - accounts for ~1 in 6 cases of adult-onset asthma

•Key distinction: workplace is the cause (not just aggravator) of asthma - distinguishes it from work-aggravated asthma

Risk Factors

Presentation

•Wheeze, dyspnoea, cough, chest tightness - mirrors non-occupational asthma

•Symptoms improve on days off/holidays and worsen on return to work - most diagnostically useful pattern

•Late asthmatic reaction - symptoms may be delayed 4-8 hours after exposure, causing missed occupational link

•Rhinitis and conjunctivitis frequently co-exist, especially with high-molecular-weight sensitisers

💡

Always ask: "Are your symptoms better on days off or during holidays?" A positive answer in a worker with adult-onset asthma should prompt immediate investigation for occupational asthma.

Investigations

🥇 First-line

•Serial peak expiratory flow (PEF) monitoring - at least 4 readings/day over 4 weeks (minimum 3 weeks at work, 1 week away); lower readings at work with recovery away confirms occupational link

•Spirometry with bronchodilator reversibility - confirms variable airflow obstruction (FEV1/FVC <0.7, ≥12% and ≥200 mL improvement post-bronchodilator)

•Skin-prick testing or specific serum IgE - identifies IgE-mediated sensitisation to high-molecular-weight agents

•FeNO - raised FeNO supports eosinophilic airway inflammation; can be measured at work and away

🏆 Gold standard

•Specific inhalation challenge (SIC) - controlled exposure to suspected agent in specialist centre with serial spirometry; used when diagnosis remains uncertain

Management

🥇 First-line

•Complete removal from exposure - single most effective intervention; earlier removal = greater chance of recovery

•Standard asthma pharmacotherapy: salbutamol 100-200 micrograms inhaled as needed (SABA) + beclometasone dipropionate 200-400 micrograms daily (ICS preventer); step up per BTS/NICE/SIGN

🥈 Second-line

•Workplace modifications - engineering controls (local exhaust ventilation), substitution of agent, respiratory protective equipment (RPE); RPE alone is not sufficient long-term

•Referral to specialist occupational/respiratory physician for SIC, fitness-for-work assessment, medicolegal support

🥉 Third-line

•Biologic therapy (e.g. anti-IL-5) for severe refractory disease persisting despite removal and optimised pharmacotherapy

📌

Occupational asthma is reportable under RIDDOR - employers must report confirmed cases to the HSE. Patients may be entitled to Industrial Injuries Disablement Benefit (IIDB) if the causative agent is on the prescribed list.

Mechanisms

Sensitiser-induced vs irritant-induced occupational asthma

Feature	Sensitiser-induced (most common)	Irritant-induced (RADS)
Mechanism	IgE-mediated (HMW) or cell-mediated (LMW)	Direct epithelial injury
Latency period	Months to years	None - single high-intensity exposure
Sensitisation required	Yes	No
Example agents	Flour, latex, isocyanates, animal dander	Chlorine gas, chemical spill, smoke

Prognosis and Complications

•Early removal (within 1-2 years of symptom onset) offers best chance of complete or near-complete lung function recovery

•Fixed airflow obstruction - continued exposure leads to irreversible airway remodelling and COPD-like disease even after eventual removal

•~1 in 6 patients with occupational asthma meet criteria for severe asthma

•Worse prognosis: longer duration to removal, more severe obstruction at diagnosis, continued smoking, older age