Key Facts

Occupational lung diseases encompass a range of respiratory conditions caused or exacerbated by inhalation of dusts, fumes, gases, or biological agents in the workplace. They represent a significant public health burden with many being preventable.

Epidemiology

• Occupational lung disease accounts for ~15% of COPD and ~15% of asthma cases
• Occupational asthma: ~3,000 new cases per year in the UK (most commonly reported occupational lung disease)
• Mesothelioma: ~2,700 cases/year (UK highest incidence globally)
• Asbestosis: declining incidence as asbestos use banned since 1999
• Silicosis: re-emerging with artificial stone/engineered quartz worktop industry

Aetiology

Pneumoconioses (mineral dust):

• Asbestosis (asbestos), silicosis (silica), coal workers' pneumoconiosis (coal dust), berylliosis (beryllium)

Occupational asthma:

• Sensitiser-induced: isocyanates (spray painting), flour/grain (bakers), wood dust, latex, laboratory animals, colophony (soldering)
• Irritant-induced (RADS): single high-level irritant exposure

Other:

• Byssinosis (cotton dust), hypersensitivity pneumonitis (farmer's lung, bird fancier's lung), COPD (mining, welding)

Pathophysiology

• Pneumoconioses: inhaled mineral particles reach alveoli → phagocytosed by macrophages → chronic inflammation → fibrosis; pattern depends on dust type and deposition site
• Occupational asthma: IgE-mediated or T-cell-mediated sensitisation to workplace allergen → airway inflammation and hyperreactivity
• Silicosis: silica particles are directly cytotoxic to macrophages → release of fibrogenic cytokines → progressive nodular fibrosis

Occupational Asthma

• Work-related symptoms: wheeze, cough, breathlessness improving on days away from work/holidays
• Latent period of sensitisation (weeks to years)
• May persist after removal from exposure

Asbestosis

• Progressive breathlessness
• Bibasal fine inspiratory crackles
• Finger clubbing
• Latency: 15-30 years

Silicosis

• Progressive breathlessness, dry cough
• Upper lobe predominant nodular fibrosis
• Accelerated/acute silicosis with high-level exposure
• Increased risk of TB (silico-tuberculosis)

Coal Workers' Pneumoconiosis

• Usually asymptomatic (simple CWP)
• Progressive massive fibrosis (PMF): severe breathlessness, melanoptysis (black sputum)
• Caplan syndrome: CWP + RA → large necrobiotic lung nodules

Red Flags

• Progressive fibrosis despite removal from exposure
• Haemoptysis in asbestos-exposed worker (mesothelioma/lung cancer risk)
• New respiratory symptoms related to workplace
• Accelerated silicosis (rapid progression)
• Symptoms of mesothelioma in asbestos-exposed

Bedside

• Detailed occupational history: essential; chronological job history, specific exposures, use of PPE
• Serial peak flow monitoring: 2-4 hourly for ≥4 weeks including time at and away from work (OASYS-2 analysis) — gold standard for occupational asthma
• Pulse oximetry: baseline

Bloods

• FBC: anaemia, eosinophilia
• CRP/ESR: may be elevated
• Autoimmune screen: if sarcoidosis or berylliosis suspected
• Specific IgE: to occupational allergens (e.g. latex, flour)

Imaging

• CXR: nodular opacities (silicosis, CWP), interstitial fibrosis (asbestosis), pleural plaques (asbestos), eggshell calcification (silicosis)
• HRCT: more sensitive than CXR; characterise pattern and distribution of disease

Special Tests

• Spirometry: restrictive (pneumoconiosis/fibrosis) or obstructive (occupational asthma/COPD)
• TLCO: reduced in fibrotic disease
• Specific inhalation challenge testing: gold standard for confirming sensitiser-induced occupational asthma (specialist centres only)
• Skin prick testing: if high molecular weight sensitiser (flour, latex, animal proteins)
• Beryllium lymphocyte proliferation test (BeLPT): for berylliosis
• BAL: asbestos bodies (ferruginous bodies) support asbestos exposure
• Lung biopsy: rarely needed; may show characteristic features (silicotic nodules, asbestos bodies)

Non-pharmacological

• Removal from exposure: most important intervention for occupational asthma (early removal improves prognosis)
• Workplace modifications: improved ventilation, dust suppression, PPE
• Health surveillance: ongoing monitoring for exposed workers (spirometry, symptom questionnaires)
• Smoking cessation: synergistic effect of smoking + occupational exposure (especially asbestos + smoking → 50× lung cancer risk)
• RIDDOR reporting: employer obligation for prescribed occupational diseases

Pharmacological

• Occupational asthma: standard asthma stepwise therapy (ICS, LABA, SABA PRN); does NOT replace exposure removal
• Silicosis/asbestosis: no specific treatment; supportive management, treat complications
• Silico-tuberculosis: standard TB treatment
• Berylliosis: corticosteroids (similar to sarcoidosis)

Surgical/Interventional

• Lung transplantation for end-stage occupational fibrosis
• Whole lung lavage: experimental treatment for silicosis

Referral Criteria

• All suspected occupational lung disease: refer to occupational lung disease specialist
• Industrial Injuries Disablement Benefit application
• Medico-legal assessment if litigation
• HSE notification for prescribed diseases

• Occupational asthma: ~30% fully recover if removed early from exposure; ~70% have persistent symptoms if exposure continues
• Asbestosis: progressive fibrosis; no reversal; increased lung cancer (especially with smoking) and mesothelioma risk
• Silicosis: progressive even after exposure ceases; increased TB risk; accelerated silicosis carries very poor prognosis
• CWP: simple CWP — stable; PMF — progressive and disabling
• Coal/silica-exposed workers with PMF: reduced life expectancy
• Prevention is key — workplace exposure controls are most effective intervention

Occupational Lung Disease Classification

Prescribed Occupational Diseases (IIDB)

Asbestos-Related Disease Spectrum