Occupational COPD

Occupational chronic obstructive pulmonary disease is persistent airflow obstruction caused or worsened by workplace exposure to dusts, gases and fumes. It is clinically and physiologically identical to COPD from smoking.

Epidemiology. Occupational exposure accounts for roughly 15% of COPD overall and a higher share among never smokers. Smoking and work exposure act together.

Exposures. Coal mine dust, silica, cement, cadmium and welding fumes, grain and cotton dust, isocyanates, diesel exhaust, vapours, gases and fumes, and construction and agricultural dusts.

Course. Progressive decline in FEV1 with exacerbations, hospital admission and early mortality when exposure continues.

Complications. Respiratory failure, cor pulmonale, lung cancer, cachexia and cardiovascular disease.

Pathophysiology.

Inhaled particles and gases cause chronic airway inflammation, mucus hypersecretion, small airway remodelling and emphysema through oxidative stress and protease antiprotease imbalance.

Fibrogenic dusts may add parenchymal change. Smoking amplifies these effects.

• Chronic cough, sputum and progressive exertional dyspnoea, with wheeze.
• Symptoms are often worse at work or after high exposure.
• Late disease: hyperinflation, pursed lip breathing, cyanosis and right heart failure signs.

Red flags.

• Haemoptysis, weight loss (cancer, tuberculosis).
• Resting hypoxaemia, hypercapnia, drowsiness or confusion.
• Rapid decline in exercise tolerance.

• Lifetime work history with agents, duration, ventilation and protection; smoking history.
• Post-bronchodilator spirometry: FEV1/FVC under 0.70 (or under the lower limit of normal) confirms obstruction. Grade by FEV1 percent predicted.
• Chest radiograph and CT for emphysema, pneumoconiosis and exclusion of other disease.
• Full lung function with gas transfer; blood eosinophil count; alpha-1 antitrypsin in appropriate patients.
• Arterial blood gas or oximetry for hypoxaemia; sputum for mycobacteria if suggestive.

Differential diagnosis. Asthma, bronchiectasis, bronchiolitis obliterans, pneumoconiosis with airflow obstruction, heart failure, tuberculosis, lung cancer.

• Remove or reduce exposure; smoking cessation; influenza, pneumococcal and COVID-19 vaccination; pulmonary rehabilitation.
• Tiotropium 18 micrograms by dry powder inhaler once daily, long term. Maximum 18 micrograms daily. Monitor dry mouth, urinary retention and glaucoma symptoms. If creatinine clearance is 60 mL/min or less, monitor anticholinergic effects closely.
• Persistent symptoms or exacerbations: combined long acting beta agonist with long acting muscarinic antagonist. Add an inhaled corticosteroid when blood eosinophils are 300 cells/microlitre or more, or exacerbations continue.
• Exacerbation: prednisolone 40 mg orally once daily for 5 days, with no taper. Maximum 40 mg daily. Monitor glucose and blood pressure. Caution in diabetes and peptic ulcer; no renal adjustment.
• Exacerbation with purulent sputum: doxycycline 200 mg orally on day 1, then 100 mg once daily for 4 days (5 days in total). Maximum 200 mg daily. Avoid in pregnancy; no renal adjustment; take upright with water.
• Long term oxygen when resting PaO2 is under 7.3 kPa, or 7.3 to 8 kPa with polycythaemia or cor pulmonale.
• Select patients: lung volume reduction or transplant assessment.

Monitoring. Spirometry and symptom review at least yearly; review after each exacerbation.

Referral and escalation. Respiratory and occupational physician; urgent admission for hypoxia, hypercapnia or severe exacerbation; notification and compensation where required.

Special groups. Older adults need review of inhaler technique and anticholinergic burden.