Malt Worker's Lung

Malt worker's lung is hypersensitivity pneumonitis caused by inhaling spores of Aspergillus clavatus (and sometimes Aspergillus fumigatus) from mouldy barley during malting.

Exposure. Malt houses, maltings, breweries and distilleries during germination, kilning and handling of moist barley.

Epidemiology. Uncommon and linked to poorly controlled mould growth in damp grain. Cases occur in clusters.

Forms. Acute, subacute and chronic. Chronic disease leads to fibrosis and obstruction.

Differences from malt asthma. Malt dust can also cause occupational asthma from barley proteins, which differs clinically from pneumonitis.

Pathophysiology.

Aspergillus spores are inhaled in high number in warm, humid malting conditions. In sensitised people, immune complexes and T helper 1 responses cause granulomatous bronchiolitis and alveolitis.

Continued exposure results in interstitial fibrosis, with traction bronchiectasis and honeycombing in chronic cases.

• Acute: fever, chills, cough, dyspnoea and malaise 4 to 8 hours after exposure, settling over 1 to 3 days.
• Subacute and chronic: progressive dyspnoea, cough, fatigue and weight loss.
• Basal crackles, and clubbing in fibrotic disease.

Red flags.

• Hypoxaemia at rest or rapid deterioration.
• Weight loss, haemoptysis or progressive fibrosis.

• Exposure history including grain moisture, malting stage and mould.
• HRCT: ground glass centrilobular nodules, mosaic attenuation with air trapping, fibrosis in chronic disease.
• Spirometry with gas transfer: restrictive or mixed, reduced DLCO.
• Serum IgG precipitins to Aspergillus clavatus show exposure; lack of antibodies does not exclude disease.
• Bronchoalveolar lavage lymphocytosis over 20 to 30%.
• Biopsy when atypical; exclude tuberculosis and fungal infection.

Differential diagnosis. Allergic bronchopulmonary aspergillosis, organic dust toxic syndrome, malt related occupational asthma, sarcoidosis, other hypersensitivity pneumonitis, idiopathic pulmonary fibrosis, infection.

• Avoid the antigen. Remove from malting areas or control mould by drying grain, ventilation and enclosure; respirators as an adjunct.
• Prednisolone 0.5 mg/kg orally once daily in the morning, maximum 40 mg daily, for 4 weeks. If symptoms, spirometry, gas transfer and imaging improve, taper to the lowest effective dose over 8 to 12 weeks, then stop. If there is no improvement, taper over 2 weeks and reconsider the diagnosis. Monitor glucose, blood pressure, weight, mood and infection, with bone protection if therapy exceeds 3 months. Exclude active tuberculosis first. Caution in diabetes and peptic ulcer; no renal adjustment.
• Chronic fibrotic disease with progression: nintedanib 150 mg orally twice daily with food, long term. Maximum 300 mg daily; reduce to 100 mg twice daily for adverse effects or mild hepatic impairment. Monitor liver enzymes monthly for 3 months, then every 3 months; manage diarrhoea. Avoid in moderate or severe hepatic impairment and in pregnancy; avoid when eGFR is under 30.
• Long term oxygen when resting PaO2 is under 7.3 kPa, or 7.3 to 8 kPa with polycythaemia or cor pulmonale.
• Lung transplant assessment in advanced fibrosis.

Monitoring. Symptoms, spirometry and gas transfer at 4 to 6 weeks, then every 3 to 6 months; HRCT at 6 to 12 months.

Referral and escalation. Respiratory and occupational physician; workplace mould assessment; transplant assessment for advanced disease; notification and compensation where required.