Wood Dust-Induced Asthma

Wood dust induced asthma is occupational asthma caused by sensitisation to wood dust, most often western red cedar (plicatic acid) and several tropical hardwoods. Many cases are not IgE-mediated.

Exposure. Sawmilling, carpentry, joinery, furniture making, flooring, boat building, and cedar shingle and cabinet work.

Epidemiology. Wood dust is a recognised cause of occupational asthma in woodworkers. Western red cedar asthma affects an appreciable minority of exposed workers in older cohorts.

Causative woods. Western red cedar, iroko, mahogany, ramin, obeche, abachi, oak, redwood and others. Contaminating moulds and preservatives also contribute.

Other wood dust disease. Rhinitis, hypersensitivity pneumonitis, dermatitis, and sinonasal adenocarcinoma with hardwood dust exposure.

Pathophysiology.

Plicatic acid acts as a hapten, binding proteins to form an antigen. Specific IgE is found in only a minority, so cell mediated and other immune mechanisms are considered important.

Other woods contain sensitising proteins and chemicals that drive IgE-mediated reactions. Persistent exposure leads to eosinophilic airway inflammation and remodelling.

• Cough, wheeze and chest tightness, often delayed until evening or night after work, with improvement on days off.
• Rhinitis and eye irritation often precede asthma.
• Late or dual asthmatic responses are common with western red cedar.

Red flags.

• Unilateral nasal obstruction, bloody discharge, epistaxis or facial swelling (sinonasal cancer).
• Severe attacks, or persistent symptoms despite treatment.

• Work history including wood species, tasks, ventilation and protection.
• Spirometry with reversibility, or methacholine challenge (PC20 under 8 mg/mL suggests asthma).
• Serial peak flow at least 4 times daily over at least 2 weeks at work and 2 weeks away.
• Specific IgE and skin tests are available for some woods but are not reliable for western red cedar.
• Specific inhalation challenge in a specialist centre; a fall in FEV1 of 20% or more is positive.
• Persistent nasal symptoms in hardwood workers need nasal endoscopy.

Differential diagnosis. Work exacerbated asthma, irritant induced asthma, hypersensitivity pneumonitis, chronic obstructive pulmonary disease, vocal cord dysfunction, chronic rhinosinusitis.

• Remove from exposure promptly. Engineering controls, local exhaust ventilation and wet methods reduce dust; respirators are an adjunct.
• Budesonide with formoterol 200/6 micrograms inhaled, 1 inhalation twice daily as maintenance plus 1 inhalation as needed (adults and adolescents 12 and over). Usual maximum 8 inhalations in 24 hours, up to 12 for a short period. Monitor symptoms, spirometry, exacerbations and oral candidiasis; rinse mouth after use. No renal adjustment; step up or down by control.
• Exacerbation: salbutamol 100 microgram metered dose through a spacer, 4 to 10 puffs, repeated every 20 minutes for the first hour, then every 4 hours as needed. Maximum 10 puffs each dose. Monitor heart rate, potassium and oxygen saturation. Caution in arrhythmia and hyperthyroidism.
• Exacerbation: prednisolone 40 to 50 mg orally once daily for 5 days, with no taper. Maximum 50 mg daily. Monitor glucose and blood pressure. Caution in diabetes and peptic ulcer; acceptable in pregnancy when needed; no renal adjustment.
• Sensitised workers who stay in exposure often worsen; persistence of asthma after removal is common.

Monitoring. Review every 3 months initially with spirometry; yearly nasal symptom review in hardwood workers.

Referral and escalation. Respiratory and occupational physician; ENT referral for persistent unilateral nasal symptoms; workplace assessment; notification and compensation where required.

Special groups. Pregnancy: continue inhaled corticosteroid and avoid exposure.