Two employees of the same mushroom farm presented to our hospital within a 5-month period. The farm is a large commercial producer of Agaricus bisporus mushrooms. Both workers were employed in the spawning shed, where mushroom compost is tipped onto a conveyor belt for mushroom spawn (sterilised grain inoculated with mushroom mycelia) distribution. The process is associated with increased levels of ambient organic dust.1 The principal means of minimising organic dust in the shed was local exhaust ventilation. Neither worker recalled receiving instructions about respiratory protection or the specific hazard of organic dust exposure during their employee-induction process.

Mushroom cultivation in Australia is a large agricultural industry, employing over 2500 people,2 yet mushroom worker’s lung has not previously been reported in the Australian medical literature, nor to an occupational lung disease notification scheme.3 It is likely that there is considerable under-recognition of this condition, as it is estimated that 5%–15% of those exposed to the causative antigens may develop hypersensitivity pneumonitis.4 In the largest cross-sectional study of workers at an Agaricus mushroom farm, 20% of those heavily exposed to organic dust reported experiencing symptoms consistent with mushroom worker’s lung.5 Unfortunately, with no thorough epidemiological studies, specifically cohort studies, it is not possible to estimate the true incidence of respiratory disease in mushroom farm workers.

Several outbreaks of mushroom worker’s lung have been reported in the international literature since the 1950s. Workers with high exposure to organic dust from mushroom compost, such as spawners and compost handlers, are commonly affected and hence the more specific term “mushroom compost worker’s lung” is occasionally used.1,6 In this form of mushroom worker’s lung, M. faeni (currently known as Saccharopolyspora rectivirgula of the class Thermoactinomycetes), which is present in mushroom compost, is the most commonly implicated allergen.1,5,7 Organic dust from mushroom compost consists of a vast array of microorganisms and organic antigens; failure to demonstrate precipitins to M. faeni, as in the patients reported here, does not exclude the diagnosis of mushroom worker’s lung.1,4,8

Japanese mushroom farm workers have been reported to suffer an alarmingly high incidence of allergic respiratory disease.9,10 In a 3-year follow-up study by Tanaka et al, 40% of workers left the industry due to intolerable respiratory symptoms.10 Japanese mushroom varieties such as Hypsizygus marmoreus (Bunashimeji) are grown on wet wood dust rather than compost and release billions of spores 4–6 μm in diameter before being harvested.10,11 The inhaled mushroom spore (rather than Thermoactinomycetes) is the causative allergen in this setting, with the term “mushroom picker’s lung” used to more accurately describe the group of workers at risk of this form of mushroom worker’s lung.11 Although commercial cultivation of “exotic” mushrooms in Australia is small (1000 tonnes per year compared with 52 250 tonnes of Agaricus mushrooms), as demand for and cultivation of these mushrooms increases, employers must be aware of the significant hazard posed by these varieties when developing safe work practices.2

The most important component of identifying hypersensitivity pneumonitis is recognition of exposure to a causative antigen, reinforcing the importance of a thorough occupational history, and identification of workplace hazards (Box 4).7,12 A temporal relationship between the development of symptoms (cough, fever, chills, dyspnoea, chest tightness and malaise) 4–8 hours after the start of exposure, and an improvement during weekends or vacations, is quite indicative of this condition.4,8 Organic dust toxic syndrome, a form of inhalation fever, may be difficult to differentiate from acute hypersensitivity pneumonitis and is estimated to be 30–50 times more common.12 Organic dust toxic syndrome may result from a single heavy exposure to organic dust, and is self-limiting, with symptoms rarely exceeding 36 hours.8

Optimal management of hypersensitivity pneumonitis requires early recognition and complete avoidance of further exposure to the causative antigen;8,7,12 a change of occupation may be necessary. Although corticosteroid therapy has been shown to result in more rapid improvement in lung function and may be warranted in severely unwell patients, it has not been shown to improve long-term outcomes.9 Recurrence of acute hypersensitivity pneumonitis is more common in patients treated with steroids; this may be due to their improved sense of wellbeing and less stringent adherence to antigen avoidance.8,13

The natural history of hypersensitivity pneumonitis has been poorly described, primarily due to a lack of longitudinal studies.8 With repeated acute or chronic low-level exposure in farmer’s lung, permanent lung damage caused by pulmonary fibrosis and emphysema has been shown to occur, with associated chronic dyspnoea and permanent impairment.8,9 Even patients who remain asymptomatic may have long-term physiological sequelae.8

Australian occupational health and safety legislation describes in broad terms employers’ responsibilities to ensure every reasonable action is taken to preserve the health and safety of workers. Obligations to control hazardous non-organic substances, such as isocyanates and silica, are further described by subordinate Occupational Health and Safety (Hazardous Substances) Regulations (Vic) and the accompanying Hazardous Substances Code of Practice. Despite organic dust clearly having the potential to harm human health, the requirement to control organic dust falls outside the domain of hazardous substance legislation in Australia. Therefore, for their duty of care to be discharged, employers in the agricultural sector must demonstrate due diligence in their identification and control of all workplace hazards, including organic dust.

The National Occupational Health and Safety Commission (now known as the Australian Safety and Compensation Council) has established limits for some organic dusts, such as cotton.14 However, organic dust in most agricultural settings is a complex and variable mixture of constituents, impairing the ability to set useful standards.8 Episodic high concentrations of dust exposure, rather than static ambient levels, may precipitate respiratory diseases, further increasing the difficulty of determining “safe” exposure standards. These factors impair our ability to advise employers how best to control this hazard. It is also difficult to determine what can reasonably be expected of employers as far as monitoring is concerned. Urgent research has been called for in this area by the American Thoracic Society.8

Employers in agricultural industries should demonstrate awareness of the hazard of organic dust, and aim to reduce exposure levels using the “as low as reasonably practicable” (ALARP) principle. Mushroom farm workers specifically should be educated about the risk of developing hypersensitivity pneumonitis and be advised of the symptoms and warning signs.5

1 Lung imaging — Patient 1

A: High resolution computed tomography (HRCT) scan of the chest of Patient 1 at presentation showing small, ill-defined centrilobular ground-glass nodules < 5 mm in diameter. Scans of the lower zones (not shown) revealed more confluent areas of ground-glass opacity, without discrete nodules. B: Repeat HRCT scan performed 1 month later (1 month without workplace exposure) showing significant improvement, but with persistence of tiny centrilobular nodules, particularly in the upper zones.

3 Lung imaging — Patient 2

High resolution computed tomography scan of Patient 2 at presentation, showing normal upper lobes (A) and patchy, centrilobular ground-glass opacities, with expiratory subsegmental air- trapping at the lung bases (B, C). This is a non-specific pattern, compatible with hypersensitivity pneumonitis.