Occupational Asthma

Occupational Asthma

Work-related asthma includes both asthma that has been caused by work (occupational asthma) and asthma that is exacerbated by work (work-exacerbated asthma). Work-related asthma is a common occupational lung disease. International estimates indicate that up to 25% of adults have work-related asthma and 15% of adult-onset asthma may be caused by hazardous occupational exposures (Hoy et al. 2017).

Work-related asthma tends to be more severe than non-work related asthma, with the potential for higher higher medication use, reduced asthma control, more rapid decline in lung function and greater socio-economic impact (Hoy et al. 2017). Occupational exposure to a range of compounds is associated with severe asthma attacks (Henneberger et al. 2015; Kim et al. 2016). However, to our knowledge no studies have specifically investigated links between work-related asthma and severe, treatment-refractory asthma.

Occupational asthma can be subdivided into sensitiser-induced and irritant-induced subtypes. Approximately 90% of cases are classified as sensitiser-induced occupational asthma. Sensitisers are agents that induce an immunological response after repeated exposures. Over 300 workplace agents have been described as causes of occupational asthma (see list here). Following development of sensitiser-induced occupational asthma, exposure to the inciting sensitiser will cause an asthma response, even at a low level of exposure. Irritant-induced occupational asthma is non-immune, resulting from exposure of the airways to irritant substances, typically at a high level such as following an industrial accident.

Sensitisers can be subdivided into 2 types:

• High molecular weight – includes proteins, with the most common being wheat flour, animal antigens and wood dust. Typically stimulate allergic immune responses, with activation of Type-2 and eosinophilic airway inflammation. For more on pathophysiology click here
• Low molecular weight – includes chemicals, such as diisocyanates, and wood dust. The immune response is less understood but can contribute to eosinophilic or neutrophilic airway inflammation.

• Occupational exposure to a respiratory sensitiser, in particular the level of exposure
• Pre-existing atopy
• Genetic pre-disposition
• Smoking status
• Occupational rhinitis, which often precedes symptoms of occupational asthma

Diagnosis of occupational asthma requires objective confirmation of the diagnosis of asthma and demonstration of an association between asthma and the workplace. The diagnosis should be made as early as possible because ongoing exposure to the causative agent at the workplace is likely to result in asthma becoming more severe, leading to rapid lung function decline (Anees et al. 2006). The diagnosis must be made accurately due to the potential negative socioeconomic implications of the management of the condition, therefore should be confirmed by a specialist with expertise in occupational asthma.

Diagnosis of occupational asthma requires a combination of investigations:

Once the diagnosis has been confirmed by a specialist, pharmacological management of occupational asthma includes a stepped approach to treatment based on asthma management guidelines.

The most important aspect of the management of sensitiser-induced occupational asthma is avoidance of the sensitiser. In some circumstances this may require relocation of the worker within the workplace or even a change of workplace. This process may require involvement of the workers compensation system. If a worker continues to work with ongoing exposure to the sensitiser they require close monitoring including regular performance of spirometry. Use of respiratory protection alone has not been demonstrated to provide sufficient protection for workers with occupational asthma.

Identification of one worker with occupational asthma indicates that other workers are at risk and there are likely to have been failings in the identification and control of respiratory hazards at the workplace. If the patient consents, there should be communication with the employer regarding the diagnosis and implementation of a review of hazard control measures.

To watch a seminar on occupational asthma on the Centre of Excellence in Severe Asthma website, click here.

For workers with sensitiser-induced occupational asthma, complete avoidance of the exposure is often necessary to improve symptoms (BMJ Best Practice). Ongoing exposure to the sensitiser is likely to lead to a progressive worsening of asthma outcomes. Improvement is generally seen within 2 years of removing the exposure, but can take up to 10 years. People with an early diagnosis of occupational asthma and shorter durations of sensitiser exposure are more likely to have improved outcomes.

For workers with irritant-induced occupational asthma, symptoms may resolve within months to year or may persist long-term. If affected people do return to work, ongoing monitoring is important to manage disease exacerbations.

However, to our knowledge no studies have specifically reported on outcomes for people with work-related asthma and severe, treatment-refractory asthma, so prognosis in this population remains unclear.