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.