Rates of silicosis and other pneumoconiosis have declined in the past several decades as control measures have reduced occupational dust exposures in settings such as underground mines and exposures to agents such as asbestos.1 Meanwhile, occupational asthma (OA) has been reported to be the most common chronic occupational lung disease in many developed countries, with epidemiological studies estimating an occupational cause to about 15% of all adult-onset asthma in the working population.2

As with all occupational diseases, OA is potentially preventable3: it mostly follows sensitisation to high-molecular or low-molecular weight sensitising agents in a susceptible subpopulation of exposed workers.4 Primary prevention (elimination or reduction of exposure in the workplace) effectively reduces OA. Although genetic and other host factors predispose to development of sensitisation and OA, knowledge of these factors is insufficient to screen out workers from exposure to specific sensitisers. Secondary prevention, when exposure to sensitisers cannot be eliminated, includes formal medical surveillance to detect affected workers early, at a time …