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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 when asthma may resolve with removal from further exposure. Additionally, health practitioners who care for patients with asthma can play a role by garnering early suspicion of OA and initiation of appropriate diagnostic tests, or referral to specialists.
Despite good rationale for these measures, as with most occupational interventions, there are no randomised control trials to confirm effectiveness, and most evaluation studies have relied on time series. Difficulties in the interpretation of these studies within individual workplaces include the frequent application of more than one intervention during the same time period (eg, concurrent reduction in worker exposures, improved education of the workforce and medical surveillance). Additionally, most have included relatively small numbers of workers with OA.
The report from Stocks and colleagues5 provides an interesting examination of time trends in the incidence of several occupational diseases, including OA, across several European countries between 2000 and 2012. Eight countries were included after excluding one that did not separate reporting of asthma from other occupational respiratory diseases. Different reporting schemes were used in the different countries, and included six physician-reporting data sets from four countries and compensation data sets from six countries, including more than one data set from four of the countries. The authors aimed to be as inclusive as possible and exceptions to case definitions were therefore allowed. Adjustments were made for changes during this time period in compensation rules or reporting methods.
Among the different countries, the authors found a small overall reduction in estimated annual recognised compensation OA claims ranging from 3.8% in Italy to 1.7% in the Czech Republic. Similarly, there was a fall in incidence of OA among the physician-reported datasets, ranging from 14.8% in France to 0.8% in the Netherlands's occupational physician reporting system.
These findings may be a reason for cautious optimism as to possible benefit from preventive measures for OA (as previously suggested with exposure control regulations in the UK.6 ,7) Nevertheless, as the authors discuss, there are several limitations to the interpretation of their findings. Reductions over time for all the occupational diseases within the physician-reported data sets may have occurred in part due to ‘reporting fatigue’ over this period, from competing demands for physician time. In addition, there likely continues to be general under-recognition of OA and therefore both physician-reported and compensation data almost certainly underestimate true rates of disease. An additional factor that can reduce incidence rates of compensated claims is the fear of job loss in economic situations where a different job may be difficult to obtain. Also, for some patients, early recognition of OA through medical surveillance, and transfer to a different job area away from exposure but with the same employer, may result in clearing of asthma and lack of initiation of a compensation claim. Conversely, physician reports may include unconfirmed cases. Data in this report did not include information regarding preventive interventions during this period in the various countries, or data on individual causes of OA.
These European results are consistent with other reports,8 ,9 and with our findings from workers’ compensation claims in Ontario, Canada, between 1980 and 2007,10 where there were initial rises in yearly total OA accepted claims to a peak of over 90 accepted claims per year between 1988 and 1990, and a fall to 25 or less per year by 2005–2007. The most common single cause in Ontario, diisocyanate-induced OA, fell from over 50% of the accepted OA claims at the peak (ie, over 50/year), down to 4–8/year in the last few years of this period, concurrent with preventive interventions.10 Conversely, asthma exacerbated but not caused by work11 (compensable in Ontario but not in most other compensation systems), rose markedly in Ontario during this period to >70% of accepted claims,12 and suggests that this also should be a focus for future preventive measures.
Acknowledgments
The author would like to thank Dr Gary Liss, MD, for helpful discussion.
References
Footnotes
Competing interests None.
Provenance and peer review Commissioned; internally peer reviewed.