Downloaded from http://oem.bmj.com/ on November 13, 2015 - Published by group.bmj.com
Commentary
Trends in incidence of occupational asthma Susan M Tarlo 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 Department of Medicine, University of Toronto, Toronto Western Hospital, Toronto, Ontario, Canada Correspondence to Dr Susan M Tarlo, Toronto Western Hospital, EW7-449, 399 Bathurst St, Toronto, Ontario, Canada M5T 2S8; [email protected] 688
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 lowmolecular 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. Occup Environ Med October 2015 Vol 72 No 10
Downloaded from http://oem.bmj.com/ on November 13, 2015 - Published by group.bmj.com
Commentary 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 com-
Occup Environ Med October 2015 Vol 72 No 10
pensated 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. Acknowledgements The author would like to thank Dr Gary Liss, MD, for helpful discussion.
Received 25 February 2015 Accepted 25 March 2015 Published Online First 20 April 2015 Occup Environ Med 2015;72:688–689. doi:10.1136/oemed-2015-102852
REFERENCES 1
2
3 4 5
6
7
8
9
10
Competing interests None. Provenance and peer review Commissioned; internally peer reviewed.
11
12
National Institute for Occupational Safety and Health Public Health Service Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, Division of Respiratory Disease Studies, Surveillance Branch. Work-Related Lung Disease Surveillance System (eWoRLD). Secondary Work-Related Lung Disease Surveillance System (eWoRLD). 2014. http://wwwn.cdc.gov/eworld/ Grouping/All_Pneumoconioses/91 Toren K, Blanc PD. Asthma caused by occupational exposures is common—a systematic analysis of estimates of the population-attributable fraction. BMC Pulm Med 2009;9:7. Tarlo SM, Liss GM. Prevention of occupational asthma. Curr Allergy Asthma Rep 2010;10:278–86. Tarlo SM, Lemiere C. Occupational asthma. N Engl J Med 2014;370:640–9. Stocks S, McNamee R, van der Molen H, et al. Trends in incidence of occupational asthma, contact dermatitis, noise-induced hearing loss, carpal tunnel syndrome and upper limb musculoskeletal disorders in European countries from 2000 to 2012. Occup Environ Med 2015;72:294–303. Stocks SJ, McNamee R, Turner S, et al. Assessing the impact of national level interventions on workplace respiratory disease in the UK: part 1–changes in workplace exposure legislation and market forces. Occup Environ Med 2013;70:476–82. Stocks SJ, McNamee R, Turner S, et al. Assessing the impact of national level interventions on workplace respiratory disease in the UK: part 2–regulatory activity by the Health and Safety Executive. Occup Environ Med 2013;70:483–90. Vandenplas O, Lantin AC, D’Alpaos V, et al. Time trends in occupational asthma in Belgium. Respir Med 2011;105:1364–72. Paris C, Ngatchou-Wandji J, Luc A, et al. Workrelated asthma in France: recent trends for the period 2001–2009. Occup Environ Med 2012;69: 391–7. Ribeiro M, Tarlo SM, Czyrka A, et al. Diisocyanate and non-diisocyanate sensitizer-induced occupational asthma frequency during 2003 to 2007 in Ontario, Canada. J Occup Environ Med 2014;56:1001–7. Henneberger PK, Redlich CA, Callahan DB, et al. An official American Thoracic Society statement: work-exacerbated asthma. Am J Respir Crit Care Med 2011;184:368–78. Lim T, Liss GM, Vernich L, et al. Work-exacerbated asthma in a workers’ compensation population. Occup Med (Lond) 2014;64:206–10.
To cite Tarlo SM. Occup Environ Med 2015;72:688– 689.
689
Downloaded from http://oem.bmj.com/ on November 13, 2015 - Published by group.bmj.com
Trends in incidence of occupational asthma Susan M Tarlo Occup Environ Med 2015 72: 688-689 originally published online April 20, 2015
doi: 10.1136/oemed-2015-102852 Updated information and services can be found at: http://oem.bmj.com/content/72/10/688
These include:
References Email alerting service
This article cites 11 articles, 5 of which you can access for free at: http://oem.bmj.com/content/72/10/688#BIBL Receive free email alerts when new articles cite this article. Sign up in the box at the top right corner of the online article.
Notes
To request permissions go to: http://group.bmj.com/group/rights-licensing/permissions To order reprints go to: http://journals.bmj.com/cgi/reprintform To subscribe to BMJ go to: http://group.bmj.com/subscribe/
Commentary
Trends in incidence of occupational asthma Susan M Tarlo 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 Department of Medicine, University of Toronto, Toronto Western Hospital, Toronto, Ontario, Canada Correspondence to Dr Susan M Tarlo, Toronto Western Hospital, EW7-449, 399 Bathurst St, Toronto, Ontario, Canada M5T 2S8; [email protected] 688
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 lowmolecular 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. Occup Environ Med October 2015 Vol 72 No 10
Downloaded from http://oem.bmj.com/ on November 13, 2015 - Published by group.bmj.com
Commentary 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 com-
Occup Environ Med October 2015 Vol 72 No 10
pensated 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. Acknowledgements The author would like to thank Dr Gary Liss, MD, for helpful discussion.
Received 25 February 2015 Accepted 25 March 2015 Published Online First 20 April 2015 Occup Environ Med 2015;72:688–689. doi:10.1136/oemed-2015-102852
REFERENCES 1
2
3 4 5
6
7
8
9
10
Competing interests None. Provenance and peer review Commissioned; internally peer reviewed.
11
12
National Institute for Occupational Safety and Health Public Health Service Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, Division of Respiratory Disease Studies, Surveillance Branch. Work-Related Lung Disease Surveillance System (eWoRLD). Secondary Work-Related Lung Disease Surveillance System (eWoRLD). 2014. http://wwwn.cdc.gov/eworld/ Grouping/All_Pneumoconioses/91 Toren K, Blanc PD. Asthma caused by occupational exposures is common—a systematic analysis of estimates of the population-attributable fraction. BMC Pulm Med 2009;9:7. Tarlo SM, Liss GM. Prevention of occupational asthma. Curr Allergy Asthma Rep 2010;10:278–86. Tarlo SM, Lemiere C. Occupational asthma. N Engl J Med 2014;370:640–9. Stocks S, McNamee R, van der Molen H, et al. Trends in incidence of occupational asthma, contact dermatitis, noise-induced hearing loss, carpal tunnel syndrome and upper limb musculoskeletal disorders in European countries from 2000 to 2012. Occup Environ Med 2015;72:294–303. Stocks SJ, McNamee R, Turner S, et al. Assessing the impact of national level interventions on workplace respiratory disease in the UK: part 1–changes in workplace exposure legislation and market forces. Occup Environ Med 2013;70:476–82. Stocks SJ, McNamee R, Turner S, et al. Assessing the impact of national level interventions on workplace respiratory disease in the UK: part 2–regulatory activity by the Health and Safety Executive. Occup Environ Med 2013;70:483–90. Vandenplas O, Lantin AC, D’Alpaos V, et al. Time trends in occupational asthma in Belgium. Respir Med 2011;105:1364–72. Paris C, Ngatchou-Wandji J, Luc A, et al. Workrelated asthma in France: recent trends for the period 2001–2009. Occup Environ Med 2012;69: 391–7. Ribeiro M, Tarlo SM, Czyrka A, et al. Diisocyanate and non-diisocyanate sensitizer-induced occupational asthma frequency during 2003 to 2007 in Ontario, Canada. J Occup Environ Med 2014;56:1001–7. Henneberger PK, Redlich CA, Callahan DB, et al. An official American Thoracic Society statement: work-exacerbated asthma. Am J Respir Crit Care Med 2011;184:368–78. Lim T, Liss GM, Vernich L, et al. Work-exacerbated asthma in a workers’ compensation population. Occup Med (Lond) 2014;64:206–10.
To cite Tarlo SM. Occup Environ Med 2015;72:688– 689.
689
Downloaded from http://oem.bmj.com/ on November 13, 2015 - Published by group.bmj.com
Trends in incidence of occupational asthma Susan M Tarlo Occup Environ Med 2015 72: 688-689 originally published online April 20, 2015
doi: 10.1136/oemed-2015-102852 Updated information and services can be found at: http://oem.bmj.com/content/72/10/688
These include:
References Email alerting service
This article cites 11 articles, 5 of which you can access for free at: http://oem.bmj.com/content/72/10/688#BIBL Receive free email alerts when new articles cite this article. Sign up in the box at the top right corner of the online article.
Notes
To request permissions go to: http://group.bmj.com/group/rights-licensing/permissions To order reprints go to: http://journals.bmj.com/cgi/reprintform To subscribe to BMJ go to: http://group.bmj.com/subscribe/
