To the Editor: Work-related asthma can be divided into occupational asthma (OA) and work-aggravated asthma (WAA).1 OA has been defined as “a disease characterized by variable airflow limitation and/or airway hyperresponsiveness due to causes and conditions attributable to a particular occupational environment and not to stimuli encountered outside the workplace.”2 This definition implies that a specific substance induces asthma at the workplace through an immunologic mechanism. WAA is defined as preexisting or concurrent asthma that is exacerbated by workplace exposures,1,3 which implies that the workplace triggers asthma but does not induce it. Although these two conditions have distinct definitions and underlying physiopathology, they are often very difficult to differentiate in clinical practice. Over the past years, there have been tremendous efforts to improve the understanding of OA. Several guidelines4,5 have been published to improve the management of this condition. In contrast, the current data available on WAA in the literature are limited. To our knowledge, there are no data describing the functional and inflammatory outcome of subjects with WAA.
WAA is likely to represent an important societal burden due to the disability of the subjects and to the high prevalence of this condition. Indeed, 21% of the asthmatic subjects complain of a worsening of their asthma when they are at work.6 Therefore, it is important to increase our understanding of WAA to assess the impact of this condition on workers and improve its management.
The aim of this study was to compare the clinical, functional, and occupational outcomes between subjects with OA and subjects with WAA 1 to 4 years after their diagnoses were made.
Materials and Methods
We conducted a cross-sectional study of the subjects previously investigated for work-related asthma in our center within 1 to 4 years after their original diagnosis of OA or WAA. Subjects were considered to have OA if they showed a positive specific inhalation challenge to an occupational agent, whereas subjects were considered as having WAA if they reported a worsening of their asthma symptoms when at work but showed a negative specific inhalation challenge to occupational agents.
We reassessed their clinical, functional, inflammatory, and occupational characteristics. Their respiratory symptoms were scored according to a Borg scale from zero (no symptoms) to 10 (worst symptoms ever).7 Their asthma maintenance treatment and their daily use of short-acting β2-agonists were also recorded. Asthma quality of life was assessed.8 The workers were asked about their employment status. Spirometry,9 methacholine challenge,10 and sputum induction11 were performed and compared with the results obtained at the time of diagnosis.
t test and the Mann-Whitney test were used to compare clinical, functional, and inflammatory parameters between the groups with OA and WAA. The analysis was performed using the SPSS 10.0 statistical package (Chicago, IL).
Eighteen subjects with OA and 10 with WAA were assessed. Their clinical characteristics are summarized in Table 1.
All subjects with OA had to change their work environment, except one worker who had developed OA due to the exposure to an occupational sensitizer used by a colleague working next to him. No subject with WAA remained at the same workplace after the diagnosis.
Subjects with WAA had asthma for a longer period of time (14.3 ± 15.8 years) than subjects with OA (9.1 ± 7.4 years, P = 0.02). Symptoms of asthma occurred before entering their new work setting in four of the 10 subjects with WAA and in one of the 18 subjects with OA. There was a similar and significant improvement in the respiratory symptoms of both groups at the time of this study.
The pulmonary function tests and the sputum cell counts were similar in subjects with OA and WAA (Table 1). Although not statistically significant, we observed a trend toward a greater improvement of PC20, a larger decrease in the dose of inhaled corticosteroids, and in the need of short-acting beta2 agonists in the subjects with OA compared with the subjects with WAA, as shown in Table 1.
Although not statistically significant, subjects with WAA tended to show a decrease of their median neutrophil counts (49.5% [36.7%]) compared with the time of their diagnosis (63.5% [42.6%], P = 0.1), whereas subjects with OA tended to have a decrease in their sputum eosinophil counts (0.50% [2.2%]) compared with the time of their diagnosis (3.5% [8.4%], P = 0.1).
All subjects with WAA and all but one subject with OA were removed from exposure after they underwent investigation for possible OA. Although subjects with WAA did not obtain any financial compensation from the Quebec Worker Compensation Board, they could not be maintained at their original workplace due to their respiratory symptoms. These data are consistent with a previous study in which the socioeconomic outcomes of the subjects with WAA were equivalent to those of the subjects with OA.12 It is unknown whether an improvement of the measures of prevention such as protective masks, improved ventilation, or increase in asthma medication would have allowed these workers with WAA to remain in their work environment.
We did not find any demographic or functional significant differences between subjects with OA and subjects with WAA a few years after the diagnosis and removal from exposure. The definition of WAA chosen in our study was based on the results of specific inhalation challenges. The occurrence of asthma after entering a new work setting did not exclude the diagnosis of WAA. This contrasts with the epidemiologic study originating from the Sentinel Event Notification Systems for Occupational Risks (SENSOR)13 in which WAA was identified if the affected individuals experienced asthma symptoms or had treatment for asthma in the 2 years before entering a new work setting and if they experienced an increase in asthma symptoms or increased use of their asthma medications after entering that new exposure setting. The patients referred to our clinic were suspected of having OA and thus, were more likely to have similar clinical characteristics than the subjects with confirmed OA. Furthermore, the subjects with preexisting asthma whose asthma was aggravated by their workplace were less likely to seek medical advice in a tertiary center because they did not attribute the onset of asthma to their workplace and did not seek any financial compensation. Therefore, the population studied in the SENSOR program is likely to differ from ours.
Although not statistically significant probably due to the low number of subjects, there was a trend toward an improvement of asthma as shown by consistent trends toward decreases in airway responsiveness, in the dose of inhaled corticosteroids necessary to control the disease, in the need of short-acting beta2 agonists, and in the sputum eosinophil counts in subjects with OA after removal from exposure. This is consistent with previous studies showing improvement of OA after removal from exposure.14
In contrast, we did not find any functional improvement in subjects with WAA, although they had a marked decrease in their respiratory symptoms. It is unknown whether subjects with WAA who would have remained at their workplace would have had a worsening of their asthma.
The functional and occupational outcomes of subjects with OA and WAA after removal from exposure seem to be similar. Although it seems that subjects with OA tend to improve to a greater extent after work removal than subjects with WAA, this needs to be confirmed by studies with a larger sample size.
The authors thank Dr Lucie Blais and Mr James Hatch for reviewing the manuscript. C Lemiere holds a scholarship from the Canadian Institutes of Health Research (CIHR). This study was funded by the Asthma Workplace Center of the CIHR.
Catherine Lemiere, MD, MSc
Sherley Pelissier, BSc
Simone Chaboillez, RT
Liza Téolis, RT
Hôpital du Sacré-Coeur de Montréal
Université de Montréal
Montreal, Quebec, Canada
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