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* From the Gage Occupational and Environmental Health Unit, University of Toronto, Toronto, Ontario, Canada.
Correspondence to: Susan M. Tarlo, MBBS, FCCP, Gage Occupational and Environmental Health Unit, 223 College St, Toronto, Ontario M5T 1R4, Canada; e-mail: susan.tarlo{at}utoronto.ca
| Abstract |
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Design: A retrospective review of data obtained from a physician-administered questionnaire, answers to which were obtained at the initial patient visit of asthmatic subjects, and which included specific questions regarding the relationship of work to symptoms. Chart review data were used to supplement information on workplace exposures and investigations.
Setting: A university-based secondary- and tertiary-referral asthma clinic.
Patients: Seven hundred thirty-one adult asthmatic subjects who were referred for assessment and management of asthma.
Interventions: Statistical analyses of asthmatic subjects with and without work-attributed symptoms and a determination, from chart review, of the likelihood of causes for symptomatic worsening of asthma at work.
Measurements and results: Sixty percent of the patients (435) had adult onset of asthma, among whom 310 patients (71%) were employed at the time of their visit. Fifty-one patients reported their asthma to be worse at work (ie, 16% of adult-onset working asthmatic subjects). Sixteen of these patients (31%) had likely or possible sensitizer-induced occupational asthma (OA), and 49% likely had aggravation of underlying asthma. The other 20% of patients had possible OA or aggravation of underlying asthma at work.
Conclusions: Adult-onset asthmatic subjects commonly report a worsening of asthma at work, more commonly on the basis of likely aggravation of underlying asthma than on the basis of likely or possible OA.
Key Words: asthma asthma prevalence occupational
| Introduction |
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Most previous studies estimating OA relative risks or prevalence7 8 9 12 13 14 have relied on patient questionnaire data that were collected during a cross-sectional survey, often many years after the subject had left work and, so, potentially subject to recall bias, especially among a disability population.7 To our knowledge, there has been no previous published study that has assessed the prevalence of OA from prospectively gathered data from among a secondary-referral and tertiary-referral asthma clinic population. The purposes of the present study are the following: (1) to assess the prevalence of probable and possible OA in a population of adult asthmatic subjects from the population of a general adult asthma clinic in which information on possible work associations had been routinely obtained in a uniform manner at the time of their initial respiratory assessment; and (2) to compare characteristics of these asthmatic subjects, with and without a work-attributed component to their asthma.
| Materials and Methods |
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Among the total of 900 patients referred to the clinic with possible
asthma, we selected the 682 adults (ie, patients aged
17
years) in whom asthma was diagnosed in the clinic by a respirologist or
clinical immunologist on the basis of history, physical examination
findings, and spirometry testing, before and after bronchodilator use.
Among these patients, the subset having adult onset of asthma symptoms
(onset age,
17 years) who were employed at the onset of their
symptoms were identified and were subdivided into the following two
groups: those who had responded that their asthma was worse at work
compared with their condition on weekends or holidays; and those who
did not report a difference. These two groups were compared according
to their work exposures and characteristics such as gender, age of
onset of asthma, smoking history, and factors reflecting severity of
asthma, using t tests and
2 tests
for statistical analyses. Severity was evaluated on the basis of the
extent of medication use, time lost from work, emergency department
visits, and hospital admissions due to asthma, as well as on the basis
of spirometry results.
For those who described adult-onset asthma while they were working and worsening of asthma symptoms at work, a retrospective chart review then was performed to identify any recorded further details of workplace exposure and the results of any investigations that may have been performed to specifically assess OA. Such specific assessment could have consisted of serial peak flow monitoring at work and away from work, skin testing with relevant workplace allergen(s), methacholine challenge testing during a working period and following a period of weeks off work, and specific occupational challenge testing. From this information these subjects were classified as having a clinical probability or possibility of OA, an aggravation of coincidental asthma, or insufficient information to categorize. A categorization of probable OA for this study was reached in those adult-onset asthmatic subjects whose asthma began while working with potential exposure to one or more respiratory sensitizers and with results from at least one objective test that supported a work relationship (ie, specific skin test response, peak expiratory flow rates, or methacholine responsiveness worsening while working or a positive specific challenge with a work sensitizer). A categorization of possible OA was reached if the objective tests to assess a work relationship had not been performed. Categorization to possible or probable aggravation of asthma was made in patients who were exposed to potential respiratory irritants at work without likely sensitizers.
| Results |
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Causes of Asthma Worse at Work
A retrospective chart review of the 51 patients reporting worsened
asthma at work indicated probable sensitizer-induced OA in 8 patients,
based on history, exposure to a recognized respiratory sensitizer
(Table 1 ), and at least one positive objective test supporting OA. The latter
included a positive result for a skin test to a relevant work
sensitizer in two patients (grain and flour), positive work-associated
changes in both serial peak expiratory flow rate recordings and
methacholine challenges in one patient, and positive results to
specific laboratory challenge tests to a work substance in five
patients. An additional eight patients had possible sensitizer-induced
OA, based on the recorded history and workplace exposure to recognized
respiratory sensitizers, but had not undergone specific objective
testing to clarify the diagnosis.
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Comparison of Asthmatic Subjects Who Were Worse at Work With Other
Adult-Onset Working Asthmatic Subjects
Comparisons were made between the recorded features of the 51
asthmatic subjects who reported worsening at work and the 259 other
adult-onset working asthmatic subjects from the clinic. The mean age
for both groups was similar (46 years), as was their smoking history
(Table 2 ), mean age at onset of asthma (40 and 39 years, respectively), and
family history of asthma (60% and 57%, respectively). Those subjects
reporting worsening of their asthma at work, however, were more likely
to be men (72% vs 54%, respectively; p < 0.05), to be laborers
(63% vs 46%, respectively; p < 0.05), and to report exposure to
fumes at work (63% vs 45%, respectively; p < 0.05). There was a
nonsignificant trend to features suggesting less severe asthma than
for the asthmatic subjects who did not report a worsening at
work: those subjects had had fewer days off work due to asthma, fewer
emergency department visits, and fewer mean hospital admissions for
asthma in the previous 2 years. They were less likely to describe
asthma symptoms with exercise (p < 0.05) (Table 2)
, and their mean
total serum IgE level showed a nonstatistical trend to be lower than
that for other asthmatics. Their FEV1 response to
a bronchodilator showed no significant difference.
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| Discussion |
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However, as with most other reported prevalence studies, detailed investigations to diagnose or exclude OA, such as peak expiratory flow rate monitoring, paired methacholine challenges after a work week and after a holiday, and specific laboratory occupational challenges as currently recommended for the clinical diagnosis of OA,15 16 were not performed in most patients. Only a subset of those subjects describing a relationship of asthma to their work (16%) received an objective diagnosis of OA. It has been shown previously that a history supporting OA is highly sensitive but poorly specific for the diagnosis,17 and it is likely that the true prevalence of OA in this population was less than the 7% of all adult asthmatic subjects in the clinic who reported a worsening of asthma at work. Probable sensitizer-induced OA (eight patients) or possible OA (eight other patients) was suggested from the exposure history and from investigations in 2.3% of the adult asthmatic subjects, while 3.7% had likely occupational aggravation of underlying asthma and another 1.5% had possible occupational aggravation of underlying asthma. Thus, aggravation of underlying asthma appeared to be over twice as prevalent as OA.
Since this study assessed asthmatic subjects in a secondary-referral and tertiary-referral clinic, it is likely that these patients represent a more severe subgroup of asthmatic subjects. Such patients would be expected to have more airway hyperresponsiveness than that of patients with milder asthma and, therefore, would be expected to have more noticeable symptomatic aggravation of asthma with workplace exposure to respiratory irritants such as dusts, fumes, and sprays. In addition, it is possible that their referral to the clinic may have been due to suboptimal control of asthma symptoms. Therefore, the 7% of adult asthma clinic patients who reported worsening of asthma at work may be an overestimate of the prevalence of asthma worsening at work among all asthmatic subjects.
Previous reported prevalence studies of work-related asthma have generally not distinguished sensitizer-induced OA from work-related aggravation of asthma, although Blanc et al,18 in a survey of 601 asthmatic subjects followed by a sample of pulmonologists and allergists, reported the exposure to potential occupational sensitizers to be about twice as common as respiratory irritants without sensitizers. In the present study, it is possible that workplace sensitizers may not have been identified in some cases on job descriptions on the questionnaire and in the clinical histories recorded. In a previous study19 of claims accepted by the Ontario Workers Compensation Board over a 4-year period, a similar number of claims was accepted on the basis of OA and on the basis of aggravation of underlying asthma. However, since patients with aggravation of asthma at work may be less likely to change their work exposure, they might be less likely to apply for compensation than those with OA, and compensation data might underestimate the true prevalence of the aggravation of underlying asthma.
It has been suggested that work-related aggravation of asthma should be included in the term occupational asthma.20 However, such symptoms in some patients may reflect undertreatment of asthma and may be better included in a definition of work-related asthma.21 Many of the agents that were considered to have aggravated asthma in this population (such as emotional stress and second-hand cigarette smoke) are not specific to the workplace and might be expected to trigger symptoms in most asthmatic subjects, especially if their treatment is suboptimal or their asthma is severe.
The asthmatic subjects in this population who described worsening of asthma at work had a trend to features that suggest milder asthma than those who noticed no worsening at work at the time of answering the questionnaire. The information used in this study was all taken from information obtained at the initial asthma clinic visit of these patients. Questions pertaining to worsening of asthma at work were asked in the present tense and would not have detected asthmatic subjects who may have had OA previously or may have had an exacerbation of asthma at work severe enough for them to have left work or changed the workplace exposure. This also may have reduced our apparent severity rates and apparent prevalence rates. Nevertheless, our findings are consistent with a recent study from our center comparing the morbidity of patients with accepted compensation claims for OA and patients with non-OA.22 In that study, there were fewer hospital admissions for asthma among those with OA as compared with other asthmatic subjects attending asthma clinics.22
Our findings support an important role for workplace exposure both in the causation of OA and in aggravating the symptoms of underlying asthma, as reported by patients with asthma. This emphasizes the need for taking a thorough occupational history in all adult asthmatic subjects and for further investigations of those whose symptoms improve on weekends or holidays off work.
| Acknowledgements |
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| Footnotes |
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Received for publication October 29, 1999. Accepted for publication June 15, 2000.
| References |
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