0
Clinical Investigations: ASTHMA |

Asthmatic Subjects Symptomatically Worse at Work*: Prevalence and Characterization Among a General Asthma Clinic Population FREE TO VIEW

Susan M. Tarlo, MBBS, FCCP; Kevin Leung, MD; Irvin Broder, MD; Frances Silverman, PhD; D. Linn Holness, MD, FCCP
Author and Funding Information

*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@utoronto.ca



Chest. 2000;118(5):1309-1314. doi:10.1378/chest.118.5.1309
Text Size: A A A
Published online

Study objectives: To assess the prevalence of a historical occupational component to asthma in an adult asthma clinic and to compare characteristics of asthmatic subjects with and without work-attributed symptoms.

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.

Occupational asthma (OA) is the most common nonacute occupational lung disease in many industrial countries, as reported from the United Kingdom,1parts of Canada (Ontario2and Quebec3), and parts of the United States (as reported to the Sensor System4). Reports from different countries using different methods and different populations have estimated that OA accounts for anywhere from 2 to 20% of all asthma cases. In 1979, a US expert committee gave an estimate, not based on a formal study, that 2% of asthma cases were due to OA.5A Japanese study in 1980 estimated that 15% of adult asthma cases were due to an occupation, particularly silk production and Maiko manufacturing.6In a US national disability survey in 1987, 15% of 468 patients with asthma attributed their condition to workplace exposure.7 Among 94 adult asthmatic subjects who were interviewed after a hospital admission, there was historical support for probable OA among 3% of subjects, and for probable or possible OA in 20% of subjects.8In the United States, among a general practice setting, Blanc and colleagues9concluded that > 1 in 10 adult asthmatic patients had a work history strongly suggestive of a potential relationship between exposure and disease, while Milton et al,10on reviewing health maintenance organization charts, suggested that 20% of new-onset asthma cases were attributable to occupational exposure. Data from nationwide registers of occupational diseases and chronic diseases in Finland were analyzed and were reported to show that 4.8% of cases of new-onset adult asthma were OA.11In a Spanish population-based study, Kogevinas et al12estimated that the risk of asthma attributable to occupational exposures was 3 to 7%, and about 1 to 2% higher when analyses were limited to cases of adult-onset asthma. Forastiere et al,13in a community sample of older women in California, found a significantly increased risk of asthma among health workers and social workers (odds ratio, 2.4) and among artists, writers, decorators, and photographers (odds ratio, 3.1). A recent multinational, population-based study estimated that 0.2 to 0.5% of young adults become asthmatic or have their asthma exacerbated because of their occupations.14

Most previous studies estimating OA relative risks or prevalence79,1214 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.

The clinic population consisted of 900 referrals to The Gage Research Institute Asthma Clinic (a secondary-referral and tertiary-referral clinic) during a 19-year period (ie, between 1972 and 1990). At the initial referral visit, a questionnaire was completed by all patients that was suitable for computer analysis. Questions included details of the nature and severity of respiratory symptoms, requirements for emergency visits and hospital admissions, triggering factors, details of the home environment, and smoking history. A description of previous and current occupations include the following categorization: (1) unskilled labor; (2) skilled labor; (3) administrative; (4) managerial; and (5) professional. The questionnaire also included the separate questions “Is asthma better, worse, or unchanged: at work, on weekends, or on holidays off work?” The computerized database also included information on medical history, family history, systematic inquiry, physical examination findings, and results of investigations, including allergy skin tests and pulmonary function tests before and after bronchodilator use.

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 χ2 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.

Prevalence of Asthma Worse at Work

Among the 682 adults who had received a clinical diagnosis of asthma, the onset of asthma, according to their history, occurred during adulthood in 435 (64%). Among the 435 patients, 310 (71%) were employed at the time of their initial asthma clinic visit. Fifty-one patients reported at their initial visit that their asthma was worse at work and was not worse on weekends or holidays off work (ie, 16% of the adult-onset employed asthmatics, 12% of all the adult-onset asthmatic subjects, and 7% of all the adult asthmatics in the clinic). Among these 51 patients who reported worsening at work, 60% reported improvement of their asthma at home, and 65% reported improvement when on vacation.

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.

Twenty-five of the 51 asthmatic subjects (49%) whose asthma was worse at work likely had work aggravation of underlying asthma, a determination that was based on their recorded history of transient worsening at work and workplace exposure to recognized respiratory aggravating factors (including emotional stress in two patients), but had no identified or likely workplace sensitizers (Table 1). An additional 10 asthmatic subjects (20%) had possible OA or possible aggravation of underlying asthma based on the recorded history, lack of further objective tests for OA, and occupations at the onset of asthma that could have included respiratory sensitizers and irritants. None of the asthmatic subjects who reported their asthma to be worse at work had a recorded history to suggest reactive airways dysfunction syndrome.

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.

Our findings of the reported prevalence of worsening asthma at work of 7% among all adult asthmatic subjects (and 16% of all adult-onset employed asthmatic subjects) in a secondary-referral and tertiary-referral asthma clinic are very similar to those of previous reports among other populations of adult asthmatic subjects.814 The advantage of this study includes the detailed, physician-administered questionnaire and the physiologic documentation of all subjects at the time of their initial visit, which included questions concerning a work relationship of their asthma, among > 100 other questions, without emphasis being given during administration of the questionnaire to any relationship of work to asthma, since that was not a specific focus of the questionnaire at the time of initial assessment.

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,1516 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,18in 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.

Abbreviation: OA = occupational asthma

Table Graphic Jump Location
Table 1. Exposures and Occupations of Those With Asthma Worse at Work*
* 

Values in parentheses signify No. of patients; values in brackets signify No. of patients with objective support for OA.

 

Thirty-one percent of asthmatics whose asthma is worse at work.

 

Forty-nine percent of asthmatics whose asthma is worse at work.

§ 

Twenty percent of asthmatics whose asthma is worse at work.

Table Graphic Jump Location
Table 2. Comparison of Study Groups*
* 

Values given as mean ± SD, unless otherwise indicated. NS = not significant; NA = not applicable.

We thank Justina Greene for assistance in data management, Drs. Arthur Leznoff, Shelley Mintz, Peter Thomas, and the late Geoff Davies for contributing to the completion of patient questionnaires, and Laurel O’Connor for secretarial assistance.

Meredith, S, Nordman, M (1996) Occupational asthma: measures of frequency from four countries.Thorax51,435-440. [CrossRef] [PubMed]
 
Liss, G, Ellinson, L Recognition of occupational asthma.Pract Allergy Immunol1994;9,252-260
 
Provencher, S, Labreche, FP, De Guire, L Physician based surveillance system for occupational respiratory diseases: the experience of PROPULSE, Quebec, Canada.Occup Environ Med1997;54,272-276. [CrossRef] [PubMed]
 
Matte, TD, Hoffman, RE, Rosenman, KD, et al Surveillance of occupational asthma under the SENSOR model.Chest1990;98,173S-178S. [PubMed]
 
Salvaggio J, ed. Occupational and environmental respiratory disease in NIAID task force report: asthma and other allergic disease. Washington DC: US Dept of Health Education and Welfare; May 1979; National Institutes of Health publication No. 79–387.
 
Kobayashi S. Different aspects of occupational asthma in Japan In: Frazier CA, ed. 1980 occupational asthma. New York, NY: Van Nostrand Reinhold, 1980; 229–244.
 
Blanc, P Occupational asthma in a national disability survey.Chest1987;92,613-617. [CrossRef] [PubMed]
 
Timmer, S, Rosenman, K Occurrence of occupational asthma.Chest1993;104,816-820. [CrossRef] [PubMed]
 
Blanc, PD, Eisner, MD, Israel, L, et al The association between occupation and asthma in general medical practice.Chest1999;115,1259-1264. [CrossRef] [PubMed]
 
Milton, DK, Solomon, G, Rosiello, RA, et al Risk and incidence of asthma attributable to occupational exposure among HMO members.Am J Ind Med1998;33,1-10. [CrossRef] [PubMed]
 
Reijula, K, Haahtela, T, Klaukka, T, et al Incidence of occupational asthma and persistent asthma in young adults has increased in Finland.Chest1996;110,58-61. [CrossRef] [PubMed]
 
Kogevinas, M, Anto, JM, Soriano, JB, et al The risk of asthma attributable to occupational exposures: a population-based study in Spain.Am J Respir Crit Care Med1996;154,137-143. [PubMed]
 
Forastiere, F, Balmes, J, Scarinci, M, et al Occupation, asthma and chronic respiratory symptoms in a community sample of older women.Am J Respir Crit Care Med1998;157,1864-1870. [PubMed]
 
Kogevinas, M, Anto, JM, Sounyer, J, et al Occupational asthma in Europe and other industrialised areas: a population -based study.Lancet1999;353,1750-1754. [CrossRef] [PubMed]
 
Tarlo, SM, Boulet, LP, Cartier, A, et al Canadian Thoracic Society guidelines on occupational asthma.Can Respir J1998;5,289-300. [PubMed]
 
American College of Chest Physicians Consensus Committee.. Assessment of asthma in the workplace.Chest1995;108,1084-1117. [CrossRef] [PubMed]
 
Malo, J-L, Ghezzo, H, L’Archeveque, J, et al Is the clinical history a satisfactory means of diagnosing occupational asthma.Am Rev Respir Dis1991;143,528-532. [PubMed]
 
Blanc, PD, Cisternas, M, Smith, S, et al Occupational asthma in a community-based survey of adult asthma.Chest1996;109(suppl),56S-57S
 
Tarlo SM, Liss G, Corey P, et al. Workers’ Compensation claims for occupational asthma: comparison of subgroups. Chest l995; 107:634–641.
 
Wagner, GR, Wegman, DH Occupational asthma: prevention by definition [editorial].Am J Ind Med1998;33,427-429. [CrossRef] [PubMed]
 
Malo, JL, Chan-Yeung, M Comment on the editorial “Occupational asthma: prevention by definition.”Am J Ind Med1999;35,207-208. [CrossRef] [PubMed]
 
Liss, G, Tarlo, SM, MacFarlane, Y, et al Hospitalization among workers compensated for occupational asthma.Am J Respir Crit Care Med2000;162,112-118. [PubMed]
 

Figures

Tables

Table Graphic Jump Location
Table 1. Exposures and Occupations of Those With Asthma Worse at Work*
* 

Values in parentheses signify No. of patients; values in brackets signify No. of patients with objective support for OA.

 

Thirty-one percent of asthmatics whose asthma is worse at work.

 

Forty-nine percent of asthmatics whose asthma is worse at work.

§ 

Twenty percent of asthmatics whose asthma is worse at work.

Table Graphic Jump Location
Table 2. Comparison of Study Groups*
* 

Values given as mean ± SD, unless otherwise indicated. NS = not significant; NA = not applicable.

References

Meredith, S, Nordman, M (1996) Occupational asthma: measures of frequency from four countries.Thorax51,435-440. [CrossRef] [PubMed]
 
Liss, G, Ellinson, L Recognition of occupational asthma.Pract Allergy Immunol1994;9,252-260
 
Provencher, S, Labreche, FP, De Guire, L Physician based surveillance system for occupational respiratory diseases: the experience of PROPULSE, Quebec, Canada.Occup Environ Med1997;54,272-276. [CrossRef] [PubMed]
 
Matte, TD, Hoffman, RE, Rosenman, KD, et al Surveillance of occupational asthma under the SENSOR model.Chest1990;98,173S-178S. [PubMed]
 
Salvaggio J, ed. Occupational and environmental respiratory disease in NIAID task force report: asthma and other allergic disease. Washington DC: US Dept of Health Education and Welfare; May 1979; National Institutes of Health publication No. 79–387.
 
Kobayashi S. Different aspects of occupational asthma in Japan In: Frazier CA, ed. 1980 occupational asthma. New York, NY: Van Nostrand Reinhold, 1980; 229–244.
 
Blanc, P Occupational asthma in a national disability survey.Chest1987;92,613-617. [CrossRef] [PubMed]
 
Timmer, S, Rosenman, K Occurrence of occupational asthma.Chest1993;104,816-820. [CrossRef] [PubMed]
 
Blanc, PD, Eisner, MD, Israel, L, et al The association between occupation and asthma in general medical practice.Chest1999;115,1259-1264. [CrossRef] [PubMed]
 
Milton, DK, Solomon, G, Rosiello, RA, et al Risk and incidence of asthma attributable to occupational exposure among HMO members.Am J Ind Med1998;33,1-10. [CrossRef] [PubMed]
 
Reijula, K, Haahtela, T, Klaukka, T, et al Incidence of occupational asthma and persistent asthma in young adults has increased in Finland.Chest1996;110,58-61. [CrossRef] [PubMed]
 
Kogevinas, M, Anto, JM, Soriano, JB, et al The risk of asthma attributable to occupational exposures: a population-based study in Spain.Am J Respir Crit Care Med1996;154,137-143. [PubMed]
 
Forastiere, F, Balmes, J, Scarinci, M, et al Occupation, asthma and chronic respiratory symptoms in a community sample of older women.Am J Respir Crit Care Med1998;157,1864-1870. [PubMed]
 
Kogevinas, M, Anto, JM, Sounyer, J, et al Occupational asthma in Europe and other industrialised areas: a population -based study.Lancet1999;353,1750-1754. [CrossRef] [PubMed]
 
Tarlo, SM, Boulet, LP, Cartier, A, et al Canadian Thoracic Society guidelines on occupational asthma.Can Respir J1998;5,289-300. [PubMed]
 
American College of Chest Physicians Consensus Committee.. Assessment of asthma in the workplace.Chest1995;108,1084-1117. [CrossRef] [PubMed]
 
Malo, J-L, Ghezzo, H, L’Archeveque, J, et al Is the clinical history a satisfactory means of diagnosing occupational asthma.Am Rev Respir Dis1991;143,528-532. [PubMed]
 
Blanc, PD, Cisternas, M, Smith, S, et al Occupational asthma in a community-based survey of adult asthma.Chest1996;109(suppl),56S-57S
 
Tarlo SM, Liss G, Corey P, et al. Workers’ Compensation claims for occupational asthma: comparison of subgroups. Chest l995; 107:634–641.
 
Wagner, GR, Wegman, DH Occupational asthma: prevention by definition [editorial].Am J Ind Med1998;33,427-429. [CrossRef] [PubMed]
 
Malo, JL, Chan-Yeung, M Comment on the editorial “Occupational asthma: prevention by definition.”Am J Ind Med1999;35,207-208. [CrossRef] [PubMed]
 
Liss, G, Tarlo, SM, MacFarlane, Y, et al Hospitalization among workers compensated for occupational asthma.Am J Respir Crit Care Med2000;162,112-118. [PubMed]
 
NOTE:
Citing articles are presented as examples only. In non-demo SCM6 implementation, integration with CrossRef’s "Cited By" API will populate this tab (http://www.crossref.org/citedby.html).

Some tools below are only available to our subscribers or users with an online account.

Related Content

Customize your page view by dragging & repositioning the boxes below.

CHEST Journal Articles
CHEST Collections
PubMed Articles
  • CHEST Journal
    Print ISSN: 0012-3692
    Online ISSN: 1931-3543