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1 Tampere Regional Institute of Occupational Health and Clinic of Occupational Medicine, Tampere University Hospital, Tampere, 2 Dept of Epidemiology and Biostatistics, Finnish Institute of Occupational Health, Helsinki, 3 Dept of Pulmonary Disease, Jorvi Hospital, Espoo, and 4 Social Insurance Institution, Helsinki, Finland
CORRESPONDENCE: K. Saarinen, Tampere Regional Institute of Occupational Health, PO Box 486, FIN-33101 Tampere, Finland. Fax: 358 32608699. E-mail: kimmo.saarinen@ttl.fi
Keywords: asthma, prevalence of work-aggravated symptoms, work environment
Received: October 31, 2002
Accepted March 28, 2003
| Abstract |
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A questionnaire was sent to 2,613 persons (aged 2065 yrs) with asthma. The analyses were restricted to the 969 respondents who were currently employed. The effect of occupational exposure on the aggravation of asthma symptoms at work was assessed according to both self-reported and expert-evaluated exposure.
Approximately 21% of the respondents reported work-aggravated asthma symptoms at least weekly during the past month. The prevalence of those with work-aggravated symptoms increased by age, self-reported occupational exposure to dusts, abnormal temperatures or poor indoor air quality, physically strenuous work, and chemicals, and expert-evaluated probability of daily occupational exposure to airborne dusts, gases or fumes.
Aggravation of asthma symptoms at work is common among employed adults with asthma. Both self-reported and expert-evaluated exposure to dusts, abnormal temperatures or poor indoor air quality, physically strenuous work, and chemicals explained the significant worsening of symptoms. The findings suggest a marked role of the work environment in the aggravation of symptoms of established asthma.
Asthma is a substantial health problem among people of working age and its prevalence appears to be increasing in many countries 1. Asthma is also a frequent cause of work disability 3.
Asthma in the workplace is usually separated into two categories: occupational asthma and work-aggravated asthma. Occupational asthma refers to cases caused by immunological sensitisation or initiated by a single high exposure to irritants. Work-aggravated asthma is pre-existing or concurrent asthma that is aggravated by irritants or physical stimuli in the workplace 4.
Only a few studies have addressed the prevalence of work-aggravated asthma symptoms among patients with physician-diagnosed asthma. Tarlo et al. 5 reported that asthma was worse at work and was not worse on weekends or holidays from work for 16% of the workers with adult-onset asthma in a general asthma clinic population.
The aim of this survey was to assess the prevalence of work-aggravated asthma symptoms, and the effect of exposures and factors of the work environment on the aggravation of symptoms of established asthma. The study focused on asthma cases without any known occupational origin.
| Material and methods |
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To be granted reimbursement rights by the Finnish Social Insurance Institution, the disease must fulfil the diagnostic and severity criteria of asthma, including objective data of reversible bronchial obstruction and a typical and persistent pattern of disease (table 1
). Among those granted special reimbursement rights for asthma medication, the reliability of the asthma diagnosis is high. In a random sample of working-aged asthmatics with granted reimbursement rights, clinically established asthma was present in 99% of subjects, but in 1% the reimbursement rights had been granted for other chronic pulmonary disease on the basis of a special individual assessment 6. Therefore, in the current study, the respondents were asked whether or not they had asthma diagnosed by a physician. The 18 (1%) without such a diagnosis and the 37 who did not reply to this question were excluded from the analyses. Patients with recognised occupational asthma do not receive reimbursement from the Social Insurance Institution but are fully compensated for asthma medication by theStatutory Accident Insurance system. Therefore, such patients were not included in the study.
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18 yrs (adult-onset) at the time of their asthma diagnosis (table 2
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Exposure assessment
In the analyses, the effect of occupational exposure on the aggravation of asthma symptoms at work was assessed according to both self-reported and expert-evaluated exposure.
Self-reported exposure
The respondents were asked about exposure to each of the following factors in their current job(yes, no, cannot say): dusts, chemical agents or factors, abnormal temperatures (cold or heat) or poor indoor air quality, mental stress, and physically strenuous work (high energetic demand).
Expert evaluation
The current occupation of the respondents was initially coded according to the 1997 Classification of Occupations of Statistics Finland 7, which is based on the International Standard Classification of Occupations, version 1988, used by the European Community, ISCO-88 (COM). The probability of nontrivial daily occupational exposure todusts, fumes or gases in each occupation was thereafter classified as probable, possible or unlikely. The assessment was made by two experts familiar with occupational conditions (K. Saarinen, A. Karjalainen). The exposure was classified asprobable for 237 occupations, possible for 200 occupations and unlikely for 188 occupations. Exposure was classified as probable for most manufacturing occupations, agricultural occupations and some service occupations (e.g. occupations related to cleaning and waste handling, and hairdressing). Exposure was classified as unlikely for office-type occupations, most teachers, most physicians and nurses, and most occupations in the human and social sciences. Exposure was classified as possible for most service, transport, sales and military occupations.
Smoking
According to the questionnaire data, the respondents were classified as current smokers, exsmokers, or nonsmokers.
Assessment of work-related aggravation of asthma symptoms
The respondents were asked about the average frequency of asthma symptoms caused or made worse by work during the last month and the last 12 months (not at all, less than once a week, one to two times a week, three to four times a week, daily or nearly daily). The frequencies were very similar for the last month and the past 12 months, and, to avoid bias caused by change of job or tasks, the authors performed the analyses according to the frequency of such symptoms during the last month.
Statistical analyses
The ordinal outcome variable was the frequency of asthma symptoms caused or made worse by work in the following four categories: not at all, less than weekly, one to two times a week, at least three times a week. Age (2034, 3544, 4554,
55 yrs), sex, smoking, use of medication (less than daily, daily), onset of asthma (child, adult) and either self-reported or expert-evaluated exposure were included as explanatory variables. A proportional odds model was used to assess the effect of the explanatory variables on the ordinal outcome variable 8. The validity of the proportional odds assumption was tested and the assumption that the estimated odds ratios (OR) were equal across all cut-off points dichotomising the outcome variable was applied. Interactions between the different self-reported occupational exposures were tested, but they were not significant and were not included in the model.
| Results |
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| Discussion |
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The case ascertainment was done through a national registry that relies on diagnoses made by chest physicians on the basis of clinical and physiological criteria, and the presence of a persistent form of asthma. The authors were interested in the aggravation of established asthma at work and, therefore, workers with a clinical history of permanent asthma were ideal subjects for the study. The study population did not include occupational asthma cases defined by Finnish legislation. The response rate was sufficiently high, but information on the nonrespondents' employment status or their characteristics was not available.
In the current study, 20% of the full-time workers reported work-aggravated asthma symptoms weekly during the pastmonth. In a study comparing the characteristics of patients with occupational and nonoccupational asthma, British researchers reported that 31% of the patients with nonoccupational asthma claimed that their asthma symptoms worsened during the weekdays, however, the study population was only small (n=29) 9. In a community sample of adults with asthma, the prevalence of respiratory symptoms at work was
20% 10. However, since a majority of the patients didnot have diagnosed asthma, the study was concerned with the prevalence of different respiratory symptoms, not the aggravation of established asthma at work.
In a study of asthma cases from a pulmonary clinic, by Tarlo et al. 5, 16% of the workers with adult-onset asthma reported their asthma to be worse at work. Altogether, 16 of these patients (31%) had likely or possible sensitiser-induced occupational asthma and underlying asthma was probably aggravated in 49%. The other 20% of the patients had possible occupational asthma or an aggravation of underlying asthma at work. Tarlo et al. 5 did not assess the frequency of symptoms. In a survey by Arif et al. 11, the prevalence of medically diagnosed asthma was 9.7% and the prevalence ofwork-related asthma was 3.7%. The authors' definition of work-related asthma was taken from positive responses to thefollowing two questions: "Has a doctor ever told you that you had asthma?" and "Are any of the symptoms wheezing, whistling, stuffy, itchy, or runny nose, watery, itchy eyes brought on by work environment?" 11. The authors did not find any study with a design resembling that of the current study, consisting of clinically diagnosed asthma cases, which would have assessed the frequency of work-related symptoms. Exposure at the workplace may cause further impairment of currently symptomatic asthma or it may trigger a relapse of pre-existing asthma. This issue is of great clinical relevance, but the literature addressing this topic is scant 12.
The design and target population in the current study include some features that must be borne in mind when the results of the study are interpreted. A comparison group of nonasthmatic adults was not used in this study, as the authors wanted to study work-aggravation of symptoms of established asthma. This approach may have led to an overestimate of the problem, since all the work-aggravated symptoms of the respondents were not necessarily due to their asthma. Awareness of a dusty working environment may influence the response of an individual with respect to a causal association (i.e. somebody working in a dusty environment may be more likely to report aggravation of asthma symptoms). The symptoms are always subjective and such a recall bias is hard to avoid. Conversely, only people in full-time employment were studied and questions were focused on their current occupation. Therefore, work-related aggravation that had already led to a discontinuation of work or a change of job was unaccounted for. This underestimates the problem. Such situations are likely to be the most severe consequences of work-aggravated asthma. Finally, the authors wish to emphasise that the aetiology of new-onset asthma was not studied. It is possible that, for some subjects, aggravating factors may have also played a role in the inception of asthma but, for many, these factors were completely unrelated to the aetiology and any conclusions in this respect cannot be drawn.
Exposure to dust and chemicals proved to be significant risk factor for work-aggravated asthma symptoms. These exposures have also been shown to increase the risk of asthma 1315. The studies in question, contrary to the current study, were mostly concerned with the aetiological factors of asthma, but it has been impossible to differentiate symptom aggravation from causative effects. In addition to sensitisation (e.g. mediated by immunoglobulin E), other causative mechanisms for occupational or work-related asthma are irritant-induced or sensitisation occurring through unknown mechanisms 4. Some of these cases are not diagnosed as occupational asthma. It is possible that, in the current study population, some of the asthma cases had been caused by these specific work-related factors. However, it is likely that this problem concerns only a small number of subjects, since the focus was mainly on the aggravation of symptoms of established asthma.
There is a lack of studies on the effects of age and smoking on the frequency of asthma symptoms. In the current study, age seemed to increase the frequency of symptoms aggravated by work. There are no data on the duration of exposure at work, and therefore no association could be made between age and duration of exposure. In the current study, smoking did not affect the frequency of asthma symptoms aggravated by work.
Surprisingly, few studies have been conducted on the symptoms of asthmatics at work. The comparison of these studies is difficult because of the differing definitions of asthma, the differing exclusion criteria and the differing concepts of the work-relatedness of asthma. The focus of other studies has been more directed at the aetiological factors inducing asthma. The findings from the current study support the assumption that the work environment plays an important role in the aggravation of symptoms of established asthma. Measures for tertiary prevention are needed at the workplace.
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