Occupational asthma in New South Wales (NSW): a population-based study
Cooperative Research Centre for Asthma, Woolcock Institute of Medical Research, NSW, Australia
Correspondence to: A. Johnson, Dust Diseases Board, 14/82 Elizabeth Street, Sydney, New South Wales 2000, Australia. Tel: 61 2 8223 6600; fax: 61 2 8223 6677; e-mail: anthonyj{at}ddb.nsw.gov.au
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Abstract |
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Background The proportion of asthma in adults that is due to occupational exposures is not known.
Aim To examine the contribution of workplace exposures to the development of asthma in adults in New South Wales (NSW) in a cross sectional, population-based study.
Methods A randomly selected population of 5331 18- to 49-year olds completed and returned a mailed questionnaire (response rate 37%). In adult-onset asthmatics we examined the association of asthma with reported exposure, within 1 year of asthma onset, to a list of occupations and exposures known to be at risk for occupational asthma (high-risk jobs and exposures).
Results Among 910 subjects (18%) with asthma, 383 (7%) subjects reported adult-onset disease. After adjusting for sex, age and smoking, working in any high-risk job or exposure at the time of asthma onset was significantly associated with adult-onset asthma (OR 1.51, 95% CI 1.19–1.92). The population attributable risk (PAR) of adult-onset asthma for either a high-risk job or an exposure was 9.5%. Sudden onset, irritant or reactive airways dysfunction syndrome type exposures were associated with adult-onset asthma (OR 4.65, 95% CI 1.64–13.2). The PAR of adult-onset asthma for these exposures was 0.2%.
Conclusion Reported adult onset of asthma is common and occupational exposures may be associated with 9.5% of prevalent cases of adult-onset asthma in NSW.
Keywords Irritant-induced asthma; occupational asthma; occupational exposures; prevalence
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Introduction |
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Occupational asthma (OA) has been defined as asthma due to causes and conditions attributable to a particular occupational environment and not to stimuli encountered outside of the workplace [1]. The prevalence of asthma in adults is increasing in industrialized countries. OA is preventable and occupational exposures have been reported as being responsible for 2–33% of asthma in adults in Europe and North America [2–10]. The contribution of occupational factors to the prevalence of asthma in Australia has not been studied. We report the association between occupational factors and adult-onset asthma in a large, population-based sample of adults in New South Wales (NSW). There is little epidemiological data on the prevalence of OA without a latency period, which has been described as ‘reactive airways dysfunction syndrome (RADS)’ or ‘irritant-induced asthma’. We also examined the association of exposures of these types with adult-onset asthma.
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Methods |
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The study was conducted in 2000 and 2001. A questionnaire was mailed to 15 000 adults, aged 18–49 years, whose names and addresses were selected at random from the NSW electoral roll. The questionnaire was a modified version of the European Community Respiratory Health Survey (ECRHS) [11] screening questionnaire. An additional battery of questions derived from a previous study [6] collected information about 36 industries, exposures and occupations known, a priori, to be at risk for inducing OA (automobile body repair, bakery, biological enzymes, chemical industry, detergent production, dry cleaning, electronic equipment manufacture, farm work, food processing, glues, grain or flour, hairdressing, hardeners/accelerators/resins, laboratory animals, latex, machining, nursing, paints, pharmaceutical industry, photographic development, plastic manufacture, platinum, nickel, chromium or cobalt, printing industry, sawmilling, seafood processing, smelter, soldering, spray painting, textile industry, vegetable gum (printing), welding and wood dust). The wording of the question was as follows: ‘Have you ever worked in any of the following industries or jobs?’ or ‘Have you worked with any of the following?’ For each positive answer, further details were collected including the time period of exposure, whether the subject's breathing was affected and if the subject had had time off work or changed jobs because of this. Information on short term, high-level exposure to irritants, such as those implicated in sudden onset, irritant-induced asthma or RADS [12] was also sought. The wording of the question was ‘Have you ever suffered from accidental exposure to a high concentration of gas, chemicals or fumes which made you sick or sent you to first aid or to the doctor?’
Up to two repeat mailings of the questionnaire were sent to subjects who did not respond to initial mailed surveys. In order to assess non-responder bias, telephone calls were made to 100 subjects randomly selected from among those who did not return a questionnaire after three mail-outs (non-responders).
Asthma was defined as answering positively to the questions ‘Have you ever had asthma?’ and ‘Was this confirmed by a doctor?’ Adult-onset asthma was defined as asthma with the first attack at age 15 years or older. Fifteen years of age was chosen, as this was the minimum first year of employment in this survey.
A case–control analysis was undertaken. Cases were subjects with adult-onset asthma and controls were subjects who never reported asthma, asthma medications use or asthma symptoms. The risk factors (exposures) were all relevant occupations, industries and/or ‘exposures’ that occurred within 1 year of asthma onset, for the cases, and within 1 year of a randomly selected time in the occupational record of the controls. As the year only was reported in the questionnaire rather than the date, it was not possible to determine if the exposure in fact preceded the development of asthma. Smoking, age and sex were controlled for in the analysis. A randomly selected year was used in the controls to enable smoking status and age to be allowed for in the analysis. Smoking and age were determined at the time of asthma onset for the cases or at the time of the randomly selected year in the controls. Chi-squared analysis or Fisher's exact test (if the expected count in one cell was <5) was used for the comparison of categorical variables. For continuous variables, two groups were compared using Student's t-test and >2 groups with one-way analysis of variance or Tukey's modified t-test [13]. A P-value <0.05 was considered significant. Odds ratios (ORs) were calculated by logistic regression.
Population attributable risk (PAR) for each exposure was calculated using the following formula: PAR = [Pe (RR–1)]/RR, where Pe is the prevalence of exposure in the controls and RR is the relative risk associated with that exposure [14]. For this purpose, the relative risk was estimated as the OR.
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Results |
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Of the 15 000 individuals selected from the electoral roll, 498 addresses were found to be inaccurate leaving 14 502 subjects eligible for the study. A total of 5331 individuals returned a completed questionnaire (37%). The majority of those who responded were female (60%) and were currently employed (82%). A total of 1018 (19%) were current smokers and 2597 (49%) had ever smoked.
Of the 100 ‘non-responders’ contacted by phone, 74 agreed to answer a limited questionnaire. There was no significant difference between responders and non-responders in the prevalence of doctor confirmed asthma, asthma symptoms, asthma medication use, age of asthma onset and the proportion that was currently employed (Table 1). Non-responders were significantly younger (32%, <30 years, versus 26%), included more males (55 versus 40%) and fewer subjects who had ever had eczema or any kind of skin allergy (9 versus 37%).
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Of the 5331 who responded to the full survey, 1002 (19%) answered yes to Have you ever had asthma? and in 910 (18%) it was confirmed by a doctor. These 910 meet the definition of asthma for the study. In 373 (41%) of these, their first asthma attack occurred at the age of 15 years or over (adult-onset asthma), in 480 (53%) it occurred at an age <15 years (childhood onset asthma) and 57 (6%) did not specify their age of asthma onset. The characteristics of these two asthma groups and the subjects who had never had asthma are shown in Table 2.
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Those with adult-onset asthma were significantly older and less likely to be male than both childhood onset asthmatics and never asthmatics. Asthmatics were not significantly less likely to be currently employed. Asthma was reported as being better on weekends or holidays for 20% of adult-onset asthmatics and 16% of childhood onset asthmatics (not significantly different). As expected, people with asthma were more likely than those without asthma to report ‘hay fever’, a usual cough and a doctor visit during the last 12 months for breathing problems or shortness of breath. Adult-onset asthmatics were significantly less likely than childhood onset asthmatics to report wheezing during the last 12 months. Adult-onset asthmatics were more likely than both childhood onset asthmatics and never asthmatics to report a RADS type exposures (11, 8 and 5%, respectively).
After adjustment for sex, age and smoking status, exposures to ammonia (OR 2.54, 95% CI 1.72–3.78) and photographic development (OR 2.25, 95% CI 1.04–4.85) were significantly associated with adult-onset asthma. Exposure to any of the listed high-risk jobs within 1 year of asthma onset was significantly associated with adult-onset asthma (OR 1.54, 95% CI 1.19–2.01), as was any high-risk exposure (OR 1.53, 95% CI 1.17–2.00) or either a high-risk job or an exposure (OR 1.51, 95% CI 1.19–1.92). Exposure to a high-risk job or exposure was reported by 34% of cases and 28% of controls. The PAR of adult-onset asthma for either a high-risk job or an exposure was 9.5%. A history of an acute exposure to irritants was strongly associated with adult-onset asthma (OR 4.65, 95% CI 1.64–13.2) but exposure in control subjects was rare, 0.3%. The PAR of adult-onset asthma for these exposures was 0.2%. Five adult-onset asthmatics reported an acute exposure to irritants during the year of their asthma onset, the substances they reported exposure to were chlorine and cleaners (1), paint and rising damp solution (1), agriculture sprays (1), laundry spray (1) and unknown (1). The median time since asthma commencement for these cases was 7.7 years (range 3–26 years) and the median duration of asthma was 4 years (range <1–16 years) as some had resolved. Only one of the five RADS exposure subjects reported asthma symptoms at the time of the survey. This subject had had asthma for 6.4 years. Only 2 of these 5 cases (40%) were currently working compared with 291 (79%) of the remaining adult-onset asthmatic cases (P = 0.03).
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Discussion |
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We examined the contribution of occupational exposures to adult-onset asthma in a large, population-based cross-sectional study of adults in Australia. After adjusting for sex, age and smoking status, working in a high-risk job or exposure to a known cause of OA at the time of asthma onset was significantly associated with adult-onset asthma (OR 1.51, 95% CI 1.19–1.92). The PAR of adult-onset asthma for either a high-risk job or an exposure was 9.5%. Irritant or RADS type exposures at the time of asthma onset were also significantly associated with adult-onset asthma (OR 4.65, 95% CI 1.64–13.2). The PAR of adult-onset asthma for these exposures was 0.2%. An estimated 9.5% of adult-onset asthma in this Australian population would be prevented if exposure to the high-risk jobs and exposures were eliminated.
The response rate in the study was low at 37%. A sample of non-responders differed from those who did respond in age, sex and prevalence of eczema and skin allergies. However, the non-responders did not differ in prevalence of asthma, asthma symptoms or asthma medication use, prevalence of current employment or prevalence of having been in another job that had affected their breathing. Therefore, in spite of the relatively low response rate, we contend that it is unlikely that response bias has significantly affected our results.
Recall bias may have affected the results of this analysis. The data on exposure were all obtained historically, without direct validation or corroboration, and is therefore susceptible to differential or non-differential recall bias.
Questionnaire data are also problematic in the diagnosis of asthma due to the absence of a gold standard. ‘Physician-diagnosed asthma’ assessed by questionnaires has low sensitivity but high specificity (99%) when validated with non-specific bronchial hyper-responsiveness [15]. This may result in an underestimation of the prevalence of asthma. However, the prevalence of asthma in this study is similar to those previously published in Australian adult populations [16].
The onset of asthma and exposure to a known cause of OA occurring at a similar time does not mean the two are causally related. Hence, in interpreting the case–control analysis and calculation of PAR, it is important to consider the possibility that a non-causal association between occupational exposures and adult-onset asthma may be relevant.
One of the strengths of our study was that it identifies subjects who had previously been diagnosed with asthma but do not have it now. Forty per cent of those who developed asthma in association with exposure to high-risk jobs or exposures reported no asthma symptoms within the previous 12 months and, therefore, would not have been included as cases in a study that only identified currently active asthma.
The estimated prevalence of OA in adult asthmatic populations varies in published studies. Blanc and Toren, who have recently reviewed the available literature, estimate that the proportion of adult asthma that is attributable to workplace factors is in the range of 2–33% (median 9%). Among the 12 studies considered to be of the highest quality, the median risk estimate was 15% [2]. Population-based studies based on the ECRHS (from New Zealand [8], Spain [3] and Europe and other industrialized countries [4]) have reported the attributable risk of occupational exposures in adult asthma. The estimates varied between 2 and 10% depending on the asthma definition used. The ECRHS study included data from Melbourne, Australia and found no excess risk of asthma for occupational exposures [4]. OA is notified in the state of Victoria, which includes Melbourne, but at a lower rate than in Europe and United Kingdom [17]. The population studied in Melbourne was likely to be different to our study as Melbourne is a large urban centre, whereas we sampled all of NSW, including urban and non-urban areas, this may explain the difference in our findings. In Finland, it was estimated that the proportion of newly diagnosed cases of asthma among adults who were attributable to an occupational aetiology was 5%.[7]. A study of Health Maintenance Organization members in the United States found that adult-onset asthma was attributable to occupational exposure in 21% (95% CI 12–32) [9]. In a study in Canada using similar methods to the current study, the PAR of occupational exposures for adult-onset asthma was 18% [6]. In a study of the entire working population of Finland, Karjalainen found the attributable fraction of occupational factors in adult-onset asthma in the employed population was 29% for men and 17% for women [10]. In a Norwegian community cohort, 14% of the incidence of asthma was attributable to dust or fumes exposure in the workplace after adjustment for sex, age, educational level and smoking [18]. It can be seen that there is considerable variability in the estimate of risk but the result found in this study is consistent with other published studies. The differences may be due to differences in measurement of exposure, differences in the type of industries and level of exposure between countries, case definition differences as well as true difference in risk in different populations.
The diagnosis of RADS is limited to individuals who experience the onset of asthma symptoms within 24 h of an acute exposure to an irritant in a very high concentration. RADS is now usually considered to be a subset of irritant-induced asthma, a broader term which includes subjects who develop asthma after both single and multiple irritant exposures [19]. Although we found that these exposures were strongly linked to adult-onset asthma symptoms, they are relatively rare and hence the PAR for asthma in our study was <1%. Most studies of RADS in the literature are of case series; this would be consistent with an uncommon disease.
In conclusion, in a population-based cross-sectional study of adults in Australia, 9.5% of adult-onset asthma may be prevented if exposure to known occupational inducing/sensitizing agents was eliminated. Exposures associated with sudden onset, irritant-induced asthma is associated with <1% of adult-onset asthma.
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Conflicts of interest |
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None declared.
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Acknowledgements |
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Supported by the NSW Government Department of Health and the Cooperative Research Centre for Asthma.
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References |
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