Abstract
Background. There are no large population-based studies on occupational asthma, and few estimates of the proportion of asthma attributed to occupation, even though asthma is the most common occupational respiratory disorder in industrialised countries. Methods. We assessed data on 15,637 people aged 20-44, randomly selected from the general population of 12 industrialised countries. Asthma was assessed by methacholine challenge test and by questionnaire data on respiratory symptoms and use of medication. Occupation was defined by job-titles and a job exposure matrix was constructed. Findings. Highest risk of asthma, defined as bronchial hyperresponsiveness and reported asthma symptoms or medication, was shown for farmers (odds ratio 2.62 [95% CI 1.29-5.35]), painters (2.34 [1.04-5.28]), plastic workers (2.20 [0.59-8.29]), cleaners (1.97 [1.33-2.92]), spray painters (1.96 [0.72-5.34]), and agricultural workers (1.79 [1.02-3.16]). Similar risks were shown for asthma defined as reported asthma symptoms or medication. The most consistent results across countries were shown for farmers and cleaners. Excess asthma risk was associated with high exposure to biological dusts, mineral dusts, and gases and fumes. The proportion of asthma among young adults attributed to occupation was 5%-10%. Interpretation. The prevalence of occupational asthma in women and in specific occupations has been underestimated. Given a mean prevalence of asthma of about 5%, about 0.2%-0.5% of young adults become asthmatics or have their asthma exacerbated because of their occupations.
Original language | English |
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Pages (from-to) | 1750-1754 |
Number of pages | 5 |
Journal | The Lancet HIV |
Volume | 353 |
Issue number | 9166 |
DOIs | |
Publication status | Published - 22 May 1999 |
Funding
Our data show that occupational asthma accounts for 5%–10% of asthma in young adults. These estimates are consistent with a study from Spain included in the ECRHS, and with estimates by Xu and Christiani, 12 who showed that the excess fraction of physician-diagnosed asthma in China was about 12% for people exposed to dust and 5% for those exposed to gases or fumes. Our study was done in several countries and used the same methods, which suggests that occupational asthma should be an important public-health issue in industrialised areas. Increased risk of asthma is associated with agents such as isocyanates, reactive dyes, grain dusts, mites, enzymes, and animal-derived allergens. 1 We showed a consistent excess risk for farmers and cleaners in nearly all countries in our study. The group of cleaners was the largest of the 16 occupational groups to show an increase in asthma risk of more than 30%. A similar excess risk was shown in a case-control study in Singapore, 6 but exposure of cleaners are not among the major recognised causes of occupational asthma. 1,9 Cleaners are commonly exposed to substances known to cause asthma, including irritants such as chlorine and acids, detergents, indoor allergens such as dusts, and outdoor pollutants such as nitrogen dioxide. Cleaners are known to have a high risk of dermatitis. 13,14 Case reports have shown that asthma can be caused by floor-cleaning products, 15,16 and in a study of 329 hospital admissions for respiratory disorders after exposure to chemical fumes and vapours, the most common occupational exposures were to chlorine, sulphur dioxide, and industrial cleaning agents. 17 Acute exposure to irritants is associated with reactive airways dysfunction syndrome, and exposure to high concentrations of chlorine gas is associated with a deterioration of airways function and with bronchial responsiveness. 18–20 Chronic exposure to low concentrations of irritants has been associated with asthma in pulp-mill workers, 21 but there is little epidemiological evidence for the importance of such exposure. 22 Underestimation of the excess asthma risk among cleaners suggests that the occupational-health risks for self-employed people, or those who work in small, transitory companies, may go unrecognised and unprevented. Moreover, exposure to non-allergens in the workplace, frequently of an irritant nature, may be a risk factor for asthma morbidity. Housewives had a small but significant excess risk of asthma, and are likely to share some of the exposures of cleaners, particularly exposure to irritant gases from cleaning materials, detergents, and other indoor allergens or air pollutants. Reilly and Rosenman 17 showed that exposure to household cleaning agents was among the most frequent causes of non-work-related hospital admission. Interpretation of an excess risk in housewives may be confounded by presence at home because of previous asthma symptoms. The risk of asthma attributable to occupational exposures among women, excluding housewives, was higher than expected. Studies of respiratory symptoms in the UK, 9 France, 23 and Italy 24 also identified a high risk of occupational asthma among women. Many occupational groups at high risk for asthma, such as textile workers, cleaners, and farmers, include a substantial proportion of female workers. Under-reporting of occupational asthma 25 may be more common among women, particularly if the potential adverse effects of household exposures on health are included. The atttributable risks that we estimated are a mean estimate for our study population of young adults in industrialised countries. Country-specific analysis shows that other occupations are also at high risk of asthma, presumably because of specific exposures in individual centres, 5 but the wide CIs in the country-specific estimates do not allow precise analysis of observed geographical variation. Exposure to biological dusts, mineral dusts, and gases and fumes was reported more frequently through selfreport than through the job-exposure matrix, possibly indicating that positive recall of exposure is influenced by previous symptoms. The questionnaire was not completed by about 40% of the people contacted, and the possibility of differential non-response cannot be excluded. Sensitivity analyses show that the effect of non-response on estimates of prevalence of bronchial reactivity in the ECRHS is likely to be minimal. 26 In another analysis of the same study, 27 adjustment for non-response had no real effect on the distribution of IgE between study centres. Non-response has to be very biased and very high to affect odds ratios markedly. 28 Our risk estimates were slightly, but not consistently higher for asthma defined as bronchial hyperresponsiveness and asthma symptoms or medication then for asthma defined by questionnaire data alone. These definitions may measure different façets of asthma. Moreover, there may have been differences in the study populations, since only 9476 of 15 637 people who responded to the questionnaire also did the methacholine-challenge test. Data on bronchial hyperresponsiveness and symptoms provide a more specific definition of asthma than questionnaire data alone, but little empirical evidence on the validity of asthma definitions in epidemiological studies compared with those used in clinical practice. 29 Occupational exposures cause between 5%–10% of cases of asthma among young men and women in European and other industrial countries. With a mean prevalence of asthma of about 5% in most areas, 30 our study shows that 0·2%–0·5% of young adults become asthmatics or have their asthma exacerbated by their occupation. Contributors Manolis Kogevinas, Josep Maria Antó, and Jordi Sunyer designed the occupational asthma analysis and wrote the paper. Aurelio Tobias did statistical analysis. Hans Kromhout did industral hygiene assessment and developed the job-exposure matrix. Peter Burney, principal investigator of the ECRHS, took part in all phases of study design and analysis. All authors participated in preparation and subsequent revision of the paper. European Community Respiratory Health Survey (ECRHS) Coordinating centre—P Burney, S Chinn, C Luczynska, D Jarvis, E Lai (London, UK). Participating centres Australia —M Abramson, J Kutin (Melbourne). Belgium —P Vermeire, F van Bastelaer (Antwerp South, Antwerp Central). Germany —H Magnussen, D Nowak (Hamburg); H E Wichmann, J Heinrich, M Wjst (Erfurt). Iceland —T Gislason, D Gislason (Reykjavik). Ireland —J Prichard, S Allwright, D MacLeod (Dublin). Italy — M Bugiani, C Bucca, C Romano (Turin); R de Marco lo Cascio, C Campello (Verona); A Marinoni, I Cerveri, L Casali (Pavia). New Zealand —J Crane, W D'Souza, N Pearce, D Barry, I Town (Wellington, Christchurch, Hawkes Bay). Norway —A Gulsvik, E Omenaas, P Bakke (Bergen). Spain — J M Antó, J Sunyer, J Soriano, M Kogevinas, A Tobias, J Roca (Barcelona); N Muniozguren, J Ramos González, A Capelastegui (Galdakao); J Martinez-Moratalla, E Almar (Albacete); J Maldonade Pérez, A Oereira, J Sánchez (Huelva); J Quirós, I Huerta (Oviedo). Sweden —G Boman, C Janson, E Björnsson (Uppsala); L Rosenhall, E Norrman, B Lundbäck (Umea); N Lindholm, P Plaschke (Göteborg). UK — M Burr, J Layzqll (Caerphilly); R Hall (Ipswich); B Harrison (Norwich); J Stark (Cambridge). USA —S Buist, W Vollmer, M Osborne (Portland). Job-exposure matrix development, occupational history assessment Hans Kromhout, Roel Vermeulen, Helianthe Dubbeld (Wageningen, Germany). Acknowledgments This work was coordinated by the European Commission. We thank the late Colette Baya, and Manuel Hallen, for their assistance, and K Vuylsteek and the members of COMAC for their support. The following grants helped to fund the local studies: Allen and Hanbury's (Australia); Belgian Science Policy Office, National Fund for Scientific Research (Belgium); GSF, and Bundesminister für Forschung und Technologie, Bonn; and GSF-National Centre for Environment and Health, Neuherberg (Germany); Ministero dell' Universita e della Ricerca Scientifica e Tecnologica, CNR, Regione Veneto grant RSF n. 381/05·93 (Italy); Asthma Foundation of New Zealand, Lotteries Grant Board, Health Research Council of New Zealand (New Zealand), Norwegian Research Council project no. 101422/310 (Norway); Ministerior Sanidad y Consumo FIS grants #91/0016060/00E-05E, #92/0319, #93/0393, #970035, Generalitat de Catalunya-CIRIT 19975 GR 00079, Hospital General de Albacete, Hospital General Juan Ramón Jiménez, Consejeria de Sanidad Principado de Asturias (Spain); The Swedish Medical Research Council, the Swedish Heart Lung Foundation, and the Swedish Association against Asthma and Allergy (Sweden); Swiss National Science Foundation grant 4026–28099 (Switzerland); National Asthma Campaign, British Lung Foundation, Department of Health, and South Thames Regional Health Authority (UK); United States Department of Health, Education and Welfare Public Health Service Grant #2 S07 RR05521–28 (USA).