We studied the relationship between occupational exposures, chronic bronchitis, and lung function in a general population survey in 14 industrialized countries, including 13,253 men and women aged 20 to 44 yr. We studied associations between occupational group, occupational exposures, bronchitis symptoms (cough and phlegm production for at least 3 mo each year), FEV1, and nonspecific bronchial responsiveness (NSBR) separately in lifetime nonsmokers, cigarette smokers, and ex-smokers. Occupational exposure to vapors, gas, dust, or fumes, estimated with a job exposure matrix (JEM), was associated with chronic bronchitis among current smokers only (prevalence ratio (PR): 1.2 to 1.7). The interaction of occupational exposure with smoking, however, was not statistically significant (p > 0.1). Self-reported exposure was related to chronic bronchitis in all smoking groups. An increased risk for chronic bronchitis was found in agricultural, textile, paper, wood, chemical, and food processing workers, being more pronounced in smokers. Lung function and NSBR were not clearly related to occupational exposures. Findings were similar for asthmatic and nonasthmatic subjects. In conclusion, occupational exposures contributed to the occurrence of chronic (industrial) bronchitis in young adults. Fixed airflow limitation was not evident, probably due to the relatively young age of this population.
Chronic airway diseases contribute considerably to the burden of chronic morbidity in adults, and occupational exposures play a role in the onset of several chronic airway diseases. Occupational asthma is the most common occupational respiratory disease in industrialized countries (1). Many different occupations and more than 200 specific occupational exposures have been associated with asthma (2). It is also known that chronic obstructive pulmonary disease (COPD) can be induced by occupational exposures (3-5). There is, however, controversy about the role of cigarette smoking in occupational respiratory disease, and about the overlap with asthma (4, 6, 7).
Cigarette smoking, typically associated with occupation, is the major determinant of COPD. Hence, smoking is likely to be a confounding factor in the relationship between occupational exposures and COPD. Even when adjusting for smoking status, a residual confounding effect can be expected, since both COPD and occupation are also associated with smoking quantity, and not only with smoking status. Thus, it is better to evaluate associations between occupational exposures and COPD separately for smokers and nonsmokers (6) and to adjust for smoking quantity within the group of smokers. In addition, earlier studies have suggested that occupational exposures may interact with smoking (6).
The role of occupational asthma as a concurrent lung disease is another important consideration. It has been suggested that COPD may arise as a consequence of longstanding asthma (6), but this is probably only apparent in older patients. Furthermore, COPD can be attributable to different types of exposures, including agents known to cause occupational asthma. Occupational exposure to these agents, especially respirable irritants, can also lead to chronic productive cough. This so-called industrial bronchitis itself does not lead to airway obstruction, but the concurrent asthma may (6). Moreover, nonspecific bronchial responsiveness (NSBR) without apparent asthma is a risk factor for decline in lung function, and NSBR itself may also be induced by occupational exposures. Thus, it is important to understand whether COPD is related to occupational exposures independently of asthma.
Evaluating relationships between occupational exposures and COPD with stratification by asthma and smoking status requires a large study population. We analyzed data from the European Community Respiratory Health Survey (ECRHS), a multicenter study among young adults, both males and females, from European and other industrialized countries. Results of two national analyses of the ECRHS, dealing with occupational exposures and COPD, have been published so far (8, 9). A study in New Zealand (8) showed increased risks for chronic bronchitis and airway obstruction in workers who had reported occupational exposure and in certain job groups. Analyses of a subset of Spanish patients (9) revealed an association between exposures as assessed with a job exposure matrix (JEM) and chronic bronchitis and lung function.
A drawback of both studies was that analyses were done on relatively small groups, which did not allow subdivision of the study population in order to evaluate modifying factors. In addition, it was not known whether occupational exposures were related to bronchitis symptoms and lung function in other countries participating in the ECRHS. We performed analyses of data from 14 countries in the ECRHS to study the relationships between specific occupations and occupational exposures and symptoms of chronic bronchitis, lung function, and NSBR. All analyses were done with stratification by current asthma and by smoking status.
The aims and methods of the ECRHS have been described elsewere (10). We used data from a random sample of the general population seen at 30 study centers in 14 countries (n = 15,111 subjects). Excluded from analyses were subjects with missing data for symptom questions (n = 283), cigar and pipe smokers and subjects with incomplete data on smoking habit (n = 680), and subjects without data about current or last-held occupation (n = 895; mainly full-time students).
The ECRHS classification was used for coding of occupations (11, 12). Subjects were classified by current occupation or, for subjects reporting a change of job because of problems with respiratory health, by occupation at that time. This was done to avoid selection bias (13). Subjects were further classified into 10 occupational groups with a high probability of exposure to vapors, gas, dust, or fumes, and into one reference group of professional, administrative, and clerical workers (11). Some potentially relevant job categories, such as mining, rubber and plastics work, and glass and ceramics work were too few (< 25) to constitute a separate group, and were not included in this part of the analyses (n = 2,336).
Occupational exposures were assessed directly from self-reported exposure to vapors, gas, dust, or fumes. We also used a JEM that provided a semiquantitative estimate (none, low, or high) of exposure to biologic dusts, mineral dusts, and gases/fumes for each occupation (9, 11).
Chronic bronchitis was defined as the regular expectoration of phlegm for at least 3 mo in each year. A second definition was a regular cough with phlegm production for at least 3 mo each year. Asthma was defined as an attack of asthma in the previous 12 mo, having been awakened by an attack of shortness of breath at any time in the previous 12 mo, or current use of asthma medication (11).
Airway obstruction was evaluated through measurement of FEV1. Subjects performed at least three acceptable reproducible lung function maneuvers done according to standard spirometric procedures. NSBR was defined as a 20% decrease in FEV1 associated with a methacholine dose of ⩽ 8 μmol, as described elsewhere (10). Values for FEV1 and NSBR were available for 84% and 62% of the population, respectively.
Analyses were performed separately for subjects with asthma (n = 1,099), and those without asthma (n = 12,154). We further stratified these two subgroups into never-smokers, ex-smokers, and current smokers. We calculated prevalence ratios (PRs) to assess the relative risks (RRs) for the categorical variables bronchitis and NSBR (14). PRs adjusted for potential confounders were calculated with Cox's proportional hazards model (15), as modified by Breslow (16), with the PHREG procedure of the Statistical Analysis System (SAS) (SAS Institute, Inc., Cary, NC) (17). Relationships between occupational exposures and FEV1 were investigated through multiple linear regression analyses (REG procedure of the SAS). All models were adjusted for gender, age, height squared, and country. Analyses of data for current smokers were additionally adjusted for number of cigarettes smoked per day. In order to investigate geographic variations, we grouped countries into six regions; these consisted of two or three adjacent countries and one region that comprised the three non-European countries in the ECRHS.
Occupational exposure to vapors, gas, dust, or fumes was more common among males than among females (Table 1). Current smokers were more often exposed than were ex-smokers or never-smokers. There was a considerable range in exposure between countries, of from 33% to 58% for self-reported exposure and from 30% to 53% for any exposure according to the JEM. The age distribution was similar for never-smokers (mean: 32.5 yr) and current smokers (33.2 yr), whereas ex-smokers (35.2 yr) were somewhat older.
|20 to 24 yr||1,578||(13.0%)||46.4%||46.3%|
|25 to 29 yr||2,475||(20.4%)||46.7%||42.5%|
|30 to 34 yr||2,625||(21.6%)||42.5%||41.4%|
|35 to 39 yr||2,562||(21.1%)||42.9%||42.2%|
|40 to 44 yr||2,914||(24.0%)||44.5%||40.5%|
Among nonasthmatic subjects, chronic bronchitis was present in 1% to 3% of never-smokers and ex-smokers, and in 5% to 9% of current smokers, depending on the definition used (Table 2). An excess risk for chronic bronchitis was found among agricultural workers in never-smokers and current smokers. Textile, wood, and food processing workers showed an excess risk predominantly for ex-smokers and current smokers, and paper and chemical workers for current smokers only. Among cleaners, an excess risk was found for ex-smokers, and possibly for never-smokers, but not for smokers. Self-reported exposure to vapors, gas, dust, or fumes was related to chronic bronchitis in all smoking groups. Occupational exposure according to the JEM was associated with chronic bronchitis in current smokers only. The interaction between occupational exposure and smoking, however, was not statistically significant (p > 0.1). When applying the JEM separately for the three types of exposure, we found comparable PRs for biologic dust, mineral dust, and gases/fumes (results not shown).
|Category||Phlegm||Cough with Phlegm|
|Never-Smokers||Ex-Smokers||Current Smokers||Never-Smokers||Ex-Smokers||Current Smokers|
|Agriculture||2.6 (1.2–5.8)‡||0.9 (0.1–6.9)||2.5 (1.4–4.4)||2.4 (0.7–8.2)||0.0 (−)||2.9 (1.4–6.1)|
|Construction||2.2 (0.8–6.1)||0.7 (0.1–5.0)||1.4 (0.8–2.5)||1.8 (0.2–14)||0.0 (−)||1.7 (0.8–3.5)|
|Metal heating||1.4 (0.4–4.5)||0.4 (0.1–3.2)||1.7 (1.0–2.9)||1.4 (0.2–11)||0.0 (−)||0.6 (0.2–2.1)|
|Other metal||1.3 (0.6–2.9)||0.9 (0.3–2.9)||1.4 (0.9–2.1)||1.6 (0.5−5.6)||1.3 (0.3–6.1)||1.7 (1.0–2.9)|
|Textile||0.6 (0.1–4.4)||2.2 (0.5–9.2)||2.5 (1.3–4.6)||1.5 (0.2−12)||4.2 (0.5–35)||2.0 (0.8–4.8)|
|Paper||0.0 (−)||0.0 (−)||1.9 (0.7–5.4)||0.0 (−)||0.0 (−)||3.8 (1.3–11)|
|Cleaning||3.0 (1.3–6.7)||3.8 (1.3–11)||1.0 (0.5–1.9)||1.1 (0.1−7.9)||3.5 (0.4–28)||1.4 (0.7–2.9)|
|Wood||0.4 (0.1–2.8)||1.6 (0.4–7.0)||2.1 (1.1–4.1)||1.1 (0.1−8.2)||3.3 (0.7–16)||2.6 (1.1–6.2)|
|Chemical||0.0 (−)||0.0 (−)||2.2 (0.9–5.4)||0.0 (−)||0.0 (−)||2.5 (0.8–8.4)|
|Food processing||1.5 (0.5–4.0)||3.4 (1.3–8.6)||2.0 (1.3–3.1)||2.2 (0.5−9.2)||3.9 (0.9–18)||1.7 (0.9–3.2)|
|Exposure to VGDF†|
|Self-reported||1.4 (1.0–2.0)||1.7 (1.1–2.8)||1.6 (1.3–2.0)||1.3 (0.8−2.3)||1.8 (0.8–4.1)||1.7 (1.3–2.3)|
|Low according to JEM||1.0 (0.7–1.4)||1.1 (0.6–1.8)||1.2 (1.0–1.5)||0.8 (0.4−1.5)||0.7 (0.3–1.8)||1.3 (0.9–1.8)|
|High according to JEM||1.4 (0.9–2.1)||1.1 (0.6–2.2)||1.6 (1.2–2.1)||1.0 (0.4−2.1)||1.0 (0.4–2.9)||1.7 (1.2–2.4)|
Figure 1 shows associations between any occupational exposure according to the JEM and cough with phlegm among current smokers in six regions. PRs for cough with phlegm ranged from 1.2 and 2.0, with a trend toward lower risks in the northern European countries. The figure further shows that the risk for bronchitis associated with occupational exposures was higher in males, although the interaction of exposure with gender was not statistically significant. For ex-smokers and never-smokers, the association between occupational exposure and chronic bronchitis was similar for males and females (results not shown).
To investigate possible residual confounding by level of cigarette consumption within the group of current smokers, we performed analyses in six strata according to the number of cigarettes smoked per day (1 to 5, 6 to 10, 11 to 15, 16 to 20, 21 to 25, and > 25). PRs for bronchitis associated with any occupational exposure assessed with the JEM were consistent among the different strata (results not shown). We found no trend toward an association of cigarette consumption with RR.
Mean FEV1 in most job categories tended to be lower than in the reference group of office workers (Table 3), although differences were not statistically significant. A consistent trend across the three smoking groups could not be observed. A high level of exposure to vapors, gas, dust, or fumes according to the JEM was associated with lower lung function only in current smokers. This decrease of 61 ml in FEV1 differed significantly (p < 0.01) from the decrease seen both in never-smokers and in ex-smokers. This was also true when biologic dusts, mineral dusts, and gases/fumes were considered separately. Self-reported occupational exposure was not associated with lung function. NSBR was not related to any of the occupational exposure indices.
|Never-Smokers||Ex-Smokers||Current Smokers||Never-Smokers||Ex-Smokers||Current Smokers|
|Agriculture||+18 (−87;+123)‡||−44 (−232;+143)||−66 (−209;+77)||1.0 (0.6–1.9)¶||1.3 (0.5–3.5)||1.2 (0.5–2.5)|
|Construction||+70 (−57;+197)||−114 (−249;+21)||−1 (−98;+97)||1.2 (0.5–2.5)||1.1 (0.5–2.4)||0.7 (0.4–1.3)|
|Metal heating||−1 (−111;+108)||−19 (−161;+123)||−86 (−195;+22)||0.8 (0.4–1.7)||1.1 (0.5–2.6)||0.8 (0.5–1.5)|
|Other metal||−44 (−122;+35)||−61 (−166;+44)||−27 (−96;+41)||0.6 (0.4–1.2)||0.6 (0.3–1.3)||1.0 (0.7–1.4)|
|Textile||−95 (−227;+37)||+73 (−128;+275)||−119 (−249;+11)||1.5 (0.8–2.8)||1.0 (0.3–3.3)||1.4 (0.8–2.3)|
|Paper||−77 (−282;+129)||−298 (−657;+61)||−10 (−202;+181)||0.8 (0.2–3.3)||1.2 (0.2–8.9)||1.0 (0.4–2.7)|
|Cleaning||−40 (−147;+67)||+15 (−153;+183)||−37 (−136;+62)||1.1 (0.6–2.2)||2.8 (1.4–5.5)||1.2 (0.7–1.9)|
|Wood||−17 (−134;+99)||−96 (−267;+74)||−114 (−254;+27)||1.2 (0.6–2.5)||1.2 (0.4–3.2)||0.9 (0.4–2.0)|
|Chemical||−218 (−460;+23)||−44 (−278;+190)||−83 (−279;+113)||1.5 (0.4–5.9)||1.3 (0.3–5.4)||0.8 (0.2–2.4)|
|Food processing||+31 (−64;+126)||−59 (−205;+87)||−107 (−198;−16)||1.2 (0.7–2.1)||0.8 (0.3–2.1)||0.9 (0.6–1.5)|
|Exposure to VGDF†|
|Self-reported||+4 (−25;+33)||−15 (−59;+29)||−10 (−42;+23)||1.1 (1.0–1.3)||1.1 (0.9–1.4)||1.0 (0.9–1.2)|
|Low according to JEM||+27 (−4;+59)||−36 (−83;+10)||+0 (−34;+35)||1.1 (0.9–1.3)||1.0 (0.8–1.3)||1.0 (0.9–1.2)|
|High according to JEM||+11 (−33;+55)||+24 (−42;+89)||−61 (−105;−16)||1.1 (0.8–1.4)||1.2 (0.8–1.7)||1.0 (0.8–1.3)|
|Overall mean / prevalence||3841§||3811||3863||20.8%||19.8%||26.5%|
Analyses were repeated for asthmatic subjects (Table 4). The prevalence of chronic bronchitis was three to six times higher in this group than among nonasthmatic subjects. Occupational exposure according to the JEM was similar to that of nonasthmatic subjects (42.3% versus 42.2%), but more asthmatic (52.6%) than nonasthmatic subjects (44.4%) had self-reported exposure. RRs for both bronchitis and NSBR, and regression coefficients for FEV1, were not essentially different for asthmatic and nonasthmatic subjects. Self-reported exposure was associated with chronic bronchitis in all smoking groups, whereas exposure according to the JEM was associated with bronchitis in current smokers only. Subject numbers were too small to evaluate associations according to occupational groups.
|Health Outcome||Never-Smokers (n = 466)||Ex-Smokers (n = 223)||Current Smokers (n = 410)|
|Self-reported exposure†||1.5 (0.9–2.6)§||2.1 (1.0–4.4)||1.7 (1.1–2.7)|
|Low exposure by JEM†||0.9 (0.5–1.6)||1.1 (0.5–2.5)||1.1 (0.7–1.7)|
|High exposure by JEM†||1.0 (0.5–2.0)||1.3 (0.5–3.6)||1.6 (1.0–2.5)|
|Cough with phlegm||7.1%||6.7%||20.7%|
|Self-reported exposure||1.1 (0.5–2.3)||2.0 (0.6–6.0)||1.4 (0.8–2.3)|
|Low exposure by JEM||1.1 (0.5–2.4)||1.0 (0.3–3.4)||1.1 (0.6–1.9)|
|High exposure by JEM||0.6 (0.2–2.1)||0.4 (0.0–3.2)||1.5 (0.9–2.6)|
|Self-reported exposure||0.9 (0.7–1.3)||0.9 (0.5–1.5)||0.8 (0.6–1.2)|
|Low exposure by JEM||1.1 (0.7–1.7)||1.3 (0.7–2.2)||1.0 (0.6–1.5)|
|High exposure by JEM||1.2 (0.7–2.0)||1.7 (0.9–3.3)||1.1 (0.7–1.7)|
|Self-reported exposure||+34 (−84;+152)‖||−29 (−206;+147)||−6 (−126;+115)|
|Low exposure by JEM||−28 (−166;+110)||+65 (−136;+266)||−110 (−243;+22)|
|High exposure by JEM||−61 (−245;+122)||+172 (−75;+420)||−84 (−234;+66)|
In this general population study, occupational exposures were related to chronic bronchitis. Associations were most obvious among cigarette smokers, but the interaction of occupational exposures with smoking was not statistically significant. Significantly increased risks for chronic bronchitis were found for agricultural workers among both smokers and never-smokers. Increased risks were also observed for other occupational groups including textile, wood, food, and paper and chemical processing workers, principally among smokers. Occupational exposures were not clearly related to either lung function or bronchial responsiveness, although smokers with a high occupational exposure had lower levels of FEV1. Results of the study suggest the occurrence of industrial bronchitis without pronounced airflow limitation.
Associations between occupational exposures and chronic bronchitis in our study are consistent with findings in previous studies. Excess risks for working in agriculture, wood and textile and paper processing confirm results of earlier, work force-based (18) and general population studies (19). Associations between self-reported exposures and chronic bronchitis were also found in analyses of national subsamples of the ECRHS (8, 9) and in other general population studies (20– 23). Relationships between chronic bronchitis and occupational exposures assessed with a JEM were also observed in the Spanish subsample of the ECRHS (9) and in a longitudinal Dutch study (19).
Results obtained with the JEM in our study were consistent with excess risks in the occupational groups examined. Exposure to biologic dust is likely in agriculture, and the paper, wood, and food processing industries, whereas mineral dust exposure occurs in agriculture (24), and exposure to gases/ fumes occurs in the chemical industry, in agriculture, and in woodworking. The JEM used in the study was not gender- or country-specific. We observed nonsignificant differences in risks between males and females, and between northern Europe and other countries. This was probably due to quantitative or qualitative differences between genders and between countries in occupational exposures within particular jobs.
In contrast with earlier general population studies (20-22), we were unable to detect a clear-cut association between occupational exposures and lung function. A statistically significant effect on FEV1 was found only for smokers with a high exposure according to the JEM. The overall lack of effects on lung function can probably be explained by our having studied a young sample, among which a considerable decline in lung function was not yet evident. A general population study in Norway (23) showed that the prevalence of chronic airflow limitation (FEV1/FVC < 0.7) ranged from 2% to 4% in subjects aged 18 to 44 yr, against 9% to 12% in the age group from 45 to 73 yr. Young age also implies a relatively low cumulative occupational exposure, and probably a more recent and cleaner work environment than that of older subjects exposed in earlier decades and included in earlier studies. In the two national subsamples of the ECRHS analyzed earlier (8, 9), however, effects of occupational exposures on lung function were suggested. This might be due to differences in occupational exposures between countries, as suggested in our study (Figure 1).
The lack of association between occupational exposures and lung function may also be due to healthy worker bias. Workers with respiratory disorders are less likely to enter high-exposure jobs, or when employed are more likely to leave high-exposure jobs. It can be expected that this effect would be strongest among nonsmokers.
We performed all analyses separately in cigarette smokers, ex-smokers, and never-smokers. In earlier studies (8, 9, 20– 23), relationships between occupational exposures and chronic bronchitis were evaluated with adjustment for smoking status. When this was done in our data set, overall risks for exposure to vapors, gas, dust, or fumes on chronic bronchitis were close to those observed within the group of current smokers only. This indicates that smoking would have caused residual confounding in unstratified analyses. Risks of chronic bronchitis were more apparent in current smokers, but we could not formally demonstrate effect modification by smoking. In analyses done on occupational groups, this was probably due to limited numbers of subjects. In analyses done with the JEM, the groups were bigger, but overall RRs were low (< 2), and differences in RR between smokers and nonsmokers were small (the largest difference being 1.7 versus 1.0, respectively). Thus, we cannot exclude the presence of effect modification by smoking; however, if it exists, it is relatively small.
Limitations of this study include misclassification in exposure assessment and possible interference by socioeconomic status (SES). The main aim of the ECRHS was not to study occupational respiratory effects. Information on occupational exposures was based on current (or last held) job and on self-reported exposure. It is unlikely that reporting of current job was influenced by respiratory health status. Therefore, the analyses by occupational group and by JEM, both of which were based on the subjects current job, were probably not biased by differential misclassification. On the other hand, it is probable that subjects with respiratory symptoms were more aware of occupational exposures in the present or in the past. This might have led to differential misclassification when using self-reported exposure. This is probably reflected by the increased RRs of bronchitis symptoms associated with self-reported exposure (Table 2).
We did not adjust for SES. Occupation and SES are strongly interrelated. Therefore, adjustment for SES may remove part of the risk that could be attributed to occupational exposures that are widespread in some SES groups (25). After we adjusted for SES in our data set (using the age of completion of full-time education), RRs did not markedly change, although standard errors increased because of colinearity. This indicated that SES did not act as a strong confounding variable within the association under study.
In conclusion, occupational exposures were associated with the occurrence of chronic (industrial) bronchitis in young adults, being more obvious among cigarette smokers. Occupational exposures were not clearly related to lung function. This may have been due to the relatively young age and therefore the limited duration of exposure among these individuals, to more recent and cleaner work environments, and to a healthy worker bias. A follow-up of this population is currently underway, and will allow us to assess whether fixed airflow limitation (COPD) develops at an older age, especially among persons suffering from chronic bronchitis.
The authors thank P. Burney, S. Chinn, C. Luczynska, D. Jarvis, E. Lai, and J. Potts from the Department of Public Health Medicine, Guy's and St. Thomas's Medical and Dental School, London, UK for coordination of the European Community Respiratory Health Survey; M. Abramson, J. Kutin (Melbourne), Australia; P. Vermeire and F. van Bastelaer (Antwerp South, Antwerp Central), Belgium; H. Magnussen and D. Nowak (Hamburg), and H.E. Wichmann and J. Heinrich, (Erfurt) Germany; T. Gislason and D. Gislason, (Reykjavik) Iceland; J. Prichard, S. Allwright and D. MacLeod, (Dublin) Ireland; M. Bugiani, C. Bucca and C. Romano, (Turin), R. de Marco lo Cascio and C. Campello (Verona), A. Marinoni, I. Cerveri, L. Casali, and L. Perfetti, (Pavia) Italy; B. Rijcken, J.P. Schouten, M. Kerkhof and H.M. Boezen, (Groningen, Bergen op Zoom, Geleen), The Netherlands; J. Crane, S. Lewis and N. Pearce, (Wellington, Christchurch, and Hawkes Bay) New Zealand; A. Gulsvik and E. Omenaas, (Bergen) Norway; J.M. Antó, J. Sunyer, J. Soriano, M. Kogevinas, A. Tobı́as and J. Roca, (Barcelona), N. Muniozguren, J. Ramos González and A. Capelastegui, (Galdakao), J. Martı́nez-Moratalla and E. Almar, (Albacete), J. Maldonado Pérez, A. Pereira and J. Sánchez, (Huelva), and J. Quirós and I. Huerta, (Oviedo), Spain; G. Boman, C. Janson, and E. Björnsson, (Uppsala), L. Rosenhall, E. Norrman, and B. Lundbäck , (Umea), and N. Lindholm, P. Plaschke, and K. Torén, (Göteborg) Sweden; N. Künzli, (Basel) Switzerland; R. Hall, (Ipswich), B. Harrison, (Norwich), and J. Stark, (Cambridge) United Kingdom; and S. Buist, W. Vollmer, and M. Osborne, (Portland) Oregon for providing occupational information; and H. Kromhout, and R. Vermeulen, Utrecht, The Netherlands, for work with the job exposure matrix.
Supported by the European Commission; Allen and Hanbury's, the Belgian Science Policy Office and Belgian National Fund for Scientific Research; GSF and the Bundesminister für Forschung und Technologie; Ministero dell'Universita e della Ricerca Scientifica e Tecnologica; Centro Nazionale per Ricerco, Regione Veneto grant RSF No. 381/05.93. Ministry of Welfare, Public Health and Culture of The Netherlands; Asthma Foundation of New Zealand, Lotteries Grant Board, and Health Research Council of New Zealand; Norwegian Research Council Project No. 101422/310; Ministerio Sanidad y Consumo de España Fondo de Investigación Sanitaria (FIS) Grants Nos. 91/0016060/00E-05E., 92/0319, 93/0393, Comissió Interdepartmental de Recerca i Innovació Tecnològica (CIRIT) 1999SGR00241, Hospital General de Albacete, Hospital General Juan Ramón Jiménez, and Consejeria de Sanidad Principado de Asturias; Swedish Medical Research Council, and Swedish Heart Lung Foundation, and Swedish Association against Asthma and Allergy; Swiss National Science Foundation Grant 4026-28099; National Asthma Campaign, British Lung Foundation, Department of Health of the United Kingdom, and South Thames Regional Health Authority; and United States Department of Health, Education and Welfare Public Health Service Grant No. 2 S07 RR05521-28.
|1.||Tarlo SM, Alexis N, Silverman F. Assessment of airway responsiveness relevant to occupational exposures. In: Banks DE, Parker JE, editors. Occupational lung disease: an international perspective. London: Chapman & Hall Medical; 1998. p. 309–325.|
|2.||Chan-Yeung M, Malo JL. Tables of major inducers of occupational asthma. In: Bernstein IL, Chan-Yeung M, Malo JL, Bernstein DI. Asthma in the workplace. New York: Marcel Dekker Inc.; 1999. p. 683–720.|
|3.||Becklake MROccupational exposures: evidence for a causal association with chronic obstructive pulmonary disease. Am Rev Respir Dis1401989S85S91|
|4.||Oxman AD, Muir DCF, Shannon HS, Stock SR, Hnizdo E, Lange HJOccupational dust exposure and chronic obstructive pulmonary disease: a systematic overview of the evidence. Am Rev Respir Dis14819933848|
|5.||Pride NB, Burrows B. Development of impaired lung function: natural history and risk factors. In: Calverley P, Pride N, editors. Chronic obstructive pulmonary disease. London: Chapman & Hall; 1995. p. 69–92.|
|6.||Hendrick DJOccupation and chronic obstructive pulmonary disease (COPD). Thorax511996947955|
|7.||Burge PSOccupation and chronic obstructive pulmonary disease (COPD). Eur Respir J7199410321034|
|8.||Fishwick D, Bradshaw LM, D'Souza W, Town I, Armstrong R, Pearce N, Crane JChronic bronchitis, shortness of breath, and airway obstruction by occupation in New Zealand. Am J Respir Crit Care Med156199714401446|
|9.||Sunyer J, Kogevinas M, Kromhout H, Antó JM, Roca J, Tobias A, Vermeulen R, Payo F, Maldonado JA, Martinez-Moratalla J, et al.Pulmonary ventilatory defects and occupational exposures in a population– based study in Spain. Am J Respir Crit Care Med1571998512517|
|10.||Burney PGJ, Luczynska C, Chinn S, Jarvis DThe European Community Respiratory Health Survey. Eur Respir J71994954960|
|11.||Kogevinas M, Antó JM, Sunyer J, Tobı́as A, Kromhout H, Burney Pthe European Community Respiratory Health Survey Study Group. A population based study on occupational asthma in Europe and other industrialised countries. Lancet353199917501754|
|12.||Office of Population Censuses and Surveys. Classification of occupations. London: HMSO; 1980.|
|13.||Checkoway H, Pearce NE, Crawford-Brown DJ. Research methods in occupational epidemiology. New York: Oxford University Press; 1989.|
|14.||Thompson ML, Myers JE, Kriebel DPrevalence odds ratio or prevalence ratio in the analysis of cross-sectional data: what is to be done? Occup Environ Med551998272277|
|15.||Cox DRRegression models and life-tables. J Stat Soc B341972187220|
|16.||Breslow NECovariance analysis of censored survival data. Biometrics3019748999|
|17.||SAS Institute, Inc. SAS User's Guide, version 6. Cary, North Carolina, 1989.|
|18.||Melbostad E, Eduard W, Magnus PChronic bronchitis in farmers. Scand J Work Environ Health231997271280|
|19.||Heederik D, Kromhout H, Burema J, Biersteker K, Kromhout DOccupational exposures and 25-year incidence rate of non-specific lung disease: The Zutphen Study. Int J Epidemiol191990945952|
|20.||Korn RJ, Dockery DW, Speizer FE, Ware JH, Ferris BGOccupational exposures and chronic respiratory symptoms: a population-based study. Am Rev Respir Dis1361987298304|
|21.||Krzyzanowksi M, Kauffmann FThe relation of respiratory symptoms and ventilatory function to moderate occupational exposure in a general population. Int J Epidemiol171988397406|
|22.||Viegi G, Prediletto R, Paoletti P, Carrozzi L, di Pede F, Vellutuni M, di Pede C, Giuntini C, Lebowitz MDRespiratory effects of occupational exposure in a general population sample in north Italy. Am Rev Respir Dis1431991510515|
|23.||Bakke PS, Baste V, Hanoa R, Gulsvik APrevalence of obstructive lung disease in a general population: relation to occupational title and exposure to some airborne agents. Thorax461991863870|
|24.||Nieuwenhuijsen MJ, Noderer KS, Schenker MB, Vallyathan V, Olenchock SPersonal exposure to dust, endotoxin and crystalline silica in California agriculture. Ann Occup Hyg4319993542|
|25.||Tüchsen F, Hannerz HSocial and occupational differences in chronic obstructive lung disease in Denmark 1981-1993. Am J Ind Med372000300306|