|
|
||||||||
Guest Access | Sign In via User Name/Password |
|||||||||
* From the Institute of Occupational and Environmental Medicine (Drs. Radon and Nowak, and Ms. Büsching), Ludwig-Maximilians-University, Munich, Germany; National Research Center for Environment and Health (Drs. Heinrich and Wichmann), Institute of Epidemiology, Neuherberg, Germany; and Krankenhaus Großhansdorf (Drs. Jörres and Magnussen), Zentrum für Pneumologie und Thoraxchirurgie, Großhansdorf, Germany.
Correspondence to: Katja Radon, PhD, Institute of Occupational and Environmental Medicine, Ziemssenstr 1, D-80336 Munich, Germany; e-mail: Katja.Radon{at}arbeits.med.uni-muenchen.de
| Abstract |
|---|
|
|
|---|
Methods: The questionnaire data of the population-based sample (n = 1,890) were analyzed. Multiple logistic regression models were carried out for current asthma (asthma symptoms or medication), chronic bronchitis (cough with phlegm for
3 months per year), and wheezing as dependent variables, and self-reported exposure to passive smoke at home and at the workplace as independent variables after adjusting for city, age, gender, active smoking, and socioeconomic status as well as occupational exposure to dusts and/or gases.
Results: The relative odds for chronic bronchitis were significantly higher in subjects reporting involuntary tobacco smoke exposure in the workplace (odds ratio [OR], 1.90; 95% confidence interval [CI], 1.16 to 3.11). Likewise, the adjusted OR for asthma was slightly elevated (OR, 1.51; 95% CI, 0.99 to 2.32). The risk of chronic bronchitis (OR, 3.07; 95% CI, 1.56 to 6.06), asthma (OR, 2.06; 95% CI, 1.07 to 3.97), and wheezing (OR, 2.12; 95% CI, 1.25 to 3.58) increased significantly with a daily exposure of > 8 h.
Conclusion: The control of passive smoke exposure in the workplace might reduce the risk of respiratory symptoms independently of exposure to other airborne contaminants.
Key Words: adults cross-sectional survey environmental air pollutants epidemiology European Community Respiratory Health Survey occupations
| Introduction |
|---|
|
|
|---|
While data on the association between passive smoke exposure during childhood and respiratory health are consistent,7 8 9 10 11 the evidence for the development and exacerbation of asthma and chronic bronchitis by chronic exposure to ETS in adults is limited and inconclusive.2 12 13 14 15 16 17 18 Although epidemiologic studies2 5 15 16 19 20 on the association between exposure to passive smoke and asthma support the hypothesis that ETS exposure may increase the risk of asthma in adults, the results of controlled exposure studies12 21 22 among asthmatic patients were inconsistent.
Most of the epidemiologic studies5 did not control for the potential confounding factor of exposure to other airborne contaminants in the workplace. Other studies19 failed to take into account passive smoke exposure in the home environment. Therefore, the aim of this secondary analysis of the data set of the European Community Respiratory Health Survey in Germany was to assess whether exposure to passive smoke is associated with an increased risk of chronic bronchitis and asthma in young adults after adjusting for workplace exposure and other potential confounding variables. Additionally, we examined the dose-response relationship between the daily duration of passive smoking exposure and the risk of chronic bronchitis and asthma.
| Materials and Methods |
|---|
|
|
|---|
Long Questionnaire
The detailed questionnaire23
contained questions on smoking exposure, respiratory symptoms, and occupational exposure to gases, fumes, and/or dusts. Based on the responses to the questionnaire, asthma was defined as a positive answer to at least one of the following questions24
:
Chronic bronchitis was defined as the existence of cough and phlegm for at least 3 months per year. Wheezing was defined as wheezing during the last 12 months without having a cold.
The following question on second-hand smoking exposure at home and at the workplace was asked of the participants23 : "Have you been regularly exposed to tobacco smoke in the last 12 months [regularly means on most days or nights]?"
If the answer to that question was "yes," the following questions were asked:
Respondents with at least a high school degree were classified as having higher educational level.
The occupational exposure to biological dusts, mineral dusts, gases, and fumes was based on a job-exposure matrix.24 The most recent job reported by the participants was coded according to the European Community socioeconomic status groups classification.25 Based on the job-exposure matrix, each of the 350 occupational types of this coding scheme then was classified as not exposed or exposed to each of the three groups of airborne pollutants.
Statistical Analysis
Logistic regression models were carried out to assess the association between passive smoke exposure and respiratory symptoms. These models were adjusted for city, age, gender, active smoking, socioeconomic status, and occupational exposure to gases, fumes, and/or dusts. Additionally, a potential effect modification by active smoking, gender, and occupational exposure to gases, fumes, and/or dusts was assessed using interaction terms.
In order to assess a dose-response relationship, subjects reporting any exposure to passive smoke were classified into four exposure categories based on the quartiles of self-reported daily duration of passive smoke exposure (1, > 0 to
2 h per day; 2, > 2 h to
4 h per day; 3, > 4 h to
8 h per day; 4, > 8 h per day). Unexposed subjects were used as a reference category. Odds ratios (ORs) with 95% confidence interval (CIs) were computed, adjusting for city, age, gender, socioeconomic status, active smoking, and occupational exposure to gases, fumes, and/or dusts.
| Results |
|---|
|
|
|---|
|
|
|
| Discussion |
|---|
|
|
|---|
Our study has several strengths. Since it is a population-based survey, it reflects the prevalence of respiratory symptoms as well as the exposure to ETS exposure in the general population. The information on exposure, outcome, and potential confounding variables was assessed in detail with a validated questionnaire instrument.23 Therefore, the analyses could be adequately controlled for potential confounding variables. Additionally, the dose-response relationship seen between the daily duration of exposure and respiratory health supports the findings of the survey. Moreover, we had the opportunity to take into account occupational exposure to other substances that potentially are associated with respiratory morbidity.24
However, some limitations to the study have to be considered. Since the survey was performed cross-sectionally, the temporality of the results cannot be estimated. Symptoms might result in a change of exposure patterns. This would result in a bias toward the null. Our finding that subjects without any exposure to passive smoke had a slightly higher risk of symptoms compared to subjects with moderate exposure supports this hypothesis. In contrast, subjects with respiratory symptoms may be more likely to report exposure. Since no objective measurements of passive smoking exposure were performed in our study, the accuracy of the self-reported exposure is difficult to estimate. However, previous studies26 have shown a high validity of self-reported exposure to ETS. Among smokers, second-hand exposure to tobacco smoke in the workplace might be a proxy for their amount of active smoking since these smokers themselves have the opportunity to smoke at the workplace. Overall, misclassification of exposure cannot be excluded in the present study.
The relatively low response rate might have resulted in a higher participation rate of symptomatic subjects.27 28 Comparing the age and gender distribution of the participants with the distribution in the target population, no differences with the target population have been observed.29 However, we could not perform a nonresponder analysis based on socioeconomic status or passive smoke exposure since we did not have any information on these parameters for nonresponders. Considering that it is unlikely that the response rates differed by exposure to ETS, it is not likely that our risk estimates were essentially overestimated due to nonresponder bias.
Some residual confounding might have occurred since subjects with passive smoke exposure may have different characteristics than subjects without such an exposure.30 Additionally, atopy might be considered a confounder for the association between passive smoking exposure and asthma.31 However, in restricting the analysis to subjects who underwent a skin-prick tests to common aeroallergens (n = 1,612), the results of the logistic regression models for asthma did not change (data not shown).
We did not find any indications for effect modification by active smoking, gender, or occupational exposure. However, the number of symptomatic subjects in each stratum was low. For instance, only 23 nonsmoking subjects reported symptoms of chronic bronchitis. Additionally, due to the limited number of symptomatic subjects in each stratum no stratified analyses could be performed.
Our finding that exposure to tobacco smoke in the workplace is a stronger predictor for respiratory morbidity than tobacco smoke exposure in the home environment is consistent with those of previous studies.2 12 The exposure levels in the workplace have been estimated to be higher than in the home environment,32 and the time spent in the work environment might be longer.2 As a result, occupational exposure to ETS might be considered an occupational health concern with respect to respiratory morbidity. Our findings indicate that there is a need for regulating tobacco smoke exposure, especially in the workplace. This might be true even for workplaces with occupational exposure to gases and/or dusts.
| Acknowledgements |
|---|
| Footnotes |
|---|
This article is part of the MD thesis of Kerstin Büsching.
This study has been supported by a grant from the Bundesministerium für Forschung und Technologie.
Received for publication September 20, 2001. Accepted for publication February 5, 2002.
| References |
|---|
|
|
|---|
This article has been cited by other articles:
![]() |
M. W. Gerbase, C. Schindler, J.-P. Zellweger, N. Kunzli, S. H. Downs, O. Brandli, J. Schwartz, M. Frey, L. Burdet, T. Rochat, et al. Respiratory Effects of Environmental Tobacco Exposure Are Enhanced by Bronchial Hyperreactivity Am. J. Respir. Crit. Care Med., November 15, 2006; 174(10): 1125 - 1131. [Abstract] [Full Text] [PDF] |
||||
![]() |
J Genuneit, G Weinmayr, K Radon, H Dressel, D Windstetter, P Rzehak, C Vogelberg, W Leupold, D Nowak, E von Mutius, et al. Smoking and the incidence of asthma during adolescence: results of a large cohort study in Germany Thorax, July 1, 2006; 61(7): 572 - 578. [Abstract] [Full Text] [PDF] |
||||
![]() |
T M L Eagan, J Hetland, and L E Aaro Decline in respiratory symptoms in service workers five months after a public smoking ban Tob. Control, June 1, 2006; 15(3): 242 - 246. [Abstract] [Full Text] [PDF] |
||||
![]() |
T. Gruning, A. B. Gilmore, and M. McKee Tobacco Industry Influence on Science and Scientists in Germany Am J Public Health, January 1, 2006; 96(1): 20 - 32. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. S. Braman Chronic Cough Due to Chronic Bronchitis: ACCP Evidence-Based Clinical Practice Guidelines Chest, January 1, 2006; 129(1_suppl): 104S - 115S. [Abstract] [Full Text] [PDF] |
||||
![]() |
D. Olivieri and E. Scoditti Impact of environmental factors on lung defences Eur. Respir. Rev., December 1, 2005; 14(95): 51 - 56. [Abstract] [Full Text] [PDF] |
||||
![]() |
L. Airoldi, P. Vineis, A. Colombi, L. Olgiati, C. Dell'Osta, R. Fanelli, L. Manzi, F. Veglia, H. Autrup, A. Dunning, et al. 4-Aminobiphenyl-Hemoglobin Adducts and Risk of Smoking-Related Disease in Never Smokers and Former Smokers in the European Prospective Investigation into Cancer and Nutrition Prospective Study Cancer Epidemiol. Biomarkers Prev., September 1, 2005; 14(9): 2118 - 2124. [Abstract] [Full Text] [PDF] |
||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |