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Original Research: COPD |

Passive Smoking Exposure Is Associated With Increased Risk of COPD in Never SmokersPassive Smoking and COPD Risk FREE TO VIEW

Stig Hagstad, MD; Anders Bjerg, MD, PhD; Linda Ekerljung, PhD; Helena Backman, MSc; Anne Lindberg, MD, PhD; Eva Rönmark, PhD; Bo Lundbäck, MD, PhD
Author and Funding Information

From the Krefting Research Centre (Drs Hagstad, Bjerg, Ekerljung, and Lundbäck), Department of Internal Medicine, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg; the Obstructive Lung Disease in Northern Sweden (OLIN) studies (Drs Hagstad, Bjerg, Lindberg, Rönmark, and Lundbäck and Ms Backman), Department of Medicine, Sunderby Central Hospital of Norrbotten, Luleå; and the Department of Public Health and Clinical Medicine (Drs Lindberg and Rönmark), Division of Medicine, Umeå University, Umeå, Sweden.

Correspondence to: Stig Hagstad, MD, University of Gothenburg, Sahlgrenska Academy, Department of Internal Medicine, Krefting Research Centre, Box 424, SE-405 30 Gothenburg, Sweden; e-mail: stig.hagstad@gu.se


Funding/Support: The authors have reported to CHEST that no funding was received for this study.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2014;145(6):1298-1304. doi:10.1378/chest.13-1349
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Background:  Passive smoking, or environmental tobacco smoke (ETS), is a risk factor for lung cancer, cardiovascular disease, and childhood asthma, but a relationship with COPD has not been fully established. Our aim was to study ETS as a risk factor for COPD in never smokers.

Methods:  Data from three cross-sectional studies within the Obstructive Lung Disease in Northern Sweden (OLIN) database were pooled. Of the 2,182 lifelong never smokers, 2,118 completed structured interviews and spirometry of acceptable quality. COPD was defined according to the GOLD (Global Initiative for Chronic Obstructive Lung Disease) criteria using postbronchodilator spirometry. The association of COPD with ETS in single and multiple settings was calculated by multivariate logistic regression adjusting for known risk factors for COPD.

Results:  COPD prevalence was associated with increased ETS exposure: 4.2% (no ETS), 8.0% (ETS ever at home), 8.3% (ETS at previous work), and 14.7% (ETS ever at home and at both previous and current work), test for trend P = .003. Exclusion of subjects aged ≥ 65 years and subjects reporting asthma yielded similar results. ETS in multiple settings, such as ever at home and at both previous and current work, was strongly associated to COPD (OR, 3.80; 95% CI, 1.29-11.2).

Conclusions:  In this population-based sample of never smokers, ETS was independently associated with COPD. The association was stronger for ETS in multiple settings. ETS in multiple settings was, after age, the strongest risk factor for COPD and comparable to personal smoking of up to 14 cigarettes/d in comparable materials. The findings strongly advocate measures against smoking in public places.

Figures in this Article

COPD is a chronic inflammatory disease characterized by progressive airflow limitation that is not fully reversible. In 2010 it was the third leading cause of death1 and is estimated to affect hundreds of millions worldwide.2

Active smoking remains the main risk factor for COPD, yet COPD occurs also in never smokers.3 Exposure to passive smoking (environmental tobacco smoke [ETS]) has been implicated as a causal factor of cardiovascular disease,4 asthma in children,5 and lung cancer6 and has been estimated to cause about 1% of overall global mortality.7 Although studies have shown associations between exposure to ETS and respiratory symptoms,8,9 a clear causal relationship between ETS and COPD has proved more difficult to establish.10

In experimental studies, the acute detrimental effects of ETS to the respiratory system have been similar to those of active smoking, suggesting the biologic plausibility of ETS as a causal factor for COPD.11,12 Inclusion of active smokers and/or relying on self-report of COPD may have contributed to the lack of a clear association with ETS in some previous studies.13,14 Moreover, none of the studies of COPD and passive smoking in never smokers used postbronchodilator spirometry,15,16 which is the gold standard to establish the diagnosis of COPD.17

We aimed to study the relationship between ETS and COPD in lifelong never smokers. Postbronchodilator spirometry was used to establish the presence of irreversible airflow limitation in accordance with current guidelines.

Study Population

The study population consisted of three cohorts derived from the general population of Norrbotten, Sweden, participating in the Obstructive Lung Disease in Northern Sweden (OLIN) studies. In 1996, a 10-year follow-up including a structured interview and spirometry was performed in 2,694 adults who originally had been surveyed in 1985 to 1986.18 In 1992, a randomly selected population sample of adults was invited to a postal questionnaire survey, after which 664 randomly selected responders participated in structured interviews and spirometry in 1994 to 1995.19 The third cohort, also examined with identical methods in 1994 to 1995, consisted of 1,997 subjects who in 1992 had reported respiratory symptoms in a postal survey of 7,735 randomly selected adults.20 The participation at the examinations of the cohorts varied from 67% to 84%. Altogether, in the three studies 5,355 subjects from the three cohorts participated in structured interviews and lung function tests.

Data from the three studies were pooled. Among the 5,355 subjects, 2,182 were lifelong never smokers (maximum smoking < 1 cigarette/d for < 1 year). Of these, 2,118 subjects (97%) had completed lung function tests of satisfactory quality. The studies were approved by the ethical committee at the University Hospital of Northern Sweden in Umeå, project number Dnr 04-045 M.

Lung Function Tests

The lung function tests were performed using a dry spirometer (Mijnhard Vicatest 5) according to American Thoracic Society guidelines21 using Swedish reference values.22 Vital capacity (VC) was defined as the best value of FVC or slow VC. The highest value of at least three attempts was used. Reversibility was tested using 0.8 mg salbutamol (Ventoline Discus) in all subjects with either FEV1/VC < 0.7 or FEV1 < 90% of the predicted value. COPD was defined using the fixed ratio definition of FEV1/VC < 0.70 and disease severity staging according to the GOLD (Global Initiative for Chronic Obstructive Lung Disease) guidelines.17 The lung function tests were performed by specially trained nurses who also conducted structured interviews.

Interview Questionnaire and Definitions

The questionnaire included questions about respiratory symptoms and diseases, comorbidity, smoking habits, occupation, socioeconomic status, and exposure to ETS. It has been used with minor modifications in all surveys of the OLIN cohorts among adults and has previously been described.23

Interview Questions Regarding ETS Exposure:

The following questions related to ETS exposure were used.

  • • Are you, or have you ever been, exposed to passive smoking at home? Alternatives: no; yes, but not currently; yes, currently.

  • • Does anyone smoke at your current work? Alternatives: no; yes, in designated places only; yes, in public spaces.

  • • With respect to longest previous employment, did anyone smoke? Alternatives: no; yes, in designated places only; yes, in public spaces.

ETS Exposure Was Categorized Accordingly:

ETS at home was defined as current or previous or either (ever ETS at home). ETS at work was defined using exposure in public settings, categorized as ETS at previous work, ETS at current work, or both (ETS at both previous and current work). A semiquantitative approach was used to account for cumulative ETS exposure in multiple settings. We postulated that ETS in multiple settings (eg, ever at home and at both previous and current work) would equal higher exposure than ETS in a single setting.

Statistical analyses were performed using PASW, version 18.0.0 (IBM). Fisher exact test was used for bivariate comparisons, and Student t test was used for normally distributed continuous data. P < .05 was considered statistically significant. As the fixed ratio definition of COPD has been considered to be age-related,24 analyses were also made excluding subjects aged > 65 years. Adjusted ORs and 95% CIs were calculated by multiple logistic regression adjusting for previously identified risk factors for COPD in the same populations (age, sex, report of asthma, family history of obstructive lung diseases, and socioeconomic group).3,25

ETS and Prevalence of COPD

Of the 2,118 never smokers (59.1% women) with complete spirometric data, 69.0% reported any ETS exposure at home, work, or both (Table 1). In total, 140 subjects (6.6%) had COPD, with 71 subjects (3.4%) having GOLD stage ≥ II. A report of asthma was present in 439 subjects, and, of these, 43 subjects had spirometric evidence of COPD. The prevalence of COPD was highly related to age (2.3% in age ≤ 45 years, 4.8% in ages 46-65 years, and 15.4% in age ≥ 66 years; test for trend P < .001) but not to sex (women 6.3%, men 7.0%; P = .534).

Table Graphic Jump Location
Table 1 —Baseline Characteristics of the Study Population

Cohort 1: age-stratified sample (n = 2,694) examined in 1996; cohort 2: random sample (n = 664) examined in 1994-1995; cohort 3: all subjects (n = 1,997) reporting respiratory symptoms in a survey in 1992, examined in 1994-1995. The study population consisted of all never smoking subjects with complete lung function data (n = 2,118). ETS = environmental tobacco smoke; GOLD = Global Initiative for Chronic Obstructive Lung Disease.

ETS and Lung Function

Subjects reporting ETS ever at home had impaired lung function compared with nonexposed subjects (FEV1, 95.9% predicted vs 98.5%; P = .002; FVC, 101.7% vs 104.7%; P = .001). Corresponding results were observed among subjects reporting exposure ever at work vs nonexposed (FEV1, 96.9% vs 98.5%; P = .045; FVC, 101.3% vs 104.7%; P < 0.001).

COPD by ETS Exposure Categories

ETS ever at home was associated with higher prevalence of COPD compared with nonexposed subjects (8.0% vs 4.2%, P = .004), as was ETS at previous work (8.3% vs 4.2%, P = .002) (Table 2). The prevalence of COPD was markedly higher among subjects reporting ETS both at work and at home, with the highest prevalence among those reporting current exposure at home in combination with both at previous and current work (18.8% vs 4.2%, P = .018). Prevalence of GOLD stage I only did not differ statistically significantly among subjects reporting ETS exposure vs nonexposed subjects. The prevalence of GOLD stage ≥ II, however, was significantly higher among subjects reporting ETS exposure in single settings. When exposure categories were aligned as mutually exclusive groups (no ETS; ETS ever at home only; ETS ever at work only; ETS ever at home and ever at work; ETS ever at home and both previous and current work), the trend of increasing COPD prevalence with increasing ETS exposure was highly statistically significant (test for trend P = .003).

Table Graphic Jump Location
Table 2 —Distribution in Prevalence of COPD According to GOLD by ETS Exposure Among Never Smokers

Difference (P value) vs no ETS exposure. See Table 1 legend for expansion of abbreviations.

When only subjects ≤ 65 years old were considered, the impact of single and combined ETS exposures was similar to that in the whole sample, with increasing degree of exposure rendering a higher prevalence of COPD (Fig 1). In subjects aged ≤ 65 years old who reported the highest exposure to ETS, COPD was six times more common than among those reporting no exposure (18.8% vs 3.0%, P = .015).

Figure Jump LinkFigure 1. Prevalence of COPD according to GOLD (Global Initiative for Chronic Obstructive Lung Disease) by ETS exposure among never smoking subjects aged ≤ 65 years old. ETS exposure was characterized as no ETS exposure, ETS I (ever at home), ETS II (at previous work), ETS III (at both previous and current work), ETS IV (ever at home and at both previous and current work), ETS V (current at home and at both previous and current work). P value vs no ETS exposure. ETS = environmental tobacco smoke.Grahic Jump Location

Risk of COPD expressed as unadjusted OR was 1.98 (95% CI, 1.23-3.18) and 2.06 (95% CI, 1.30-3.27) from ETS ever at home or previous work, respectively, and 3.94 (95% CI, 1.41-11.0) for exposure both at home and at work (Table 3). ETS at current work conferred no additional risk to ETS at previous work. Current exposure at home in combination with both at previous and current work yielded unadjusted OR of 5.27 (95% CI, 1.41-19.7).

Table Graphic Jump Location
Table 3 —Associations of ETS Exposure and COPD Among Never Smokers

Crude and adjusted ORs, 95% CIs, and P values. Each exposure category was tested separately against the reference group of no ETS exposure, as the exposure categories were partially overlapping. See Table 1 legend for expansion of abbreviation.

a 

Adjusted for age, sex, report of asthma, family history of obstructive airway diseases, and socioeconomic group.

The high risk of COPD from combined ETS exposures remained after adjusting for age, sex, socioeconomic status based on occupation, family history of obstructive lung diseases, and report of asthma (Table 3). Adjusting for area of domicile, proxy for living in areas of varying degrees of air pollution, did not alter the results (data not shown). ETS currently at home and at both current and previous work was strongly associated with COPD (adjusted OR, 5.73; 95% CI, 1.46-22.5). The adjusted OR of ETS ever at home and at both current and previous work was 3.80 (95% CI, 1.29-11.2). ETS exposure in single settings was associated, however, not significantly, with COPD. Age ≥ 66 years and report of asthma were associated with COPD, yielding adjusted ORs of 8.29 to 8.83 and 2.01 to 2.02, respectively, depending on the ETS variable used. Testing for GOLD stage ≥ II yielded similar results, yet statistical significance was not reached because of few cases (data not shown). Stratified by sex, among men, ETS ever at home and at both previous and current work was strongly associated with COPD (OR, 5.97; 95% CI, 1.75-20.5) and GOLD stage ≥ II (OR, 9.09; 95% CI, 1.37-60.2). Among women, statistical significance was not reached.

Sensitivity Analysis

When the analyses were repeated excluding subjects with a previous report of asthma, the same overall pattern was observed. Among those reporting ETS ever at home and at both previous and current work, the prevalence of COPD was 20.0% compared with 3.8% among nonexposed (P = .004), and the corresponding OR was 7.24 (95% CI, 2.26-23.2) after adjusting for age, sex, socioeconomic status, and family history of obstructive lung disease.

In this cross-sectional, population-based study of lifelong never smokers, ETS was associated with an increased risk of COPD. The prevalence of COPD was two times higher in subjects exposed to ETS in single settings. ETS in multiple settings (ie, both at home and at work) was strongly associated with COPD even after adjusting for other known risk factors. In fact, exposure to ETS in multiple settings was, after belonging to the oldest age group, the strongest risk factor for COPD in never smokers.

COPD is a disease that develops progressively over time. Analogous to active smoking, prolonged and repeated exposure to passive smoking would be expected to develop pathology among never smokers. In this study population, ETS exposure in multiple settings conferred an adjusted OR of 4 to 6. In current smokers with on average 20 to 30 pack-years smoking history living in the same area, this risk of COPD corresponds to personal smoking of up to 14 cigarettes/d.26 We also found ETS exposure in multiple settings to be strongly associated with increased prevalence of COPD in younger age groups, arguing for the importance of passive smoking also in the development of early-onset disease.

We found a clear relationship between ETS exposure and lower lung function, in-line with previous studies.10,27 Because of our large study sample of never smokers, we could also show an association with spirometrically defined COPD. Although only a minority of those exposed was subjected to ETS in multiple settings in this population, the high risk of COPD in these groups and the possible dose-response relationship strongly argue for the causative role of passive smoking in COPD development. Even though active smoking remains by far the most important risk factor for COPD, the fact remains that subjects exposed to passive smoking become sick through involuntary exposure. The 2006 US Surgeon General report acknowledged that there is no safe level of exposure to tobacco smoke.28 Policymakers should, thus, err on the side of caution when regulating the use of tobacco to protect those potentially at risk.

The prevalence of COPD was significantly associated with ETS exposure at previous but not current work, analogous to the healthy worker effect.29 At the time of data collection, passive smoke exposure at work in Sweden was more common than today. Over the past decade, Sweden and an increasing number of countries and organizations have implemented legislation restricting tobacco use in public places. Despite this, in many countries tobacco smoking in public places remains unregulated.30

We used the GOLD criteria (ie, fixed-ratio definition) to diagnose COPD. One criticism voiced against the fixed ratio concerns the risk for overdiagnosis among elderly subjects.31 However, we found the same overall prevalence of COPD in groups reporting exposure in multiple settings also after excluding the oldest age group. The ERS task force’s recommendations allow both the fixed-ratio definition and the lower limit of normal to be used in epidemiologic studies but emphasizes the importance of using postbronchodilator spirometry to exclude reversible airway obstruction.24

Strengths and Limitations

Among the strengths of our study are the large number of never smokers, carefully performed spirometry, and valid interview data. Unlike previous studies on COPD and passive smoking,15,16 COPD was defined using the gold standard (ie, postbronchodilator spirometry). By excluding current or ex-smokers, we avoided the impact of active smoking. Limitations include the broad categories of ETS exposure, owing in part to the wording of the interview questions and lack of precise temporal data on exposure. Although this approach limits the resolution, it greatly reduces the risk of recall bias and also the uncertainties inherent in weighing exposures in various settings during a lifetime. In addition, the rationale was not to establish a threshold level for passive smoking but to investigate whether an association with COPD existed. We note that our study sample of never smokers was of sufficient size to support this association with appropriate statistical strength.

Another strength is the population-based study design. One of the cohorts was enriched in subjects with airway symptoms, which explains the slightly higher prevalence of self-reported asthma compared with other Swedish studies.32 Importantly, this should not bias the association of ETS with COPD, and this was evident also after excluding subjects with a report of asthma. There are, however, several reasons that subjects reporting asthma should be included. First, long duration of asthma has been implied in the development of irreversible airflow obstruction and COPD.33 Second, COPD may have been misclassified as asthma, as COPD was not a fully defined and well-known disease entity in this region of Sweden when the data were collected. In fact, even among ever smokers with COPD from the same cohorts, one-fourth had a report of asthma, and more than one-half had no diagnosed respiratory disease (data not shown). In subjects not specifically belonging to a risk group, such as never smokers, misclassification and underdiagnosis could be expected to be even more pronounced.

We conclude from this study that exposure to passive smoke is a risk factor among never smokers to develop COPD. The relationship becomes stronger with increasing exposure. In multiple ETS exposure settings, the risk of developing COPD is even comparable to moderate smoking. This lends strength to the argument calling for tobacco-free environment in public settings.

Author contributions: Drs Hagstad and Lundbäck guarantee the integrity of the entire study, and Dr Lundbäck is the guarantor of the study.

Dr Hagstad: contributed to study concept and design, drafted the article, performed the data analysis, and approved the submission of this version for publication.

Dr Bjerg: contributed to study concept and design, data analysis, and critical revision of the article and approved submission of this version for publication.

Dr Ekerljung: contributed to data analysis and critical revision of the article and approved submission of this version for publication.

Ms Backman: contributed to data analysis and critical revision of the article and approved submission of this version for publication.

Dr Lindberg: contributed to study concept and design, data analysis, and critical revision of the article and approved submission of this version for publication.

Dr Rönmark: contributed to study concept and design, data acquisition and analysis, and critical revision of the article and approved submission of this version for publication.

Dr Lundbäck: contributed to study design, data acquisition and analysis, and critical revision of the article and approved submission of this version for publication.

Financial/nonfinancial disclosures: The authors have reported to CHEST the following conflicts of interest: Dr Lindberg participated at speaking activities and industry advisory committees sponsored by Takeda Pharmaceuticals International GmbH (formerly Nycomed), Boehringer-Ingelheim GmbH, Novartis Corp, and AstraZeneca. Dr Lundbäck has received funding from AstraZeneca to the Swedish OLIN Studies for epidemiologic research. He has further received payment for lectures and/or advisory board participation from GlaxoSmithKline; AstraZeneca; Merck & Co, Inc; Mundipharma International; and Takeda Pharmaceuticals International GmbH. Drs Hagstad, Bjerg, Ekerljung, and Rönmark and Ms Backman have reported that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

ETS

environmental tobacco smoke

GOLD

Global Initiative for Chronic Obstructive Lung Disease

VC

vital capacity

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Heidrich J, Wellmann J, Heuschmann PU, Kraywinkel K, Keil U. Mortality and morbidity from coronary heart disease attributable to passive smoking. Eur Heart J. 2007;28(20):2498-2502.
 
Bjerg-Bäcklund A, Perzanowski MS, Platts-Mills T, Sandström T, Lundbäck B, Rönmark E. Asthma during the primary school ages—prevalence, remission and the impact of allergic sensitization. Allergy. 2006;61(5):549-555.
 
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Figures

Figure Jump LinkFigure 1. Prevalence of COPD according to GOLD (Global Initiative for Chronic Obstructive Lung Disease) by ETS exposure among never smoking subjects aged ≤ 65 years old. ETS exposure was characterized as no ETS exposure, ETS I (ever at home), ETS II (at previous work), ETS III (at both previous and current work), ETS IV (ever at home and at both previous and current work), ETS V (current at home and at both previous and current work). P value vs no ETS exposure. ETS = environmental tobacco smoke.Grahic Jump Location

Tables

Table Graphic Jump Location
Table 1 —Baseline Characteristics of the Study Population

Cohort 1: age-stratified sample (n = 2,694) examined in 1996; cohort 2: random sample (n = 664) examined in 1994-1995; cohort 3: all subjects (n = 1,997) reporting respiratory symptoms in a survey in 1992, examined in 1994-1995. The study population consisted of all never smoking subjects with complete lung function data (n = 2,118). ETS = environmental tobacco smoke; GOLD = Global Initiative for Chronic Obstructive Lung Disease.

Table Graphic Jump Location
Table 2 —Distribution in Prevalence of COPD According to GOLD by ETS Exposure Among Never Smokers

Difference (P value) vs no ETS exposure. See Table 1 legend for expansion of abbreviations.

Table Graphic Jump Location
Table 3 —Associations of ETS Exposure and COPD Among Never Smokers

Crude and adjusted ORs, 95% CIs, and P values. Each exposure category was tested separately against the reference group of no ETS exposure, as the exposure categories were partially overlapping. See Table 1 legend for expansion of abbreviation.

a 

Adjusted for age, sex, report of asthma, family history of obstructive airway diseases, and socioeconomic group.

References

Lozano R, Naghavi M, Foreman K, et al. Global and regional mortality from 235 causes of death for 20 age groups in 1990 and 2010: a systematic analysis for the Global Burden of Disease Study 2010. Lancet. 2012;380(9859):2095-2128.
 
Soriano JB, Rodríguez-Roisin R. Chronic obstructive pulmonary disease overview: epidemiology, risk factors, and clinical presentation. Proc Am Thorac Soc. 2011;8(4):363-367.
 
Salvi SS, Barnes PJ. Chronic obstructive pulmonary disease in non-smokers. Lancet. 2009;374(9691):733-743.
 
Heidrich J, Wellmann J, Heuschmann PU, Kraywinkel K, Keil U. Mortality and morbidity from coronary heart disease attributable to passive smoking. Eur Heart J. 2007;28(20):2498-2502.
 
Bjerg-Bäcklund A, Perzanowski MS, Platts-Mills T, Sandström T, Lundbäck B, Rönmark E. Asthma during the primary school ages—prevalence, remission and the impact of allergic sensitization. Allergy. 2006;61(5):549-555.
 
Brennan P, Buffler PA, Reynolds P, et al. Secondhand smoke exposure in adulthood and risk of lung cancer among never smokers: a pooled analysis of two large studies. Int J Cancer. 2004;109(1):125-131.
 
Öberg M, Jaakkola MS, Woodward A, Peruga A, Prüss-Ustün A. Worldwide burden of disease from exposure to second-hand smoke: a retrospective analysis of data from 192 countries. Lancet. 2011;377(9760):139-146.
 
Zheng P, Li W, Chapman S, Zhang Z, Gao J, Fu H. Workplace exposure to secondhand smoke and its association with respiratory symptoms—a cross-sectional study among workers in Shanghai. Tob Control. 2011;20(1):58-63.
 
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