Passive smoking and cardiorespiratory health in a general population in the west of Scotland.

Hole, David; Gillis, Charles R.; Chopra, Charu; Hawthorne, Victor M.

doi:10.1136/bmj.299.6696.423

Cited by 168 publications

(88 citation statements)

References 15 publications

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“…Among adults, the impact of ETS on pulmonary function has been less clear. In several studies, self-reported ETS exposure was associated with decreased FEV 1 , FVC, or FEV 1 /FVC ratio (27)(28)(29)(30)(31)(32)(33). Supporting these deleterious effects of ETS, we found an increase in pulmonary function among 53 bartenders after reduction in workplace ETS exposure during an 8-week period (34).…”

Section: Discussionsupporting

confidence: 62%

Environmental tobacco smoke exposure and pulmonary function among adults in NHANES III: impact on the general population and adults with current asthma.

Eisner

2002

Environ Health Perspect

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The impact of environmental tobacco smoke (ETS) exposure on adult pulmonary function has not been clearly determined. Because adults with asthma have chronic airway inflammation, they may be a particularly susceptible group. Using data from the Third National Health and Nutrition Examination Survey (NHANES III), I examined the cross-sectional relationship between serum cotinine, a biomarker of ETS exposure, and pulmonary function among 10,581 adult nonsmokers and 440 nonsmoking adults with asthma whose cotinine and spirometry data were available. I generated residuals, which are observed minus predicted values (based on Crapo equations), for forced expiratory volume in 1 sec (FEV1), forced vital capacity (FVC), and FEV1/FVC ratio to adjust for age, sex, and height. In addition, I used multivariate linear regression to control for sociodemographic characteristics and previous smoking history. Most adults with and without asthma had detectable serum cotinine levels, indicating recent ETS exposure (85.7% and 83.4%, respectively). Among nonsmoking male participants, I found no evidence that ETS exposure was related to decreased pulmonary function. In the nonsmoking female stratum, the highest cotinine tertile was associated with a lower FEV1 [-100 mL; 95% confidence interval (CI), -143 to -56 mL], FVC (-119 mL; 95% CI, -168 to -69 mL), and FEV1/FVC ratio (-1.77%; 95% CI, -2.18% to -1.36%). Among women with asthma, the highest cotinine tertile was also associated with decreased FEV1 (-261 mL; 95% CI, -492 to -30 mL), FVC (-291 mL; 95% CI, -601 to 20 mL), and FEV1/FVC ratio (-1.6%; 95% CI, -3.3% to 0.19%). In conclusion, ETS exposure is associated with decreased pulmonary function in adult females, especially those with asthma. This analysis should provide further impetus for public policies that promote smoke-free environments.

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Section: Discussionsupporting

confidence: 62%

Environmental tobacco smoke exposure and pulmonary function among adults in NHANES III: impact on the general population and adults with current asthma.

Eisner

2002

Environ Health Perspect

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“…Concern about confounding is further reduced by the results of five other studies that show both age-adjusted and multivariate RR estimates for CHD associated with spousal smoking (3,12,13,18,22). In three of these studies the RR estimate increased after multivariate adjustment (12,13,22); in the remaining two (3,18), the RR estimate decreased slightly, as it did in the Nurses' Health Study (4 (42).…”

Section: Confoundingmentioning

confidence: 89%

“…In three of these studies the RR estimate increased after multivariate adjustment (12,13,22); in the remaining two (3,18), the RR estimate decreased slightly, as it did in the Nurses' Health Study (4 (42). The age-adjusted prevalence of self-reported hypertension, diabetes, and increased cholesterol was slightly (1-3%) higher among ETS-exposed nurses than among the unexposed.…”

Section: Confoundingmentioning

confidence: 90%

“…Spousal environmental tobacco smoke and coronary heart disease: case-control studies (listed by first author). Hirayama, 1984 (6) Svendsen, 1987 (9) Butler, 1988 (spouse-pairs) (10) Butler, 1988 (AHSMOG men) (10) Butler, 1988 (AHSMOG women) (10) SandIer, 1989 (men) ( 11) SandIer, 1989 (women) (11) Hole, 1989 (12) Humble, 1990 (13) Steenland, 1996 (men) (3) Steenland, 1996 (women) (3) Kawachi, 1997 (4) Time I (3,4,9,12,13,18,22), four showed an increase in the RR estimate when adjusted for multiple factors besides age (9,12,13,22), whereas three showed a decrease in the RR (3,4,18).…”

Section: Methodsmentioning

confidence: 99%

“…To ensure completeness, we reviewed published and unpublished studies of nonfatal myocardial infarction (MI) and/or death from ischemic heart disease (IHD) among lifelong nonsmokers whose potential ETS exposure was defined by the smoking status of the spouses. Ultimately we included nine cohort (3,4,(6)(7)(8)(9)(10)(11)(12)(13) and eight case-control (14)(15)(16)(17)(18)(19)(20)(21)(22) studies in the overview. Two of the cohort studies (3,4) and three case-control studies (20)(21)(22) were new since OSHA last summarized the literature (5).…”

Section: Methodsmentioning

confidence: 99%

See 2 more Smart Citations

Epidemiologic Studies of Fatal and Nonfatal Cardiovascular Disease and ETS Exposure from Spousal Smoking

Thun¹,

Henley²,

Apicella³

1999

Environmental Health Perspectives

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This article reviews the epidemiologic studies of the association of ischemic heart disease risk and environmental tobacco smoke (ETS) exposure from a spouse who smokes. Seventeen studies (nine cohort, eight case-control) comprising more than 485,000 lifelong nonsmokers and 7,345 coronary heart disease (CHD) events were included in a meta-analysis. Together, these studies include 36% more CHD events and 58% more study subjects than were available for review by the U.S. Occupational Safety and Health Administration (OSHA) in 1994. The relative risk (RR) for fatal or nonfatal coronary events among never smokers married to smokers, compared to those whose spouses did not smoke, was RR = 1.25 (95% confidence interval [95% Cl], 1.17-1.33) across the combined studies. This association was statistically similar in men (RR = 1.24; 95% Cl, 1.15-1.32) and women (RR = 1.23; 95% Cl, 1.15-1.32); in studies of cohort (RR = 1.23; 95% Cl, 1.15-1.31) and case-control (RR = 1.47; 95% Cl, 1.19-1.81) design; in the United States (RR =1.22; 95% Cl, 1.13-1.30) and other countries (RR = 1.41; 95% Cl, 1.21-1.65); and in studies of fatal (RR = 1.22; 95% Cl, 1.14-1.30) and nonfatal (RR = 1.32; 95% Cl, 1.04-1.67) heart disease. In three studies that presented data separately for nonsmokers married to current or former smokers, the association was stronger when the spouses continued to smoke (RR = 1.16, 1.06-1.28) than with former smokers (RR = 0.98; 95% Cl, 0.89-1.08). The aggregate data are unlikely to be attributable to chance, publication bias, confounding, or misclassification of exposure. The evidence linking heart disease and ETS exposure from a spouse has become substantially stronger since OSHA first proposed including heart disease in its risk assessment of ETS in 1994. Key words: environmental tobacco smoke, heart disease. -Environ Health Perspect 107(suppl 6):841-846 (1999). http.//ehpnetl.niehs.nih.gov/docs/1999/suppl6/84 1-846thun/abstract. html

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Passive Smoking and Cardiovascular Risk

Kritz¹,

Schmid²,

Sinzinger³

1995

Arch Intern Med

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A possible relationship between passive smoking and coronary heart disease has been widely debated during the past decade. Convincing evidence links environmental (passive) tobacco smoke exposure to heart disease morbidity as well as mortality. In the United States, 37,000 coronary heart disease deaths per year are attributed to environmental tobacco smoke exposure, accounting for 70% of all deaths caused by environmental tobacco smoke. The analysis of 10 epidemiologic studies indicated a consistent dose-response effect related to exposure, but more proof is still needed. Evidence indicates that nonsmokers are more sensitive to smoke, including cardiovascular effects, and that sidestream smoke contains higher concentrations of gas constituents, including carbon monoxide. Pathophysiological and biochemical data after short- and long-term environmental tobacco smoke exposure show changes in endothelial and platelet function as well as exercise capacity similar to those in active smoking. Therefore, passive smoking is a relevant risk factor for heart disease morbidity and mortality.

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Passive smoking and cardiorespiratory health in a general population in the west of Scotland.

Cited by 168 publications

References 15 publications

Environmental tobacco smoke exposure and pulmonary function among adults in NHANES III: impact on the general population and adults with current asthma.

Environmental tobacco smoke exposure and pulmonary function among adults in NHANES III: impact on the general population and adults with current asthma.

Epidemiologic Studies of Fatal and Nonfatal Cardiovascular Disease and ETS Exposure from Spousal Smoking

Passive Smoking and Cardiovascular Risk

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