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Liu K, Jiang J, Lin Y, Liu W, Zhu X, Zhang Y, Jiang H, Yu K, Liu X, Zhou M, Yuan Y, Long P, Wang Q, Zhang X, He M, Chen W, Guo H, Wu T. Exposure to polycyclic aromatic hydrocarbons, DNA methylation and heart rate variability among non-current smokers. ENVIRONMENTAL POLLUTION (BARKING, ESSEX : 1987) 2021; 288:117777. [PMID: 34265559 DOI: 10.1016/j.envpol.2021.117777] [Citation(s) in RCA: 7] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Received: 02/11/2021] [Revised: 04/28/2021] [Accepted: 07/09/2021] [Indexed: 06/13/2023]
Abstract
Polycyclic aromatic hydrocarbons (PAHs) exposure is associated with heart rate variability (HRV) reduction, a widely used marker of cardiovascular autonomic dysfunction. The role of DNA methylation in the relationship between PAHs exposure and decreased HRV is largely unknown. This study aims to explore epigenome-wide DNA methylation changes associated with PAHs exposure and further evaluate their associations with HRV alternations among non-current smokers. We measured 10 mono-hydroxylated PAHs (OH-PAHs) in urine and DNA methylation levels in blood leukocytes among participants from three panels of Chinese non-current smokers (152 in WHZH, 99 in SY, and 53 in COW). We conducted linear regression analyses between DNA methylation and OH-PAHs metabolites with adjustment for age, gender, body mass index, drinking, blood cell counts, and surrogate variables in each panel separately, and combined the results by using inverse-variance weighted fixed-effect meta-analysis to obtain estimates of effect size. The median value of total OH-PAHs ranged from 0.92 × 10-2 in SY panel (62.6% men) to 13.82 × 10-2 μmol/mmol creatinine in COW panel (43.4% men). The results showed that methylation levels of cg18223625 (COL20A1) and cg07805771 (SLC16A1) were significantly or marginally significantly associated with urinary 2-hydroxynaphthalene [β(SE) = 0.431(0.074) and 0.354(0.068), FDR = 0.016 and 0.056, respectively], while methylation level of cg09235308 (PLEC1) was positively associated with urinary total OH-PAHs [β(SE) = 0.478(0.079), FDR = 0.004]. Hypermethylations of cg18223625, cg07805771, and cg09235308 were inversely associated with HRV indices among the WHZH and COW non-current smokers. However, we did not observe significant epigenome-wide associations for the other 9 urinary OH-PAHs. These findings provide new evidence that PAHs exposure is linked to differential DNA methylation, which may help better understand the influences of PAHs exposure on HRV alternations.
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Affiliation(s)
- Kang Liu
- Department of Occupational and Environmental Health, Key Laboratory of Environment and Health, Ministry of Education and State Key Laboratory of Environmental Health (Incubating), School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China
| | - Jing Jiang
- Department of Occupational and Environmental Health, Key Laboratory of Environment and Health, Ministry of Education and State Key Laboratory of Environmental Health (Incubating), School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China
| | - Yuhui Lin
- Department of Occupational and Environmental Health, Key Laboratory of Environment and Health, Ministry of Education and State Key Laboratory of Environmental Health (Incubating), School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China
| | - Wei Liu
- Department of Occupational and Environmental Health, Key Laboratory of Environment and Health, Ministry of Education and State Key Laboratory of Environmental Health (Incubating), School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China
| | - Xiaoyan Zhu
- Department of Occupational and Environmental Health, Key Laboratory of Environment and Health, Ministry of Education and State Key Laboratory of Environmental Health (Incubating), School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China; Suzhou Center for Disease Prevention and Control, Suzhou, 215004, China
| | - Yizhi Zhang
- Department of Occupational and Environmental Health, Key Laboratory of Environment and Health, Ministry of Education and State Key Laboratory of Environmental Health (Incubating), School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China
| | - Haijing Jiang
- Department of Occupational and Environmental Health, Key Laboratory of Environment and Health, Ministry of Education and State Key Laboratory of Environmental Health (Incubating), School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China
| | - Kuai Yu
- Department of Occupational and Environmental Health, Key Laboratory of Environment and Health, Ministry of Education and State Key Laboratory of Environmental Health (Incubating), School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China
| | - Xuezhen Liu
- Department of Occupational and Environmental Health, Key Laboratory of Environment and Health, Ministry of Education and State Key Laboratory of Environmental Health (Incubating), School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China
| | - Min Zhou
- Department of Occupational and Environmental Health, Key Laboratory of Environment and Health, Ministry of Education and State Key Laboratory of Environmental Health (Incubating), School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China
| | - Yu Yuan
- Department of Occupational and Environmental Health, Key Laboratory of Environment and Health, Ministry of Education and State Key Laboratory of Environmental Health (Incubating), School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China
| | - Pinpin Long
- Department of Occupational and Environmental Health, Key Laboratory of Environment and Health, Ministry of Education and State Key Laboratory of Environmental Health (Incubating), School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China
| | - Qiuhong Wang
- Department of Occupational and Environmental Health, Key Laboratory of Environment and Health, Ministry of Education and State Key Laboratory of Environmental Health (Incubating), School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China
| | - Xiaomin Zhang
- Department of Occupational and Environmental Health, Key Laboratory of Environment and Health, Ministry of Education and State Key Laboratory of Environmental Health (Incubating), School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China
| | - Meian He
- Department of Occupational and Environmental Health, Key Laboratory of Environment and Health, Ministry of Education and State Key Laboratory of Environmental Health (Incubating), School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China
| | - Weihong Chen
- Department of Occupational and Environmental Health, Key Laboratory of Environment and Health, Ministry of Education and State Key Laboratory of Environmental Health (Incubating), School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China
| | - Huan Guo
- Department of Occupational and Environmental Health, Key Laboratory of Environment and Health, Ministry of Education and State Key Laboratory of Environmental Health (Incubating), School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
| | - Tangchun Wu
- Department of Occupational and Environmental Health, Key Laboratory of Environment and Health, Ministry of Education and State Key Laboratory of Environmental Health (Incubating), School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China
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Association of secondhand smoke exposure with mental health in men and women: Cross-sectional and prospective analyses using the UK Health and Lifestyle Survey. Eur Psychiatry 2020; 28:276-81. [DOI: 10.1016/j.eurpsy.2012.04.001] [Citation(s) in RCA: 25] [Impact Index Per Article: 5.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 06/22/2011] [Revised: 04/02/2012] [Accepted: 04/03/2012] [Indexed: 11/18/2022] Open
Abstract
AbstractObjectives:We examine cross-sectional and prospective associations between objectively measured SHS exposure and mental health using data from the Health and Lifestyle Survey (HALS), a large, UK-wide, general population-based, prospective cohort study with measurements of carbon monoxide or salivary cotinine levels.Methods:Mental health was assessed using the 30-item version of the General Health Questionnaire (GHQ). Multivariate logistic regression models adjusting for age, sex, height, body mass index, alcohol intake, social status, and longstanding illness were used to analyze the association between exposure to SHS (exhaled CO and salivary cotinine categories) and psychological distress (≥ 5 GHQ).Results:Fully adjusted cross-sectional analysis revealed a positive relationship between exhaled carbon monoxide and psychological distress among smokers (OR 1.36; 95% CI 1.04-1.78) but not among non-smoking adults. In a similar cross-sectional analysis between cotinine level and psychological distress, non-significant associations were found among smokers and non-smokers. Prospective analyses of the cotinine-psychological distress relationship among participants without psychological distress at baseline showed no significant increased risk of psychological distress among both smokers and non-smokers. In a prospective analysis of poor mental health outcome with respect to self-report smoking and SHS status, smokers had an increased risk of psychological distress while SHS and non-smokers did not.Conclusions:A non-significant association between objectively measured SHS exposure and poor mental health was found in this study. Our findings show discrepancies with recent studies suggesting the need for additional future research in this growing field of study.
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Passive smoking and cardiometabolic risk factors in Iranian children and adolescents: CASPIAN-V study. J Diabetes Metab Disord 2019; 18:401-408. [PMID: 31890665 DOI: 10.1007/s40200-019-00429-8] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/31/2018] [Accepted: 08/04/2019] [Indexed: 02/08/2023]
Abstract
Background Smoking behavior as a harmful trend among adolescents and young adults has increased over last two decades. Many children and adolescents are at the risk of "second-hand" smoking at home due to their exposure to parents' or siblings' smoking. These second hand smokers are called "passive smokers" and are at risk of several health complications like cardiometabolic risk factors. Objectives The present study aims to evaluate the association between passive smoking and increase of cardiometabolic risk factors in a sample of Iranian's children and adolescents, aged 7-18 years. Methods This multicenter cross-sectional study was carried out over 14,400 students (aged 7-18 years). Blood sampling were randomly collected from a sub-sample of 4200 selected pupils. According to their degree of exposure to smoke for both cigarette and hookah, water pipes that are used to smoke specially made tobacco that comes in different flavors, all participants were divided to the two separate groups of positive and negative exposure. Metabolic syndrome (MetS) is defined as a constellation of at least three out of five cardiometabolic risk factors, including abdominal obesity, elevated blood pressure, elevated fasting plasma glucose concentration, high serum levels of triglycerides (TG), and depressed high-density cholesterol (HDL-C) levels. Results The mean and standard deviation (SD) age of participants was 12.3 ± 2.24 years. 49.4% were girls and 71.4% of them were urban residents. The mean SD for BMI of participants was 18.5 (4.7) Kg/m2. The mean TG levels were considerably higher among passive smoker children and adolescents. MetS and being overweight were found to have a major association with passive smoking (OR 1.63 CI 95% 1.17-2.29 P Value 0.004 and OR 1.21 95% CI 1.06-1.37 P Value 0.004, respectively). Conclusion This study confirms that passive smoking or second-hand smoking is linked with the increased prevalence of cardiometabolic risk factors and places children and adolescents at a higher risk of being overweight. Preventive strategies could be incorporated against passive smoking to recognize it as a health priority among children and adolescents.
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Kunutsor SK, Spee JM, Kieneker LM, Gansevoort RT, Dullaart RPF, Voerman AJ, Touw DJ, Bakker SJL. Self-Reported Smoking, Urine Cotinine, and Risk of Cardiovascular Disease: Findings From the PREVEND (Prevention of Renal and Vascular End-Stage Disease) Prospective Cohort Study. J Am Heart Assoc 2018; 7:JAHA.118.008726. [PMID: 29720504 PMCID: PMC6015309 DOI: 10.1161/jaha.118.008726] [Citation(s) in RCA: 14] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/16/2022]
Abstract
BACKGROUND We aimed to compare the associations of smoking exposure as assessed by self-reports and urine cotinine with cardiovascular disease (CVD) risk and determine the potential utility of cotinine for CVD risk prediction. METHODS AND RESULTS Smoking status by self-reports and urine cotinine were assessed at baseline in 4737 participants (mean age, 53 years) of the PREVEND (Prevention of Renal and Vascular End-Stage Disease) prospective study. Participants were classified as never, former, light current (≤10 cigarettes/day), and heavy current smokers (>10 cigarettes/day) according to self-reports and analogous cutoffs for urine cotinine. During a median follow-up of 8.5 years, 296 first CVD events were recorded. Compared with self-reported never smokers, the hazard ratios (95% confidence interval) of CVD for former, light current, and heavy current smokers were 0.86 (0.64-1.17), 1.28 (0.83-1.97), and 1.80 (1.27-2.57) in multivariate analysis. Compared with urine cotinine-assessed never smokers, the corresponding hazard ratios of CVD for urine cotinine-assessed former, light current, and heavy current smokers were 1.70 (1.03-2.81), 1.62 (1.15-2.28), and 1.95 (1.39-2.73) respectively. The C-index change on adding urine cotinine-assessed smoking status to a standard CVD risk prediction model (without self-reported smoking status) was 0.0098 (0.0031-0.0164; P=0.004). The corresponding C-index change for self-reported smoking status was 0.0111 (0.0042-0.0179; P=0.002). CONCLUSIONS Smoking status as assessed by self-reports and urine cotinine is associated with CVD risk; however, the nature of the association of urine cotinine with CVD is consistent with a dose-response relationship. The ability of urine cotinine to improve CVD risk assessment is similar to that of self-reported smoking status.
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Affiliation(s)
- Setor K Kunutsor
- Translational Health Sciences, Bristol Medical School, Southmead Hospital University of Bristol, United Kingdom .,National Institute for Health Research Bristol Biomedical Research Centre, University Hospitals Bristol NHS Foundation Trust University of Bristol, United Kingdom
| | - Julia M Spee
- Department of Internal Medicine, University of Groningen and University Medical Center Groningen, The Netherlands
| | - Lyanne M Kieneker
- Department of Internal Medicine, University of Groningen and University Medical Center Groningen, The Netherlands
| | - Ron T Gansevoort
- Department of Internal Medicine, University of Groningen and University Medical Center Groningen, The Netherlands
| | - Robin P F Dullaart
- Department of Internal Medicine, University of Groningen and University Medical Center Groningen, The Netherlands
| | - Albert-Jan Voerman
- Department of Pharmacy and Clinical Pharmacology, University of Groningen and University Medical Center Groningen, The Netherlands
| | - Daan J Touw
- Department of Pharmacy and Clinical Pharmacology, University of Groningen and University Medical Center Groningen, The Netherlands
| | - Stephan J L Bakker
- Department of Internal Medicine, University of Groningen and University Medical Center Groningen, The Netherlands.,Top Institute Food and Nutrition, Wageningen, The Netherlands
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Lee PN, Forey BA, Hamling JS, Thornton AJ. Environmental tobacco smoke exposure and heart disease: A systematic review. World J Meta-Anal 2017; 5:14. [DOI: 10.13105/wjma.v5.i2.14] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/06/2016] [Revised: 01/10/2017] [Accepted: 03/02/2017] [Indexed: 02/05/2023] Open
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Zeng YN, Li YM. Secondhand smoke exposure and mental health in adults: a meta-analysis of cross-sectional studies. Soc Psychiatry Psychiatr Epidemiol 2016; 51:1339-48. [PMID: 26661619 DOI: 10.1007/s00127-015-1164-5] [Citation(s) in RCA: 26] [Impact Index Per Article: 2.9] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/29/2015] [Accepted: 11/29/2015] [Indexed: 01/09/2023]
Abstract
PURPOSE Previous studies assessing secondhand smoke (SHS) and risk of mental health problems have yielded inconsistent results. We performed a meta-analysis to statistically assess the association between SHS exposure, depressive symptoms and psychological distress among adults. METHODS A systematically search of Pubmed (1946-2015) and EMBASE (1976-2015) was conducted and supplemented by bibliographies of all retrieved articles to find additional relevant citations. Odds ratios (OR) and associated 95 % confidence interval (CI) of each eligible study were extracted and pooled in our meta-analysis. RESULTS A total of 11 studies comprising 86,739 participants met the inclusion criteria. A random-effect model was used in meta-analysis since considerable heterogeneity was expected. Our results indicate that SHS exposure was significantly associated with depressive symptoms (OR 1.60, 95 % CI 1.35-1.90) and psychological distress (OR 1.32, 95 % CI 1.11-1.56). CONCLUSION Exposure to SHS among non-smoker is associated with depressive symptoms and psychological distress, emphasizing the significance of reducing SHS exposure at a population level.
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Affiliation(s)
- Yan-Ni Zeng
- Department of Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan Province, China
| | - Ya-Min Li
- Department of Nursing, The Second Xiangya Hospital, Central South University, Changsha, Hunan Province, China.
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Kelishadi R, Noori A, Qorbani M, Rahimzadeh S, Djalalinia S, Shafiee G, Motlagh ME, Ardalan G, Ansari H, Asayesh H, Ahadi Z, Heshmat R. Are active and passive smoking associated with cardiometabolic risk factors in adolescents? The CASPIAN-III Study. Paediatr Int Child Health 2016; 36:181-8. [PMID: 26055078 DOI: 10.1179/2046905515y.0000000039] [Citation(s) in RCA: 25] [Impact Index Per Article: 2.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 10/31/2022]
Abstract
BACKGROUND Smoking is an important risky behavior in adolescents worldwide. Active and passive smoking have adverse health effects at public and individual levels. OBJECTIVE This study aimed to evaluate the association of active and passive smoking with cardiometabolic risk factors in a national sample of Iranian adolescents. METHODS Participants consisted of 5625 students, aged 10-18 years, studied in the third survey of a national school-based surveillance system. Participants were classified into three groups based on smoking pattern: active smoker, passive smoker, and exposure to smoke (active or passive or both of them). Considering the Adult Treatment Panel III criteria modified for the paediatric age group, metabolic syndrome (MetS) was defined as the co-existence of three out of five components of abdominal obesity, elevated blood pressure, elevated fasting plasma glucose, high serum triglycerides, and depressed high-density cholesterol (HDL-C) levels. RESULTS The mean (SD) age of participants was 14.7 (2.4) years. Mean level of HDL-C was significantly lower in all types of smoking compared to non-smokers. Low HDL-C and MetS had significant association with active smoking (OR 2.10, 95% CI 1.33-3.31 and OR 5.24, 95% CI 2.41-11.37), passive smoking (OR 1.19, 95% CI 1.01-1.43 and OR 1.79, 95% CI 1.09-2.96), and smoking exposure (OR 1.20, 95% CI 1.01-1.43 and OR 2.02, 95% CI 1.22-3.31), respectively. CONCLUSION This study confirms that both smoking and exposure to smoke are associated with an increased risk of MetS and some of the cardiometabolic risk factors in adolescents. Preventive measures against passive smoking should be considered as a health priority in the paediatric age groups.
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Affiliation(s)
- Roya Kelishadi
- a Child Growth and Development Research Center, Research Institute for Primordial Prevention of Non-communicable Disease , Isfahan University of Medical Sciences , Isfahan
| | - Atefeh Noori
- b Non-communicable Diseases Research Center, Endocrinology and Metabolism Population Sciences Institute , Tehran University of Medical Sciences
| | - Mostafa Qorbani
- c Department of Community Medicine , Alborz University of Medical Sciences , Karaj.,d Chronic Diseases Research Center, Endocrinology and Metabolism Population Sciences Institute, Endocrinology and Metabolism Research Institute , Tehran University of Medical Sciences , Tehran
| | - Shadi Rahimzadeh
- b Non-communicable Diseases Research Center, Endocrinology and Metabolism Population Sciences Institute , Tehran University of Medical Sciences
| | - Shirin Djalalinia
- b Non-communicable Diseases Research Center, Endocrinology and Metabolism Population Sciences Institute , Tehran University of Medical Sciences.,e Development of Research and Technology Center, Deputy of Research and Technology , Ministry of Health and Medical Education , Tehran
| | - Gita Shafiee
- d Chronic Diseases Research Center, Endocrinology and Metabolism Population Sciences Institute, Endocrinology and Metabolism Research Institute , Tehran University of Medical Sciences , Tehran
| | | | - Gelayol Ardalan
- a Child Growth and Development Research Center, Research Institute for Primordial Prevention of Non-communicable Disease , Isfahan University of Medical Sciences , Isfahan
| | - Hossein Ansari
- g Health Promotion Research Center , Zahedan University of Medical Sciences
| | - Hamid Asayesh
- h Department of Medical Emergencies , Qom University of Medical Sciences , Qom , Iran
| | - Zeinab Ahadi
- d Chronic Diseases Research Center, Endocrinology and Metabolism Population Sciences Institute, Endocrinology and Metabolism Research Institute , Tehran University of Medical Sciences , Tehran
| | - Ramin Heshmat
- d Chronic Diseases Research Center, Endocrinology and Metabolism Population Sciences Institute, Endocrinology and Metabolism Research Institute , Tehran University of Medical Sciences , Tehran
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Lai CH, Han CK, Shibu MA, Pai PY, Ho TJ, Day CH, Tsai FJ, Tsai CH, Yao CH, Huang CY. Lumbrokinase from earthworm extract ameliorates second-hand smoke-induced cardiac fibrosis. ENVIRONMENTAL TOXICOLOGY 2015; 30:1216-1225. [PMID: 24706507 DOI: 10.1002/tox.21993] [Citation(s) in RCA: 12] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Received: 01/27/2014] [Revised: 03/19/2014] [Accepted: 03/23/2014] [Indexed: 06/03/2023]
Abstract
Exposure to tobacco smoke has epidemiologically been linked to the occurrence of cardiovascular disease among nonsmokers but the associated molecular events are not well elucidated yet. When Sprague Dawley rats were exposed to second-hand tobacco cigarette smoke twice a day for a 30 days period at an exposure rate of 10 cigarettes/30 min, they showed adverse effects including reduced left ventricle weight, increased cardiac damages, deteriorated cardiac features, and cardiac fibrosis. Exposure to second-hand smoking (SHS) increased the molecular markers of cardiac fibrosis such as urokinase plasminogen activator and matrix metallopeptidases. The modulations in the protein levels were led by the activation of extracellular signal-regulated kinases (ERK1/2), the transcription factor-specificity protein 1 (SP1), and the fibrogenic master switch-connective for epithelial-mesenchymal transition tissue growth factor there by indicating their effective role in SHS-induced myocardial infraction. Dilong, an edible earthworm extract used in Chinese medicine and its bioactive fibrinolytic enzyme product-lumbrokinase, when administered in rats, restricted the SHS exposure induced cardiac fibrosis and provided cardio-protection. The results show that lumbrokinase and dilong administration can efficiently prevent epidemiological incidence of cardiac disease among SHS-exposed nonsmokers.
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Affiliation(s)
- Chao-Hung Lai
- Graduate Institute of Aging Medicine, China Medical University, Taichung, Taiwan
- Division of Cardiology, Department of Internal Medicine, Armed Force Taichung General Hospital, Taichung, Taiwan
| | - Chien-Kuo Han
- Department of Health and Nutrition Biotechnology, Asia University, Taichung, Taiwan
| | | | - Pei Ying Pai
- Division of Cardiology, China Medical University Hospital, Taichung, Taiwan
| | - Tsung-Jung Ho
- Graduate Institute of Chinese Medical Science, China Medical University, Taichung, Taiwan
- Department of Chinese Medicine, China Medical University Beigang Hospital, Taiwan
| | | | - Fuu-Jen Tsai
- Graduate Institute of Chinese Medical Science, China Medical University, Taichung, Taiwan
| | - Chang-Hai Tsai
- Department of Healthcare Administration, Asia University, Taichung, Taiwan
| | - Chun-Hsu Yao
- Department of Biomedical Imaging and Radiological Science, China Medical University, Taichung, Taiwan
| | - Chih-Yang Huang
- Department of Health and Nutrition Biotechnology, Asia University, Taichung, Taiwan
- Graduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan
- Graduate Institute of Chinese Medical Science, China Medical University, Taichung, Taiwan
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Ueno M, Ohara S, Sawada N, Inoue M, Tsugane S, Kawaguchi Y. The association of active and secondhand smoking with oral health in adults: Japan public health center-based study. Tob Induc Dis 2015. [PMID: 26225132 PMCID: PMC4518564 DOI: 10.1186/s12971-015-0047-6] [Citation(s) in RCA: 11] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/30/2022] Open
Abstract
Background Smoking is one of the major risk factors for oral diseases, and many studies have found that active smoking is closely associated with the prevalence or severity of periodontal disease and fewer remaining teeth. In contrast to the established association between active smoking and oral health, there have been very few studies investigating the effects of secondhand smoking on oral health, and whether secondhand smoking deteriorates oral health has not been fully clarified. The purpose of the present study was to examine whether active and secondhand smoking were associated with the prevalence of severe periodontal disease and number of teeth among Japanese adults. Methods Subjects were 1,164 dentate adults aged 55–75 years as of May 2005 who participated in both the Japan Public Health Center-Based Study Cohort I in 1990 and a dental survey in 2005. The dental survey was implemented in the Yokote health center jurisdiction, Akita Prefecture. Participating subjects completed a self-administered questionnaire and a clinical oral examination. The association of smoking status with prevalence of periodontal disease was analyzed using a logistic regression, and with number of teeth or functional tooth units of natural teeth (n-FTUs) using a generalized linear model. Results After adjusting for age, education level, history of diabetes, BMI, alcohol consumption, perceived mental stress, presence of a family dentist, and oral hygiene, the odds ratio (OR) of risk for periodontal disease in male subjects was significantly increased in non-smokers with secondhand smoking only at home (OR = 3.14, 95 % CI: 1.08−9.12, p = 0.036), non-smokers with secondhand smoking both at home and other places (OR = 3.61, 95 % CI: 1.33−9.81, p = 0.012) and current smokers (OR = 3.31, 95 % CI: 1.54−7.08, p = 0.002), compared to non-smokers without secondhand smoking. Further in men, current smokers had significantly fewer numbers of teeth (19.7 ± 6.82) and n-FTUs (4.92 ± 4.12) than non-smokers without secondhand smoking (22.2 ± 6.92, p = 0.014 and 6.56 ± 4.18, p = 0.007). Such significant relationships of smoking status with periodontal disease and dentition were not observed in women. Conclusions The present study indicates that active smoking as well as secondhand smoking may have harmful effects on periodontal health in men. Therefore, it is imperative for health and oral health professionals to enlighten people about the negative influence of smoking, not only on their own health but also on others’ health.
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Affiliation(s)
- Masayuki Ueno
- Department of Oral Health Promotion, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan
| | - Satoko Ohara
- Department of Comprehensive Oral Health Care, Faculty of Dentistry, Tokyo Medical and Dental University, Tokyo, Japan
| | - Norie Sawada
- Epidemiology and Prevention Division, Research Center for Cancer Prevention and Screening, National Cancer Center, Tokyo, Japan
| | - Manami Inoue
- Epidemiology and Prevention Division, Research Center for Cancer Prevention and Screening, National Cancer Center, Tokyo, Japan ; AXA Department of Health and Human Security, Graduate School of Medicine, University of Tokyo, Tokyo, Japan
| | - Shoichiro Tsugane
- Epidemiology and Prevention Division, Research Center for Cancer Prevention and Screening, National Cancer Center, Tokyo, Japan
| | - Yoko Kawaguchi
- Department of Oral Health Promotion, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan
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Modeling the effects of indoor passive smoking at home, work, or other households on adult cardiovascular and mental health: the Scottish Health Survey, 2008-2011. INTERNATIONAL JOURNAL OF ENVIRONMENTAL RESEARCH AND PUBLIC HEALTH 2014; 11:3096-107. [PMID: 24633145 PMCID: PMC3987022 DOI: 10.3390/ijerph110303096] [Citation(s) in RCA: 15] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Subscribe] [Scholar Register] [Received: 02/04/2014] [Revised: 02/27/2014] [Accepted: 03/04/2014] [Indexed: 02/07/2023]
Abstract
Passive smoking has contributed increased risks of cardiovascular disease, mental health, and mortality, but the cumulative effects from work or other households were less studied. Therefore, it was aimed to model the effects of indoor passive smoking from own home, work, and other households in a country-wide, population-based setting. Data in the Scottish Health Survey between 2008 and 2011 after the law banning smoking in public places were analyzed. Information including demographics, lifestyle factors, and self-reported cardiovascular disease and mental health was obtained by household interview. Analyses included chi-square test and survey-weighted logistic regression modeling. After full adjustment, it was observed that being exposed to indoor passive smoking, in particular in more than two places of exposure, was significantly associated with risks of stroke, angina, heart attack, abnormal heart rhythms, and GHQ ≥ 12. The significance remained for angina, GHQ ≥ 12 and probably heart attack in never smokers. The cumulative risks also impacted on sleep problems, self-recognition, making decisions, self-confidence, under strain constantly, depressed, happiness and self-worth. The significance remained for sleep problems, self-confidence, under strain constantly, depressed, and happiness in never smokers. Elimination of indoor passive smoking from different sources should still be a focus in future public health programs.
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Avila-Tang E, Al-Delaimy WK, Ashley DL, Benowitz N, Bernert JT, Kim S, Samet JM, Hecht SS. Assessing secondhand smoke using biological markers. Tob Control 2013; 22:164-71. [PMID: 22940677 PMCID: PMC3639350 DOI: 10.1136/tobaccocontrol-2011-050298] [Citation(s) in RCA: 174] [Impact Index Per Article: 14.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/01/2011] [Accepted: 07/29/2012] [Indexed: 01/13/2023]
Abstract
Secondhand smoke exposure (SHSe) is a known cause of many adverse health effects in adults and children. Increasingly, SHSe assessment is an element of tobacco control research and implementation worldwide. In spite of decades of development of approaches to assess SHSe, there are still unresolved methodological issues; therefore, a multidisciplinary expert meeting was held to catalogue the approaches to assess SHSe and with the goal of providing a set of uniform methods for future use by investigators and thereby facilitate comparisons of findings across studies. The meeting, held at Johns Hopkins, in Baltimore, Maryland, USA, was supported by the Flight Attendant Medical Research Institute (FAMRI). A series of articles were developed to summarise what is known about self-reported, environmental and biological SHSe measurements. Non-smokers inhale toxicants in SHS, which are mainly products of combustion of organic materials and are not specific to tobacco smoke exposure. Biomarkers specific to SHSe are nicotine and its metabolites (e.g., cotinine), and metabolites of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). Cotinine is the preferred blood, saliva and urine biomarker for SHSe. Cotinine and nicotine can also be measured in hair and toenails. NNAL (4-[methylnitrosamino]-1-[3-pyridyl]-1-butanol), a metabolite of NNK, can be determined in the urine of SHS-exposed non-smokers. The selection of a particular biomarker of SHSe and the analytic biological medium depends on the scientific or public health question of interest, study design and setting, subjects, and funding. This manuscript summarises the scientific evidence on the use of biomarkers to measure SHSe, analytical methods, biological matrices and their interpretation.
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Affiliation(s)
- Erika Avila-Tang
- 1Department of Epidemiology, Institute for Global Tobacco Control, Johns Hopkins Bloomberg School of Public Health, 2213 McElderry Street, 4th Floor, Baltimore, MD 21205, USA.
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Abstract
In this review, we have sought to examine the epidemiological, basic science, and public health data regarding the association between second-hand smoke (SHS) exposure and the development of coronary heart disease (CHD). SHS increases the risk of CHD by 25-30% according to multiple cohort, case-control, and meta-analytical studies. Physiologic and basic science research suggest that the mechanisms by which SHS affects the cardiovascular system are multiple and include increased thrombogenesis and low-density lipoprotein oxidation, decreased exercise tolerance, dysfunctional flow-mediated vasodilatation, and activation of inflammatory pathways with concomitant oxidative damage and impaired vascular repair. As a result, chronic exposure promotes atherogenesis and the development of cardiovascular disease, increasing the risk of having an acute coronary syndrome (ACS). With the implementation of statewide and nationwide public smoke-free legislation across the United States and Europe, respectively, over the last 10-15 years, there has been a significant and reciprocal decline in the incidence of emergency admissions for ACS by an average 17% despite persistent attempts on the part of the tobacco industry to diminish the correlation between SHS exposure and CHD. These findings underscore the importance of the effects of smoking legislation on community health.
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Affiliation(s)
- Andrew Dunbar
- Department of Internal Medicine, New York Presbyterian/Weill Cornell Medical Center, New York, NY, USA
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13
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Young D, Borland R, Coghill K. An actor-network theory analysis of policy innovation for smoke-free places: understanding change in complex systems. Am J Public Health 2010; 100:1208-17. [PMID: 20466949 PMCID: PMC2882392 DOI: 10.2105/ajph.2009.184705] [Citation(s) in RCA: 30] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Accepted: 12/17/2009] [Indexed: 11/04/2022]
Abstract
Complex, transnational issues like the tobacco epidemic are major challenges that defy analysis and management by conventional methods, as are other public health issues, such as those associated with global food distribution and climate change. We examined the evolution of indoor smoke-free regulations, a tobacco control policy innovation, and identified the key attributes of those jurisdictions that successfully pursued this innovation and those that to date have not. In doing so, we employed the actor-network theory, a comprehensive framework for the analysis of fundamental system change. Through our analysis, we identified approaches to help overcome some systemic barriers to the solution of the tobacco problem and comment on other complex transnational problems.
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Affiliation(s)
- David Young
- VicHealth Centre for Tobacco Control, Cancer Council Victoria, Carlton, Australia.
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Lightwood JM, Glantz SA. Declines in acute myocardial infarction after smoke-free laws and individual risk attributable to secondhand smoke. Circulation 2009; 120:1373-9. [PMID: 19770392 DOI: 10.1161/circulationaha.109.870691] [Citation(s) in RCA: 200] [Impact Index Per Article: 12.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/14/2023]
Abstract
BACKGROUND The estimated effects of recent pubic and workplace smoking restriction laws suggest that they produce significant declines in community rates of heart attack. The consistency of these declines with existing estimates of the relative risk of heart attack in individuals attributable to passive smoking exposure is poorly understood. The objective is to determine the consistency of estimates of reductions in community rates of heart attacks resulting from smoking restriction laws with estimates of the relative risk of heart disease in individuals exposed to passive smoking. METHODS AND RESULTS Meta-analyses of existing estimates of declines in community rates were compared with a mathematical model of the relationship between individual risk and community rates. The outcome measure is the ratio of community rates of acute myocardial infarction (after divided by before implementation of a smoking restriction law). There is a significant drop in the rate of acute myocardial infarction hospital admissions associated with the implementation of strong smoke-free legislation. The primary reason for heterogeneity in results of different studies is the duration of follow-up after adoption of the law. The pooled random-effects estimate of the rate of acute myocardial infarction hospitalization 12 months after implementation of the law is 0.83 (95% confidence interval, 0.80 to 0.87), and this benefit grows with time. This drop in admissions is consistent with a range of plausible individual risk and exposure scenarios. CONCLUSIONS Passage of strong smoke-free legislation produces rapid and substantial benefits in terms of reduced acute myocardial infarctions, and these benefits grow with time.
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Affiliation(s)
- James M Lightwood
- Department of Clinical Pharmacy, University of California, 3333 California St, Suite 420, San Francisco, CA 94118, USA.
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Lightwood JM, Coxson PG, Bibbins-Domingo K, Williams LW, Goldman L. Coronary heart disease attributable to passive smoking: CHD Policy Model. Am J Prev Med 2009; 36:13-20. [PMID: 19095162 PMCID: PMC3940697 DOI: 10.1016/j.amepre.2008.09.030] [Citation(s) in RCA: 18] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/26/2007] [Revised: 07/08/2008] [Accepted: 09/08/2008] [Indexed: 11/17/2022]
Abstract
BACKGROUND Passive smoking is a major risk factor for coronary heart disease (CHD), and existing estimates are out of date due to recent and substantial changes in the level of exposure. OBJECTIVE To estimate the annual clinical burden and cost of CHD treatment attributable to passive smoking. OUTCOME MEASURES Annual attributable CHD deaths, myocardial infarctions (MI), total CHD events, and the direct cost of CHD treatment. METHODS A Monte Carlo simulation estimated the CHD events and costs as a function of the prevalence of CHD risk factors, including passive-smoking prevalence and a low (1.26) and high (1.65) relative risk of CHD due to passive smoking. Estimates were calculated using the CHD Policy Model, calibrated to reproduce key CHD outcomes in the baseline Year 2000 in the U.S. RESULTS At 1999-2004 levels, passive smoking caused 21,800 (SE=2400) to 75,100 (SE=8000) CHD deaths and 38,100 (SE=4300) to 128,900 (SE=14,000) MIs annually, with a yearly CHD treatment cost of $1.8 (SE=$0.2) to $6.0 (SE=$0.7) billion. If recent trends in the reduction in the prevalence of passive smoking continue from 2000 to 2008, the burden would be reduced by approximately 25%-30%. CONCLUSIONS Passive smoking remains a substantial clinical and economic burden in the U.S.
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Affiliation(s)
- James M Lightwood
- Department of Clinical Pharmacy, University of California San Francisco, San Francisco, California, USA.
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Al-Delaimy WK, Willett WC. Measurement of tobacco smoke exposure: comparison of toenail nicotine biomarkers and self-reports. Cancer Epidemiol Biomarkers Prev 2008; 17:1255-61. [PMID: 18483348 DOI: 10.1158/1055-9965.epi-07-2695] [Citation(s) in RCA: 34] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/16/2022] Open
Abstract
BACKGROUND Accurate measurement tools of exposure for use in large epidemiologic studies are lacking. Biomarkers of tobacco exposure provide additional advantages to self-reports and there is a need to further develop and validate them. The objective is to compare toenail nicotine levels, a novel biomarker of tobacco exposure, with self-reports of tobacco exposure from a large cohort study. METHODS In this cross-sectional analysis, toenail samples were collected from 2,485 women participating in the Nurses' Health Study in 1982. Detailed self-reports of smoking habits and reported exposure to secondhand smoke (SHS) were collected from these women near the time of toenail collection. The toenail samples were analyzed by a high-performance liquid chromatography method for measuring nicotine. RESULTS The 5 to 95 percentile range of toenail nicotine was from 0.06 to 4.06 ng/mg toenail and the median level was 0.21 ng/mg. There was a significant difference in toenail nicotine levels according to reported smoking status (the median level for nonsmokers with no SHS was 0.10 ng/mg, the median level for nonsmokers with SHS was 0.14 ng/mg, and the median level for active smokers was 1.77 ng/mg). However there was considerable overlap in nicotine levels according to reported smoking status. Toenail nicotine level was strongly associated with reported smoking level (Spearman r = 0.63), but there was no complete concordance, suggesting that the two methods are measuring different aspects of the same exposure. CONCLUSION Our findings show that toenail nicotine levels capture the overall burden of tobacco smoke exposure and provide additional information on exposure not captured by reported history.
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Affiliation(s)
- Wael K Al-Delaimy
- Moores UCSD Cancer Center, Department of Family and Preventive Medicine, University of California-San Diego, La Jolla, CA 92093, USA.
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Wu FY, Chiu HT, Wu HDI, Lin CJ, Lai JS, Kuo HW. Comparison of urinary and plasma cotinine levels during the three trimesters of pregnancy. Paediatr Perinat Epidemiol 2008; 22:296-301. [PMID: 18426525 DOI: 10.1111/j.1365-3016.2008.00927.x] [Citation(s) in RCA: 23] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/30/2022]
Abstract
Assays of metabolised cotinine are considered to be an accurate measure of exposure to cigarette smoke among pregnant women. We investigated the association and differences between the cotinine levels in maternal urine and blood, and the umbilical cord blood of three tobacco exposure groups at different stages of pregnancy. A prospective study was conducted among 398 pregnant women undergoing prenatal care in different trimesters at two medical centres and one regional hospital in central Taiwan. All 398 subjects (including 25 smokers, 191 passive smokers and 182 non-smokers) remained in the study up to the time of delivery; 384 of them delivered singleton live births. Cotinine levels were assayed in the maternal plasma and urine of the mothers at each trimester and in the cord blood of the newborns. All specimens were measured using a sensitive high-performance liquid chromatography. Cotinine concentrations in plasma and urine showed a significant dose-dependent difference among the three groups (non-smoker, passive and active smoker) and a trend that increased with gestation among the pregnant women. Significant correlations between cotinine concentrations in plasma and urine among the pregnant women in each trimester were found. In addition, the level of cotinine in umbilical cord blood was significantly correlated with that in maternal blood at term (r = 0.89, P < 0.001). A pattern of elevated cotinine concentrations in the plasma and urine of pregnant women from the beginning to the end of pregnancy was found, and this correlated significantly with the cotinine levels in the umbilical cord blood.
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Affiliation(s)
- Fang Y Wu
- Institute of Environmental Health, College of Public Health, China Medical University, Taiwan
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Looney SW, Hagan JL. 4 Statistical Methods for Assessing Biomarkers and Analyzing Biomarker Data. HANDBOOK OF STATISTICS 2007. [DOI: 10.1016/s0169-7161(07)27004-x] [Citation(s) in RCA: 8] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 12/12/2022]
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Boffetta P, Clark S, Shen M, Gislefoss R, Peto R, Andersen A. Serum cotinine level as predictor of lung cancer risk. Cancer Epidemiol Biomarkers Prev 2006; 15:1184-8. [PMID: 16775179 DOI: 10.1158/1055-9965.epi-06-0032] [Citation(s) in RCA: 67] [Impact Index Per Article: 3.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/16/2022] Open
Abstract
BACKGROUND No prospective studies are available on serum cotinine level as a marker of lung cancer risk. METHODS We analyzed serum cotinine level among 1,741 individuals enrolled since the 1970s in a prospective study of Norwegian volunteers who developed lung cancer during the follow-up and 1,741 matched controls free from lung cancer. Serum cotinine was measured with a competitive immunoassay. Regression dilution was corrected for based on repeated measures on samples from 747 subjects. RESULTS Mean serum cotinine level was higher in cases than in controls. Compared with subjects with a cotinine level of < or = 5 ng/mL, the odds ratio of lung cancer was increasing linearly, reaching 55.1 (95% confidence interval, 35.7-85.0) among individuals with a serum cotinine level of > 378 ng/mL. There was no clear suggestion of a plateau in risk at high exposure levels. Odds ratios were very similar in men and women. We found no association between serum cotinine level (range, 0.1-9.9 ng/mL) and lung cancer risk among self-reported nonsmokers and long-term quitters (79 cases and 350 controls). DISCUSSION The association between tobacco smoking and lung cancer risk might be stronger than is estimated from questionnaire-based studies. Serum cotinine level is a predictor of risk of lung cancer among smokers. The reported plateau in risk at high doses is likely due mainly to artifacts. There is no difference between men and women in the carcinogenicity of tobacco smoking.
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Repace J, Al-Delaimy WK, Bernert JT. Correlating atmospheric and biological markers in studies of secondhand tobacco smoke exposure and dose in children and adults. J Occup Environ Med 2006; 48:181-94. [PMID: 16474267 DOI: 10.1097/01.jom.0000184883.72902.d4] [Citation(s) in RCA: 29] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/25/2022]
Abstract
OBJECTIVE We sought to directly compare secondhand smoke (SHS) atmospheric markers to each other and to SHS dosimetric biomarkers, permitting intercomparison of clinical and atmospheric studies. METHODS We used atmospheric and pharmacokinetic (PK) models for the quantitative estimation of SHS exposure and dose for infants, children, and adults, based on building smoker density and air exchange rate, and from exposure duration, default PK parameters, and respiration rates. RESULTS We estimate the SHS serum cotinine doses for the typical and most-exposed individuals in the U.S. population; predictions compare well to measurements on a national probability sample. Using default respiration rates, we estimate serum cotinine dose from SHS nicotine exposure for 40 adults exposed to SHS in an environmental chamber; predictions agreed with observations. We correlate urine cotinine and hair nicotine levels for 127 infants exposed to parental smoking, and estimate corresponding atmospheric nicotine exposure via PK modeling. CONCLUSIONS Our "Rosetta Stone" Equations allow the SHS atmospheric markers, respirable particles, nicotine, and carbon monoxide, to be related to the SHS biomarkers, cotinine in blood, urine, and saliva and nicotine in hair, permitting intercomparison of clinical and atmospheric studies of SHS for the first time.
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Affiliation(s)
- James Repace
- Tufts University School of Medicine, and Repace Associates Inc., 101 Felicia Lane, Bowie, MD 20720, USA.
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Kaur S, Cohen A, Dolor R, Coffman CJ, Bastian LA. The impact of environmental tobacco smoke on women's risk of dying from heart disease: a meta-analysis. J Womens Health (Larchmt) 2005; 13:888-97. [PMID: 15671704 DOI: 10.1089/jwh.2004.13.888] [Citation(s) in RCA: 18] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/14/2023] Open
Abstract
OBJECTIVE To review systematically and analyze the association between environmental tobacco smoke (ETS) exposure and the risk of dying from heart disease in women. METHODS We searched the English-language literature using MEDLINE (1966-April 2004), CINAHL, PsychInfo, and bibliographies of selected studies. We included studies that specifically addressed the association of ETS and heart disease mortality in women and had adequate controls and retrievable risk estimates. We looked for either cohort studies or randomized controlled trials. Studies were evaluated independently by two of the authors. Nine cohort studies were finally selected for analysis. We estimated the summary relative risk (RR) and associated 95% confidence intervals (95% CI) using a random-effects model. RESULTS Mean follow-up periods for these cohorts ranged from 6 to 39 years. Among non-smoking women, exposure to ETS was associated with a 15% increase in the risk of dying from heart disease compared with nonsmoking women not exposed to ETS (RR = 1.15, 95% CI 1.03-1.28, p < 0.05). CONCLUSIONS Among nonsmoking women, exposure to passive smoke increases the risk of dying from heart disease. In accordance with the newly developed guidelines by the American Heart Association for prevention of cardiovascular disease (CVD) in women, we recommend counseling women on reducing or avoiding ETS exposure.
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Affiliation(s)
- Suneet Kaur
- Health Services Research and Development, Durham Veterans Affairs Medical Center, Durham, North Carolina 27705, USA.
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Chen R, Tunstall-Pedoe H, Tavendale R. Best estimates of coronary risk of passive smoking are needed. BMJ 2004; 329:918. [PMID: 15485986 PMCID: PMC523163 DOI: 10.1136/bmj.329.7471.918-b] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/03/2022]
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Whincup PH, Gilg JA, Emberson JR, Jarvis MJ, Feyerabend C, Bryant A, Walker M, Cook DG. Passive smoking and risk of coronary heart disease and stroke: prospective study with cotinine measurement. BMJ 2004; 329:200-5. [PMID: 15229131 PMCID: PMC487731 DOI: 10.1136/bmj.38146.427188.55] [Citation(s) in RCA: 192] [Impact Index Per Article: 9.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/29/2022]
Abstract
OBJECTIVE To examine the associations between a biomarker of overall passive exposure to tobacco smoke (serum cotinine concentration) and risk of coronary heart disease and stroke. DESIGN Prospective population based study in general practice (the British regional heart study). PARTICIPANTS 4729 men in 18 towns who provided baseline blood samples (for cotinine assay) and a detailed smoking history in 1978-80. MAIN OUTCOME MEASURE Major coronary heart disease and stroke events (fatal and non-fatal) during 20 years of follow up. RESULTS 2105 men who said they did not smoke and who had cotinine concentrations < 14.1 ng/ml were divided into four equal sized groups on the basis of cotinine concentrations. Relative hazards (95% confidence intervals) for coronary heart disease in the second (0.8-1.4 ng/ml), third (1.5-2.7 ng/ml), and fourth (2.8-14.0 ng/ml) quarters of cotinine concentration compared with the first (> or = 0.7 ng/ml) were 1.45 (1.01 to 2.08), 1.49 (1.03 to 2.14), and 1.57 (1.08 to 2.28), respectively, after adjustment for established risk factors for coronary heart disease. Hazard ratios (for cotinine 0.8-14.0 nu > or = 0.7 ng/ml) were particularly increased during the first (3.73, 1.32 to 10.58) and second five year follow up periods (1.95, 1.09 to 3.48) compared with later periods. There was no consistent association between cotinine concentration and risk of stroke. CONCLUSION Studies based on reports of smoking in a partner alone seem to underestimate the risks of exposure to passive smoking. Further prospective studies relating biomarkers of passive smoking to risk of coronary heart disease are needed.
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Affiliation(s)
- Peter H Whincup
- Department of Community Health Sciences, St George's Hospital Medical School, London SW17 0RE.
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Moshammer H, Neuberger M, Nebot M. Nicotine and surface of particulates as indicators of exposure to environmental tobacco smoke in public places in Austria. Int J Hyg Environ Health 2004; 207:337-43. [PMID: 15471097 DOI: 10.1078/1438-4639-00299] [Citation(s) in RCA: 12] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/18/2022]
Abstract
As part of a Europe-wide project the amount of exposure to environmental tobacco smoke (ETS) in public places like schools, restaurants, and public transport facilities was investigated. Three methods were applied: nicotine passive samplers (with a filter treated with sodium bisulphate), the same filters with an active sampling device, and the measurement of fine particles' active surface by unipolar diffusion charging. Settings were selected where either high or low ETS concentrations were expected and where non-smokers would have to stay or at least to pass by. Highest ETS concentrations were found in discos (mean nicotine concentration 154.4 maximum 487.1 microg/m3) and intermediate concentrations in restaurants with no significant difference between smoking (21.3 +/- 6.1 microg/m3) and non-smoking areas (23.3 +/- 15.9 microg/m3) but on average higher values in restaurants with no separation between smoking and non-smoking areas (38.0 +/- 60.6 microg/m3). Concentrations usually below 10 microg/m3 were found in transport facilities (8.9 +/- 8.0 microg/m3, maximum 20.6 in the restaurant section of a railway station's waiting room) and in schools (3.0 +/- 4.6 microg/m3). In hospitals "problem spots" were sought and so concentrations from very low to as high as 45.1 microg/m3 next to a smoking area with no physical barrier or separation and 47.7 microg/m3 inside a smoking room could be documented (21.4 +/- 39.3 microg/m3). The fine particle's surface correlated well with the nicotine concentration (r = 0.8; p < 0.001). Only in one instance (in a pizza restaurant on a busy road with heavy duty diesel traffic and the sampling spot next to the pizza stove) high concentration of fine particles was detected without high nicotine. Tobacco smoke is a key source of indoor fine particles. Health policy must intervene to change the situation found at present in many public places in Austria.
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Pitsavos C, Panagiotakos DB, Chrysohoou C, Skoumas J, Tzioumis K, Stefanadis C, Toutouzas P. Association between exposure to environmental tobacco smoke and the development of acute coronary syndromes: the CARDIO2000 case-control study. Tob Control 2002; 11:220-5. [PMID: 12198272 PMCID: PMC1759016 DOI: 10.1136/tc.11.3.220] [Citation(s) in RCA: 55] [Impact Index Per Article: 2.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/14/2023]
Abstract
OBJECTIVE To investigate the association between environmental tobacco smoke (ETS) exposure (at least 30 minutes a day) and the risk of developing acute coronary syndromes (ACS). DESIGN AND SETTING The CARDIO2000 is a case-control study which was conducted in Greece from 2000 to 2001. Cases included 847 individuals with a first event of ACS and 1078 cardiovascular disease-free controls. Cases and controls were frequency matched on age (within three years of age), sex, and region. MAIN OUTCOME MEASURES ACS was defined as a diagnosis of first acute myocardial infarction or unstable angina. Main independent variable: Exposure to ETS was measured by self report as follows: after the second day of hospitalisation for the cases, and at the entry for the controls, participants were asked whether they were currently exposed to tobacco smoke from other people (home and/or work) for more than 30 minutes a day. The responses were categorised into three levels: no exposure, occasional exposure (< 3 times per week), and regular exposure. In addition participants were asked how many years they had been exposed. Because these were self reported assessments and prone to bias, the results were compared to reports obtained from subjects' relatives or friends, using the Kendal's tau coefficient that showed high agreement. RESULTS 731 (86%) of the patients and 605 (56%) of the controls reported current exposure of 30 minutes per day or more to ETS. Among current non-smokers, cases were 47% more likely to report regular exposure to ETS (odds ratio (OR) 1.47, 95% confidence interval (CI) 1.26 to 1.80) compared to controls. Exposure to ETS at work was associated with a greater risk of ACS compared to home exposure (+97% v +33%). The risk of ACS was also raised in active smokers (OR 2.83, 95% CI 2.07 to 3.31) regularly exposed to ETS. CONCLUSIONS This study supports the hypothesis that exposure to ETS increases the risk of developing ACS. The consistency of these findings with the existing totality of evidence presented in the literature supports the role of ETS in the aetiology of ACS.
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Affiliation(s)
- C Pitsavos
- Section of Preventive Cardiology, Department of Cardiology, School of Medicine, University of Athens, Greece
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Panagiotakos DB, Chrysohoou C, Pitsavos C, Papaioannou I, Skoumas J, Stefanadis C, Toutouzas P. The association between secondhand smoke and the risk of developing acute coronary syndromes, among non-smokers, under the presence of several cardiovascular risk factors: The CARDIO2000 case-control study. BMC Public Health 2002; 2:9. [PMID: 12031093 PMCID: PMC116572 DOI: 10.1186/1471-2458-2-9] [Citation(s) in RCA: 28] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/11/2001] [Accepted: 05/24/2002] [Indexed: 11/29/2022] Open
Abstract
BACKGROUND The purpose of this study was to investigate the association between secondhand smoke and the risk of developing a first event of acute coronary syndromes (ACS), i.e. acute myocardial infarction or unstable angina, among non-smokers, in relation to the presence of several other cardiovascular risk factors. METHODS Eight hundred and forty-eight patients with first event of ACS and 1078 cardiovascular disease-free matched controls completed a detailed questionnaire regarding their exposure to secondhand smoke, among other investigated parameters. RESULTS Two hundred and ninety-seven (35%) of the patients and 259 (24%) of the controls were defined as secondhand smokers. After controlling for several potential confounders, the results showed that non-smokers occasionally (< 3 time per week) exposed to cigarette smoke were associated with 26% higher risk of ACS (OR = 1.26, P-value < 0.01) compared to non-smokers not exposed to smoke, while regular exposure is associated with 99% higher risk of developing ACS (OR = 1.99, P-value < 0.001). Moreover, the previous risk increases progressively from 15% to 256% if one or more of the classical cardiovascular risk factors (i.e. hypertension, hypercholesterolemia, diabetes mellitus, sedentary life and family history of premature coronary heart disease) are present. CONCLUSIONS Consequently, this study supports the hypothesis that even occasional secondhand smoke increases the risk of developing acute coronary syndromes, especially when other risk factors are present. Given the high prevalence of cigarette smoking, the public health consequences of passive smoking with regard to coronary heart disease are important.
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Affiliation(s)
- Demosthenes B Panagiotakos
- Section of Preventive Cardiology, Department of Cardiology, School of Medicine, University of Athens, Athens, Greece
| | - Christina Chrysohoou
- Section of Preventive Cardiology, Department of Cardiology, School of Medicine, University of Athens, Athens, Greece
| | - Christos Pitsavos
- Section of Preventive Cardiology, Department of Cardiology, School of Medicine, University of Athens, Athens, Greece
| | - Ioanna Papaioannou
- Section of Preventive Cardiology, Department of Cardiology, School of Medicine, University of Athens, Athens, Greece
| | - John Skoumas
- Section of Preventive Cardiology, Department of Cardiology, School of Medicine, University of Athens, Athens, Greece
| | - Christodoulos Stefanadis
- Section of Preventive Cardiology, Department of Cardiology, School of Medicine, University of Athens, Athens, Greece
| | - Pavlos Toutouzas
- Section of Preventive Cardiology, Department of Cardiology, School of Medicine, University of Athens, Athens, Greece
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Vartiainen E, Seppälä T, Lillsunde P, Puska P. Validation of self reported smoking by serum cotinine measurement in a community-based study. J Epidemiol Community Health 2002; 56:167-70. [PMID: 11854334 PMCID: PMC1732104 DOI: 10.1136/jech.56.3.167] [Citation(s) in RCA: 395] [Impact Index Per Article: 17.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/15/2023]
Abstract
STUDY OBJECTIVE The validity of self reported smoking in population surveys remains an important question. An associated question is what would be the value of measuring serum cotinine concentrations in such surveys to obtain validated smoking data. DESIGN Cross sectional analysis of data on self reported smoking and serum cotinine among a random population sample of 5846 persons aged 25 to 64 years, who participated in the FINRISK-92 survey. MAIN RESULTS Among self reported regular smokers, 97.2% of men and 94.9% of women had a cotinine concentration of 10 ng/ml or higher in serum. Of those participants who reported to have smoked at any time during their life but not during the previous month, 6.3% of men and 5.2% of women had a serum cotinine concentration of at least 10 ng/ml. Among never smokers 2.5% of men and 2.7% of women had detectable level of cotinine in their serum. The validity of self reporting was similar among subjects from different areas, ages, and socioeconomic groups. CONCLUSIONS In a sample of the general population in Finland the validity of self reported smoking is high, and most of the few self reported non-smokers who had cotinine in their serum had only low or moderate levels.
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Affiliation(s)
- E Vartiainen
- National Public Health Institute, Helsinki, Finland.
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28
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Chen R, Tunstall-Pedoe H, Tavendale R. Environmental tobacco smoke and lung function in employees who never smoked: the Scottish MONICA study. Occup Environ Med 2001; 58:563-8. [PMID: 11511742 PMCID: PMC1740185 DOI: 10.1136/oem.58.9.563] [Citation(s) in RCA: 35] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/04/2022]
Abstract
OBJECTIVES To investigate the relation between lung function in employees and exposure to environmental tobacco smoke (ETS) at work and elsewhere. METHODS Never smokers in employment (301) were identified from the fourth Scottish MONICA survey. They completed a self administered health record, which included details of exposure to ETS, and attended a survey clinic for physical and lung function measurements, and for venepuncture for estimation of serum cotinine. Differences in lung function in groups exposed to ETS were tested by analysis of variance (ANOVA), the exposure-response relation by a linear regression model, and a case-control analysis undertaken with a logistic regression model. RESULTS Both men and women showed effects on forced expiratory volume in the first second (FEV(1)) and forced vital capacity (FVC) from exposure to ETS-higher exposure going with poorer lung function. This was found at work, and in total exposure estimated from ETS at work, at home, and at other places. Linear regression showed an exposure-response relation, significant for ETS at work, total exposure, and exposure time/day, but not at home or elsewhere. Compared with those not exposed to ETS at work, those who were exposed a lot had a 254 ml (95% confidence interval (95% CI) 84 to 420) reduction in FEV(1), and a 273 ml (60 to 480) reduction in FVC after adjusting for confounders. Although lung function was not significantly associated with serum cotinine in all the data, a significant inverse relation between cotinine concentration and FVC occurred in men who had had blood collected in the morning. Case-control analysis also showed a significant exposure-response relation between ETS, mainly at work, and lung function. A higher exposure measured both by self report and serum cotinine went with lower lung function. CONCLUSION The exposure-response relation shows a reduction in pulmonary function of workers associated with passive smoking, mainly at work. These findings endorse current policies of strictly limiting smoking in shared areas, particularly working environments.
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Affiliation(s)
- R Chen
- Cardiovascular Epidemiology Unit, University of Dundee, Ninewells Hospital and Medical School, Dundee DD1 9SY, Scotland, UK.
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Abstract
Passive smoking is defined as an involuntary exposure to a combined but diluted cigarette sidestream smoke (SS, gas and particle phases that are evolved from the smoldering end of a cigarette while the smoker is not puffing) and the exhaled smoke from smokers. SS contains numerous cytotoxic substances such as polycyclic aromatic hydrocarbons (PAHs), aromatic amines, nitrosamines, heavy metals, poisonous gases, pesticide residues, and radioactive elements in quantities much higher than those found from the cigarette mainstream smoke (MS) which is puffed by smokers. Passive smoking is found to be the cause of death from cancers and cardiac disease. Furthermore, it damagingly involves reproductive organs, the nervous system, genetic materials, and is particularly hazardous to mother and child during pregnancy and to those with a history of asthma, chronic infections, induced or earned immune deficiency, or predisposed susceptibility.
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Affiliation(s)
- E Nelson
- Institute of Hygiene and Occupational Medicine, University Medical Center, Essen, Germany
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Woodward A, al-Delaimy W. Measures of exposure to environmental tobacco smoke. Validity, precision, and relevance. Ann N Y Acad Sci 2000; 895:156-72. [PMID: 10676415 DOI: 10.1111/j.1749-6632.1999.tb08083.x] [Citation(s) in RCA: 22] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/28/2022]
Abstract
It is often not clear what the best measures of exposure are for a risk assessment, or even how one should answer this question. Environmental tobacco smoke (ETS) provides a good example for an exploration of uncertainty. There are a variety of methods for estimating exposure and each has short-comings. In this paper we summarize the physical characteristics of ETS and the principal methods for assessing exposure. We review the accuracy and applicability of these methods, and explore major sources of uncertainty in the assessment of ETS.
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Affiliation(s)
- A Woodward
- Department of Public Health, Wellington School of Medicine, New Zealand.
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Thun M, Henley J, Apicella L. Epidemiologic studies of fatal and nonfatal cardiovascular disease and ETS exposure from spousal smoking. ENVIRONMENTAL HEALTH PERSPECTIVES 1999; 107 Suppl 6:841-846. [PMID: 10592140 PMCID: PMC1566204 DOI: 10.1289/ehp.99107s6841] [Citation(s) in RCA: 40] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 05/23/2023]
Abstract
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% CI], 1.17-1.33) across the combined studies. This association was statistically similar in men (RR = 1.24; 95% CI, 1.15-1.32) and women (RR = 1.23; 95% CI, 1.15-1.32); in studies of cohort (RR = 1.23; 95% CI, 1.15-1. 31) and case-control (RR = 1.47; 95% CI, 1.19-1.81) design; in the United States (RR =1.22; 95% CI, 1.13-1.30) and other countries (RR = 1.41; 95% CI, 1.21-1.65); and in studies of fatal (RR = 1.22; 95% CI, 1.14-1.30) and nonfatal (RR = 1.32; 95% CI, 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% CI, 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.
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Affiliation(s)
- M Thun
- American Cancer Society, Atlanta, Georgia 30329, USA.
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Steenland K. Risk assessment for heart disease and workplace ETS exposure among nonsmokers. ENVIRONMENTAL HEALTH PERSPECTIVES 1999; 107 Suppl 6:859-863. [PMID: 10592143 PMCID: PMC1566202 DOI: 10.1289/ehp.99107s6859] [Citation(s) in RCA: 70] [Impact Index Per Article: 2.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Figures] [Subscribe] [Scholar Register] [Indexed: 05/23/2023]
Abstract
In 1994 the U.S. Occupational Health and Safety Administration (OSHA) published a study of risk assessment for heart disease and lung cancer resulting from workplace exposure to environmental tobacco smoke (ETS) among nonsmokers. This assessment is currently being revised. The present article considers different possible approaches to a risk assessment for heart disease among nonsmokers resulting from workplace ETS exposure, reviews the approach taken by OSHA in 1994, and suggests some modifications to that approach. Since 1994 the literature supporting an association between ETS exposure and heart disease among never smokers (sometimes including long-term former smokers) has been strengthened by new studies, including some studies that have specifically considered workplace exposure. A number of these studies are appropriate for inclusion in a meta-analysis, whereas a few may not be due to methodological problems or problems in exposure definition. A meta-analysis of eight relative risks (either rate ratios or odds ratios) for heart disease resulting from workplace ETS exposure, based on one reasonable selection of appropriate studies, yields a combined relative risk of 1.21 (95% confidence interval [CI], 1.04-1.41). This relative risk, which is similar to that used by OSHA in 1994, yields an excess risk of death from heart disease by age 70 of 7 per 1000 (95% CI 0.001-0.013) resulting from ETS exposure in the workplace. This excess risk exceeds OSHA's usual threshold for regulation of 1 per 1000. Approximately 1,710 excess ischemic heart disease deaths per year would be expected among nonsmoking U.S. workers 35-69 years of age exposed to workplace ETS.
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Affiliation(s)
- K Steenland
- National Institute for Occupational Safety and Health, Cincinnati, Ohio 45226, USA.
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Benowitz NL. Biomarkers of environmental tobacco smoke exposure. ENVIRONMENTAL HEALTH PERSPECTIVES 1999; 107 Suppl 2:349-55. [PMID: 10350520 PMCID: PMC1566286 DOI: 10.1289/ehp.99107s2349] [Citation(s) in RCA: 224] [Impact Index Per Article: 8.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 05/18/2023]
Abstract
Biomarkers are desirable for quantitating human exposure to environmental tobacco smoke (ETS) and for predicting potential health risks for exposed individuals. A number of biomarkers of ETS have been proposed. At present cotinine, measured in blood, saliva, or urine, appears to be the most specific and the most sensitive biomarker. In nonsmokers with significant exposure to ETS, cotinine levels in the body are derived primarily from tobacco smoke, can be measured with extremely high sensitivity, and reflect exposure to a variety of types of cigarettes independent of machine-determined yield. Under conditions of sustained exposure to ETS (i.e., over hours or days), cotinine levels reflect exposure to other components of ETS. Supporting the validity of cotinine as a biomarker, cotinine levels have been positively correlated to the risks of some ETS-related health complications in children who are not cigarette smokers.
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Affiliation(s)
- N L Benowitz
- Division of Clinical Pharmacology and Experimental Therapeutics, University of California, San Francisco, California, USA.
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He J, Vupputuri S, Allen K, Prerost MR, Hughes J, Whelton PK. Passive smoking and the risk of coronary heart disease--a meta-analysis of epidemiologic studies. N Engl J Med 1999; 340:920-6. [PMID: 10089185 DOI: 10.1056/nejm199903253401204] [Citation(s) in RCA: 374] [Impact Index Per Article: 14.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/14/2023]
Abstract
BACKGROUND The effect of passive smoking on the risk of coronary heart disease is controversial. We conducted a meta-analysis of the risk of coronary heart disease associated with passive smoking among nonsmokers. METHODS We searched the Medline and Dissertation Abstracts Online data bases and reviewed citations in relevant articles to identify 18 epidemiologic (10 cohort and 8 case-control) studies that met prestated inclusion criteria. Information on the designs of the studies, the characteristics of the study subjects, exposure and outcome measures, control for potential confounding factors, and risk estimates was abstracted independently by three investigators using a standardized protocol. RESULTS Overall, nonsmokers exposed to environmental smoke had a relative risk of coronary heart disease of 1.25 (95 percent confidence interval, 1.17 to 1.32) as compared with nonsmokers not exposed to smoke. Passive smoking was consistently associated with an increased relative risk of coronary heart disease in cohort studies (relative risk, 1.21; 95 percent confidence interval, 1.14 to 1.30), in case-control studies (relative risk, 1.51; 95 percent confidence interval, 1.26 to 1.81), in men (relative risk, 1.22; 95 percent confidence interval, 1.10 to 1.35), in women (relative risk, 1.24; 95 percent confidence interval, 1.15 to 1.34), and in those exposed to smoking at home (relative risk, 1.17; 95 percent confidence interval, 1.11 to 1.24) or in the workplace (relative risk, 1.11; 95 percent confidence interval, 1.00 to 1.23). A significant dose-response relation was identified, with respective relative risks of 1.23 and 1.31 for nonsmokers who were exposed to the smoke of 1 to 19 cigarettes per day and those who were exposed to the smoke of 20 or more cigarettes per day, as compared with nonsmokers not exposed to smoke (P=0.006 for linear trend). CONCLUSIONS Passive smoking is associated with a small increase in the risk of coronary heart disease. Given the high prevalence of cigarette smoking, the public health consequences of passive smoking with regard to coronary heart disease may be important.
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Affiliation(s)
- J He
- Department of Biostatistics and Epidemiology, Prevention Research Center, Tulane University School of Public Health and Tropical Medicine, New Orleans, LA 70112, USA.
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Repace JL, Jinot J, Bayard S, Emmons K, Hammond SK. Air nicotine and saliva cotinine as indicators of workplace passive smoking exposure and risk. RISK ANALYSIS : AN OFFICIAL PUBLICATION OF THE SOCIETY FOR RISK ANALYSIS 1998; 18:71-83. [PMID: 9523445 DOI: 10.1111/j.1539-6924.1998.tb00917.x] [Citation(s) in RCA: 42] [Impact Index Per Article: 1.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 05/22/2023]
Abstract
We model nicotine from environmental tobacco smoke (ETS) in office air and salivary cotinine in nonsmoking U.S. workers. We estimate that: an average salivary cotinine level of 0.4 ng/ml corresponds to an increased lifetime mortality risk of 1/1000 for lung cancer, and 1/100 for heart disease; > 95% of ETS-exposed office workers exceed OSHA's significant risk level for heart disease mortality, and 60% exceed significant risk for lung cancer mortality; 4000 heart disease deaths and 400 lung cancer deaths occur annually among office workers from passive smoking in the workplace, at the current 28% prevalence of unrestricted smoking in the office workplace.
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Affiliation(s)
- J L Repace
- Office of Air and Radiation, U.S. Environmental Protection Agency, Washington, DC 20460, USA.
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Abstract
OBJECTIVES This review sought to determine whether passive smoking in the workplace has roughly the same association with heart disease as passive smoking at home and to update a previous 1994 review on the effects of home-based passive exposure on the heart. BACKGROUND To predict the effects of passive smoking at work on heart disease, public agencies have had to assume that workplace exposure to tobacco smoke was equivalent to home exposure. With the availability of more workplace exposure data, it is now possible to make a direct comparison. METHODS The odds ratios and relative risks (RRs) of the eight studies that contained data on workplace exposure (1,699 cases) were arranged in what was believed to be the order of the quality of their tobacco smoke exposure measurements. A meta-analysis was performed to obtain combined RRs. Data from seven new studies on largely home-based exposure and heart disease that were not included in the 1994 review were also evaluated. RESULTS The combined RR for the three top-rated workplace studies was 1.50 (95% confidence interval [CI] 1.12 to 2.01). Adding four lower rated studies reduced the RR to 1.35 (95% CI 1.09 to 1.67). Adding the largest study but the one with questionable exposure history reduced the combined RR to 1.18 (95% CI 1.04 to 1.34). Adding the seven new, largely home-based studies increased the home-based morbidity RR to 1.49 (95% CI 1.29 to 1.72) compared with 1.42 in 1994 while leaving the mortality RR unchanged at 1.23 (95% CI 1.14 to 1.32). CONCLUSIONS The RRs for heart disease from passive smoking at work are roughly equal to those from home-based exposure.
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Abstract
1. Whether passive smoking or environmental tobacco smoke (ETS) can cause coronary heart disease (CHD) is controversial. We have undertaken a comprehensive review of the epidemiological studies regarding the relationship between ETS and CHD. 2. We searched for all original papers and reviews and calculated pooled odds ratio using the Mantel-Haenszel method. 3. Ten prospective studies, nine case-control studies and one cross-sectional study were found. Almost all studies showed positive associations between ETS and CHD and a few were statistically significant, with dose-response relationships being evident. Six review papers calculated pooled estimates of the relative risks, which ranged from 1.23 to 1.51. Other studies also showed that ETS could have other cardiovascular effects. 4. The association observed is likely to be real. The criteria for causation of time sequence, consistency, coherence and biological plausibility are satisfied. We conclude that ETS may cause CHD, particularly in women who have never smoked.
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Affiliation(s)
- T H Lam
- Department of Community Medicine, University of Hong Kong, Hong Kong.
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38
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Lee PN. Environmental tobacco smoke and heart disease. JAMA 1992; 267:3284; author reply 3285-6. [PMID: 1597905 DOI: 10.1007/978-1-4471-0769-9_57] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/27/2022]
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