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Lai H, Liu Q, Ye Q, Liang Z, Long Z, Hu Y, Wu Q, Jiang M. Impact of smoking cessation duration on lung cancer mortality: A systematic review and meta-analysis. Crit Rev Oncol Hematol 2024; 196:104323. [PMID: 38462148 DOI: 10.1016/j.critrevonc.2024.104323] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/09/2023] [Revised: 02/11/2024] [Accepted: 03/06/2024] [Indexed: 03/12/2024] Open
Abstract
BACKGROUND Smoking history is a heterogeneous situation for different populations, and numerous studies suggest that smoking cessation is conducive to reduce the mortality of lung cancer. However, no quantitative meta-analysis regarding smoking cessation duration based on different populations has demonstrated it clearly. METHODS We systematically searched four electronic databases (PubMed, Embase, the Cochrane Central Register of Controlled Trials, and Scoups) till February 2023. Eligible studies reported the association between lung cancer survival and duration of smoking cessation. Additionally, we stratified the study population according to whether they had lung cancer at the time they quit smoking. Studies were pooled with the random-effects model. RESULTS Out of the 11,361 potential studies initially identified, we included 24 studies involving 969,560 individuals in our analysis. Lung cancer mortality varied across two groups: general quitters and peri-diagnosis quitters. For general quitters, those who had quit smoking for less than 10 years exhibited an RR of 0.64 (95% CI [0.55-0.76]), while those who quit for 10-20 years had an RR of 0.33 (0.25-0.43), over 20 years had an RR of 0.16 (0.11-0.24), and never-smokers had an RR at 0.11 (0.07-0.15). Among peri-diagnosis quitters, the 1-year Overall Survival (OS) showed an RR of 0.80 (0.67-0.96), the 2-year OS had an RR of 0.89 (0.80-0.98), the 3-year OS had an RR of 0.93 (0.84-1.03), and the 5-year OS had an RR of 0.85 (0.76-0.96). CONCLUSIONS Earlier and longer smoking cessation is associated with reduced lung cancer mortality, no matter in which cessation stage for two different populations.
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Affiliation(s)
- Hongkun Lai
- National Clinical Research Center for Respiratory Disease, State Key Laboratory of Respiratory Disease, Guangzhou Institute of Respiratory Health, the First Affiliated Hospital, Guangzhou Medical College, Guangzhou, Guangdong, China; Guangzhou Medical University, Guangzhou 510180, China
| | - Quanzhen Liu
- National Clinical Research Center for Respiratory Disease, State Key Laboratory of Respiratory Disease, Guangzhou Institute of Respiratory Health, the First Affiliated Hospital, Guangzhou Medical College, Guangzhou, Guangdong, China; Nanshan College, Guangzhou Medical University, Guangzhou, Guangdong 510180, China
| | - Qianxian Ye
- National Clinical Research Center for Respiratory Disease, State Key Laboratory of Respiratory Disease, Guangzhou Institute of Respiratory Health, the First Affiliated Hospital, Guangzhou Medical College, Guangzhou, Guangdong, China; Guangzhou Medical University, Guangzhou 510180, China
| | - Ziyang Liang
- National Clinical Research Center for Respiratory Disease, State Key Laboratory of Respiratory Disease, Guangzhou Institute of Respiratory Health, the First Affiliated Hospital, Guangzhou Medical College, Guangzhou, Guangdong, China; Guangzhou Medical University, Guangzhou 510180, China
| | - Zhiwei Long
- National Clinical Research Center for Respiratory Disease, State Key Laboratory of Respiratory Disease, Guangzhou Institute of Respiratory Health, the First Affiliated Hospital, Guangzhou Medical College, Guangzhou, Guangdong, China; Guangzhou Medical University, Guangzhou 510180, China
| | - Yinghong Hu
- National Clinical Research Center for Respiratory Disease, State Key Laboratory of Respiratory Disease, Guangzhou Institute of Respiratory Health, the First Affiliated Hospital, Guangzhou Medical College, Guangzhou, Guangdong, China; Guangzhou Medical University, Guangzhou 510180, China
| | - Qianlong Wu
- National Clinical Research Center for Respiratory Disease, State Key Laboratory of Respiratory Disease, Guangzhou Institute of Respiratory Health, the First Affiliated Hospital, Guangzhou Medical College, Guangzhou, Guangdong, China; Guangzhou Medical University, Guangzhou 510180, China
| | - Mei Jiang
- National Clinical Research Center for Respiratory Disease, State Key Laboratory of Respiratory Disease, Guangzhou Institute of Respiratory Health, the First Affiliated Hospital, Guangzhou Medical College, Guangzhou, Guangdong, China.
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Mwenda V, Odeny L, Mohamed S, Gathecha G, Kendagor A, Kiptui D, Jaguga F, Mugi B, Mithi C, Okinda K, Mwai D, Njuguna D, Awuor W, Kitonyo-Devotsu R, Ong’ang’o JR. Prevalence, patterns, and factors associated with tobacco use among patients with priority tobacco related illnesses at four Kenyan national referral hospitals, 2022. PLOS GLOBAL PUBLIC HEALTH 2023; 3:e0002002. [PMID: 37948351 PMCID: PMC10637644 DOI: 10.1371/journal.pgph.0002002] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Grants] [Track Full Text] [Subscribe] [Scholar Register] [Received: 05/11/2023] [Accepted: 10/13/2023] [Indexed: 11/12/2023]
Abstract
Tobacco use is a risk factor for many chronic health conditions. Quantifying burden of tobacco use among people with tobacco-related illnesses (TRI) can strengthen cessation programs. This study estimated prevalence, patterns and correlates of tobacco use among patients with TRI at four national referral hospitals in Kenya. We conducted a cross-sectional study among patients with five TRI (cancer, cardiovascular diseases, cerebrovascular disease, chronic obstructive pulmonary disease, and pulmonary tuberculosis) during January-July 2022. Cases identified from medical records were interviewed on socio-demographic, tobacco use and cessation information. Descriptive statistics were used to characterize patterns of tobacco use. Multiple logistic regression models were used to identify associations with tobacco use. We identified 2,032 individuals with TRI; 46% (939/2,032) had age ≥60 years, and 61% (1,241/2,032) were male. About 45% (923/2,032) were ever tobacco users (6% percent current and 39% former tobacco users). Approximately half of smokers and 58% of smokeless tobacco users had attempted quitting in the last month; 42% through cessation counselling. Comorbidities were present in 28% of the participants. Most (92%) of the patients had been diagnosed with TRI within the previous five years. The most frequent TRI were oral pharyngeal cancer (36% [725/2,032]), nasopharyngeal cancer (12% [246/2.032]) and lung cancer (10% [202/2,032]). Patients >60 years (aOR 2.24, 95% CI: 1.84, 2.73) and unmarried (aOR 1.21, 95% CI: 1.03, 1.42) had higher odds of tobacco use. Female patients (aOR 0.35, 95% CI: 0.30, 0.41) and those with no history of alcohol use (aOR 0.27, 95% CI: 0.23, 0.31), had less odds of tobacco use. Our study shows high prevalence of tobacco use among patients with TRI in Kenya, especially among older, male, less educated, unmarried, and alcohol users. We recommend tobacco use screening and cessation programs among patients with TRI as part of clinical care.
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Affiliation(s)
- Valerian Mwenda
- Department of Non-communicable Diseases, Ministry of Health, Nairobi, Kenya
| | | | - Shukri Mohamed
- African Population and Health Research Center, Nairobi, Kenya
| | - Gladwell Gathecha
- Department of Non-communicable Diseases, Ministry of Health, Nairobi, Kenya
| | - Anne Kendagor
- Department of Non-communicable Diseases, Ministry of Health, Nairobi, Kenya
| | - Dorcas Kiptui
- Department of Non-communicable Diseases, Ministry of Health, Nairobi, Kenya
| | | | | | - Caroline Mithi
- Kenyatta University Teaching, Referral and Research Hospital, Nairobi, Kenya
| | - Kennedy Okinda
- Kenyatta National Hospital-Othaya Referral Hospital, Othaya, Kenya
| | | | - David Njuguna
- Department of Planning and Health Financing, Ministry of Health, Nairobi, Kenya
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Baghery F, Lau LDW, Mohamadi M, Vazirinejad R, Ahmadi Z, Javedani H, Eslami H, Nazari A. Risk of urinary tract cancers following arsenic exposure and tobacco smoking: a review. ENVIRONMENTAL GEOCHEMISTRY AND HEALTH 2023; 45:5579-5598. [PMID: 37248359 DOI: 10.1007/s10653-023-01627-3] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Received: 02/28/2023] [Accepted: 05/18/2023] [Indexed: 05/31/2023]
Abstract
Bladder cancer, prostate cancer, and kidney cancer, due to their high morbidity and mortality rates, result in significant economic and health care costs. Arsenic exposure affects the drinking water of millions of people worldwide. Long-term exposure to arsenic, even in low concentrations, increases the risk of developing various cancers. Smoking is also one of the leading causes of bladder, prostate and kidney cancers. Accordingly, this research reviews the relationship between arsenic exposure and smoking with three kinds of urinary tract cancers (bladder cancer, prostate cancer, and kidney cancer) due to their widespread concern for their negative impact on public health globally. In this review, we have gathered the most current information from scientific databases [PubMed, Scopus, Google Scholar, ISI web of science] regarding the relationship between arsenic exposure and tobacco smoking with the risk of bladder, prostate, and kidney cancer. In several studies, a significant relationship was determined between the incidence and mortality rate of the above-mentioned cancers in humans with arsenic exposure and tobacco smoking. The decrease or cessation of smoking and consumption of arsenic-free water significantly declined the incidence of bladder, prostate, and kidney cancers.
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Affiliation(s)
- Fatemeh Baghery
- Pistachio Safety Research Center, Rafsanjan University of Medical Sciences, Rafsanjan, Iran
| | | | - Maryam Mohamadi
- Occupational Safety and Health Research Center, NICICO, WorldSafety Organization and Rafsanjan University of Medical Sciences, Rafsanjan, Iran
| | - Reza Vazirinejad
- Social Determinants of Health Research Center, Rafsanjan University of Medical Sciences, Rafsanjan, Iran
| | - Zahra Ahmadi
- Pistachio Safety Research Center, Rafsanjan University of Medical Sciences, Rafsanjan, Iran
| | - Hossein Javedani
- Immunology of Infectious Diseases Research Center, Research Institute of Basic Medical Sciences, Rafsanjan University of Medical Sciences, Rafsanjan, Iran
| | - Hadi Eslami
- Occupational Safety and Health Research Center, NICICO, WorldSafety Organization and Rafsanjan University of Medical Sciences, Rafsanjan, Iran
| | - Alireza Nazari
- Social Determinants of Health Research Center, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.
- Department of Surgery, School of Medicine, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.
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Dong W, Bensken WP, Kim U, Rose J, Fan Q, Schiltz NK, Berger NA, Koroukian SM. Variation in and Factors Associated With US County-Level Cancer Mortality, 2008-2019. JAMA Netw Open 2022; 5:e2230925. [PMID: 36083583 PMCID: PMC9463612 DOI: 10.1001/jamanetworkopen.2022.30925] [Citation(s) in RCA: 16] [Impact Index Per Article: 5.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/14/2022] Open
Abstract
IMPORTANCE The association between cancer mortality and risk factors may vary by geography. However, conventional methodological approaches rarely account for this variation. OBJECTIVE To identify geographic variations in the association between risk factors and cancer mortality. DESIGN, SETTING, AND PARTICIPANTS This geospatial cross-sectional study used county-level data from the National Center for Health Statistics for individuals who died of cancer from 2008 to 2019. Risk factor data were obtained from County Health Rankings & Roadmaps, Health Resources and Services Administration, and Centers for Disease Control and Prevention. Analyses were conducted from October 2021 to July 2022. MAIN OUTCOMES AND MEASURES Conventional random forest models were applied nationwide and by US region, and the geographical random forest model (accounting for local variation of association) was applied to assess associations between a wide range of risk factors and cancer mortality. RESULTS The study included 7 179 201 individuals (median age, 70-74 years; 3 409 508 women [47.5%]) who died from cancer in 3108 contiguous US counties during 2008 to 2019. The mean (SD) county-level cancer mortality rate was 177.0 (26.4) deaths per 100 000 people. On the basis of the variable importance measure, the random forest models identified multiple risk factors associated with cancer mortality, including smoking, receipt of Supplemental Nutrition Assistance Program (SNAP) benefits, and obesity. The geographical random forest model further identified risk factors that varied at the county level. For example, receipt of SNAP benefits was a high-importance factor in the Appalachian region, North and South Dakota, and Northern California; smoking was of high importance in Kentucky and Tennessee; and female-headed households were high-importance factors in North and South Dakota. Geographic areas with certain high-importance risk factors did not consistently have a corresponding high prevalence of the same risk factors. CONCLUSIONS AND RELEVANCE In this cross-sectional study, the associations between cancer mortality and risk factors varied by geography in a way that did not correspond strictly to risk factor prevalence. The degree to which other place-specific characteristics, observed and unobserved, modify risk factor effects should be further explored, and this work suggests that risk factor importance may be a preferable paradigm for selecting cancer control interventions compared with risk factor prevalence.
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Affiliation(s)
- Weichuan Dong
- Department of Population and Quantitative Health Sciences, Case Western Reserve University School of Medicine, Cleveland, Ohio
| | - Wyatt P. Bensken
- Department of Population and Quantitative Health Sciences, Case Western Reserve University School of Medicine, Cleveland, Ohio
| | - Uriel Kim
- Kellogg School of Management, Northwestern University, Evanston, Illinois
| | - Johnie Rose
- Department of Population and Quantitative Health Sciences, Case Western Reserve University School of Medicine, Cleveland, Ohio
- Case Comprehensive Cancer Center, Case Western Reserve University, Cleveland, Ohio
- Center for Community Health Integration, School of Medicine, Case Western Reserve University, Cleveland, Ohio
| | - Qinjin Fan
- Surveillance and Health Equity Science, American Cancer Society, Kennesaw, Georgia
| | - Nicholas K. Schiltz
- Department of Population and Quantitative Health Sciences, Case Western Reserve University School of Medicine, Cleveland, Ohio
- Center for Community Health Integration, School of Medicine, Case Western Reserve University, Cleveland, Ohio
- Frances Payne Bolton School of Nursing, Case Western Reserve University, Cleveland, Ohio
| | - Nathan A. Berger
- Case Comprehensive Cancer Center, Case Western Reserve University, Cleveland, Ohio
- Center for Science, Health, and Society, School of Medicine, Case Western Reserve University School of Medicine, Cleveland, Ohio
| | - Siran M. Koroukian
- Department of Population and Quantitative Health Sciences, Case Western Reserve University School of Medicine, Cleveland, Ohio
- Case Comprehensive Cancer Center, Case Western Reserve University, Cleveland, Ohio
- Center for Community Health Integration, School of Medicine, Case Western Reserve University, Cleveland, Ohio
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Lin BM, Wang M, Stankovic KM, Eavey R, McKenna MJ, Curhan GC, Curhan SG. Cigarette Smoking, Smoking Cessation, and Risk of Hearing Loss in Women. Am J Med 2020; 133:1180-1186. [PMID: 32387319 PMCID: PMC7541613 DOI: 10.1016/j.amjmed.2020.03.049] [Citation(s) in RCA: 22] [Impact Index Per Article: 4.4] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/29/2020] [Revised: 03/25/2020] [Accepted: 03/28/2020] [Indexed: 11/21/2022]
Abstract
BACKGROUND Previous studies demonstrated higher risk of hearing loss among cigarette smokers, but longitudinal data on whether the risk is influenced by smoking cessation are limited. We prospectively investigated relations between smoking, smoking cessation, and risk of self-reported moderate or worse hearing loss among 81,505 women in the Nurses' Health Study II (1991-2013). METHODS Information on smoking and hearing status was obtained from validated biennial questionnaires. Cox proportional hazards regression was used to estimate multivariable-adjusted relative risks (MVRR, 95% confidence interval). RESULTS During 1,533,214 person-years of follow-up, 2760 cases of hearing loss were reported. Smoking was associated with higher risk of hearing loss and the risk tended to be higher with greater number of pack-years smoked. Compared with never smokers, the MVRR (95% confidence interval) among past smokers with 20+ pack-years of smoking was 1.30 (1.09-1.55) and 1.21 (1.02-1.43) for current smokers. The magnitude of elevated risk diminished with greater time since smoking cessation. Compared with never smokers, the MVRR among smokers who quit <5 years prior was 1.43 (1.17-1.75); 5-9 years prior was 1.27 (1.03-1.56); 10-14 years prior was 1.17 (0.96-1.41); and plateaued thereafter. Additional adjustment for pack-years smoking attenuated the results. CONCLUSIONS The higher risk of hearing loss associated with smoking may diminish over time after quitting.
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Affiliation(s)
- Brian M Lin
- Department of Otolaryngology-Head and Neck Surgery, Johns Hopkins University School of Medicine, Baltimore, Md; Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Mass.
| | - Molin Wang
- Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Mass; Department of Epidemiology; Department of Biostatistics, Harvard T.H. Chan School of Public Health, Boston, Mass
| | - Konstantina M Stankovic
- Department of Otolaryngology-Head and Neck Surgery, Massachusetts Eye and Ear, Boston, Mass; Harvard Medical School, Boston, Mass
| | - Roland Eavey
- Vanderbilt Bill Wilkerson Center for Otolaryngology and Communications Sciences, Vanderbilt University School of Medicine, Nashville, Tenn
| | - Michael J McKenna
- Department of Otolaryngology-Head and Neck Surgery, Massachusetts Eye and Ear, Boston, Mass; Harvard Medical School, Boston, Mass
| | - Gary C Curhan
- Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Mass; Department of Epidemiology; Harvard Medical School, Boston, Mass; Renal Division, Department of Medicine, Brigham and Women's Hospital, Boston, Mass
| | - Sharon G Curhan
- Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Mass; Harvard Medical School, Boston, Mass
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Schubauer-Berigan MK, Berrington de Gonzalez A, Cardis E, Laurier D, Lubin JH, Hauptmann M, Richardson DB. Evaluation of Confounding and Selection Bias in Epidemiological Studies of Populations Exposed to Low-Dose, High-Energy Photon Radiation. J Natl Cancer Inst Monogr 2020; 2020:133-153. [PMID: 32657349 PMCID: PMC7355263 DOI: 10.1093/jncimonographs/lgaa008] [Citation(s) in RCA: 27] [Impact Index Per Article: 5.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/03/2023] Open
Abstract
BACKGROUND Low-dose, penetrating photon radiation exposure is ubiquitous, yet our understanding of cancer risk at low doses and dose rates derives mainly from high-dose studies. Although a large number of low-dose cancer studies have been recently published, concern exists about the potential for confounding to distort findings. The aim of this study was to describe and assess the likely impact of confounding and selection bias within the context of a systematic review. METHODS We summarized confounding control methods for 26 studies published from 2006 to 2017 by exposure setting (environmental, medical, or occupational) and identified confounders of potential concern. We used information from these and related studies to assess evidence for confounding and selection bias. For factors in which direct or indirect evidence of confounding was lacking for certain studies, we used a theoretical adjustment to determine whether uncontrolled confounding was likely to have affected the results. RESULTS For medical studies of childhood cancers, confounding by indication (CBI) was the main concern. Lifestyle-related factors were of primary concern for environmental and medical studies of adult cancers and for occupational studies. For occupational studies, other workplace exposures and healthy worker survivor bias were additionally of interest. For most of these factors, however, review of the direct and indirect evidence suggested that confounding was minimal. One study showed evidence of selection bias, and three occupational studies did not adjust for lifestyle or healthy worker survivor bias correlates. Theoretical adjustment for three factors (smoking and asbestos in occupational studies and CBI in childhood cancer studies) demonstrated that these were unlikely to explain positive study findings due to the rarity of exposure (eg, CBI) or the relatively weak association with the outcome (eg, smoking or asbestos and all cancers). CONCLUSION Confounding and selection bias are unlikely to explain the findings from most low-dose radiation epidemiology studies.
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Affiliation(s)
- Mary K Schubauer-Berigan
- Evidence Synthesis and Classification Section, International Agency for Research on Cancer, Lyon, France
| | | | - Elisabeth Cardis
- Radiation Programme, Barcelona Institute for Global Health (ISGlobal), Barcelona, Spain
- Universitat Pompeu Fabra (UPF), Barcelona, Spain
- CIBER Epidemiología y Salud Pública (CIBERESP), Madrid, Spain
| | - Dominique Laurier
- Institut de Radioprotection et de Sûreté Nucléaire (IRSN), Fontenay-aux-Roses, France
| | - Jay H Lubin
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD
| | - Michael Hauptmann
- Division of Epidemiology and Biostatistics, Netherlands Cancer Institute, Amsterdam, The Netherlands (MH); Brandenburg Medical School, Institute of Biostatistics and Registry Research, Neuruppin, Germany
| | - David B Richardson
- Department of Epidemiology, University of North Carolina, School of Public Health, Chapel Hill, NC, USA
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Ni Y, Shi G, Qu J. Indoor PM 2.5, tobacco smoking and chronic lung diseases: A narrative review. ENVIRONMENTAL RESEARCH 2020; 181:108910. [PMID: 31780052 DOI: 10.1016/j.envres.2019.108910] [Citation(s) in RCA: 63] [Impact Index Per Article: 12.6] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Received: 09/03/2019] [Revised: 11/05/2019] [Accepted: 11/07/2019] [Indexed: 06/10/2023]
Abstract
The lung is one of the most important organs exposed to environmental agents. People spend approximately 90% of their time indoors, and risks to health may thus be greater from exposure to poor air quality indoors than outdoors. Multiple indoor pollutants have been linked to chronic respiratory diseases. Environmental tobacco smoke (ETS) is known as an important source of multiple pollutants, especially in indoor environments. Indoor PM2.5 (particulate matter with aerodynamic diameter < 2.5 μm) was reported to be the most reliable marker of the presence of tobacco smoke. Recent studies have demonstrated that PM2.5 is closely correlated with chronic lung diseases. In this paper, we reviewed the relationship of tobacco smoking and indoor PM2.5 and the mechanism that underpin the link of tobacco smoke, indoor PM2.5 and chronic lung diseases.
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Affiliation(s)
- Yingmeng Ni
- Department of Pulmonary and Critical Care Medicine, Rui Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China; Institute of Respiratory Diseases, Shanghai Jiao Tong University School of Medicine, Shanghai, China
| | - Guochao Shi
- Department of Pulmonary and Critical Care Medicine, Rui Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China; Institute of Respiratory Diseases, Shanghai Jiao Tong University School of Medicine, Shanghai, China
| | - Jieming Qu
- Department of Pulmonary and Critical Care Medicine, Rui Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China; Institute of Respiratory Diseases, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
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Kim K, Choi S, Lee G, Jeong SM, Kim SM, Son JS, Yun JM, Kim YY, Park SY, Park SM. Cancer risk among young men with weight gain after smoking cessation: A population-based cohort study. Cancer Epidemiol 2019; 60:86-92. [PMID: 30933889 DOI: 10.1016/j.canep.2019.03.005] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/19/2018] [Revised: 03/04/2019] [Accepted: 03/11/2019] [Indexed: 01/10/2023]
Abstract
BACKGROUND Smoking cessation may help the current smokers to reduce cancer risk. However, weight gain following smoking cessation may attenuate the protective association of cessation with cancer. PATIENTS AND METHODS Our study included 1,278,794 men who were aged 20-39 years and underwent two consecutive health examinations by the National Health Insurance Service, without previous diagnosis of cancer. Participants were categorized into continual smokers, quitters with different degree of body weight change, and never smokers based on the biennial national health screening program (2002-2003 and 2004-2005) and were followed from January 1, 2006 to December 31, 2015. Cox proportional hazard models and restricted cubic spline model was used to evaluate the association of post-cessation weight change and cancer risk after adjustment for potential confounders. RESULTS During the 10 years of follow-up, the analyses included 1,278,794 men with 21,494 cancer incidences. Compared to continual smokers, quitters without weight gain of 2.0 kg had significantly lower risk of obesity-related cancer (hazard ratio [HR], 0.88; 95% confidence interval [CI], 0.79-0.97), smoking-related cancer (HR, 0.90; 95% CI, 0.83 to 0.98), and gastrointestinal cancer (HR, 89; 95% CI, 0.80 to 0.98). Weight gain among quitters attenuated the risk reduction of cancer compared to continual smoking. Among quitters, weight gain up to 5.0 kg with smoking cessation showed protective association with cancer risk among quitters without weight gain. CONCLUSION Excessive weight gain with smoking cessation among quitters was not associated with reduced risk of several cancer types. This association should be taken into account when recommending smoking cessation to prevent cancer.
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Affiliation(s)
- Kyuwoong Kim
- Department of Biomedical Sciences, Seoul National University Graduate School, Seoul, Republic of Korea
| | - Seulggie Choi
- Department of Biomedical Sciences, Seoul National University Graduate School, Seoul, Republic of Korea
| | - Gyeongsil Lee
- Department of Family Medicine, Seoul National University Hospital, Seoul, Republic of Korea
| | - Su-Min Jeong
- Department of Family Medicine, Seoul National University Hospital, Seoul, Republic of Korea
| | - Sung Min Kim
- Department of Biomedical Sciences, Seoul National University Graduate School, Seoul, Republic of Korea
| | - Joung Sik Son
- Department of Family Medicine, Seoul National University Hospital, Seoul, Republic of Korea
| | - Jae-Moon Yun
- Department of Family Medicine, Seoul National University Hospital, Seoul, Republic of Korea
| | - Yeon-Yong Kim
- Department of Family Medicine, College of Medicine, Seoul National University, Seoul, Republic of Korea; Big Data Steering Department, National Health Insurance Service, Wonju, Republic of Korea
| | - Seong Yong Park
- Department of Family Medicine, College of Medicine, Seoul National University, Seoul, Republic of Korea; Big Data Steering Department, National Health Insurance Service, Wonju, Republic of Korea
| | - Sang Min Park
- Department of Biomedical Sciences, Seoul National University Graduate School, Seoul, Republic of Korea; Department of Family Medicine, Seoul National University Hospital, Seoul, Republic of Korea; Department of Family Medicine, College of Medicine, Seoul National University, Seoul, Republic of Korea.
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Yang JJ, Yu D, Wen W, Shu XO, Saito E, Rahman S, Gupta PC, He J, Tsugane S, Xiang YB, Gao YT, Koh WP, Tamakoshi A, Irie F, Sadakane A, Tsuji I, Kanemura S, Matsuo K, Nagata C, Chen CJ, Yuan JM, Shin MH, Park SK, Pan WH, Qiao YL, Pednekar MS, Gu D, Sawada N, Li HL, Gao J, Cai H, Grant E, Tomata Y, Sugawara Y, Ito H, Wada K, Shen CY, Wang R, Ahn YO, You SL, Yoo KY, Ashan H, Chia KS, Boffetta P, Inoue M, Kang D, Potter JD, Zheng W. Tobacco Smoking and Mortality in Asia: A Pooled Meta-analysis. JAMA Netw Open 2019; 2:e191474. [PMID: 30924901 PMCID: PMC6450311 DOI: 10.1001/jamanetworkopen.2019.1474] [Citation(s) in RCA: 123] [Impact Index Per Article: 20.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/17/2023] Open
Abstract
IMPORTANCE Understanding birth cohort-specific tobacco smoking patterns and their association with total and cause-specific mortality is important for projecting future deaths due to tobacco smoking across Asian populations. OBJECTIVES To assess secular trends of tobacco smoking by countries or regions and birth cohorts and evaluate the consequent mortality in Asian populations. DESIGN, SETTING, AND PARTICIPANTS This pooled meta-analysis was based on individual participant data from 20 prospective cohort studies participating in the Asia Cohort Consortium. Between September 1, 2017, and March 31, 2018, a total of 1 002 258 Asian individuals 35 years or older were analyzed using Cox proportional hazards regression analysis and random-effects meta-analysis. The pooled results were presented for mainland China; Japan; Korea, Singapore, and Taiwan; and India. EXPOSURES Tobacco use status, age at starting smoking, number of cigarettes smoked per day, and age at quitting smoking. MAIN OUTCOMES AND MEASURES Country or region and birth cohort-specific mortality and the population attributable risk for deaths from all causes and from lung cancer. RESULTS Of 1 002 258 participants (51.1% women and 48.9% men; mean [SD] age at baseline, 54.6 [10.4] years), 144 366 deaths (9158 deaths from lung cancer) were ascertained during a mean (SD) follow-up of 11.7 (5.3) years. Smoking prevalence for men steadily increased in China and India, whereas it plateaued in Japan and Korea, Singapore, and Taiwan. Among Asian male smokers, the mean age at starting smoking decreased in successive birth cohorts, while the mean number of cigarettes smoked per day increased. These changes were associated with an increasing relative risk of death in association with current smoking in successive birth cohorts of pre-1920, 1920s, and 1930 or later, with hazard ratios for all-cause mortality of 1.26 (95% CI, 1.17-1.37) for the pre-1920 birth cohort, 1.47 (95% CI, 1.35-1.61) for the 1920s birth cohort, and 1.70 (95% CI, 1.57-1.84) for the cohort born in 1930 or later. The hazard ratios for lung cancer mortality were 3.38 (95% CI, 2.25-5.07) for the pre-1920 birth cohort, 4.74 (95% CI, 3.56-6.32) for the 1920s birth cohort, and 4.80 (95% CI, 3.71-6.19) for the cohort born in 1930 or later. Tobacco smoking accounted for 12.5% (95% CI, 8.4%-16.3%) of all-cause mortality in the pre-1920 birth cohort, 21.1% (95% CI, 17.3%-24.9%) of all-cause mortality in the 1920s birth cohort, and 29.3% (95% CI, 26.0%-32.3%) of all-cause mortality for the cohort born in 1930 or later. Tobacco smoking among men accounted for 56.6% (95% CI, 44.7%-66.3%) of lung cancer mortality in the pre-1920 birth cohort, 66.6% (95% CI, 58.3%-73.5%) of lung cancer mortality in the 1920s birth cohort, and 68.4% (95% CI, 61.3%-74.4%) of lung cancer mortality for the cohort born in 1930 or later. For women, tobacco smoking patterns and lung cancer mortality varied substantially by countries and regions. CONCLUSIONS AND RELEVANCE In this study, mortality associated with tobacco smoking continued to increase among Asian men in recent birth cohorts, indicating that tobacco smoking will remain a major public health problem in most Asian countries in the coming decades. Implementing comprehensive tobacco-control programs is warranted to end the tobacco epidemic.
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Affiliation(s)
- Jae Jeong Yang
- Division of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center, Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, Tennessee
| | - Danxia Yu
- Division of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center, Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, Tennessee
| | - Wanqing Wen
- Division of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center, Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, Tennessee
| | - Xiao-Ou Shu
- Division of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center, Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, Tennessee
| | - Eiko Saito
- Division of Cancer Statistics Integration, Center for Cancer Control and Information Services, National Cancer Center, Tokyo, Japan
| | - Shafiur Rahman
- Department of Global Health Policy, Graduate School of Medicine, University of Tokyo, Tokyo, Japan
| | - Prakash C. Gupta
- Healis-Sekhsaria Institute for Public Health, Mahape, Navi Mumbai, India
| | - Jiang He
- Department of Epidemiology, Tulane University School of Public Health and Tropical Medicine, New Orleans, Louisiana
| | - Shoichiro Tsugane
- Epidemiology and Prevention Group, Center for Public Health Sciences, National Cancer Center, Tokyo, Japan
| | - Yong-Bing Xiang
- State Key Laboratory of Oncogene and Related Genes, Department of Epidemiology, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, People’s Republic of China
| | - Yu-Tang Gao
- State Key Laboratory of Oncogene and Related Genes, Department of Epidemiology, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, People’s Republic of China
| | - Woon-Puay Koh
- Duke-NUS Medical School Singapore, Singapore, Republic of Singapore
- Saw Swee Hock School of Public Health, National University of Singapore, Singapore, Republic of Singapore
| | - Akiko Tamakoshi
- Graduate School of Medicine, Hokkaido University, Sapporo, Japan
| | - Fujiko Irie
- Ibaraki Chikusei Public Health Center, Chikusei City, Japan
| | | | - Ichiro Tsuji
- Tohoku University Graduate School of Medicine, Sendai, Japan
| | - Seiki Kanemura
- Tohoku University Graduate School of Medicine, Sendai, Japan
| | - Keitaro Matsuo
- Division of Molecular and Clinical Epidemiology, Aichi Cancer Center Research Institute, Nagoya, Japan
- Department of Epidemiology, Nagoya University Graduate School of Medicine, Nagoya, Japan
| | - Chisato Nagata
- Graduate School of Medicine, Gifu University, Gifu City, Japan
| | | | - Jian-Min Yuan
- Graduate School of Public Health, University of Pittsburgh, Pittsburgh, Pennsylvania
| | - Myung-Hee Shin
- Department of Social and Preventive Medicine, Sungkyunkwan University School of Medicine, Seoul, South Korea
| | - Sue K. Park
- Department of Preventive Medicine, Seoul National University College of Medicine, Seoul, South Korea
- Department of Biomedical Sciences, Seoul National University Graduate School, Seoul, South Korea
- Cancer Research Institute, Seoul National University, Seoul, South Korea
| | - Wen-Harn Pan
- Institute of Biomedical Sciences, Academia Sinica, Taipei City, Taiwan
| | - You-Lin Qiao
- Cancer Foundation of China, Beijing, People’s Republic of China
| | | | - Dongfeng Gu
- Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, People’s Republic of China
| | - Norie Sawada
- Epidemiology and Prevention Group, Center for Public Health Sciences, National Cancer Center, Tokyo, Japan
| | - Hong-Lan Li
- State Key Laboratory of Oncogene and Related Genes, Department of Epidemiology, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, People’s Republic of China
| | - Jing Gao
- State Key Laboratory of Oncogene and Related Genes, Department of Epidemiology, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, People’s Republic of China
| | - Hui Cai
- Division of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center, Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, Tennessee
| | - Eric Grant
- Radiation Effects Research Foundation, Hiroshima, Japan
| | - Yasutake Tomata
- Tohoku University Graduate School of Medicine, Sendai, Japan
| | - Yumi Sugawara
- Tohoku University Graduate School of Medicine, Sendai, Japan
| | - Hidemi Ito
- Division of Molecular and Clinical Epidemiology, Aichi Cancer Center Research Institute, Nagoya, Japan
- Department of Epidemiology, Nagoya University Graduate School of Medicine, Nagoya, Japan
| | - Keiko Wada
- Graduate School of Medicine, Gifu University, Gifu City, Japan
| | - Chen-Yang Shen
- Taiwan Biobank, Institute of Biomedical Sciences, Academia Sinica, Taipei City, Taiwan
- Graduate Institute of Environmental Science, China Medical University, Taichung, Taiwan
| | - Renwei Wang
- Graduate School of Public Health, University of Pittsburgh, Pittsburgh, Pennsylvania
| | - Yoon-Ok Ahn
- Department of Preventive Medicine, Seoul National University College of Medicine, Seoul, South Korea
| | - San-Lin You
- School of Medicine, Big Data Research Center, Fu Jen Catholic University, Taipei City, Taiwan
| | - Keun-Young Yoo
- Department of Preventive Medicine, Seoul National University College of Medicine, Seoul, South Korea
- Armed Forces Capital Hospital, Seoul National University College of Medicine, Seoul, South Korea
| | - Habibul Ashan
- Cancer Research Center, Department of Health Studies, University of Chicago, Chicago, Illinois
- Cancer Research Center, Department of Medicine, University of Chicago, Chicago, Illinois
- Cancer Research Center, Department of Human Genetics, University of Chicago, Chicago, Illinois
| | - Kee Seng Chia
- Saw Swee Hock School of Public Health, National University of Singapore, Singapore, Republic of Singapore
| | - Paolo Boffetta
- Icahn School of Medicine at Mount Sinai, New York, New York
| | - Manami Inoue
- Epidemiology and Prevention Group, Center for Public Health Sciences, National Cancer Center, Tokyo, Japan
| | - Daehee Kang
- Department of Preventive Medicine, Seoul National University College of Medicine, Seoul, South Korea
- Department of Biomedical Sciences, Seoul National University Graduate School, Seoul, South Korea
- Cancer Research Institute, Seoul National University, Seoul, South Korea
| | - John D. Potter
- Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington
- Centre for Public Health Research, Massey University, Wellington, New Zealand
- Department of Epidemiology, University of Washington, Seattle
| | - Wei Zheng
- Division of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center, Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, Tennessee
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Indirect adjustment of relative risks of an exposure with multiple categories for an unmeasured confounder. Ann Epidemiol 2018; 28:801-807. [PMID: 30297163 DOI: 10.1016/j.annepidem.2018.09.003] [Citation(s) in RCA: 7] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/07/2018] [Revised: 09/04/2018] [Accepted: 09/10/2018] [Indexed: 01/24/2023]
Abstract
PURPOSE With observational epidemiologic studies, there is often concern that an unmeasured variable might confound an observed association. Investigators can assess the impact from such unmeasured variables on an observed relative risk (RR) by utilizing externally sourced information and applying an indirect adjustment procedure, for example, the "Axelson adjustment." Although simple and easy to use, this approach applies to exposure and confounder variables that are binary. Other approaches eschew specific values and provide only bounds on the potential bias. METHODS For both multiplicative and additive RR models, we present formulae for indirect adjustment of observed RRs for unmeasured potential confounding variables when there are multiple categories. In addition, we suggest an alternative strategy to identify the characteristics that the confounder must have to explain fully the observed association. RESULTS AND CONCLUSIONS We provide examples involving studies of pediatric computer tomography scanning and leukemia and nuclear radiation workers and smoking to demonstrate that with externally sourced information, an investigator can assess whether confounding from unmeasured factors is likely to occur.
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11
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Abdel-Rahman O, Helbling D, Schöb O, Eltobgy M, Mohamed H, Schmidt J, Giryes A, Mehrabi A, Iype S, John H, Tekbas A, Zidan A, Oweira H. Cigarette smoking as a risk factor for the development of and mortality from hepatocellular carcinoma: An updated systematic review of 81 epidemiological studies. J Evid Based Med 2017; 10:245-254. [PMID: 28891275 DOI: 10.1111/jebm.12270] [Citation(s) in RCA: 73] [Impact Index Per Article: 9.1] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/05/2017] [Accepted: 08/13/2017] [Indexed: 01/11/2023]
Abstract
BACKGROUND AND AIMS Hepatocellular carcinoma (HCC) is the sixth most common cancer worldwide and its incidence has increased during the past decade. While hepatitis B and C virus infections and alcohol were established risk factors, the impact of smoking on the incidence and mortality of HCC was needed to be confirmed. METHODS We reviewed cohort and case-control studies evaluating the association between cigarette smoking and incidence and mortality of HCC from MEDLINE and Google Scholar. We also checked reference lists of original studies and review articles manually for cross-references up to February 2016. We extracted the relevant information on participant characteristics and study outcomes, as well as information on the methodology of the studies. We also assessed the quality of the included trials using critical appraisal skills program checklists. Meta-analysis was performed by using RevMan 5.3 software. RESULTS A total of 81 studies were included in the systematic review. Pooled OR for HCC development with current smokers was 1.55 (95% CI: 1.46 to 1.65; P < 0.00001). Pooled OR for HCC development with former smokers was 1.39 (95% CI: 1.26 to 1.52; P < 0.00001) and pooled OR for HCC development with heavy smokers was 1.90 (95% CI: 1.68 to 2.14; P < 0.00001). Pooled OR for the mortality of current smokers with HCC was 1.29 (95% CI: 1.23 to 1.34; P < 0.00001); and for former smokers with HCC, it was 1.20 (95% CI: 1.00 to 1.42; P = 0.04). CONCLUSIONS Cigarette smoking increases the incidence and mortality of HCC. Further studies are needed to evaluate possible impact of quitting smoking on decreasing this risk.
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Affiliation(s)
- Omar Abdel-Rahman
- Clinical Oncology Department, Faculty of Medicine, Ain Shams University, Cairo, Egypt
- Department of Medical Oncology, Gastrointestinal Tumor Center Zurich, Zurich, Switzerland
| | - Daniel Helbling
- Department of Medical Oncology, Gastrointestinal Tumor Center Zurich, Zurich, Switzerland
| | - Othmar Schöb
- Surgical Center Zurich, Hirslanden Hospital Zurich, Zurich, Switzerland
| | - Mostafa Eltobgy
- Clinical Oncology Department, Faculty of Medicine, Ain Shams University, Cairo, Egypt
| | - Hadeer Mohamed
- Clinical Oncology Department, Faculty of Medicine, Ain Shams University, Cairo, Egypt
| | - Jan Schmidt
- Surgical Center Zurich, Hirslanden Hospital Zurich, Zurich, Switzerland
| | - Anwar Giryes
- Department of Medical Oncology, Gastrointestinal Tumor Center Zurich, Zurich, Switzerland
| | - Arianeb Mehrabi
- Department of General, Visceral and Transplant Surgery, University of Heidelberg, Heidelberg, Germany
| | - Satheesh Iype
- Department of Surgery, Cambridge University Hospital, Cambridge, United Kingdom
| | - Hannah John
- Department of Surgery, Cambridge University Hospital, Cambridge, United Kingdom
| | - Aysun Tekbas
- Department of General, Visceral and Transplant Surgery, University of Heidelberg, Heidelberg, Germany
| | - Ahmad Zidan
- Department of HPB and Liver Transplantation, Rajhy Liver Hospital, Assiut University, Assiut, Egypt
| | - Hani Oweira
- Surgical Center Zurich, Hirslanden Hospital Zurich, Zurich, Switzerland
- Department of General, Visceral and Transplant Surgery, University of Heidelberg, Heidelberg, Germany
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12
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Jung KJ, Jeon C, Jee SH. The effect of smoking on lung cancer: ethnic differences and the smoking paradox. Epidemiol Health 2016; 38:e2016060. [PMID: 28092929 PMCID: PMC5309724 DOI: 10.4178/epih.e2016060] [Citation(s) in RCA: 31] [Impact Index Per Article: 3.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/12/2016] [Accepted: 12/20/2016] [Indexed: 01/30/2023] Open
Abstract
The objectives of this review were to determine whether the smoking paradox still exists and to summarize possible explanations for the smoking paradox. Based on published data, we compared the risk of cigarette smoking for lung cancer in Western and Asian countries. We extracted data from the relevant studies about annual tobacco consumption, lung cancer mortality rates according to smoking status from each country, and possible explanations for the smoking paradox. A significantly greater risk of lung cancer death was found among current smokers in Asian countries than among nonsmokers, with relative risks (RRs) of 4.0 to 4.6 for Koreans, 3.7 to 5.1 for Japanese, and 2.4 to 6.5 for Chinese. Although a significantly greater risk of lung cancer was present among current smokers in Asian countries, the RRs in Asian countries were much lower than those reported in Western countries (range, 9.4 to 23.2). Possible explanations for the smoking paradox included epidemiologic characteristics, such as the smoking amount, age at smoking initiation, and the use of filtered or mild tobacco. The smoking paradox definitely exists, but may be explained by major epidemiologic characteristics. Therefore, the smoking paradox should not be interpreted as indicating that tobacco is safer or less harmful for Asians.
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Affiliation(s)
- Keum Ji Jung
- Institute for Health Promotion, Department of Epidemiology and Health Promotion, Graduate School of Public Health, Yonsei University, Seoul, Korea
| | - Christina Jeon
- Institute for Health Promotion, Department of Epidemiology and Health Promotion, Graduate School of Public Health, Yonsei University, Seoul, Korea.,Department of Public Health, Graduate School, Yonsei University, Seoul, Korea
| | - Sun Ha Jee
- Institute for Health Promotion, Department of Epidemiology and Health Promotion, Graduate School of Public Health, Yonsei University, Seoul, Korea
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13
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Nordlund LA, Carstensen JM, Pershagen G. Are male and female smokers at equal risk of smoking-related cancer: evidence from a Swedish prospective study. Scand J Public Health 2016. [DOI: 10.1177/14034948990270010301] [Citation(s) in RCA: 15] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/15/2022]
Abstract
This study examines sex differences in the relative risks of lung cancer and other smoking-related cancers (i.e. cancers of the upper respiratory tract, oesophagus, pancreas, bladder, and renal pelvis). Data on smoking habits in 1963 from a random sample of 56,000 men and women were linked with information on new cases of cancer for 1964 - 89. Compared with people who have never smoked, the relative risks of lung cancer at different levels of pack-years completed in 1963 (>5, 6 - 15, 16 - 25 and 25+ pack-years) were 1.6, 4.4, 14.2, and 17.9 for men, and 2.1, 6.3, 10.3, and 16.5 for women. The corresponding relative risks of other smoking-related cancers were 1.8, 3.0 5.4, and 6.4 for men, and 2.0, 3.1, 5.0, and 6.5 for women. These results suggest that men and women have similar relative risks of smoking-related cancers at different levels of smoking.
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Affiliation(s)
- L. Anders Nordlund
- Department of Health and Society, Tema Research, Linköpings University, Linköping,
| | - John M. Carstensen
- Department of Health and Society, Tema Research, Linköpings University, Linköping
| | - Göran Pershagen
- Institute of Environmental Medicine, Karolinska Institute, Stockholm, Sweden
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14
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Berthiller J, Straif K, Agudo A, Ahrens W, Bezerra Dos Santos A, Boccia S, Cadoni G, Canova C, Castellsague X, Chen C, Conway D, Curado MP, Dal Maso L, Daudt AW, Fabianova E, Fernandez L, Franceschi S, Fukuyama EE, Hayes RB, Healy C, Herrero R, Holcatova I, Kelsey K, Kjaerheim K, Koifman S, Lagiou P, La Vecchia C, Lazarus P, Levi F, Lissowska J, Macfarlane T, Mates D, McClean M, Menezes A, Merletti F, Morgenstern H, Muscat J, Olshan AF, Purdue M, Ramroth H, Rudnai P, Schwartz SM, Serraino D, Shangina O, Smith E, Sturgis EM, Szeszenia-Dabrowska N, Thomson P, Vaughan TL, Vilensky M, Wei Q, Winn DM, Wünsch-Filho V, Zhang ZF, Znaor A, Ferro G, Brennan P, Boffetta P, Hashibe M, Lee YCA. Low frequency of cigarette smoking and the risk of head and neck cancer in the INHANCE consortium pooled analysis. Int J Epidemiol 2016; 45:835-45. [PMID: 26228584 PMCID: PMC5005938 DOI: 10.1093/ije/dyv146] [Citation(s) in RCA: 34] [Impact Index Per Article: 3.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Accepted: 06/26/2015] [Indexed: 01/14/2023] Open
Abstract
BACKGROUND Cigarette smoking is a major risk factor for head and neck cancer (HNC). To our knowledge, low cigarette smoking (<10 cigarettes per day) has not been extensively investigated in fine categories or among never alcohol drinkers. METHODS We conducted a pooled analysis of individual participant data from 23 independent case-control studies including 19 660 HNC cases and 25 566 controls. After exclusion of subjects using other tobacco products including cigars, pipes, snuffed or chewed tobacco and straw cigarettes (tobacco product used in Brazil), as well as subjects smoking more than 10 cigarettes per day, 4093 HNC cases and 13 416 controls were included in the analysis. The lifetime average frequency of cigarette consumption was categorized as follows: never cigarette users, >0-3, >3-5, >5-10 cigarettes per day. RESULTS Smoking >0-3 cigarettes per day was associated with a 50% increased risk of HNC in the study population [odds ratio (OR) = 1.52, 95% confidence interval (CI): (1.21, 1.90). Smoking >3-5 cigarettes per day was associated in each subgroup from OR = 2.01 (95% CI: 1.22, 3.31) among never alcohol drinkers to OR = 2.74 (95% CI: 2.01, 3.74) among women and in each cancer site, particularly laryngeal cancer (OR = 3.48, 95% CI: 2.40, 5.05). However, the observed increased risk of HNC for low smoking frequency was not found among smokers with smoking duration shorter than 20 years. CONCLUSION Our results suggest a public health message that low frequency of cigarette consumption contributes to the development of HNC. However, smoking duration seems to play at least an equal or a stronger role in the development of HNC.
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Affiliation(s)
- Julien Berthiller
- International Agency for Research on Cancer, Lyon, France, Pôle Information Médicale Evaluation Recherche, Hospices Civils de Lyon, France
| | - Kurt Straif
- International Agency for Research on Cancer, Lyon, France
| | - Antonio Agudo
- Catalan Institute of Oncology (ICO-IDIBELL), L'Hospitalet de Llobregat, Barcelona, Spain
| | - Wolfgang Ahrens
- Bremen Institute for Prevention Research and Social Medicine (BIPS), Bremen, Germany
| | | | - Stefania Boccia
- Institute of Public Health, Section of Hygiene, Università Cattolica del Sacro Cuore, Rome, Italy, L'Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS), Rome, Italy
| | - Gabriella Cadoni
- Head and Neck Surgery Department, Institute of Otorhinolaryngology, Università Cattolica del Sacro Cuore, Rome, Italy
| | | | - Xavier Castellsague
- Catalan Institute of Oncology (ICO)-IDIBELL, L'Hospitalet de Llobregat, Barcelona, Spain, CIBER de Epidemiología y Salud Pública (CIBERESP), Barcelona, Spain
| | - Chu Chen
- Fred Hutchinson Cancer Research Center, Seattle, WA, USA
| | - David Conway
- Dental School, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, UK
| | | | | | | | | | - Leticia Fernandez
- Institute of Oncology and Radiobiology, La Havana, Cuba, Instituto do Câncer do Estado de Sao Paulo (ICESP), Sao Paulo, Brazil
| | | | - Erica E Fukuyama
- Instituto do Câncer do Estado de Sao Paulo (ICESP), Sao Paulo, Brazil
| | - Richard B Hayes
- Division of Epidemiology, New York University School Of Medicine, New York, NY, USA
| | - Claire Healy
- Trinity College School of Dental Science, Dublin, Ireland
| | | | - Ivana Holcatova
- Institute of Hygiene and Epidemiology, Prague, Czech Republic
| | | | | | - Sergio Koifman
- Escola Nacional de Saude Publica, Fundacao Oswaldo Cruz, Rio de Janeiro, Brazil
| | - Pagona Lagiou
- University of Athens School of Medicine, Athens, Greece
| | - Carlo La Vecchia
- Istituto Di Ricovero e Cura a Carattere Scientific IRCCS, Milan, Italy
| | - Philip Lazarus
- Washington State University College of Pharmacy, Spokane, WA, USA
| | - Fabio Levi
- Institute of Social and Preventive Medicine (IUMSP), Lausanne University Hospital (CHUV), Lausanne, Switzerland
| | - Jolanta Lissowska
- M. Skasodowska-Curie Memorial Cancer Center and Institute of Oncology, Department of Cancer Epidemiology and Prevention, Warsaw, Poland
| | | | - Dana Mates
- National Institute of Public Health, Bucharest, Romania
| | | | - Ana Menezes
- Universidade Federal de Pelotas, Pelotas, Brazil
| | | | - Hal Morgenstern
- Departments of Epidemiology, Environmental Health Sciences, and Urology, Schools of Public Health and Medicine, and Comprehensive Cancer Center, University of Michigan, Ann Arbor, MI, USA
| | | | | | - Mark Purdue
- National Cancer Institute, National Institutes of Health, Bethesda, MD, USA
| | | | - Peter Rudnai
- National Institute of Environmental Health, Budapest, Hungary
| | | | | | | | - Elaine Smith
- College of Public Health, University of Iowa, Iowa City, IA, USA
| | | | | | | | | | - Marta Vilensky
- Institute of Oncology Angel H. Roffo, University of Buenos Aires, Buenos Aires, Argentina
| | - Qingyi Wei
- UT-M.D. Anderson Cancer Center, Houston, TX, USA
| | - Deborah M Winn
- National Cancer Institute, National Institutes of Health, Bethesda, MD, USA
| | | | | | - Ariana Znaor
- Croatian National Cancer Registry, Zagreb, Croatia
| | - Gilles Ferro
- International Agency for Research on Cancer, Lyon, France
| | - Paul Brennan
- International Agency for Research on Cancer, Lyon, France
| | - Paolo Boffetta
- Tisch Cancer Institute and Institute of Translational Epidemiology, Icahn School of Medicine at Mount Sinai, New York, NY, USA
| | - Mia Hashibe
- Huntsman Cancer Institute, University of Utah School of Medicine, Salt Lake City, UT, USA and University of Utah School of Medicine, Salt Lake City, UT, USA
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15
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Bergman BP, Mackay DF, Morrison D, Pell JP. Smoking-related cancer in military veterans: retrospective cohort study of 57,000 veterans and 173,000 matched non-veterans. BMC Cancer 2016; 16:311. [PMID: 27178424 PMCID: PMC4868009 DOI: 10.1186/s12885-016-2347-5] [Citation(s) in RCA: 15] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/24/2014] [Accepted: 05/11/2016] [Indexed: 11/15/2022] Open
Abstract
Background Serving military personnel are more likely to smoke, and to smoke more heavily, than civilians. The aim of our study was to examine whether veterans have an increased risk of a range of smoking-related cancers compared with non-veterans, using a large, national cohort of veterans. Methods We conducted a retrospective cohort study of 57,000 veterans resident in Scotland and 173,000 age, sex and area of residence matched civilians. We used Cox proportional hazard models to compare the risk of any cancer, lung cancer and other smoking-related cancers overall, by sex and by birth cohort, adjusting for the potential confounding effect of socioeconomic deprivation. Results Over a mean of 29 years follow-up, 445 (0.79 %) veterans developed lung cancer compared with 1106 (0.64 %) non-veterans (adjusted hazard ratio 1.16, 95 % confidence intervals 1.04–1.30, p = 0.008). Other smoking-related cancers occurred in 737 (1.31 %) veterans compared with 1883 (1.09 %) non-veterans (adjusted hazard ratio 1.18, 95 % confidence intervals 1.08–1.29, p < 0.001). A significantly increased risk was observed among veterans born 1950–1954 for lung cancer and 1945–1954 for other smoking-related cancers. The risk of lung cancer was decreased among veterans born 1960 onwards. In comparison, there was no difference in the risk of any cancer overall (adjusted hazard ratio 0.98, 95 % confidence intervals 0.94–1.01, p = 0.171), whilst younger veterans were at reduced risk of any cancer (adjusted hazard ratio 0.88, 95 % confidence intervals 0.81–0.97, p = 0.006). Conclusions Military veterans living in Scotland who were born before 1955 are at increased risk of smoking-related cancer compared with non-veterans, but younger veterans are not. The differences may reflect changing patterns of smoking behaviour over time in military personnel which may, in turn, be linked to developments in military health promotion policy and a changing military operational environment, as well as to wider societal factors.
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Affiliation(s)
- Beverly P Bergman
- Institute of Health and Wellbeing, University of Glasgow, Glasgow, G12 8RZ, UK.
| | - Daniel F Mackay
- Institute of Health and Wellbeing, University of Glasgow, Glasgow, G12 8RZ, UK
| | - David Morrison
- Institute of Health and Wellbeing, University of Glasgow, Glasgow, G12 8RZ, UK
| | - Jill P Pell
- Institute of Health and Wellbeing, University of Glasgow, Glasgow, G12 8RZ, UK
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Yang CS, Chen X, Tu S. Etiology and Prevention of Esophageal Cancer. Gastrointest Tumors 2016; 3:3-16. [PMID: 27722152 DOI: 10.1159/000443155] [Citation(s) in RCA: 60] [Impact Index Per Article: 6.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 12/06/2015] [Accepted: 12/07/2015] [Indexed: 12/13/2022] Open
Abstract
BACKGROUND Esophageal cancer (EC) occurs commonly, especially in Asia, and is the sixth leading cause of cancer deaths worldwide. Recently, great progress has been made in research on the etiology and prevention of EC. SUMMARY The major risk factors for esophageal squamous cell carcinoma (ESCC) are tobacco smoking and alcohol drinking, which act synergistically. Dietary parameters, including dietary carcinogens and insufficiency of micronutrients, could also be important risk factors in certain areas. A common etiological factor for both EC and some other cancers are low levels of intake of fruits and vegetables. With improvements in diet and drinking water in developing countries, the incidence of ESCC decreased. However, in economically well-developed countries, the incidence of esophageal adenocarcinoma (EAC) has markedly increased in the past 40 years. The major etiological factor for EAC is gastroesophageal reflux, which is also an etiological factor for gastric cardia adenocarcinoma (GCA). In certain areas of China, the occurrence of GCA is closely related to ESCC. Susceptibility genes for EC are starting to be discovered, and this may help to identify high-risk groups that have more need for preventive measures. Mitigation of the risk factors, early detection and treatment of precancerous lesions are effective approaches for prevention. Smoking cessation, avoidance of excessive alcohol, meat and caloric consumption, increasing physical activity and frequent consumption of vegetables and fruits are prudent lifestyle modifications for the prevention of EC as well as other diseases. KEY MESSAGE The etiology of EC includes tobacco smoking, alcohol drinking, low levels of intake of fruits and vegetables as well as gastroesophageal reflux and susceptibility genes. PRACTICAL IMPLICATIONS A healthy lifestyle including smoking cessation, increasing physical activity, consumption of vegetables as well as reduction of alcohol intake and caloric consumption are major approaches to the prevention of EC.
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Affiliation(s)
- Chung S Yang
- Department of Chemical Biology, Susan Lehman Cullman Laboratory for Cancer Research, Ernest Mario School of Pharmacy, Rutgers, The State University of New Jersey, Piscataway, N.J, USA
| | - Xiaoxin Chen
- Julius L. Chambers Biomedical/Biotechnology Research Institute, North Carolina Central University, Durham, N.C, USA; Center for Esophageal Diseases and Swallowing, Division of Gastroenterology and Hepatology, Department of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, N.C., USA
| | - Shuiping Tu
- Department of Oncology, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, PR China
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Khalil EM, Anwar MM, M.Abdelfattah S. Pattern of treatment and clinico-epidemiological analysis of 804 lung and pleura cancer patients treated in radiation oncology department, NCI-Egypt. EGYPTIAN JOURNAL OF CHEST DISEASES AND TUBERCULOSIS 2016. [DOI: 10.1016/j.ejcdt.2015.08.008] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/28/2022] Open
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Abstract
To systematically assess the relationship between smoking and glioma risk.A dose-response meta-analysis of case-control and cohort studies was performed. Pertinent studies were identified by searching database and reference lists. Random-effects model was employed to pool the estimates of the relative risks (RRs) with corresponding 95% confidence intervals (CIs).A total of 19 case-control and 6 cohort studies were included. Overall, compared with those who never smoked, the pooled RR and 95% CI was 0.98 (0.92-1.05) for ever smoker. The subgroups were not significantly different regarding risk of glioma except the group of age at start smoking (RR = 1.17, 95% CI: 0.93-1.48 for age < 20; RR = 1.25, 95% CI: 1.02-1.52 for age ≥ 20). Dose-response analysis also suggested no significant association between smoking and the risk of glioma, although some evidence for a linear relationship between smoking and glioma risk was observed.In conclusion, this meta-analysis provides little support for a causal relationship between smoking and risk of glioma.
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Affiliation(s)
- Chuan Shao
- From the Department of Neurosurgery, The Second Clinical Medical College of North Sichuan Medical College, Nanchong, Sichuan, China (CS, WZ, JH); and Department of Neurosurgery, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, China (ZQ)
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19
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Olaleye O, Ekrikpo U, Lyne O, Wiseberg J. Incidence and survival trends of lip, intra-oral cavity and tongue base cancers in south-east England. Ann R Coll Surg Engl 2015; 97:229-34. [PMID: 26263810 DOI: 10.1308/003588414x14055925061676] [Citation(s) in RCA: 11] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/15/2022] Open
Abstract
BACKGROUND Oral cavity cancers are on the increase in the UK. Understanding site-specific epidemiological trends is important for cancer control measures. This study demonstrates the changing epidemiological trends in lip, intra-oral cavity and tongue base cancers in south-east England from 1987 to 2006. AIM METHODS This was a retrospective study using anonymised data obtained from the Thames Cancer Registry (TCR) London. Data were analysed using SPSS v.17 and survival analyses with Kaplan-Meier and Cox regression. Age standardisation of the incidence rates was performed. It was conducted in south-east England, which has an average population of 12 million. The study analysed 9,318 cases (ICD-10 code C00-C06, C14). Kent Research Ethics Committee UK granted ethical approval. RESULTS Oral cancers were more common in men, with male: female ratio of 1.6:1. Tongue cancers had the highest frequency at 3,088 (33.1%). Incidence varied with each cancer type. Mean incidence (per 1,000,000) ranged from 2.3 (lip cancer) to 13.8 (tongue cancer). There has been a statistically significant increase in incidence for cancers of the tongue base, other parts of tongue, gum and palate (p<0.001). Median survival time varied by sub-site, with lip cancer having the best median survival time (11.09 years) compared with tongue base cancer (2.42 years). Survival analyses showed worse prognosis for men, older age at diagnosis, and presence of synchronous tumours (p<0.001). CONCLUSION There is a rising incidence of tongue and tongue base, gum and palate cancers in south-east England with wide variability in survival. Oral cancer awareness and screening programmes should be encouraged.
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Affiliation(s)
- O Olaleye
- 1 School of Cancer Sciences, University of Birmingham , United Kingdom
| | - U Ekrikpo
- 2 University of Uyo Teaching Hospital , Nigeria
| | - O Lyne
- 3 School of Mathematics, Statistics and Actuarial Science, University of Kent, Canterbury , United Kingdom
| | - J Wiseberg
- 4 University of Liverpool, Liverpool , United Kingdom
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20
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Ohno T, Kakinuma S, Kato S, Tsujii H, Shimada Y. Risk of second cancers after radiotherapy for cervical cancer. Expert Rev Anticancer Ther 2014; 6:49-57. [PMID: 16375644 DOI: 10.1586/14737140.6.1.49] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/08/2022]
Abstract
Radiotherapy for cervical cancer has both beneficial and detrimental effects: improvement of patient survival and potential induction of a second cancer among long-term survivors. Large epidemiological studies have demonstrated small, but significant, increases of second cancers with radiotherapy compared with the general population. The risk of second cancer has been characterized by organ sites, dose, time since radiotherapy and age at the time of radiotherapy. Analyses of genetic susceptibility and molecular carcinogenesis can be used to develop more appropriate strategies for radiation therapy for cervical cancers.
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Affiliation(s)
- Tatsuya Ohno
- Research Center for Charged Particle Therapy, National Institute of Radiological Sciences, 4-9-1 Anagawa, Chiba, Japan.
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21
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Cigarette smoking, alcohol intake, and risk of glioma in the NIH-AARP Diet and Health Study. Br J Cancer 2013; 110:242-8. [PMID: 24335921 PMCID: PMC3887282 DOI: 10.1038/bjc.2013.611] [Citation(s) in RCA: 29] [Impact Index Per Article: 2.4] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/29/2013] [Revised: 09/10/2013] [Accepted: 09/12/2013] [Indexed: 11/09/2022] Open
Abstract
BACKGROUND Although cigarette smoking and alcohol drinking increase the risk of several cancers and certain components of cigarette smoke and alcohol can penetrate the blood-brain barrier, it remains unclear whether these exposures influence the risk of glioma. METHODS We examined the associations between cigarette smoking, alcohol intake, and risk of glioma in the National Institutes of Health-AARP Diet and Health Study, a prospective study of 477,095 US men and women ages 50-71 years at baseline. Hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated using models with age as the time metric and adjusted for sex, race/ethnicity, education, and marital status. RESULTS During a median 10.5 person-years of follow-up, 492 men and 212 women were diagnosed with first primary glioma. Among men, current, heavier smoking was associated with a reduced risk of glioma compared with never smoking, but this was based on only nine cases. No associations were observed between smoking behaviours and glioma risk in women. Greater alcohol consumption was associated with a decreased risk of glioma, particularly among men (>2 drinks per day vs <1 drink per week: HR=0.67, 95% CI=0.51-0.90). CONCLUSION Smoking and alcohol drinking do not appear to increase the risk of glioma.
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Dar NA, Shah IA, Bhat GA, Makhdoomi MA, Iqbal B, Rafiq R, Nisar I, Bhat AB, Nabi S, Masood A, Shah SA, Lone MM, Zargar SA, Islami F, Boffetta P. Socioeconomic status and esophageal squamous cell carcinoma risk in Kashmir, India. Cancer Sci 2013; 104:1231-6. [PMID: 23721087 PMCID: PMC7657212 DOI: 10.1111/cas.12210] [Citation(s) in RCA: 69] [Impact Index Per Article: 5.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/21/2013] [Revised: 05/21/2013] [Accepted: 05/24/2013] [Indexed: 01/22/2023] Open
Abstract
Studies have persistently associated esophageal squamous cell carcinoma (ESCC) risk with low socioeconomic status (SES), but this association is unexplored in Kashmir, an area with a high incidence of ESCC in the northernmost part of India. We carried out a case-control study to assess the association of multiple indicators of SES and ESCC risk in the Kashmir valley. A total number of 703 histologically confirmed ESCC cases and 1664 controls matched to the cases for age, sex, and district of residence were recruited from October 2008 to January 2012. Conditional logistic regression models were used to calculate unadjusted and adjusted odds ratios and 95% confidence intervals. Composite wealth scores were constructed based on the ownership of several appliances using multiple correspondence analyses. Higher education, living in a kiln brick or concrete house, use of liquefied petroleum gas and electricity for cooking, and higher wealth scores all showed an inverse association with ESCC risk. Compared to farmers, individuals who had government jobs or worked in the business sector were at lower risk of ESCC, but this association disappeared in fully adjusted models. Occupational strenuous physical activity was strongly associated with ESCC risk. In summary, we found a strong relationship of low SES and ESCC in Kashmir. The findings need to be studied further to understand the mechanisms through which such SES parameters increase ESCC risk.
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Affiliation(s)
- Nazir A Dar
- Department of Biochemistry, University of Kashmir, Srinagar, India.
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23
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Kamper-Jørgensen M, Rostgaard K, Glaser SL, Zahm SH, Cozen W, Smedby KE, Sanjosé S, Chang ET, Zheng T, La Vecchia C, Serraino D, Monnereau A, Kane EV, Miligi L, Vineis P, Spinelli JJ, McLaughlin JR, Pahwa P, Dosman JA, Vornanen M, Foretova L, Maynadie M, Staines A, Becker N, Nieters A, Brennan P, Boffetta P, Cocco P, Hjalgrim H. Cigarette smoking and risk of Hodgkin lymphoma and its subtypes: a pooled analysis from the International Lymphoma Epidemiology Consortium (InterLymph). Ann Oncol 2013; 24:2245-55. [PMID: 23788758 DOI: 10.1093/annonc/mdt218] [Citation(s) in RCA: 38] [Impact Index Per Article: 3.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/21/2022] Open
Abstract
BACKGROUND The etiology of Hodgkin lymphoma (HL) remains incompletely characterized. Studies of the association between smoking and HL have yielded ambiguous results, possibly due to differences between HL subtypes. PATIENTS AND METHODS Through the InterLymph Consortium, 12 case-control studies regarding cigarette smoking and HL were identified. Pooled analyses on the association between smoking and HL stratified by tumor histology and Epstein-Barr virus (EBV) status were conducted using random effects models adjusted for confounders. Analyses included 3335 HL cases and 14 278 controls. RESULTS Overall, 54.5% of cases and 57.4% of controls were ever cigarette smokers. Compared with never smokers, ever smokers had an odds ratio (OR) of HL of 1.10 [95% confidence interval (CI) 1.01-1.21]. This increased risk reflected associations with mixed cellularity cHL (OR = 1.60, 95% CI 1.29-1.99) and EBV-positive cHL (OR = 1.81, 95% CI 1.27-2.56) among current smokers, whereas risk of nodular sclerosis (OR = 1.09, 95% CI 0.90-1.32) and EBV-negative HL (OR = 1.02, 95% CI 0.72-1.44) was not increased. CONCLUSION These results support the notion of etiologic heterogeneity between HL subtypes, highlighting the need for HL stratification in future studies. Even if not relevant to all subtypes, our study emphasizes that cigarette smoking should be added to the few modifiable HL risk factors identified.
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Affiliation(s)
- M Kamper-Jørgensen
- Department of Public Health, University of Copenhagen, Copenhagen, K, Denmark
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Nakamura H, Saji H. Worldwide trend of increasing primary adenocarcinoma of the lung. Surg Today 2013; 44:1004-12. [PMID: 23754705 DOI: 10.1007/s00595-013-0636-z] [Citation(s) in RCA: 79] [Impact Index Per Article: 6.6] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/06/2013] [Accepted: 05/13/2013] [Indexed: 01/15/2023]
Abstract
The four major histological types of lung cancer are adenocarcinoma, squamous cell carcinoma (SQ), large cell carcinoma and small cell carcinoma. Over the past few decades, the incidence of lung adenocarcinoma has increased gradually in most countries as the most frequently occurring histological type, displacing SQ. Adenocarcinoma is the predominant type of lung cancer among lifelong non-smokers and among females. Especially in East Asian countries, the cause(s) of the increase in adenocarcinomas are not clear. Several genetic mutations specific to lung adenocarcinomas have been found, representing attractive targets for molecular therapy. Recently, the pathological classification of lung adenocarcinoma was revised by integrating the newer clinical and biological knowledge concerning this prevailing type. Additional epidemiological, pathological and genetic studies are required to better understand this type of lung cancer.
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Affiliation(s)
- Haruhiko Nakamura
- Department of Chest Surgery, St. Marianna University School of Medicine, 2-16-1 Sugao, Miyamae-ku, Kawasaki, Kanagawa, 216-8511, Japan,
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25
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Utility of biochemical verification of tobacco cessation in the Department of Veterans Affairs. Addict Behav 2013; 38:1792-5. [PMID: 23261494 DOI: 10.1016/j.addbeh.2012.11.006] [Citation(s) in RCA: 30] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/11/2012] [Revised: 09/14/2012] [Accepted: 11/12/2012] [Indexed: 11/20/2022]
Abstract
Research on the validity of self-report tobacco use has varied by the population studied and has yet to be examined among smokers serviced by the Department of Veterans Affairs (VA). The purpose of this study was to determine the predictors of returning a biochemical urine test and the specificity and sensitivity of self-reported tobacco use status compared to biochemical verification. This was a sub-analysis of the larger Tobacco Tactics research study, a pre-/post-non-randomized control design study to implement and evaluate a smoking cessation intervention in three large VA hospitals. Inpatient smokers completed baseline demographic, health history and tobacco use measures. Patients were sent a follow-up survey at six-months to assess tobacco use and urine cotinine levels. A total of 645 patients returned six-month surveys of which 578 also returned a urinary cotinine strip at six-months. Multivariate analysis of the predictors of return rate revealed those more likely to return biochemical verification of their smoking status were younger, more likely to be thinking about quitting smoking, have arthritis, and less likely to have heart disease. The sensitivity and specificity of self-report tobacco use were 97% (95% confidence interval=0.95-0.98) and 93% (95% confidence interval=0.84-0.98) respectively. The misclassification rate among self-reported quitters was 21%. The misclassification rate among self-reported tobacco users was 1%. The sensitivity and specificity of self-report tobacco use were high among veteran smokers, yet among self-report quitters that misclassification rate was high at 21% suggesting that validating self-report tobacco measures is warranted in future studies especially in populations that are prone to misclassification.
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Greenberg AK, Tsay JC, Tchou-Wong KM, Jorgensen A, Rom WN. Chemoprevention of lung cancer: prospects and disappointments in human clinical trials. Cancers (Basel) 2013; 5:131-48. [PMID: 24216701 PMCID: PMC3730305 DOI: 10.3390/cancers5010131] [Citation(s) in RCA: 17] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/06/2012] [Revised: 01/15/2013] [Accepted: 01/17/2013] [Indexed: 12/14/2022] Open
Abstract
Decreasing the risk of lung cancer, or preventing its development in high-risk individuals, would have a huge impact on public health. The most effective means to decrease lung cancer incidence is to eliminate exposure to carcinogens. However, with recent advances in the understanding of pulmonary carcinogenesis and the identification of intermediate biomarkers, the prospects for the field of chemoprevention research have improved dramatically. Here we review the most recent research in lung cancer chemoprevention-focusing on those agents that have been investigated in human clinical trials. These agents fall into three major categories. First, oxidative stress plays an important role in pulmonary carcinogenesis; and therefore, antioxidants (including vitamins, selenium, green tea extracts, and isothiocyanates) may be particularly effective in preventing the development of lung cancer. Second, inflammation is increasingly accepted as a crucial factor in carcinogenesis, and many investigators have focused on anti-inflammatory agents, such as glucocorticoids, NSAIDs, statins, and PPARγ agonists. Finally, the PI3K/AKT/mTOR pathway is recognized to play a central role in tobacco-induced carcinogenesis, and inhibitors of this pathway, including myoinositol and metformin, are promising agents for lung cancer prevention. Successful chemoprevention will likely require targeting of multiple pathways to carcinogenesis-both to minimize toxicity and maximize efficacy.
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Affiliation(s)
- Alissa K Greenberg
- Division of Pulmonary, Critical Care, and Sleep Medicine, Departments of Medicine and Environmental Medicine, New York University School of Medicine, New York, NY 10016, USA.
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Fry JS. Dose-response relationship of lung cancer to amount smoked, duration and age starting. World J Meta-Anal 2013; 1:57. [DOI: 10.13105/wjma.v1.i2.57] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/02/2013] [Revised: 05/09/2013] [Accepted: 08/06/2013] [Indexed: 02/05/2023] Open
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Retrospective cohort study of smoking and lung cancer incidence in rural prefecture, Japan. Environ Health Prev Med 2012; 12:178-82. [PMID: 21432062 DOI: 10.1007/bf02897988] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/21/2006] [Accepted: 05/17/2007] [Indexed: 10/22/2022] Open
Abstract
OBJECTIVES We conducted an epidemiological study of the relationship between lung cancer incidence and smoking, with special reference to the benefits of smoking cessation for reducing lung cancer incidence, to promote a local smoking control program. METHODS The study was a retrospective cohort study. The population studied was 16,383 male examinees of lung cancer health examinations in 1995 in Tottori Prefecture, Japan. Smoking status from the questionnaire during the health examination was used as the exposure variable. Endpoint (lung cancer incidence) was obtained from the Tottori population-based cancer registry. A multivariable analysis using the Cox proportional hazard model was adapted for statistical analysis. The average follow-up period was 4.3 years. RESULTS The hazard ratio of current smokers for the incidence of lung cancer was 4.9, whereas that of ex-smokers was 2.2. The dose-response relationship between lung cancer incidence and lifetime cigarette consumption (pack year) was determined. The ratio increased among younger subjects (under 65 years old). The hazard ratio of ex-smokers decreased with years just after quitting smoking, and reached the level of never smokers after 10-19 years from smoking cessation. CONCLUSIONS We reconfirmed that the magnitude of risk estimates of smoking for lung cancer incidence was similar to those of previous studies, and smoking cessation was effective for reducing lung cancer risk.
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Lee PN, Forey BA, Coombs KJ. Systematic review with meta-analysis of the epidemiological evidence in the 1900s relating smoking to lung cancer. BMC Cancer 2012; 12:385. [PMID: 22943444 PMCID: PMC3505152 DOI: 10.1186/1471-2407-12-385] [Citation(s) in RCA: 180] [Impact Index Per Article: 13.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/04/2012] [Accepted: 07/18/2012] [Indexed: 02/07/2023] Open
Abstract
BACKGROUND Smoking is a known lung cancer cause, but no detailed quantitative systematic review exists. We summarize evidence for various indices. METHODS Papers published before 2000 describing epidemiological studies involving 100+ lung cancer cases were obtained from Medline and other sources. Studies were classified as principal, or subsidiary where cases overlapped with principal studies. Data were extracted on design, exposures, histological types and confounder adjustment. RRs/ORs and 95% CIs were extracted for ever, current and ex smoking of cigarettes, pipes and cigars and indices of cigarette type and dose-response. Meta-analyses and meta-regressions investigated how relationships varied by study and RR characteristics, mainly for outcomes exactly or closely equivalent to all lung cancer, squamous cell carcinoma ("squamous") and adenocarcinoma ("adeno"). RESULTS 287 studies (20 subsidiary) were identified. Although RR estimates were markedly heterogeneous, the meta-analyses demonstrated a relationship of smoking with lung cancer risk, clearly seen for ever smoking (random-effects RR 5.50, CI 5.07-5.96) current smoking (8.43, 7.63-9.31), ex smoking (4.30, 3.93-4.71) and pipe/cigar only smoking (2.92, 2.38-3.57). It was stronger for squamous (current smoking RR 16.91, 13.14-21.76) than adeno (4.21, 3.32-5.34), and evident in both sexes (RRs somewhat higher in males), all continents (RRs highest for North America and lowest for Asia, particularly China), and both study types (RRs higher for prospective studies). Relationships were somewhat stronger in later starting and larger studies. RR estimates were similar in cigarette only and mixed smokers, and similar in smokers of pipes/cigars only, pipes only and cigars only. Exceptionally no increase in adeno risk was seen for pipe/cigar only smokers (0.93, 0.62-1.40). RRs were unrelated to mentholation, and higher for non-filter and handrolled cigarettes. RRs increased with amount smoked, duration, earlier starting age, tar level and fraction smoked and decreased with time quit. Relationships were strongest for small and squamous cell, intermediate for large cell and weakest for adenocarcinoma. Covariate-adjustment little affected RR estimates. CONCLUSIONS The association of lung cancer with smoking is strong, evident for all lung cancer types, dose-related and insensitive to covariate-adjustment. This emphasises the causal nature of the relationship. Our results quantify the relationships more precisely than previously.
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Affiliation(s)
- Peter N Lee
- P N Lee Statistics and Computing Ltd, Sutton, Surrey, United Kingdom
| | - Barbara A Forey
- P N Lee Statistics and Computing Ltd, Sutton, Surrey, United Kingdom
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The association between cigarette smoking and non-Hodgkin lymphoid neoplasms in a large US cohort study. Cancer Causes Control 2012; 23:1231-40. [DOI: 10.1007/s10552-012-0001-3] [Citation(s) in RCA: 14] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/12/2012] [Accepted: 05/18/2012] [Indexed: 12/14/2022]
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Keith RL. Lung cancer chemoprevention. PROCEEDINGS OF THE AMERICAN THORACIC SOCIETY 2012; 9:52-6. [PMID: 22550242 PMCID: PMC3359111 DOI: 10.1513/pats.201107-038ms] [Citation(s) in RCA: 10] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Received: 07/08/2011] [Accepted: 08/11/2011] [Indexed: 12/11/2022]
Abstract
Lung cancer is the leading cause of cancer death in the United States, and the majority of diagnoses are made in former smokers. Although avoidance of tobacco abuse and smoking cessation clearly will have the greatest impact on lung cancer development, effective chemoprevention could prove to be more effective than treatment of established, advanced-stage disease. Chemoprevention is the use of dietary or pharmaceutical agents to reverse or block the carcinogenic process and has been successfully applied to common malignancies other than lung (including recent reports on the prevention of breast cancer in high-risk individuals). Despite previous studies in lung cancer chemoprevention failing to identify effective agents, our ability to define the highest-risk populations and the understanding of lung tumor and premalignant biology continue to make advances. Squamous cell carcinogenesis in the bronchial epithelium starts with normal epithelium and progresses through hyperplasia, metaplasia, dysplasia, and carcinoma in situ to invasive cancer. Precursor lesions also have been identified for adenocarcinoma, and these premalignant lesions are targeted by chemopreventive agents in current and future trials. Chemopreventive agents can currently only be recommended as part of well-designed clinical trials, and multiple trials have recently been completed or are enrolling subjects.
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Affiliation(s)
- Robert L Keith
- Division of Pulmonary Sciences and Critical Care Medicine, Department of Medicine, Veterans Affairs Eastern Colorado Healthcare System, University of Colorado at Denver–School of Medicine, Denver, Colorado, USA.
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Olaleye O, Moorthy R, Lyne O, Black M, Mitchell D, Wiseberg J. A 20-year retrospective study of tonsil cancer incidence and survival trends in South East England: 1987-2006. Clin Otolaryngol 2012; 36:325-35. [PMID: 21696555 DOI: 10.1111/j.1749-4486.2011.02361.x] [Citation(s) in RCA: 17] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/28/2022]
Abstract
BACKGROUND There has been an increasing incidence of tonsil cancer worldwide. Documenting these changes is crucial to cancer prevention and control measures, resource allocation and understanding disease aetiology. OBJECTIVE To analyse the changing epidemiology of tonsil cancer in South East England over a 20-year period between 1987 and 2006. DESIGN A retrospective, quantitative study using secondary anonymised data obtained from the Thames Cancer Registry, London. Data were analysed using spss v.17 and survival analyses with Kaplan-Meier and Cox regression. SETTING This study was conducted in South East of England comprising London, Kent, Surrey and Sussex counties with an average population of 12 million. This population increased from 10.7 to 11.8 million (a 10% increase) between 1987 and 2006. PARTICIPANTS All patients with tonsil cancer in South East England registered with the Thames Cancer Registry (ICD-10 code C09) between 1987 and 2006. A total of 1794 patients' data were analysed. Ethical Considerations: Ethical approval was granted by the Kent Research Ethics Committee. MAIN OUTCOME MEASURES Data were analysed for demographic trends including gender, age at diagnosis, yearly incidence and survival. RESULTS Tonsil cancer incidence has increased significantly from 0.60 to 1.45 per 100,000 in the 20 years (P < 0.001). This increase is mainly amongst men and age groups 40-59 years with a significant reduction in age at diagnosis by 2 years from 61.6 years in the first decade to 59.6 years in the second decade (P < 0.001). Survival was worse in men, older age groups and in the presence of synchronous tumours (P < 0.001). There has been a statistically significant increase in median survival times from tonsil cancer by about 3 years from 2.7 years in the first decade to 5.7 years in the second decade of this study (P < 0.001). CONCLUSIONS Tonsil cancer incidence has increased in the 20 years of this study in South East England, especially amongst men and age groups 40-59 years. There has also been significant reduction in the mean age at diagnosis and an increase in median survival times for tonsil cancer. Further studies are needed to explain these trends.
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Affiliation(s)
- O Olaleye
- Department of Otolaryngology, Russells Hall Hospital, Dudley, West Midlands UK.
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Winkler V, Ng N, Tesfaye F, Becher H. Predicting lung cancer deaths from smoking prevalence data. Lung Cancer 2011; 74:170-7. [DOI: 10.1016/j.lungcan.2011.02.011] [Citation(s) in RCA: 9] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/15/2010] [Revised: 02/14/2011] [Accepted: 02/19/2011] [Indexed: 10/18/2022]
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Abstract
BACKGROUND Smoking has been related to esophageal and gastric cardia adenocarcinoma, but the magnitude of the association is uncertain. METHODS We conducted a meta-analysis of 33 studies published up to January 2010. We derived summary estimates using random-effects models. RESULTS Compared with never-smokers, the pooled relative risk (RR) was 1.76 (95% confidence interval = 1.54-2.01) for ever-smokers, 2.32 (1.96-2.75) for current smokers, and 1.62 (1.40-1.87) for ex-smokers. There was no important difference between esophageal (RR = 1.85 for ever- vs. never-smokers) and gastric cardia (RR = 1.76) adenocarcinoma. We found a direct association with dose (RR = 2.48 [2.14-2.86] for ≥ 20 cigarettes/d) and duration (RR = 2.32 [1.92-2.82] for ≥ 40 years) of cigarette consumption. CONCLUSIONS This meta-analysis estimates the excess of esophageal and gastric cardia adenocarcinoma risk for smokers. This risk was similar for the 2 cancer sites.
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Katanoda K, Saika K, Yamamoto S, Tanaka S, Oshima A, Nakamura M, Satoh H, Tajima K, Suzuki T, Tamakoshi A, Tsugane S, Sobue T. Projected Cancer Mortality Among Japanese Males Under Different Smoking Prevalence Scenarios: Evidence for Tobacco Control Goal Setting. Jpn J Clin Oncol 2011; 41:483-9. [DOI: 10.1093/jjco/hyq247] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/12/2022] Open
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Saillant J, Biat I, Boudet G, Maublant C, Chamoux A. À propos de trois cas groupés d’oncocytomes rénaux sur un même site industriel chimique. ARCH MAL PROF ENVIRO 2010. [DOI: 10.1016/j.admp.2010.06.005] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/25/2022]
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Kvale E, Ekundayo OJ, Zhang Y, Akhter S, Aban I, Love TE, Ritchie C, Ahmed A. History of cancer and mortality in community-dwelling older adults. Cancer Epidemiol 2010; 35:30-6. [PMID: 20708995 DOI: 10.1016/j.canep.2010.07.011] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/15/2009] [Revised: 07/02/2010] [Accepted: 07/13/2010] [Indexed: 10/19/2022]
Abstract
BACKGROUND The association between a history of cancer and mortality has not been studied in a propensity-matched population of community-dwelling older adults. METHODS Of the 5795 participants in the Cardiovascular Health Study, 827 (14%) had self-reported physician-diagnosed cancer at baseline. Propensity scores for cancer were used to assemble a cohort of 789 and 3118 participants with and without cancer respectively who were balanced on 45 baseline characteristics. Cox regression models were used to determine the association between cancer and all-cause mortality among matched patients, and to identify independent predictors of mortality among unmatched cancer patients. RESULTS Matched participants had a mean (SD) age of 74 (6) years, 57% were women, 10% were African Americans, and 38% died from all causes during 12 years of follow-up. All-cause mortality occurred in 41% and 37% of matched participants with and without a history of cancer respectively (hazard ratio when cancer was compared with no cancer, 1.16; 95% confidence interval, 1.02-1.31; P=0.019). Among those with cancer, older age, male gender, smoking, lower than college education, fair-to-poor self-reported health, coronary artery disease, diabetes mellitus, chronic kidney disease, left ventricular hypertrophy, increased heart rate, low hemoglobin and low baseline albumin were associated with increased risk of mortality. CONCLUSIONS Among community-dwelling older adults, a history of cancer was associated with increased mortality and among those with cancer, several socio-demographic variables and morbidities predicted mortality. These findings suggest that addressing traditional risk factors for cardiovascular mortality may help improve outcomes in older adults with a history of cancer.
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Ansary-Moghaddam A, Huxley RR, Lam TH, Woodward M. The risk of upper aero digestive tract cancer associated with smoking, with and without concurrent alcohol consumption. ACTA ACUST UNITED AC 2010; 76:392-403. [PMID: 19642154 DOI: 10.1002/msj.20125] [Citation(s) in RCA: 24] [Impact Index Per Article: 1.6] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/17/2022]
Abstract
BACKGROUND Smoking and alcohol are major causal factors for upper aerodigestive tract cancer, but reliable quantification of the combined impact of smoking and alcohol on this cancer and its major subtypes has not been performed. METHODS A meta-analysis of studies that had published quantitative estimates of smoking and upper aerodigestive tract cancer by January 2007 was performed. Pooled estimates of relative risks were obtained. Publication bias was investigated through funnel plots and corrected if found to be present. RESULTS Overall, 85 studies with information on 53,940 individuals with upper aerodigestive tract cancer were included. The pooled estimate for the association between smoking and the risk of this cancer was 3.47 (95% confidence interval, 3.06-3.92). The risk remained elevated for a decade after smoking cessation but declined thereafter. Individuals who both smoked and consumed alcohol had double the risk of upper aerodigestive tract cancer in comparison with those who only smoked: the relative risk was 6.93 (95% confidence interval, 4.99-9.62) for the former and 2.56 (95% confidence interval, 2.20-2.97) for the latter (P < 0.001). CONCLUSIONS Public health interventions that simultaneously discourage smoking and heavy drinking would have greater benefits than would be expected from those that target only one of these risk factors.
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Report of Three Cases of Renal Oncocytoma in the Same French Chemical Industrial Factory. J Occup Environ Med 2009; 51:1113-5. [DOI: 10.1097/jom.0b013e3181ad49eb] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/26/2022]
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Lee YCA, Cohet C, Yang YC, Stayner L, Hashibe M, Straif K. Meta-analysis of epidemiologic studies on cigarette smoking and liver cancer. Int J Epidemiol 2009; 38:1497-511. [PMID: 19720726 DOI: 10.1093/ije/dyp280] [Citation(s) in RCA: 192] [Impact Index Per Article: 12.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/12/2022] Open
Abstract
BACKGROUND Whereas the International Agency for Research on Cancer (IARC) Monograph concluded that the evidence for the relationship between cigarette smoking and liver cancer is sufficient, the US Surgeon General's report summarized the data as suggestive but not sufficient. METHODS A meta-analysis of previous epidemiologic studies may help to clarify the potential association. We identified 38 cohort studies and 58 case-control studies in a systematic literature search for studies on liver cancer and cigarette smoking. The meta-relative risk (mRR) of liver cancer and dose-response trends were calculated. Tests for heterogeneity, publication bias assessment and influence analyses were performed. RESULTS Compared with never smokers, the adjusted mRR was 1.51 [95% confidence interval (CI) 1.37-1.67] for current smokers and 1.12 (95% CI 0.78-1.60) for former smokers. The increased liver cancer risk among current smokers appeared to be consistent in strata of different regions, study designs, study sample sizes and publication periods. CONCLUSION The results of our meta-analysis show that tobacco smoking is associated with liver cancer development, which supports the conclusion by the IARC Monograph. This conclusion has an important public health message for areas with high smoking prevalence and high liver cancer incidence such as China.
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Mandelzweig L, Novikov I, Sadetzki S. Smoking and risk of glioma: a meta-analysis. Cancer Causes Control 2009; 20:1927-38. [DOI: 10.1007/s10552-009-9386-z] [Citation(s) in RCA: 24] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/19/2009] [Accepted: 06/10/2009] [Indexed: 11/29/2022]
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Kilfoy BA, Zheng T, Lan Q, Han X, Qin Q, Rothman N, Holford T, Zhang Y. Genetic polymorphisms in glutathione S-transferases and cytochrome P450s, tobacco smoking, and risk of non-Hodgkin lymphoma. Am J Hematol 2009; 84:279-82. [PMID: 19338043 DOI: 10.1002/ajh.21386] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/10/2022]
Abstract
We investigated variation in glutathione S-transferases (GSTs) and cytochrome P450s (CYPs), and smoking in a population-based case-control study of NHL including 1,115 women. Although risk of NHL was not altered by variant polymorphisms in GSTs or CYPs, it was significantly changed for DLBCL when considered in conjunction with smoking behavior, though only in nonsmokers. An increased risk of DLBCL in nonsmokers was associated with the variant G allele for GSTP1 (OR = 1.6, 95% CI 1.0-2.3) and CYP1A1 (OR = 2.4; 95% CI 1.0-5.7), but a decreased risk for the variant G allele for CYP1B1 (OR = 0.6, 95% CI 0.4-1.0). Our results confer support investigation of the gene-environment interaction in a larger study population of DLBCL.
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MESH Headings
- Adult
- Aged
- Aged, 80 and over
- Alleles
- Aryl Hydrocarbon Hydroxylases/genetics
- Biomarkers, Tumor
- Case-Control Studies
- Cytochrome P-450 CYP1A1/genetics
- Cytochrome P-450 CYP1B1
- Female
- Glutathione S-Transferase pi/genetics
- Humans
- Lymphoma, Large B-Cell, Diffuse/enzymology
- Lymphoma, Large B-Cell, Diffuse/etiology
- Lymphoma, Large B-Cell, Diffuse/genetics
- Lymphoma, Non-Hodgkin/enzymology
- Lymphoma, Non-Hodgkin/etiology
- Lymphoma, Non-Hodgkin/genetics
- Middle Aged
- Polymorphism, Genetic
- Risk
- Risk Factors
- Smoking/adverse effects
- Young Adult
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Affiliation(s)
- Briseis A Kilfoy
- Department of Environmental Health Sciences, School of Epidemiology and Public Health, Yale University, New Haven, Connecticut 06520-8034, USA
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Smoking and the risk of upper aero digestive tract cancers for men and women in the Asia-Pacific region. INTERNATIONAL JOURNAL OF ENVIRONMENTAL RESEARCH AND PUBLIC HEALTH 2009; 6:1358-70. [PMID: 19440523 PMCID: PMC2681196 DOI: 10.3390/ijerph6041358] [Citation(s) in RCA: 11] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 12/24/2008] [Accepted: 04/01/2009] [Indexed: 11/16/2022]
Abstract
Although smoking is an established causal factor for upper aero digestive tract cancer (UADTC), most of the evidence originates from the West. Thus, we analysed data from 455,409 subjects in the Asia Pacific Cohort Studies Collaboration. Over a median of around six years follow-up, 371 deaths from UADTC were observed. The hazard ratio (95% confidence interval) for current smokers, compared with those who had never smoked, was 2.36 (1.76 – 3.16), adjusted for age and alcohol drinking. Tobacco control policies are urgently required in Asia to prevent millions of deaths from UADTC that smoking will otherwise cause.
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Abstract
This article reviews the environmental risk factors and predisposing conditions for the two main histologic types of esophageal cancer. Tobacco smoking, excessive alcohol consumption, drinking maté, low intake of fresh fruits and vegetables, achalasia, and low socioeconomic status increase the risk of esophageal squamous cell carcinoma. Results of investigations on other potential risk factors, including opium consumption, intake of hot drinks, eating pickled vegetables, poor oral health, and exposure to human papillomavirus, polycyclic aromatic hydrocarbons, N-nitroso compounds, acetaldehyde, and fumonisins are discussed. Gastroesophageal reflux, obesity, tobacco smoking, hiatal hernia, achalasia, and, probably, absence of H pylori in the stomach increase the risk of esophageal adenocarcinoma. Results of studies investigating other factors are also discussed.
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Affiliation(s)
- Farin Kamangar
- Division of Cancer Epidemiology and Genetics, NCI, 6120 Executive Blvd., Room 3034, Bethesda, MD 20892-7232, Phone: (301) 594-2936,
| | - Wong-Ho Chow
- Division of Cancer Epidemiology and Genetics, NCI, 6120 Executive Blvd., Room 8100, Bethesda, MD 20892-7240, Phone: (301) 435-4708,
| | - Christian Abnet
- Division of Cancer Epidemiology and Genetics, NCI, 6120 Executive Blvd., Room 3042, Bethesda, MD 20892-7232, Phone: (301) 594-1511,
| | - Sanford Dawsey
- Division of Cancer Epidemiology and Genetics, NCI, 6120 Executive Blvd., Room 3024, Bethesda, MD 20892-7232, Phone: (301) 594-2930,
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Doobaree IU, Landis SH, Linklater KM, El-Hariry I, Moller H, Tyczynski J. Head and neck cancer in South East England between 1995-1999 and 2000-2004: An estimation of incidence and distribution by site, stage and histological type. Oral Oncol 2009; 45:809-14. [PMID: 19251472 DOI: 10.1016/j.oraloncology.2008.12.009] [Citation(s) in RCA: 33] [Impact Index Per Article: 2.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/25/2008] [Revised: 12/18/2008] [Accepted: 12/18/2008] [Indexed: 11/29/2022]
Abstract
Population-based data on head and neck cancer (HNC) stage and histological type are poorly described for England; these data are essential for clinical management and research. The aim of this study was to describe the distribution and incidence of all HNC and selected anatomical sites by sex, age, stage and histological type using a population-based cancer registry in South East England, and determine if the incidence changed between 1995-1999 and 2000-2004. We identified all HNC cancer cases registered by the Thames Cancer Registry for 1995-1999 and 2000-2004. Frequency distributions and age-standardised incidence rates were calculated by sex, age, stage and histological type and trends in incidence between the two time periods were described using incidence rate ratios and 95% confidence intervals. A total of 8700 HNC cases were reported in 2000-2004, representing an age-standardised incidence rate of 8.59 per 100000, which did not change significantly from 1995-1999. The three commonest HNC sites were intra-oral cavity, larynx and tonsil. Males were two to six times as likely as females to be diagnosed with HNC and there was a trend toward younger age at diagnosis over time. Significant increases in the incidence rate of intra-oral cavity cancer for both sexes and tonsillar cancer among males were observed. Conversely, laryngeal cancer incidence decreased over time. Staging data was only available for about 40% of HNC cases. Seventy six percent of HNC cases were squamous cell carcinomas. Trends in incidence varied between HNC sites, highlighting the importance of presenting data for individual HNC sites. The high proportion of unstaged cancers may result from incomplete recording in medical records; thus, the reporting of staging data should be made a priority.
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Abstract
Tobacco smoking is the main known cause of urinary bladder cancer in humans. In most populations, over half of cases in men and a sizeable proportion in women are attributable to this habit. Epidemiological studies conducted in different populations have shown a linear relationship between intensity and duration of smoking and risk. Quitting smoking reduces the risk of bladder cancer. Smoking black (air-cured) cigarettes results in a higher risk than smoking blond (flue-cured) tobacco cigarettes; results on inhalation patterns and use of filter are not consistent. Cigar and pipe smoking also increases the risk of bladder cancer; data on other tobacco products are limited. The evidence for non-transitional bladder carcinoma is limited, but consistent with an increased risk. The available evidence does not point towards a different carcinogenic effect of tobacco smoking in men and women or in whites and blacks. Data on involuntary smoke and use of smokeless tobacco products are limited, but do not suggest an increased risk of bladder cancer.
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Affiliation(s)
- Paolo Boffetta
- International Agency for Research on Cancer, 150 cours Albert Thomas, Lyon, France.
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Predicting lung cancer death in Africa and Asia: differences with WHO estimates. Cancer Causes Control 2009; 20:721-30. [PMID: 19123056 DOI: 10.1007/s10552-008-9285-8] [Citation(s) in RCA: 10] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/21/2008] [Accepted: 12/09/2008] [Indexed: 10/21/2022]
Abstract
OBJECTIVE Reliable cancer burden estimates are rarely available from most developing countries where cancer registration is lacking. This study provided estimates on the current and future number of lung cancer deaths in Indonesia, Vietnam and Ethiopia, and Sub-Saharan Africa at large. METHODS The number of lung cancer deaths was estimated from detailed smoking prevalence data (obtained from surveys among 8,726 rural individuals aged 25-74 years in Indonesia, Vietnam, and Ethiopia in 2005-2006) and on lung cancer rate estimates among non-smokers. RESULTS Our estimate for lung cancer deaths in Sub-Saharan Africa is 44,076 in 2005, which is 2.6 times the most recent WHO estimate in 2003 (17,000 deaths). A similar ratio is found for the country-specific estimate in Ethiopia. Our estimates are only slightly higher than the WHO's in Indonesia, and Vietnam. The attributable risk of smoking for lung cancer death among men was 39% in Ethiopia, 80% in Indonesia and 85% in Vietnam. We expect the annual number of lung cancer deaths to double by 2025, even if the smoking prevalence is assumed not to increase further. CONCLUSIONS WHO estimates on lung cancer deaths in Asia appear to be slightly lower than our study results; however, in Africa, the burden appears to be largely underestimated.
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Hassan MM, Spitz MR, Thomas MB, El-Deeb AS, Glover KY, Nguyen NT, Chan W, Kaseb A, Curley SA, Vauthey JN, Ellis LM, Abdalla E, Lozano RD, Patt YZ, Brown TD, Abbruzzese JL, Li D. Effect of different types of smoking and synergism with hepatitis C virus on risk of hepatocellular carcinoma in American men and women: case-control study. Int J Cancer 2008; 123:1883-91. [PMID: 18688864 PMCID: PMC2673571 DOI: 10.1002/ijc.23730] [Citation(s) in RCA: 65] [Impact Index Per Article: 3.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/16/2022]
Abstract
The International Agency for Research on Cancer has declared smoking to be a risk factor for hepatocellular carcinoma (HCC). However, passive exposure to cigarette smoke and use of noncigarette tobacco products on the risk of HCC has not been examined. Therefore, we evaluated the independent effects of different types of smoking exposure along with multiple risk factors for HCC and determined whether the magnitude of smoking was modified by other risk factors in men and women. We conducted a case-control study at The University of Texas M. D. Anderson Cancer Center where 319 HCC patients and 1,061 healthy control subjects were personally interviewed for several HCC risk factors. Multivariate logistic regression analysis was performed to estimate the adjusted odds ratio (AOR) and 95% confidence interval (CI) for each potential risk factor. Use of smokeless tobacco (chewing tobacco and snuff), cigars, pipes and passive smoking exposure were not related to HCC among noncigarette smokers. However, regular cigarette smoking was associated with HCC in men: AOR, 1.9 (95% CI, 1.1-3.1). Heavy alcohol consumption was associated with HCC in women: AOR, 7.7 (95% CI, 2.3-25.1). Cigarette smoking interacted synergistically with chronic infection of hepatitis C virus in men: AOR, 136.3 (95% CI, 43.2-429.6) and with heavy alcohol consumption in women: AOR, 13.7 (95% CI, 3.2-57.9). We conclude that sex differences were observed in HCC relationship with cigarette smoking and alcohol consumption. Controlling for smoking exposure might be a prudent approach to the prevention of HCC, especially in patients with chronic viral hepatitis infections.
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Affiliation(s)
- Manal M Hassan
- Department of Gastrointestinal Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
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Ladeiras-Lopes R, Pereira AK, Nogueira A, Pinheiro-Torres T, Pinto I, Santos-Pereira R, Lunet N. Smoking and gastric cancer: systematic review and meta-analysis of cohort studies. Cancer Causes Control 2008; 19:689-701. [PMID: 18293090 DOI: 10.1007/s10552-008-9132-y] [Citation(s) in RCA: 332] [Impact Index Per Article: 19.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/31/2007] [Accepted: 02/09/2008] [Indexed: 12/20/2022]
Abstract
OBJECTIVE We conducted a systematic review of studies addressing the relation between cigarette smoking and gastric cancer to estimate the magnitude of the association for different levels of exposure and cancer locations. METHODS Published cohort, case-cohort, and nested case-control studies were identified through PubMed, Scopus, and Web of Science searches, from inception to July 2007. Relative risk (RR) estimates referring to the comparison of two categories of exposure (e.g., current smokers vs. never smokers) were combined using a random effects model. Generalized least squares regression was used for trend estimation. Heterogeneity was quantified using the I (2) statistic. RESULTS Forty-two articles were considered for the systematic review. Comparing current smokers with never smokers: the summary RR estimates were 1.62 in males (95% CI: 1.50-1.75; I (2) = 46.0%; 18 studies) and 1.20 in females (95% CI: 1.01-1.43; I (2) = 49.8%; nine studies); the RR increased from 1.3 for the lowest consumptions to 1.7 for the smoking of approximately 30 cigarettes per day in the trend estimation analysis; smoking was significantly associated with both cardia (RR = 1.87; 95% CI: 1.31-2.67; I (2) = 73.2%; nine studies) and non-cardia (RR = 1.60; 95% CI: 1.41-1.80; I (2) = 18.9%; nine studies) cancers. CONCLUSION Our study provides solid evidence to classify smoking as the most important behavioral risk factor for gastric cancer.
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Affiliation(s)
- Ricardo Ladeiras-Lopes
- Department of Hygiene and Epidemiology, Porto University Medical School, Porto, Portugal
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