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Onwuka JU, Zahed H, Feng X, Alcala K, Erhunmwunsee L, Williams RM, Aldrich MC, Ahluwalia JS, Albanes D, Arslan AA, Bassett JK, Brennan P, Cai Q, Chen C, Dimou N, Ferrari P, Freedman ND, Huang WY, Jones ME, Jones MR, Kaaks R, Koh WP, Langhammer A, Liao LM, Malekzadeh R, Milne RL, Rohan TE, Sánchez MJ, Sheikh M, Sinha R, Shu XO, Stevens VL, Tinker LF, Visvanathan K, Wang Y, Wang R, Weinstein SJ, White E, Yuan JM, Zheng W, Johansson M, Robbins HA. Association between socioeconomic position and lung cancer incidence in 16 countries: a prospective cohort consortium study. EClinicalMedicine 2025; 82:103152. [PMID: 40212049 PMCID: PMC11985077 DOI: 10.1016/j.eclinm.2025.103152] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/02/2024] [Revised: 02/17/2025] [Accepted: 02/25/2025] [Indexed: 04/13/2025] Open
Abstract
Background Studies have reported higher lung cancer incidence among groups with lower socioeconomic position (SEP). However, it is not known how this difference in lung cancer incidence between SEP groups varies across different geographical settings. Furthermore, most prior studies that assessed the association between SEP and lung cancer incidence were conducted without detailed adjustment for smoking. Therefore, we aimed to assess this relationship across world regions. Methods In this international prospective cohort consortium study, we used data from the Lung Cancer Cohort Consortium (LC3), which includes 20 prospective population cohorts from 16 countries in North America, Europe, Asia, and Australia. Participants were enrolled between 1985 and 2010 and followed for cancer outcomes using registry linkages and/or active follow-up. We estimated hazard ratios (HRs) for the association between educational level (our primary measure of SEP, in 4 categories) and incident lung cancer using Cox proportional hazards models separately for participants with and without a smoking history. The models were adjusted for age, sex, cohort (when multiple cohorts were included), smoking duration, cigarettes per day, and time since cessation. Findings Among 2,487,511 participants, 53,830 developed lung cancer during a 13.5-year median follow-up (IQR = 6.5-15.0 years). Among participants with a smoking history, higher education was associated with decreased lung cancer incidence in nearly every cohort after detailed smoking adjustment. By world region, this association was observed in North America (HR per one-category increase in education [HRtrend] = 0.88, 95% CI = 0.87-0.89), Europe (HRtrend = 0.89, 95% CI = 0.88-0.91), and Asia (HRtrend = 0.91, 95% CI = 0.86-0.96), but not in the Australian study (HRtrend = 1.02, 95% CI = 0.95-1.09). By histological subtype, education associated most strongly with squamous cell carcinoma and more weakly with adenocarcinoma (p-heterogeneity < 0.0001). Among participants who never smoked, there was no association between education and lung cancer incidence in any cohort (all p-trend > 0.05), except the USA Southern Community Cohort Study (HRtrend = 0.75, 95% CI = 0.62-0.90). Interpretation Based on longitudinal data from 2.5 million participants from 16 countries, our findings suggest that higher educational attainment was associated with lower lung cancer risk among participants with a smoking history, but not among participants who never smoked. Limitations of our study include that cohort participants cannot fully represent the general populations of the geographical regions included, and education was the only measure of SEP consistently available across our consortium. Funding This study was supported in part by the National Cancer Institute (NCI), the Lung Cancer Research Foundation (LCRF), and the World Cancer Research Fund (WCRF).
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Affiliation(s)
| | - Hana Zahed
- Genomic Epidemiology Branch, International Agency for Research on Cancer, Lyon, France
| | - Xiaoshuang Feng
- Genomic Epidemiology Branch, International Agency for Research on Cancer, Lyon, France
| | - Karine Alcala
- Genomic Epidemiology Branch, International Agency for Research on Cancer, Lyon, France
| | - Loretta Erhunmwunsee
- Division of Thoracic Surgery, Department of Surgery, City of Hope Comprehensive Cancer Center, Duarte, CA, USA
| | - Randi M. Williams
- Department of Oncology, Cancer Prevention and Control Program, Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, DC, USA
| | - Melinda C. Aldrich
- Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA
| | - Jasjit S. Ahluwalia
- Center for Alcohol and Addiction Studies, Brown University School of Public Health and Alpert School of Medicine, Providence, RI, USA
| | - Demetrius Albanes
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD, USA
| | - Alan A. Arslan
- Departments of Obstetrics and Gynecology and Population Health, New York University Grossman School of Medicine, New York, NY, USA
| | - Julie K. Bassett
- Cancer Epidemiology Division, Cancer Council Victoria, Melbourne, Australia
- Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, University of Melbourne, Parkville, Australia
| | - Paul Brennan
- Genomic Epidemiology Branch, International Agency for Research on Cancer, Lyon, France
| | - Qiuyin Cai
- Division of Epidemiology, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA
| | - Chu Chen
- Program in Epidemiology and the Women’s Health Initiative Clinical Coordinating Center, Division of Public Health Sciences, Fred Hutchinson Cancer Center, Seattle, WA, USA
| | - Niki Dimou
- Nutrition and Metabolism Branch, International Agency for Research on Cancer, Lyon, France
| | - Pietro Ferrari
- Nutrition and Metabolism Branch, International Agency for Research on Cancer, Lyon, France
| | - Neal D. Freedman
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD, USA
| | - Wen-Yi Huang
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD, USA
| | - Michael E. Jones
- Division of Genetics and Epidemiology, Institute of Cancer Research, London, United Kingdom
| | - Miranda R. Jones
- Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA
| | - Rudolf Kaaks
- Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany
| | - Woon-Puay Koh
- Healthy Longevity Translational Research Program, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore
- Singapore Institute for Clinical Sciences, Agency for Science Technology and Research (A∗STAR), Singapore, Singapore
| | - Arnulf Langhammer
- Department of Public Health and Nursing, HUNT Research Center, NTNU Norwegian University of Science and Technology, Levanger, Norway
- Levanger Hospital, Nord-Trøndelag Hospital Trust, Levanger, Norway
| | - Linda M. Liao
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD, USA
| | - Reza Malekzadeh
- Digestive Disease Research Institute, Tehran University of Medical Sciences, Tehran, Iran
| | - Roger L. Milne
- Cancer Epidemiology Division, Cancer Council Victoria, Melbourne, Australia
- Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, University of Melbourne, Parkville, Australia
- School of Clinical Sciences at Monash Health, Monash University, Melbourne, Australia
| | - Thomas E. Rohan
- Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, NY, USA
| | - Maria-José Sánchez
- Escuela Andaluza de Salud Pública, Granada, Spain
- Instituto de Investigación Biosanitaria ibs.GRANADA, Granada, Spain
- Centro de Investigación Biomédica en Red de Epidemiología y Salud Pública (CIBERESP), Madrid, Spain
| | - Mahdi Sheikh
- Genomic Epidemiology Branch, International Agency for Research on Cancer, Lyon, France
| | - Rashmi Sinha
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD, USA
| | - Xiao-Ou Shu
- Division of Epidemiology, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA
| | | | - Lesley F. Tinker
- Division of Public Health Sciences, Women’s Health Initiative Clinical Coordinating Center, Fred Hutchinson Cancer Center, Seattle, WA, USA
| | - Kala Visvanathan
- Division of Cancer Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA
- Johns Hopkins Women's Malignancies Program, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA
| | - Ying Wang
- American Cancer Society, Atlanta, GA, USA
| | - Renwei Wang
- UPMC Hillman Cancer Center, University of Pittsburgh, Pittsburgh, PA, USA
| | - Stephanie J. Weinstein
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD, USA
| | - Emily White
- Cancer Prevention Research Program, Fred Hutchinson Cancer Center, Seattle, WA, USA
| | - Jian-Min Yuan
- Department of Epidemiology, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA, USA
- Division of Cancer Control and Population Sciences, UPMC Hillman Cancer Centre, University of Pittsburgh, Pittsburgh, PA, USA
| | - Wei Zheng
- Division of Epidemiology, Department of Medicine, Vanderbilt University Medical Center, Vanderbilt-Ingram Cancer Center, Nashville, TN, USA
| | - Mattias Johansson
- Genomic Epidemiology Branch, International Agency for Research on Cancer, Lyon, France
| | - Hilary A. Robbins
- Genomic Epidemiology Branch, International Agency for Research on Cancer, Lyon, France
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Lam ACL, Hueniken K, Pienkowski M, Lee JJW, Dong M, Diergaarde B, Olshan AF, Brennan P, Virani S, Saunders D, Santi SA, Conlon MSC, Waterboer T, Hayes DN, Pring M, Macfarlane GJ, Lagiou P, Lagiou A, Polesel J, Agudo A, Alemany L, Ahrens W, Healy CM, Conway DI, Nygard M, Canova C, Hornakova A, Richiardi L, Znaor A, Hung RJ, Xu W, Liu G. Performance of 8 Smoking Metrics for Modeling Survival in Head and Neck Squamous Cell Carcinoma. JAMA Otolaryngol Head Neck Surg 2025; 151:360-370. [PMID: 39976935 PMCID: PMC11843462 DOI: 10.1001/jamaoto.2024.5392] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/28/2024] [Accepted: 12/19/2024] [Indexed: 02/23/2025]
Abstract
Importance Cigarette smoking is a strong risk factor for mortality in patients diagnosed with head and neck squamous cell carcinoma (HNSCC). However, little evidence supports which smoking metric best models the association between smoking and survival in HNSCC. Objective To determine which smoking metric best models a linear association between smoking exposure and overall survival (OS) in patients with HNSCC. Design, Setting, and Participants A retrospective multicenter cohort study of 6 clinical epidemiological studies was performed. Five were part of the Human Papillomavirus, Oral and Oropharyngeal Cancer Genomic Research (VOYAGER) consortium. Participants included patients 18 years and older with pathologically confirmed HNSCC. Data were collected from January 2002 to December 2019, and data were analyzed between January 2022 to November 2024. Main Outcomes and Measures The primary outcome was OS. The performance of 8 smoking metrics, including pack-years, duration, and log cig-years (calculated as log10[cigarettes smoked per day + 1] × number of years smoked) for modeling OS were compared. Metric performance was measured by the strength of association in Cox proportional hazard models, linearity based on P for linear trend, Akaike information criterion (AIC; lower value indicates better model fit), and visual assessment of spline curves. Secondary outcomes included modeling OS in clinicodemographic subgroups and HNSCC anatomic subsites. Exploratory outcomes included cancer-specific survival and noncancer survival. Results In total, 8875 patients with HNSCC (2114 [24%] female; median [IQR] age, 61 [54-69] years) were included. Of 8 smoking metrics evaluated, smoking duration (adjusted hazard ratio [aHR], 1.11 [95% CI, 1.03-1.19]) and log cig-years (aHR, 1.11 [95% CI, 1.04-1.18]) had the highest aHRs; both had a statistically significant linear association with OS. Log cig-years had the lowest AIC linear value and the most visually linear spline curve when modeling OS. Duration and log cig-years outperformed pack-years for modeling OS regardless of age, smoking status, and cancer stage. Both performed well in lip and oral cavity, laryngeal (only duration was significant), and human papillomavirus-negative oropharyngeal subsites. In an exploratory analysis, duration had the highest aHR (1.15 [95% CI, 1.02-1.29]), and log cig-years had the lowest AIC linear value when modeling noncancer survival. Conclusions and Relevance In this cohort study, smoking duration and log cig-years best modeled a linear relationship with OS for patients with HNSCC. Both metrics maintained robust performance within specific clinicodemographic subgroups and anatomic subsites. Although most HNSCC survival models control for smoking exposure using smoking status or pack-years, duration and log cig-years may be superior metrics to account for the effects of smoking on survival.
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Affiliation(s)
- Andrew C. L. Lam
- Department of Medicine, University of Toronto, Toronto, Ontario, Canada
| | - Katrina Hueniken
- Division of Medical Oncology, Princess Margaret Cancer Centre, Toronto, Ontario, Canada
| | - Martha Pienkowski
- Division of Medical Oncology, Princess Margaret Cancer Centre, Toronto, Ontario, Canada
| | - John J. W. Lee
- Department of Otolaryngology–Head and Neck Surgery, Sinai Health Systems, University of Toronto, Toronto, Ontario, Canada
| | - Mei Dong
- Department of Biostatistics, Dalla Lana School of Public Health, University of Toronto, Toronto, Ontario, Canada
| | - Brenda Diergaarde
- Department of Human Genetics, School of Public Health, University of Pittsburgh, and UPMC Hillman Cancer Center, Pittsburgh, Pennsylvania
| | - Andrew F. Olshan
- Department of Epidemiology, Gillings School of Global Public Health, University of North Carolina, Chapel Hill
| | - Paul Brennan
- Genetic Epidemiology Group, World Health Organization, International Agency for Research on Cancer, Lyon, France
| | - Shama Virani
- Genetic Epidemiology Group, World Health Organization, International Agency for Research on Cancer, Lyon, France
| | - Deborah Saunders
- Department of Dental Oncology, Shirley and Jim Fielding Northeast Cancer Centre, Health Sciences North, Sudbury, Ontario, Canada
- Northern Ontario School of Medicine University, Sudbury, Ontario, Canada
| | - Stacey A. Santi
- Health Sciences North Research Institute, Sudbury, Ontario, Canada
| | | | - Tim Waterboer
- Division of Infections and Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany
| | - D. Neil Hayes
- University of Tennessee Health Science Center, Center for Cancer Research, Memphis
| | - Miranda Pring
- Bristol Dental Hospital and School, University of Bristol, Bristol, United Kingdom
| | - Gary J. Macfarlane
- Epidemiology Group, School of Medicine, Medical Sciences and Nutrition, University of Aberdeen, Aberdeen, Scotland, United Kingdom
| | - Pagona Lagiou
- School of Medicine, National and Kapodistrian University of Athens, Athens, Greece
| | - Areti Lagiou
- School of Public Health, University of West Attica, Athens, Greece
| | - Jerry Polesel
- Unit of Cancer Epidemiology, Centro di Riferimento Oncologico di Aviano (CRO) IRCCS, Aviano, Italy
| | - Antonio Agudo
- Catalan Institute of Oncology (ICO), and Bellvitge Biomedical Research Institute (IDIBELL), Barcelona, Spain
| | - Laia Alemany
- Catalan Institute of Oncology, Bellvitge Biomedical Research Institute (IDIBELL), Barcelona, Spain
- Centro de Investigación Biomédica en Red de Epidemiología y Salud Pública, Madrid, Spain
| | | | - Claire M. Healy
- School of Dental Science, Trinity College Dublin, Dublin, Ireland
| | - David I. Conway
- School of Medicine, Dentistry, and Nursing, University of Glasgow, Scotland, United Kingdom
| | - Mari Nygard
- Department of Research, Cancer Registry of Norway, Norwegian Institute of Public Health, Oslo, Norway
| | | | - Anna Hornakova
- Institute of Hygiene & Epidemiology, 1st Faculty of Medicine, Charles University, Prague, Czech Republic
| | - Lorenzo Richiardi
- Cancer Epidemiology Unit, Department of Medical Sciences, University of Turin, Turin, Italy
| | - Ariana Znaor
- International Agency for Research on Cancer, Lyon, France
| | - Rayjean J. Hung
- Prosserman Centre for Population Health Research, Lunenfeld-Tanenbaum Research Institute, Sinai Health System, Toronto, Ontario, Canada
| | - Wei Xu
- Department of Biostatistics, Dalla Lana School of Public Health, University of Toronto, Toronto, Ontario, Canada
| | - Geoffrey Liu
- Medicine, Medical Biophysics, Pharmacology and Toxicology, Institute of Medical Science, Temerty Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada
- Epidemiology, Dalla Lana School of Public Health, Toronto, Ontario, Canada
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Kang H, Cheon E, Hwang J, Jo S, Na K, Park SY, Cho SI. Risk of all-cause mortality by various cigarette smoking indices: A longitudinal study using the Korea National Health Examination Baseline Cohort in South Korea. Tob Induc Dis 2025; 23:TID-23-05. [PMID: 39877382 PMCID: PMC11773640 DOI: 10.18332/tid/199670] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/08/2024] [Revised: 12/30/2024] [Accepted: 01/03/2025] [Indexed: 01/31/2025] Open
Abstract
INTRODUCTION Smoking behaviors can be quantified using various indices. Previous studies have shown that these indices measure and predict health risks differently. Additionally, the choice of measure differs depending on the health outcome of interest. We compared how each smoking index predicted all-cause mortality and assessed the goodness-of-fit of each model. METHODS A population-based retrospective cohort, the Korea National Health Examination Baseline Cohort, was used (N=6001607). Data from 2009 were utilized, and the participants were followed until 2021. Cox proportional hazards regression analyses were performed among all participants and ever smokers, respectively, to estimate all-cause mortality. Model fit was assessed by the Akaike Information Criterion. RESULTS For men, smoking intensity showed the strongest effect size (hazard ratio HR=1.16; 95% CI: 1.14-1.18), while pack-years provided the best model fit for all-cause mortality. Among women, smoking intensity showed both the strongest effect size (HR=1.49; 95% CI: 1.28-1.74) and the best model fit. Smoking status (never/former/current) also showed comparable effect sizes (men, HR=1.14; 95% CI: 1.13-1.15; women, HR=1.14; 95% CI: 1.11- 1.18) with fair model fit. Analyses of people who ever smoked indicated that a model incorporating smoking status, duration, and intensity best described the mortality data. CONCLUSIONS The smoking indices showed varying effect sizes and model fits by sex, making it challenging to recommend a single optimal measure. Smoking intensity may be preferred for capturing cumulative exposure, whereas smoking status is notable for its simplicity, comparable effect size, and model fit. Further research that includes biochemical measurements, additional health outcomes, and longer follow-up periods is needed to refine these findings.
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Affiliation(s)
- Heewon Kang
- Institute of Health and Environment, Graduate School of Public Health, Seoul National University, Seoul, Republic of Korea
| | - Eunsil Cheon
- Department of Public Health Science, Graduate School of Public Health, Seoul National University, Seoul, Republic of Korea
| | - Jieun Hwang
- Department of Health Administration, College of Health Science, Dankook University, Cheonan, Republic of Korea
| | - Suyoung Jo
- Institute of Health and Environment, Graduate School of Public Health, Seoul National University, Seoul, Republic of Korea
| | - Kyoungin Na
- Division of Climate Change and Health Hazard, Korea Disease Control and Prevention Agency, Osong, Republic of Korea
| | - Seong Yong Park
- Department of Big Data Service, National Health Insurance Service, Wonju, Republic of Korea
| | - Sung-il Cho
- Institute of Health and Environment, Graduate School of Public Health, Seoul National University, Seoul, Republic of Korea
- Department of Public Health Science, Graduate School of Public Health, Seoul National University, Seoul, Republic of Korea
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Thomson B, Jemal A, Islami F. Association of Age at Smoking Initiation, Age at Smoking Cessation, and Lower Respiratory Mortality: Prospective Study of 500,000 Adults in the United States. Chest 2024; 166:1151-1154. [PMID: 38801857 DOI: 10.1016/j.chest.2024.04.022] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/18/2024] [Revised: 04/11/2024] [Accepted: 04/12/2024] [Indexed: 05/29/2024] Open
Affiliation(s)
- Blake Thomson
- Department of Surveillance and Health Equity Science, American Cancer Society, Atlanta, GA.
| | - Ahmedin Jemal
- Department of Surveillance and Health Equity Science, American Cancer Society, Atlanta, GA
| | - Farhad Islami
- Department of Surveillance and Health Equity Science, American Cancer Society, Atlanta, GA
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Kearney LE, Belancourt P, Katki HA, Tanner NT, Wiener RS, Robbins HA, Landy R, Caverly TJ. The Development and Performance of Alternative Criteria for Lung Cancer Screening. Ann Intern Med 2024; 177:1222-1232. [PMID: 39159457 DOI: 10.7326/m23-3250] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 08/21/2024] Open
Abstract
BACKGROUND The recommendation for lung cancer screening (LCS) developed by the U.S. Preventive Services Task Force (USPSTF) may exclude some high-benefit people. OBJECTIVE To determine whether alternative criteria can identify these high-benefit people. DESIGN Model-based projections. SETTING United States. PARTICIPANTS People from the 1997-2014 National Health Interview Survey (NHIS) to develop alternative criteria using fast-and-frugal tree algorithms and from the 2014-2018 NHIS and the 2022 Behavioral Risk Factor Surveillance System for comparisons of USPSTF criteria versus alternative criteria. MEASUREMENTS Life-years gained from LCS were estimated using the life-years gained from screening computed tomography (LYFS-CT) model. "High-benefit" was defined as gaining an average of at least 16.2 days of life from 3 annual screenings, which reflects high lung cancer risk and substantial life gains if lung cancer is detected by screening. RESULTS The final alternative criteria were 1) people who smoked any amount each year for at least 40 years, or 2) people aged 60 to 80 years with at least 40 pack-years of smoking. The USPSTF and alternative criteria selected similar numbers of people for LCS. Compared with the USPSTF criteria, the alternative criteria had higher sensitivity (91% vs. 78%; P < 0.001) and specificity (86% vs. 84%; P < 0.001) for identifying high-benefit people. For racial and ethnic minorities, the alternative criteria provided greater gains in sensitivity than the USPSTF criteria (Black: 83% vs. 56% [P < 0.001]; Hispanic: 95% vs. 73% [P = 0.086]; Asian: 94% vs. 68% [P = 0.171]) at similar specificity. The alternative criteria identify high-risk, high-benefit groups excluded by the USPSTF criteria (those with a smoking duration of ≥40 years but <20 pack-years and a quit history of >15 years), many of whom are members of racial and ethnic minorities. LIMITATION The results were based on model projections. CONCLUSION These results suggest that simple alternative LCS criteria can identify substantially more high-benefit people, especially in some racial and ethnic groups. PRIMARY FUNDING SOURCE U.S. Department of Veterans Affairs Lung Precision Oncology Program.
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Affiliation(s)
- Lauren E Kearney
- Center for Healthcare Organization & Implementation Research, VA Boston Healthcare System, and The Pulmonary Center, Boston University Chobanian & Avedisian School of Medicine, Boston, Massachusetts (L.E.K.)
| | - Patrick Belancourt
- VA Ann Arbor Healthcare System and Center for Clinical Management Research, Ann Arbor, Michigan (P.B.)
| | - Hormuzd A Katki
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland (H.A.K., R.L.)
| | - Nichole T Tanner
- Health Equity and Rural Outreach Innovation Center, Ralph H. Johnson Veterans Affairs Healthcare System, and Division of Pulmonary, Critical Care and Sleep Medicine, Medical University of South Carolina, Charleston, South Carolina (N.T.T.)
| | - Renda Soylemez Wiener
- Center for Healthcare Organization & Implementation Research, VA Boston Healthcare System, Boston, Massachusetts; The Pulmonary Center, Boston University Chobanian & Avedisian School of Medicine, Boston, Massachusetts; and National Center for Lung Cancer Screening, Veterans Health Administration, Washington, DC (R.S.W.)
| | - Hilary A Robbins
- International Agency for Research on Cancer, Lyon, France (H.A.R.)
| | - Rebecca Landy
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland (H.A.K., R.L.)
| | - Tanner J Caverly
- VA Ann Arbor Healthcare System, Ann Arbor, Michigan; National Center for Lung Cancer Screening, Veterans Health Administration, Washington, DC; and University of Michigan Medical School, Ann Arbor, Michigan (T.J.C.)
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Potter AL, Xu NN, Senthil P, Srinivasan D, Lee H, Gazelle GS, Chelala L, Zheng W, Fintelmann FJ, Sequist LV, Donington J, Palmer JR, Yang CFJ. Pack-Year Smoking History: An Inadequate and Biased Measure to Determine Lung Cancer Screening Eligibility. J Clin Oncol 2024; 42:2026-2037. [PMID: 38537159 PMCID: PMC11191064 DOI: 10.1200/jco.23.01780] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/16/2023] [Revised: 12/21/2023] [Accepted: 02/02/2024] [Indexed: 05/03/2024] Open
Abstract
PURPOSE Pack-year smoking history is an imperfect and biased measure of cumulative tobacco exposure. The use of pack-year smoking history to determine lung cancer screening eligibility in the current US Preventive Services Task Force (USPSTF) guideline may unintentionally exclude many high-risk individuals, especially those from racial and ethnic minority groups. It is unclear whether using a smoking duration cutoff instead of a smoking pack-year cutoff would improve the selection of individuals for screening. METHODS We analyzed 49,703 individuals with a smoking history from the Southern Community Cohort Study (SCCS) and 22,126 individuals with a smoking history from the Black Women's Health Study (BWHS) to assess eligibility for screening under the USPSTF guideline versus a proposed guideline that replaces the ≥20-pack-year criterion with a ≥20-year smoking duration criterion. RESULTS Under the USPSTF guideline, only 57.6% of Black patients with lung cancer in the SCCS would have qualified for screening, whereas a significantly higher percentage of White patients with lung cancer (74.0%) would have qualified (P < .001). Under the proposed guideline, the percentage of Black and White patients with lung cancer who would have qualified for screening increased to 85.3% and 82.0%, respectively, eradicating the disparity in screening eligibility between the groups. In the BWHS, using a 20-year smoking duration cutoff instead of a 20-pack-year cutoff increased the percentage of Black women with lung cancer who would have qualified for screening from 42.5% to 63.8%. CONCLUSION Use of a 20-year smoking duration cutoff instead of a 20-pack-year cutoff greatly increases the proportion of patients with lung cancer who would qualify for screening and eliminates the racial disparity in screening eligibility between Black versus White individuals; smoking duration has the added benefit of being easier to calculate and being a more precise assessment of smoking exposure compared with pack-year smoking history.
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Affiliation(s)
- Alexandra L. Potter
- Division of Thoracic Surgery, Department of Surgery, Massachusetts General Hospital, Boston, MA
| | - Nuo N. Xu
- Slone Epidemiology Center at Boston University, Boston, MA
| | - Priyanka Senthil
- Division of Thoracic Surgery, Department of Surgery, Massachusetts General Hospital, Boston, MA
| | - Deepti Srinivasan
- Division of Thoracic Surgery, Department of Surgery, Massachusetts General Hospital, Boston, MA
| | - Hang Lee
- Biostatistics Center, Massachusetts General Hospital, Boston, MA
| | - G. Scott Gazelle
- Department of Radiology, Massachusetts General Hospital, Boston, MA
- Institute for Technology Assessment, Massachusetts General Hospital, Boston, MA
| | - Lydia Chelala
- Department of Radiology, University of Chicago Pritzker School of Medicine, Chicago, IL
| | - Wei Zheng
- Division of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center, Nashville, TN
- Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, TN
| | | | - Lecia V. Sequist
- Mass General Cancer Center, Massachusetts General Hospital, Boston, MA
| | - Jessica Donington
- Section of Thoracic Surgery, Department of Surgery, University of Chicago Hospital, Chicago, IL
| | | | - Chi-Fu Jeffrey Yang
- Division of Thoracic Surgery, Department of Surgery, Massachusetts General Hospital, Boston, MA
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Rissanen I, Nerg I, Oura P, Huikari S, Korhonen M. Productivity costs of lifelong smoking-the Northern Finland Birth Cohort 1966 study. Eur J Public Health 2024; 34:572-577. [PMID: 38552215 PMCID: PMC11161164 DOI: 10.1093/eurpub/ckae057] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 06/09/2024] Open
Abstract
BACKGROUND Smoking is one of the leading causes of impaired health and mortality. Loss of paid and unpaid work and replacements due to morbidity and mortality result in productivity costs. Our aim was to investigate the productivity costs of lifelong smoking trajectories and cumulative exposure using advanced human capital method (HCM) and friction cost method (FCM). METHODS Within the Northern Finland Birth Cohort 1966 (NFBC1966), 10 650 persons were followed from antenatal period to age 55 years. The life course of smoking behaviour was assessed with trajectory modelling and cumulative exposure with pack-years. Productivity costs were estimated with advanced HCM and FCM models by using detailed, national register-based data on care, disability, mortality, education, taxation, occupation and labour market. A two-part regression model was used to predict productivity costs associated with lifelong smoking and cumulative exposure. RESULTS Of the six distinct smoking trajectories, lifetime smokers had the highest productivity costs followed by late starters, late adult quitters, young adult quitters and youth smokers. Never-smokers had the lowest productivity costs. The higher the number of pack-years, the higher the productivity costs. Uniform patterns were found in both men and women and when estimated with HCM and FCM. The findings were independent of other health behaviours. CONCLUSIONS Cumulative exposure to smoking is more crucial to productivity costs than starting or ending age of smoking. This suggests that the harmful effects of smoking depend on dose and duration of smoking and are irrespective of age when smoking occurred.
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Affiliation(s)
- Ina Rissanen
- Research Unit of Population Health, Faculty of Medicine, University of Oulu, Oulu, Finland
- Medical Research Center Oulu, Oulu University Hospital and University of Oulu, Oulu, Finland
- Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht and Utrecht University, Utrecht, The Netherlands
| | - Iiro Nerg
- Research Unit of Population Health, Faculty of Medicine, University of Oulu, Oulu, Finland
- Department of Economics, Oulu Business School, University of Oulu, Oulu, Finland
| | - Petteri Oura
- Medical Research Center Oulu, Oulu University Hospital and University of Oulu, Oulu, Finland
- Research Unit of Health Sciences and Technology, University of Oulu, Oulu, Finland
| | - Sanna Huikari
- Department of Economics, Oulu Business School, University of Oulu, Oulu, Finland
| | - Marko Korhonen
- Department of Economics, Oulu Business School, University of Oulu, Oulu, Finland
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8
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Laguna JC, Tagliamento M, Lambertini M, Hiznay J, Mezquita L. Tackling Non-Small Cell Lung Cancer in Young Adults: From Risk Factors and Genetic Susceptibility to Lung Cancer Profile and Outcomes. Am Soc Clin Oncol Educ Book 2024; 44:e432488. [PMID: 38788188 DOI: 10.1200/edbk_432488] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 05/26/2024]
Abstract
Lung cancer has traditionally been associated with advanced age; however, its increasing incidence among young adults raises concerning questions regarding its etiology and unique considerations for this population. In contrast to the older population, the onset of lung cancer at younger age may be attributed to a complex interplay of incompletely understood individual susceptibility and prevalent environmental risk factors beyond tobacco smoke exposure, such as radon gas and air pollution, which are widespread globally. Consequently, this leads to distinct clinical and molecular profiles, requiring a tailored approach. Furthermore, a diagnosis of cancer represents a threatening event during the prime years of a young person's life, prompting concern about career development, social aspects, fertility aspirations, and physical independence. This poses significant additional challenges for health care professionals in a field that remains underexplored. This comprehensive review recognizes lung cancer in young adults as a distinct entity, exploring its clinical and molecular characteristics, diverse predisposing factors, and priorities in terms of quality of life, with the aim of providing practical support to oncologists and enhancing our understanding of this under-researched population.
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Affiliation(s)
- Juan Carlos Laguna
- Medical Oncology Department, Hospital Clinic of Barcelona, Barcelona, Spain
- Laboratory of Translational Genomics and Targeted Therapies in Solid Tumors, IDIBAPS, Barcelona, Spain
| | - Marco Tagliamento
- Department of Internal Medicine and Medical Specialties (DIMI), School of Medicine, University of Genova, Genova, Italy
- Department of Medical Oncology, Clinica di Oncologia Medica, IRCCS Ospedale Policlinico San Martino, Genova, Italy
| | - Matteo Lambertini
- Department of Internal Medicine and Medical Specialties (DIMI), School of Medicine, University of Genova, Genova, Italy
- Department of Medical Oncology, Clinica di Oncologia Medica, IRCCS Ospedale Policlinico San Martino, Genova, Italy
| | | | - Laura Mezquita
- Medical Oncology Department, Hospital Clinic of Barcelona, Barcelona, Spain
- Laboratory of Translational Genomics and Targeted Therapies in Solid Tumors, IDIBAPS, Barcelona, Spain
- Department of Medicine, University of Barcelona, Barcelona, Spain
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9
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Joannès C, Kelly-Irving M, Couarraze S, Castagné R. The effect of smoking initiation in adolescence on the subsequent smoking trajectories of people who smoke, and the role of adverse childhood experiences: Results from the 1958 British cohort study. Public Health Nurs 2024; 41:127-138. [PMID: 37953700 DOI: 10.1111/phn.13261] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/28/2023] [Revised: 10/02/2023] [Accepted: 10/23/2023] [Indexed: 11/14/2023]
Abstract
OBJECTIVE To examine the association between smoking initiation in adolescence and subsequent different smoking trajectories of people who smoke, and to examine the combined effect of adverse childhood experiences (ACEs) and smoking initiation in adolescence on smoking trajectories of people who smoke. DESIGN AND SAMPLE Data are from 8757 individuals in Great Britain from the birth cohort National Child Development Study and who reported being smokers or former smokers by age 23. MEASUREMENTS Smoking initiation in adolescence was measured at 16 y and smoking trajectories were derived from smoking variables from ages 23 to 55. We modelled the relationship between smoking initiation in adolescence with or without ACEs and smoking trajectories. RESULTS Individuals who initiated smoking in adolescence were more likely to quit later than quitting in twenties (RRR quitting in thirties = 3.43 [2.40; 4.89] p < .001; RRR quitting in forties = 5.25 [3.38; 8.14] p < .001; RRR quitting in fifties = 4.48 [2.95; 6.79] p < .001), to relapse (RRR Relapse = 3.66 [2.82; 4.76] p < .001) and to be persistent smokers (RRR persistent = 5.25 [3.81; 7.25] p < .001) compared to those who had initiated smoking in young adulthood. These effects were particularly pronounced in case of ACEs. CONCLUSION Smoking prevention programs aimed at reducing smoking initiation should be promoted to adolescents to limit the burden of smoking, especially for people who have suffered adversity during childhood.
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Affiliation(s)
- Camille Joannès
- EQUITY Research Team, Center for Epidemiology & Research in POPulation Health (CERPOP), UMR 1295, University Toulouse III Paul Sabatier, Toulouse, France
| | - Michelle Kelly-Irving
- EQUITY Research Team, Center for Epidemiology & Research in POPulation Health (CERPOP), UMR 1295, University Toulouse III Paul Sabatier, Toulouse, France
| | - Sébastien Couarraze
- Department of Medicine, Maieutics and Paramedicine, Faculty of Health, Center for Epidemiology & Research in POPulation Health (CERPOP), UMR 1295, University Toulouse III Paul Sabatier, Toulouse, France
| | - Raphaële Castagné
- EQUITY Research Team, Center for Epidemiology & Research in POPulation Health (CERPOP), UMR 1295, University Toulouse III Paul Sabatier, Toulouse, France
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10
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Turati F, Rossi M, Spinazzè A, Pira E, Cavallo DM, Patel L, Mensi C, La Vecchia C, Negri E. Occupational asbestos exposure and ovarian cancer: updated systematic review. Occup Med (Lond) 2023; 73:532-540. [PMID: 38072464 DOI: 10.1093/occmed/kqad122] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/30/2024] Open
Abstract
BACKGROUND The association between asbestos exposure and ovarian cancer has been questioned given the possible misdiagnosis of peritoneal mesothelioma as ovarian cancer. AIMS To update a systematic review on ovarian cancer risk in women occupationally exposed to asbestos, exploring the association with the time since first exposure and the duration of exposure. METHODS We searched PubMed from 2008 onwards, screened previous systematic reviews, combined standardized mortality ratios (SMR) using random effect models and quantified heterogeneity using the I2 statistic. To assess tumour misclassification, we compared the distribution of observed excess ovarian cancers (OEOC) to that expected (EEOC) from the distribution of peritoneal cancers in strata of latency and exposure duration. RESULTS Eighteen publications (20 populations), including a pooled analysis of 21 cohorts, were included. The pooled SMR was 1.79 (95% confidence interval 1.38-2.31), with moderate heterogeneity between studies (I2 = 42%), based on 144 ovarian cancer deaths/cases. The risk was increased for women with indirect indicators of higher exposure, longer duration and latency, and lower for chrysotile than for crocidolite exposure. The effect of duration and latency could not be completely disentangled, since no multivariate analysis was available for time-related variables. The dissimilarity index between OEOC and EEOC for the time since first exposure was small suggesting a similar pattern of risk. CONCLUSIONS While some misclassification between ovarian and peritoneal cancers cannot be excluded, the observed excess risk of ovarian cancer should be added to the overall disease burden of asbestos.
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Affiliation(s)
- F Turati
- Department of Clinical Sciences and Community Health, University of Milan, 20133 Milan, Italy
| | - M Rossi
- Department of Clinical Sciences and Community Health, University of Milan, 20133 Milan, Italy
| | - A Spinazzè
- Department of Science and High Technology, University of Insubria, 22100 Como, Italy
| | - E Pira
- Department of Sciences of Public Health and Pediatrics, University of Turin, 10126 Turin, Italy
| | - D M Cavallo
- Department of Science and High Technology, University of Insubria, 22100 Como, Italy
| | - L Patel
- Department of Clinical Sciences and Community Health, University of Milan, 20133 Milan, Italy
| | - C Mensi
- Occupational Health Unit, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, 20122 Milan, Italy
| | - C La Vecchia
- Department of Clinical Sciences and Community Health, University of Milan, 20133 Milan, Italy
| | - E Negri
- Department of Medical and Surgical Sciences, University of Bologna, 40138 Bologna, Italy
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11
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Balmain A. Peto's paradox revisited: black box vs mechanistic approaches to understanding the roles of mutations and promoting factors in cancer. Eur J Epidemiol 2023; 38:1251-1258. [PMID: 36512199 PMCID: PMC10757908 DOI: 10.1007/s10654-022-00933-x] [Citation(s) in RCA: 3] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/05/2022] [Accepted: 10/10/2022] [Indexed: 12/15/2022]
Affiliation(s)
- Allan Balmain
- Helen Diller Family Comprehensive Cancer Center, University of California, San FranciscoSan Francisco, CA, 1450 3rd Street94143, USA.
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12
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Ma Z, Lv J, Zhu M, Yu C, Ma H, Jin G, Guo Y, Bian Z, Yang L, Chen Y, Chen Z, Hu Z, Li L, Shen H. Lung cancer risk score for ever and never smokers in China. Cancer Commun (Lond) 2023; 43:877-895. [PMID: 37410540 PMCID: PMC10397566 DOI: 10.1002/cac2.12463] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/09/2023] [Revised: 05/23/2023] [Accepted: 06/28/2023] [Indexed: 07/07/2023] Open
Abstract
BACKGROUND Most lung cancer risk prediction models were developed in European and North-American cohorts of smokers aged ≥ 55 years, while less is known about risk profiles in Asia, especially for never smokers or individuals aged < 50 years. Hence, we aimed to develop and validate a lung cancer risk estimate tool for ever and never smokers across a wide age range. METHODS Based on the China Kadoorie Biobank cohort, we first systematically selected the predictors and explored the nonlinear association of predictors with lung cancer risk using restricted cubic splines. Then, we separately developed risk prediction models to construct a lung cancer risk score (LCRS) in 159,715 ever smokers and 336,526 never smokers. The LCRS was further validated in an independent cohort over a median follow-up of 13.6 years, consisting of 14,153 never smokers and 5,890 ever smokers. RESULTS A total of 13 and 9 routinely available predictors were identified for ever and never smokers, respectively. Of these predictors, cigarettes per day and quit years showed nonlinear associations with lung cancer risk (Pnon-linear < 0.001). The curve of lung cancer incidence increased rapidly above 20 cigarettes per day and then was relatively flat until approximately 30 cigarettes per day. We also observed that lung cancer risk declined sharply within the first 5 years of quitting, and then continued to decrease but at a slower rate in the subsequent years. The 6-year area under the receiver operating curve for the ever and never smokers' models were respectively 0.778 and 0.733 in the derivation cohort, and 0.774 and 0.759 in the validation cohort. In the validation cohort, the 10-year cumulative incidence of lung cancer was 0.39% and 2.57% for ever smokers with low (< 166.2) and intermediate-high LCRS (≥ 166.2), respectively. Never smokers with a high LCRS (≥ 21.2) had a higher 10-year cumulative incidence rate than those with a low LCRS (< 21.2; 1.05% vs. 0.22%). An online risk evaluation tool (LCKEY; http://ccra.njmu.edu.cn/lckey/web) was developed to facilitate the use of LCRS. CONCLUSIONS The LCRS can be an effective risk assessment tool designed for ever and never smokers aged 30 to 80 years.
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Affiliation(s)
- Zhimin Ma
- Department of EpidemiologyCenter for Global HealthSchool of Public HealthNanjing Medical UniversityNanjingJiangsuP. R. China
- Jiangsu Key Lab of Cancer BiomarkersPrevention and TreatmentCollaborative Innovation Center for Cancer Personalized MedicineNanjing Medical UniversityNanjingJiangsuP. R. China
- Department of EpidemiologySchool of Public HealthSoutheast UniversityNanjingJiangsuP. R. China
| | - Jun Lv
- Department of Epidemiology & BiostatisticsSchool of Public HealthPeking UniversityBeijingP. R. China
- Ministry of EducationKey Laboratory of Molecular Cardiovascular Sciences (Peking University)BeijingP. R. China
| | - Meng Zhu
- Department of EpidemiologyCenter for Global HealthSchool of Public HealthNanjing Medical UniversityNanjingJiangsuP. R. China
- Jiangsu Key Lab of Cancer BiomarkersPrevention and TreatmentCollaborative Innovation Center for Cancer Personalized MedicineNanjing Medical UniversityNanjingJiangsuP. R. China
| | - Canqing Yu
- Department of Epidemiology & BiostatisticsSchool of Public HealthPeking UniversityBeijingP. R. China
| | - Hongxia Ma
- Department of EpidemiologyCenter for Global HealthSchool of Public HealthNanjing Medical UniversityNanjingJiangsuP. R. China
- Jiangsu Key Lab of Cancer BiomarkersPrevention and TreatmentCollaborative Innovation Center for Cancer Personalized MedicineNanjing Medical UniversityNanjingJiangsuP. R. China
| | - Guangfu Jin
- Department of EpidemiologyCenter for Global HealthSchool of Public HealthNanjing Medical UniversityNanjingJiangsuP. R. China
- Jiangsu Key Lab of Cancer BiomarkersPrevention and TreatmentCollaborative Innovation Center for Cancer Personalized MedicineNanjing Medical UniversityNanjingJiangsuP. R. China
| | - Yu Guo
- Chinese Academy of Medical SciencesBeijingP. R. China
| | - Zheng Bian
- Chinese Academy of Medical SciencesBeijingP. R. China
| | - Ling Yang
- Clinical Trial Service Unit & Epidemiological Studies Unit (CTSU)Nuffield Department of Population HealthUniversity of OxfordOxfordOxfordshireUK
| | - Yiping Chen
- Clinical Trial Service Unit & Epidemiological Studies Unit (CTSU)Nuffield Department of Population HealthUniversity of OxfordOxfordOxfordshireUK
| | - Zhengming Chen
- Clinical Trial Service Unit & Epidemiological Studies Unit (CTSU)Nuffield Department of Population HealthUniversity of OxfordOxfordOxfordshireUK
| | - Zhibin Hu
- Department of EpidemiologyCenter for Global HealthSchool of Public HealthNanjing Medical UniversityNanjingJiangsuP. R. China
- Jiangsu Key Lab of Cancer BiomarkersPrevention and TreatmentCollaborative Innovation Center for Cancer Personalized MedicineNanjing Medical UniversityNanjingJiangsuP. R. China
| | - Liming Li
- Department of Epidemiology & BiostatisticsSchool of Public HealthPeking UniversityBeijingP. R. China
- Clinical Trial Service Unit & Epidemiological Studies Unit (CTSU)Nuffield Department of Population HealthUniversity of OxfordOxfordOxfordshireUK
| | - Hongbing Shen
- Department of EpidemiologyCenter for Global HealthSchool of Public HealthNanjing Medical UniversityNanjingJiangsuP. R. China
- Jiangsu Key Lab of Cancer BiomarkersPrevention and TreatmentCollaborative Innovation Center for Cancer Personalized MedicineNanjing Medical UniversityNanjingJiangsuP. R. China
- Research Units of Cohort Study on Cardiovascular Diseases and CancersChinese Academy of Medical SciencesBeijingP. R. China
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Dragani TA, Muley T, Schneider MA, Kobinger S, Eichhorn M, Winter H, Hoffmann H, Kriegsmann M, Noci S, Incarbone M, Tosi D, Franzi S, Colombo F. Lung Adenocarcinoma Diagnosed at a Younger Age Is Associated with Advanced Stage, Female Sex, and Ever-Smoker Status, in Patients Treated with Lung Resection. Cancers (Basel) 2023; 15:cancers15082395. [PMID: 37190323 DOI: 10.3390/cancers15082395] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/31/2023] [Revised: 04/06/2023] [Accepted: 04/19/2023] [Indexed: 05/17/2023] Open
Abstract
To date, the factors which affect the age at diagnosis of lung adenocarcinoma are not fully understood. In our study, we examined the relationships of age at diagnosis with smoking, pathological stage, sex, and year of diagnosis in a discovery (n = 1694) and validation (n = 1384) series of lung adenocarcinoma patients who had undergone pulmonary resection at hospitals in the Milan area and at Thoraxklinik (Heidelberg), respectively. In the discovery series, younger age at diagnosis was associated with ever-smoker status (OR = 1.5, p = 0.0035) and advanced stage (taking stage I as reference: stage III OR = 1.4, p = 0.0067; stage IV OR = 1.7, p = 0.0080), whereas older age at diagnosis was associated with male sex (OR = 0.57, p < 0.001). Analysis in the validation series confirmed the ever versus never smokers' association (OR = 2.9, p < 0.001), the association with highest stages (stage III versus stage I OR = 1.4, p = 0.0066; stage IV versus stage I OR = 2.0, p = 0.0022), and the male versus female sex association (OR = 0.78, p = 0.032). These data suggest the role of smoking in affecting the natural history of the disease. Moreover, aggressive tumours seem to have shorter latency from initiation to clinical detection. Finally, younger age at diagnosis is associated with the female sex, suggesting that hormonal status of young women confers risk to develop lung adenocarcinoma. Overall, this study provided novel findings on the mechanisms underlying age at diagnosis of lung adenocarcinoma.
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Affiliation(s)
- Tommaso A Dragani
- Department of Research, Fondazione IRCCS Istituto Nazionale dei Tumori, 20133 Milan, Italy
| | - Thomas Muley
- Translational Research Unit (STF), Thoraxklinik, Heidelberg University Hospital, 69126 Heidelberg, Germany
- Translational Lung Research Center (TLRC), German Center for Lung Research (DZL), 69120 Heidelberg, Germany
| | - Marc A Schneider
- Translational Research Unit (STF), Thoraxklinik, Heidelberg University Hospital, 69126 Heidelberg, Germany
- Translational Lung Research Center (TLRC), German Center for Lung Research (DZL), 69120 Heidelberg, Germany
| | - Sonja Kobinger
- Department of Thoracic Surgery, Thoraxklinik, Heidelberg University Hospital, 69126 Heidelberg, Germany
| | - Martin Eichhorn
- Department of Thoracic Surgery, Thoraxklinik, Heidelberg University Hospital, 69126 Heidelberg, Germany
| | - Hauke Winter
- Translational Lung Research Center (TLRC), German Center for Lung Research (DZL), 69120 Heidelberg, Germany
- Department of Thoracic Surgery, Thoraxklinik, Heidelberg University Hospital, 69126 Heidelberg, Germany
| | - Hans Hoffmann
- Department of Thoracic Surgery, Klinikum Rechts der Isar, Technische Universität München, 81675 Munich, Germany
| | - Mark Kriegsmann
- Translational Lung Research Center (TLRC), German Center for Lung Research (DZL), 69120 Heidelberg, Germany
- Institute of Pathology, Heidelberg University Hospital, 69120 Heidelberg, Germany
| | - Sara Noci
- Department of Research, Fondazione IRCCS Istituto Nazionale dei Tumori, 20133 Milan, Italy
| | - Matteo Incarbone
- Department of Surgery, IRCCS Multimedica, 20099 Sesto San Giovanni, Italy
| | - Davide Tosi
- Thoracic Surgery and Lung Transplantation, Foundation IRCCS Ca' Granda Ospedale Maggiore Policlinico, 20122 Milan, Italy
| | - Sara Franzi
- Thoracic Surgery and Lung Transplantation, Foundation IRCCS Ca' Granda Ospedale Maggiore Policlinico, 20122 Milan, Italy
| | - Francesca Colombo
- Department of Research, Fondazione IRCCS Istituto Nazionale dei Tumori, 20133 Milan, Italy
- Institute for Biomedical Technologies, CNR, 20054 Segrate, Italy
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14
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Wang Q, Gümüş ZH, Colarossi C, Memeo L, Wang X, Kong CY, Boffetta P. SCLC: Epidemiology, Risk Factors, Genetic Susceptibility, Molecular Pathology, Screening, and Early Detection. J Thorac Oncol 2023; 18:31-46. [PMID: 36243387 PMCID: PMC10797993 DOI: 10.1016/j.jtho.2022.10.002] [Citation(s) in RCA: 100] [Impact Index Per Article: 50.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/09/2022] [Revised: 10/03/2022] [Accepted: 10/04/2022] [Indexed: 11/13/2022]
Abstract
We review research regarding the epidemiology, risk factors, genetic susceptibility, molecular pathology, and early detection of SCLC, a deadly tumor that accounts for 14% of lung cancers. We first summarize the changing incidences of SCLC globally and in the United States among males and females. We then review the established risk factor (i.e., tobacco smoking) and suspected nonsmoking-related risk factors for SCLC, and emphasize the importance of continued effort in tobacco control worldwide. Review of genetic susceptibility and molecular pathology suggests different molecular pathways in SCLC development compared with other types of lung cancer. Last, we comment on the limited utility of low-dose computed tomography screening in SCLC and on several promising blood-based molecular biomarkers as potential tools in SCLC early detection.
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Affiliation(s)
- Qian Wang
- University Hospitals Seidman Cancer Center, Cleveland, Ohio.
| | - Zeynep H Gümüş
- Department of Genetics and Genomics, Icahn School of Medicine at Mount Sinai, New York, New York; Center for Thoracic Oncology, Tisch Cancer Center, Icahn School of Medicine at Mount Sinai, New York, New York
| | - Cristina Colarossi
- Pathology Unit, Department of Experimental Oncology, Mediterranean Institute of Oncology, Catania, Italy
| | - Lorenzo Memeo
- Pathology Unit, Department of Experimental Oncology, Mediterranean Institute of Oncology, Catania, Italy
| | - Xintong Wang
- Department of Pathology, Icahn School of Medicine at Mount Sinai, New York, New York
| | - Chung Yin Kong
- Division of General Internal Medicine, Icahn School of Medicine at Mount Sinai, New York, New York
| | - Paolo Boffetta
- Department of Family, Population & Preventive Medicine, Stony Brook University, Stony Brook, New York; Department of Medical and Surgical Sciences, University of Bologna, Bologna, Italy
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15
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Langley-Evans SC. Early life programming of health and disease: the long-term consequences of obesity in pregnancy: a narrative review. J Hum Nutr Diet 2022; 35:816-832. [PMID: 35475555 PMCID: PMC9540012 DOI: 10.1111/jhn.13023] [Citation(s) in RCA: 9] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/31/2022] [Accepted: 04/06/2022] [Indexed: 11/28/2022]
Abstract
The prevalence of overweight and obesity is rising in all parts of the world and among young women it presents a very clear danger during pregnancy. Women who are overweight or who gain excessive weight during pregnancy are at greater risk of complications in pregnancy and labour, and are more likely to lose their child to stillbirth, or themselves die during pregnancy. This narrative review considers the evidence that in addition to increasing risk of poor pregnancy outcomes, obesity has the capacity to programme fetuses to be at greater risk of cardiometabolic disorders later in life. An extensive body of evidence from prospective and retrospective cohorts, and record linkage studies demonstrates associations of maternal obesity and/or gestational diabetes with cardiovascular disease, type-1 and type-2 diabetes. Studies in animals suggest that these associations are underpinned by adaptations that occur in fetal life, which remodel the structures of major organs including the brain, kidney and pancreas. This article is protected by copyright. All rights reserved.
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Affiliation(s)
- Simon C Langley-Evans
- School of Biosciences, University of Nottingham, Sutton Bonington Campus, Loughborough, LE12 5RD
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16
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Bates JHT, Hamlington KL, Garrison G, Kinsey CM. Prediction of lung cancer risk based on age and smoking history. COMPUTER METHODS AND PROGRAMS IN BIOMEDICINE 2022; 216:106660. [PMID: 35114461 PMCID: PMC8920760 DOI: 10.1016/j.cmpb.2022.106660] [Citation(s) in RCA: 5] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Subscribe] [Scholar Register] [Received: 06/10/2021] [Revised: 01/21/2022] [Accepted: 01/23/2022] [Indexed: 06/14/2023]
Abstract
BACKGROUND AND OBJECTIVE The CISNET models provide predictions for dying of lung cancer in any year of life as a function of age and smoking history, but their predictions are quite variable and the models themselves can be complex to implement. Our goal was to develop a simple empirical model of the risk of dying of lung cancer that is mathematically constrained to produce biologically appropriate probability predictions as a function of current age, smoking start age, quit age, and smoking intensity. METHODS The six adjustable parameters of the model were evaluated by fitting its predictions of cancer death risk versus age to the mean of published predictions made by the CISNET models for the never smoker and for six different scenarios of lifetime smoking burden. RESULTS The mean RMS fitting error of the model was 6.16 × 10 -2 (% risk of dying of cancer per year of life) between 55 and 80 years of age. The model predictions increased monotonically with current age, quit age and smoking intensity, and decreased with increasing start age. CONCLUSIONS Our simple model of the risk of dying of lung cancer in any given year of life as a function of smoking history is easily implemented and thus may serve as a useful tool in situations where the mortality risks of smoking need to be estimated.
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Affiliation(s)
- Jason H T Bates
- Pulmonary/Critical Care Division, Department of Medicine, University of Vermont, Burlington VT 05405, USA.
| | - Katharine L Hamlington
- Department of Pediatrics, University of Colorado at Children's Hospital Colorado, Aurora, CO 80045, USA
| | - Garth Garrison
- Pulmonary/Critical Care Division, Department of Medicine, University of Vermont, Burlington VT 05405, USA
| | - C Matthew Kinsey
- Pulmonary/Critical Care Division, Department of Medicine, University of Vermont, Burlington VT 05405, USA
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Farkas G, Kocsis ZS, Székely G, Dobozi M, Kenessey I, Polgár C, Jurányi Z. Smoking, chromosomal aberrations, and cancer incidence in healthy subjects. Mutat Res 2021; 867:503373. [PMID: 34266629 DOI: 10.1016/j.mrgentox.2021.503373] [Citation(s) in RCA: 8] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/10/2021] [Revised: 06/14/2021] [Accepted: 06/15/2021] [Indexed: 12/15/2022]
Abstract
Chromosomal aberrations (CAs) in peripheral blood lymphocytes can be used as biomarkers of cancer risk. Cytogenetic tests were conducted on 2396 healthy Hungarian individuals and cancer incidence was followed up from 1989 to 2018. Venous blood samples were obtained from the subjects and metaphases from lymphocyte cultures were prepared. We compared the CA frequencies of the various smoking (1-5; 6-10; 11-19; or 20-40 cigarettes/day) and exposure (irradiation; chemical industry; chemical research laboratory) groups. Chromatid break (p = 0.0002), total aberration (p = 0.002), and aberrant cell (p = 0.001) frequencies were higher in smokers than in non-smokers. For very heavy smokers, total CAs were significantly higher than for non-smokers (<0.001) or less intensive smokers (p = 0.003-0.0006). Intensity of smoking was a predictor of chromosomal aberrations, while duration was not. During follow-up, 177 (7.3 %) cancer cases were found. A Cox-regression model showed that subjects with cell values ≥2 CAs developed cancer more frequently (hazard ratio = 1.39; 95 % CI, 1.02-1.90). The relative risks of cancer were 1.06 (95 % CI 0.53-2.06) for light smokers and 1.74 (95 % CI 1.08-2.77) for very heavy smokers. The distributions of cancer sites showed differences between smoker and non-smoker groups: in male smokers, lung cancer, in non-smokers, prostate, and in females (both groups) breast cancer were most common. Cancer incidence correlated with chromosome aberrations; smoking was not a confounder in this relationship.
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Affiliation(s)
- Gyöngyi Farkas
- National Institute of Oncology, Centre of Radiotherapy, Department of Radiobiology and Diagnostic Onco-Cytogenetics, Ráth György u. 7-9, 1122, Budapest, Hungary
| | - Zsuzsa S Kocsis
- National Institute of Oncology, Centre of Radiotherapy, Department of Radiobiology and Diagnostic Onco-Cytogenetics, Ráth György u. 7-9, 1122, Budapest, Hungary
| | - Gábor Székely
- National Institute of Oncology, Centre of Radiotherapy, Department of Radiobiology and Diagnostic Onco-Cytogenetics, Ráth György u. 7-9, 1122, Budapest, Hungary
| | - Mária Dobozi
- National Institute of Oncology, National Cancer Registry, Ráth György u. 7-9, 1122, Budapest, Hungary
| | - István Kenessey
- National Institute of Oncology, National Cancer Registry, Ráth György u. 7-9, 1122, Budapest, Hungary
| | - Csaba Polgár
- National Institute of Oncology, Centre of Radiotherapy, Ráth György u. 7-9, 1122, Budapest, Hungary; Semmelweis University, Department of Oncology, Ráth György u. 7-9, 1122, Budapest, Hungary
| | - Zsolt Jurányi
- National Institute of Oncology, Centre of Radiotherapy, Department of Radiobiology and Diagnostic Onco-Cytogenetics, Ráth György u. 7-9, 1122, Budapest, Hungary.
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18
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Ten Haaf K, van der Aalst CM, de Koning HJ, Kaaks R, Tammemägi MC. Personalising lung cancer screening: An overview of risk-stratification opportunities and challenges. Int J Cancer 2021; 149:250-263. [PMID: 33783822 PMCID: PMC8251929 DOI: 10.1002/ijc.33578] [Citation(s) in RCA: 45] [Impact Index Per Article: 11.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/18/2020] [Revised: 03/04/2021] [Accepted: 03/12/2021] [Indexed: 12/17/2022]
Abstract
Randomised clinical trials have shown the efficacy of computed tomography lung cancer screening, initiating discussions on whether and how to implement population‐based screening programs. Due to smoking behaviour being the primary risk‐factor for lung cancer and part of the criteria for determining screening eligibility, lung cancer screening is inherently risk‐based. In fact, the selection of high‐risk individuals has been shown to be essential in implementing lung cancer screening in a cost‐effective manner. Furthermore, studies have shown that further risk‐stratification may improve screening efficiency, allow personalisation of the screening interval and reduce health disparities. However, implementing risk‐based lung cancer screening programs also requires overcoming a number of challenges. There are indications that risk‐based approaches can negatively influence the trade‐off between individual benefits and harms if not applied thoughtfully. Large‐scale implementation of targeted, risk‐based screening programs has been limited thus far. Consequently, questions remain on how to efficiently identify and invite high‐risk individuals from the general population. Finally, while risk‐based approaches may increase screening program efficiency, efficiency should be balanced with the overall impact of the screening program. In this review, we will address the opportunities and challenges in applying risk‐stratification in different aspects of lung cancer screening programs, as well as the balance between screening program efficiency and impact.
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Affiliation(s)
- Kevin Ten Haaf
- Department of Public Health, Erasmus MC-University Medical Center Rotterdam, Rotterdam, The Netherlands
| | - Carlijn M van der Aalst
- Department of Public Health, Erasmus MC-University Medical Center Rotterdam, Rotterdam, The Netherlands
| | - Harry J de Koning
- Department of Public Health, Erasmus MC-University Medical Center Rotterdam, Rotterdam, The Netherlands
| | - Rudolf Kaaks
- Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany.,Translational Lung Research Center (TLRC) Heidelberg, Member of the German Center for Lung Research (DZL), Heidelberg, Germany
| | - Martin C Tammemägi
- Department of Health Sciences, Brock University, St. Catharines, Ontario, Canada
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19
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Grignon M, Renaud T, Guerrouche K. Prise en compte de la durée et de l’intensité du tabagisme dans l’estimation de la mortalité attribuable au tabac : une nouvelle méthode appliquée au cancer du poumon en France. POPULATION 2021. [DOI: 10.3917/popu.2004.0561] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/14/2022]
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20
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Alexander DD, Pastula ST, Riordan AS. Epidemiology of lung cancer among acrylonitrile-exposed study populations: A meta-analysis. Regul Toxicol Pharmacol 2021; 122:104896. [PMID: 33617939 DOI: 10.1016/j.yrtph.2021.104896] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/16/2020] [Revised: 02/02/2021] [Accepted: 02/15/2021] [Indexed: 10/22/2022]
Abstract
PURPOSE To conduct a systematic review and meta-analysis of lung cancer among acrylonitrile-exposed workers. METHODS A literature search through April 2020 was performed to identify relevant cohort and case-control studies. Data from these studies were meta-analyzed to generate summary relative risk estimates (SRREs). Heterogeneity was examined in sub-group and sensitivity analyses, and by meta-regression. RESULTS Twenty-two studies were reviewed systematically, and 10 cohort studies and one case-control study were meta-analyzed. Individual relative risk estimates reported across studies were heterogeneous, with most being relatively weak in statistical strength and non-statistically significant on both sides of the null value. Meta-analysis of these data resulted in an SRRE of 1.04 (95% CI: 0.89-1.21; overall model, largely consisting of all workers exposed to acrylonitrile). Sub-group analyses and meta-regression did not support patterns of positive dose-response relationships by duration of exposure/employment or cumulative exposure. CONCLUSIONS Although some positive associations have been reported in internal comparison analyses based on increasing exposure categories, few associations are statistically significant, there are no apparent or consistent patterns of dose-response, and the confounding influence of cigarette smoking was not adequately controlled. Thus, findings from this review and meta-analysis do not support an increased risk of lung cancer among acrylonitrile workers.
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21
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Hajdu SI. Pathfinders in oncology from the first clinical use of single-agent chemotherapy to the introduction of mammography. Cancer 2021; 127:12-26. [PMID: 33095913 DOI: 10.1002/cncr.33223] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/03/2020] [Revised: 09/01/2020] [Accepted: 09/03/2020] [Indexed: 01/18/2023]
Abstract
During the period from 1942 to 1962, treatment attempts with single-agent chemotherapy such as nitrogen mustard and urethan gained limited application. However, the groundbreaking success with aminopterin in the treatment of patients with pediatric acute leukemia and methotrexate in the treatment of gestational choriocarcinoma established single-agent chemotherapy as a pioneering contribution to oncology. The landmark discovery that early-stage Hodgkin disease is curable with radiation made radiotherapy into an essential specialty of oncology. Although radical surgical treatment dominated the field of surgery, the excision of localized cancers with or without adjuvant radiation emerged as new modality in therapy. Cytopathology and surgical pathology became new fields in medicine and pathologists became an integral part of the preoperative, intraoperative, and postoperative care of patients with cancer. The discovery of multiple new drugs demonstrated promising results and widened the field of oncology from the laboratory to the clinic. In the etiology of cancer, precancerous conditions were named and carcinoma of the lung was definitively linked to cigarette smoking. All things considered, the progress made between 1942 and 1962 came about through the dedicated work of many individuals. However, there were 7 distinguished pathfinders (2 pathologists, 1 pediatric pathologist-oncologist, 1 radiation therapist, 1 physician-actuary, 1 gynecologist-oncologist, and 1 chemist) who, despite their different backgrounds, interests, and sex, made groundbreaking contributions to oncology.
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22
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Piva F, Tartari F, Giulietti M, Aiello MM, Cheng L, Lopez-Beltran A, Mazzucchelli R, Cimadamore A, Cerqueti R, Battelli N, Montironi R, Santoni M. Predicting future cancer burden in the United States by artificial neural networks. Future Oncol 2020; 17:159-168. [PMID: 33305617 DOI: 10.2217/fon-2020-0359] [Citation(s) in RCA: 6] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [Key Words] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/04/2023] Open
Abstract
Aims: To capture the complex relationships between risk factors and cancer incidences in the US and predict future cancer burden. Materials & methods: Two artificial neural network (ANN) algorithms were adopted: a multilayer feed-forward network (MLFFNN) and a nonlinear autoregressive network with eXogenous inputs (NARX). Data on the incidence of the four most common tumors (breast, colorectal, lung and prostate) from 1992 to 2016 (available from National Cancer Institute online datasets) were used for training and validation, and data until 2050 were predicted. Results: The rapid decreasing trend of prostate cancer incidence started in 2010 will continue until 2018-2019; it will then slow down and reach a plateau after 2050, with several differences among ethnicities. The incidence of breast cancer will reach a plateau in 2030, whereas colorectal cancer incidence will reach a minimum value of 35 per 100,000 in 2030. As for lung cancer, the incidence will decrease from 50 per 100,000 (2017) to 31 per 100,000 in 2030 and 26 per 100,000 in 2050. Conclusion: This up-to-date prediction of cancer burden in the US could be a crucial resource for planning and evaluation of cancer-control programs.
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Affiliation(s)
- Francesco Piva
- Department of Specialistic Clinical & Odontostomatological Sciences, Polytechnic University of Marche, 60126, Ancona, Italy
| | - Francesca Tartari
- Department of Economics & Law, University of Macerata, via Crescimbeni, 20, 62100, Macerata, Italy
| | - Matteo Giulietti
- Department of Specialistic Clinical & Odontostomatological Sciences, Polytechnic University of Marche, 60126, Ancona, Italy
| | | | - Liang Cheng
- Department of Pathology & Laboratory Medicine, Indiana University School of Medicine, Indianapolis, IN 46202, USA
| | | | - Roberta Mazzucchelli
- Section of Pathological Anatomy, Polytechnic University of the Marche Region, School of Medicine, United Hospitals, 60126, Ancona, Italy
| | - Alessia Cimadamore
- Section of Pathological Anatomy, Polytechnic University of the Marche Region, School of Medicine, United Hospitals, 60126, Ancona, Italy
| | - Roy Cerqueti
- Department of Social & Economic Sciences, Sapienza University of Rome, Piazzale Aldo Moro, 5 - I-00185, Rome, Italy.,School of Business, London South Bank University, London, SE1 0AA, UK
| | | | - Rodolfo Montironi
- Section of Pathological Anatomy, Polytechnic University of the Marche Region, School of Medicine, United Hospitals, 60126, Ancona, Italy
| | - Matteo Santoni
- Oncology Unit, Macerata Hospital, 62012, Macerata, Italy
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23
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Genomic instability in chronic obstructive pulmonary disease and lung cancer: A systematic review and meta-analysis of studies using the micronucleus assay. MUTATION RESEARCH-REVIEWS IN MUTATION RESEARCH 2020; 787:108344. [PMID: 34083053 DOI: 10.1016/j.mrrev.2020.108344] [Citation(s) in RCA: 9] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Subscribe] [Scholar Register] [Received: 06/17/2020] [Revised: 10/26/2020] [Accepted: 10/27/2020] [Indexed: 12/22/2022]
Abstract
Respiratory tissues are highly susceptible to diseases due to the constant exposure to physical and chemical airborne pollutants. Chronic obstructive pulmonary disease (COPD) and lung cancer are among the most common causes of serious illness and death worldwide. The inflammatory environment associated with these respiratory diseases has long been accepted as the major player in the development of airway abnormalities. The presence and relevance of DNA damage and genomic instability makes the micronucleus assay a suitable candidate to quantitatively estimate these early pathogenetic events. A systematic review and meta-analysis were planned to determine underlying common mechanisms that can explain the relationships between COPD and lung cancer. A total of 17 studies from Jan 1999 to Dec 2019 comparing micronucleus frequency in patients affected by respiratory diseases vs healthy controls were analysed. Our results confirmed the presence of significant association between MN frequency and the diseases investigated, and suggested a circle of events linking inflammation induced oxidative stress to the risk of disease through genomic instability and hypoxia. Therefore, using non-invasive, robust and cost effective genomic instability assays such as the micronucleus assay, would allow us to capture unique phenotypic and biological changes that would allow the identification of subjects at high risk of developing lung diseases and improve early detection strategies.
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24
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Oura P, Rissanen I, Junno JA, Harju T, Paananen M. Lifelong smoking trajectories of Northern Finns are characterized by sociodemographic and lifestyle differences in a 46-year follow-up. Sci Rep 2020; 10:16365. [PMID: 33004859 PMCID: PMC7529914 DOI: 10.1038/s41598-020-73334-3] [Citation(s) in RCA: 10] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/16/2020] [Accepted: 09/16/2020] [Indexed: 01/07/2023] Open
Abstract
Smoking remains among the leading causes of mortality worldwide. Obtaining a comprehensive understanding of a population’s smoking behaviour is essential for tobacco control. Here, we aim to characterize lifelong smoking patterns and explore underlying sociodemographic and lifestyle factors in a population-based birth cohort population followed up for 46 years. Our analysis is based on 5797 individuals from the Northern Finland Birth Cohort 1966 who self-reported their tobacco smoking behaviour at the ages of 14, 31 and 46. Data on sex, education, employment, body mass index, physical activity, alcohol consumption, and substance addiction were also collected at the follow-ups. We profile each individual’s annual smoking history from the age of 5 to 47, and conduct a latent class trajectory analysis on the data. We then characterize the identified smoking trajectory classes in terms of the background variables, and compare the heaviest smokers with other classes in order to reveal specific predictors of non-smoking and discontinued smoking. Six smoking trajectories are identified in our sample: never-smokers (class size 41.0%), youth smokers (12.6%), young adult quitters (10.8%), late adult quitters (10.5%), late starters (4.3%), and lifetime smokers (20.7%). Smoking is generally associated with male sex, lower socioeconomic status and unhealthier lifestyle. Multivariable between-class comparisons identify unemployment (odds ratio [OR] 1.28–1.45) and physical inactivity (OR 1.20–1.52) as significant predictors of lifetime smoking relative to any other class. Female sex increases the odds of never-smoking and youth smoking (OR 1.29–1.33), and male sex increases the odds of adult quitting (OR 1.30–1.41), relative to lifetime smoking. We expect future initiatives to benefit from our data by exploiting the identified predictors as direct targets of intervention, or as a means of identifying individuals who may benefit from such interventions.
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Affiliation(s)
- Petteri Oura
- Center for Life Course Health Research, Faculty of Medicine, University of Oulu, PO Box 5000, 90014, Oulu, Finland. .,Kerava Health Care Center, Metsolantie 2, 04200, Kerava, Finland.
| | - Ina Rissanen
- Departments of Neurology and Neurosurgery, Oulu University Hospital, PO Box 50, 90029, Oulu, Finland.,Medical Research Center Oulu (MRC Oulu), Northern Ostrobothnia Hospital District, University of Oulu, PO Box 5000, 90014, Oulu, Finland.,Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, PO Box 85500, 3508 GA, Utrecht, The Netherlands
| | - Juho-Antti Junno
- Cancer Research and Translational Medicine Research Unit, University of Oulu, PO Box 5000, 90014, Oulu, Finland
| | - Terttu Harju
- Research Unit of Internal Medicine, Faculty of Medicine, University of Oulu, PO Box 5000, 90014, Oulu, Finland
| | - Markus Paananen
- Center for Life Course Health Research, Faculty of Medicine, University of Oulu, PO Box 5000, 90014, Oulu, Finland.,Kerava Health Care Center, Metsolantie 2, 04200, Kerava, Finland
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25
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Schlage WK, Titz B, Iskandar A, Poussin C, Van der Toorn M, Wong ET, Pratte P, Maeder S, Schaller JP, Pospisil P, Boue S, Vuillaume G, Leroy P, Martin F, Ivanov NV, Peitsch MC, Hoeng J. Comparing the preclinical risk profile of inhalable candidate and potential candidate modified risk tobacco products: A bridging use case. Toxicol Rep 2020; 7:1187-1206. [PMID: 32995294 PMCID: PMC7502378 DOI: 10.1016/j.toxrep.2020.09.004] [Citation(s) in RCA: 5] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/23/2020] [Revised: 06/24/2020] [Accepted: 09/01/2020] [Indexed: 11/25/2022] Open
Abstract
Heated tobacco products tested for reduced exposure and reduced risk properties. Bridging opportunities for nonclinical results from two heated tobacco products. Similarly reduced impact on apical and molecular endpoints relative to cigarettes. Evidence evaluated along a “causal chain of events leading to disease” (CELSD). Representative assays along CELSD could support nonclinical substantial equivalence. Cigarette smoking causes major preventable diseases, morbidity, and mortality worldwide. Smoking cessation and prevention of smoking initiation are the preferred means for reducing these risks. Less harmful tobacco products, termed modified-risk tobacco products (MRTP), are being developed as a potential alternative for current adult smokers who would otherwise continue smoking. According to a regulatory framework issued by the US Food and Drug Administration, a manufacturer must provide comprehensive scientific evidence that the product significantly reduces harm and the risk of tobacco-related diseases, in order to obtain marketing authorization for a new MRTP. For new tobacco products similar to an already approved predicate product, the FDA has foreseen a simplified procedure for assessing “substantial equivalence”. In this article, we present a use case that bridges the nonclinical evidence from previous studies demonstrating the relatively reduced harm potential of two heat-not-burn products based on different tobacco heating principles. The nonclinical evidence was collected along a “causal chain of events leading to disease” (CELSD) to systematically follow the consequences of reduced exposure to toxicants (relative to cigarette smoke) through increasing levels of biological complexity up to disease manifestation in animal models of human disease. This approach leverages the principles of systems biology and toxicology as a basis for further extrapolation to human studies. The experimental results demonstrate a similarly reduced impact of both products on apical and molecular endpoints, no novel effects not seen with cigarette smoke exposure, and an effect of switching from cigarettes to either MRTP that is comparable to that of complete smoking cessation. Ideally, a subset of representative assays from the presented sequence along the CELSD could be sufficient for predicting similarity or substantial equivalence in the nonclinical impact of novel products; this would require further validation, for which the present use case could serve as a starting point.
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Key Words
- BIF, biological impact factor
- CELSD, causal chain of events leading to disease
- CHTP, carbon heated tobacco product
- CS, cigarette smoke
- CVD, cardiovascular disease
- GVP, gas/vapor phase
- HPHC, harmful and potentially harmful constituents
- MRTP, modified risk tobacco product
- Modified risk tobacco product (MRTP)
- NPA, network perturbation amplitude
- PMI, Philip Morris International
- RBIF, relative BIF
- Substantial equivalence
- Systems toxicology
- THS, Tobacco Heating System
- TPM, total particulate matter
- Tobacco harm reduction
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Affiliation(s)
| | - Bjoern Titz
- PMI R&D, Philip Morris Products S.A., Quai Jeanrenaud 5, CH-2000, Neuchâtel, Switzerland
| | - Anita Iskandar
- PMI R&D, Philip Morris Products S.A., Quai Jeanrenaud 5, CH-2000, Neuchâtel, Switzerland
| | - Carine Poussin
- PMI R&D, Philip Morris Products S.A., Quai Jeanrenaud 5, CH-2000, Neuchâtel, Switzerland
| | - Marco Van der Toorn
- PMI R&D, Philip Morris Products S.A., Quai Jeanrenaud 5, CH-2000, Neuchâtel, Switzerland
| | - Ee Tsin Wong
- PMI R&D, Philip Morris International Research Laboratories Pte. Ltd., Science Park II, Singapore
| | - Pascal Pratte
- PMI R&D, Philip Morris Products S.A., Quai Jeanrenaud 5, CH-2000, Neuchâtel, Switzerland
| | - Serge Maeder
- PMI R&D, Philip Morris Products S.A., Quai Jeanrenaud 5, CH-2000, Neuchâtel, Switzerland
| | - Jean-Pierre Schaller
- PMI R&D, Philip Morris Products S.A., Quai Jeanrenaud 5, CH-2000, Neuchâtel, Switzerland
| | - Pavel Pospisil
- PMI R&D, Philip Morris Products S.A., Quai Jeanrenaud 5, CH-2000, Neuchâtel, Switzerland
| | - Stephanie Boue
- PMI R&D, Philip Morris Products S.A., Quai Jeanrenaud 5, CH-2000, Neuchâtel, Switzerland
| | - Grégory Vuillaume
- PMI R&D, Philip Morris Products S.A., Quai Jeanrenaud 5, CH-2000, Neuchâtel, Switzerland
| | - Patrice Leroy
- PMI R&D, Philip Morris Products S.A., Quai Jeanrenaud 5, CH-2000, Neuchâtel, Switzerland
| | - Florian Martin
- PMI R&D, Philip Morris Products S.A., Quai Jeanrenaud 5, CH-2000, Neuchâtel, Switzerland
| | - Nikolai V Ivanov
- PMI R&D, Philip Morris Products S.A., Quai Jeanrenaud 5, CH-2000, Neuchâtel, Switzerland
| | - Manuel C Peitsch
- PMI R&D, Philip Morris Products S.A., Quai Jeanrenaud 5, CH-2000, Neuchâtel, Switzerland
| | - Julia Hoeng
- PMI R&D, Philip Morris Products S.A., Quai Jeanrenaud 5, CH-2000, Neuchâtel, Switzerland
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26
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Hammouz RY, Kostanek JK, Dudzisz A, Witas P, Orzechowska M, Bednarek AK. Differential expression of lung adenocarcinoma transcriptome with signature of tobacco exposure. J Appl Genet 2020; 61:421-437. [PMID: 32564237 PMCID: PMC7413900 DOI: 10.1007/s13353-020-00569-1] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/13/2020] [Revised: 05/12/2020] [Accepted: 06/09/2020] [Indexed: 12/17/2022]
Abstract
Smoking accounts for almost 80-90% of lung cancer cases, which is also the most frequent cause of cancer-related deaths in humans. With over 60 carcinogens in tobacco smoke, cells dividing at the time of carcinogen exposure are at particular risk of neoplasia. The present study aimed to investigate global gene expression differences in lung adenocarcinoma (LUAD) tumour samples of current smokers and non-smokers, in an attempt to elucidate biological mechanisms underlying divergent smoking effects. Current and non-smoker tumour samples were analysed using bioinformatics tools, examining differences in molecular drivers of cancer initiation and progression, as well as evaluating the effect of smoking and sex on epithelial mesenchymal transition (EMT). As a result, we identified 1150 differentially expressed genes showing visible differences in the expression profiles between the smoking subgroups. The genes were primarily involved in cell cycle, DNA replication, DNA repair, VEGF, GnRH, ErbB and T cell receptor signalling pathways. Our results show that smoking clearly affected E2F transcriptional activity and DNA repair pathways including mismatch repair, base excision repair and homologous recombination. We observed that sex could modify the effects of PLA2G2A and PRG4 in LUAD tumour samples, whereas sex and smoking status might possibly have a biological effect on the EMT-related genes: HEY2, OLFM1, SFRP1 and STRAP. We also identified potential epigenetic changes smoking solely might have on EMT-related genes, which may serve as potential diagnostic and prognostic biomarkers for LUAD patients.
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Affiliation(s)
- Raneem Y. Hammouz
- Department of Molecular Carcinogenesis, Medical University of Lodz, Zeligowskiego 7/9, 90-752 Lodz, Poland
| | - Joanna K. Kostanek
- Department of Molecular Carcinogenesis, Medical University of Lodz, Zeligowskiego 7/9, 90-752 Lodz, Poland
| | - Aleksandra Dudzisz
- Department of Molecular Carcinogenesis, Medical University of Lodz, Zeligowskiego 7/9, 90-752 Lodz, Poland
| | - Piotr Witas
- Department of Molecular Carcinogenesis, Medical University of Lodz, Zeligowskiego 7/9, 90-752 Lodz, Poland
| | - Magdalena Orzechowska
- Department of Molecular Carcinogenesis, Medical University of Lodz, Zeligowskiego 7/9, 90-752 Lodz, Poland
| | - Andrzej K. Bednarek
- Department of Molecular Carcinogenesis, Medical University of Lodz, Zeligowskiego 7/9, 90-752 Lodz, Poland
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27
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Chen CK, Chang YJ, Fang HY. Patients with spontaneous pneumothorax have a higher risk of developing lung cancer: A STROBE-compliant article. Medicine (Baltimore) 2020; 99:e21411. [PMID: 32791756 PMCID: PMC7387064 DOI: 10.1097/md.0000000000021411] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/28/2022] Open
Abstract
Lung cancer is a common malignancy worldwide, and risk factors include bronchitis, asthma, tuberculosis, smoking, and air pollution. These are also risk factors for spontaneous pneumothorax, a benign disease. We hypothesized that patients who experience a spontaneous pneumothorax have a greater risk to develop lung cancer, and designed a study to determine if this is so.We used the population-based Taiwan Health Insurance Research Database to perform a retrospective cohort study. The database includes more than 99% of the population of Taiwan. We established a 27,405-person pneumothorax cohort and a 109,620 person comparison cohort with data from 2000 to 2009 to evaluate the relationship between spontaneous pneumothorax and lung cancer.Multivariable analysis showed that patients who have had a spontaneous pneumothorax have a greater relative risk to develop lung cancer. The overall hazard ratio was 2.09 (95% confidence interval 1.69-2.58) adjusted by age, gender, hypertension, diabetes mellitus, and chronic lung diseases such as chronic obstructive pulmonary disease, tuberculosis, asthma, bronchitis, and emphysema. A dose effect was present; a high frequency of spontaneous pneumothorax was associated with a greater relative risk to develop lung cancer. If the spontaneous pneumothorax frequency was greater than 2 times per year, the hazard ratio was 34.09 (95% confidence interval 22.74-51.10)Patients with spontaneous pneumothorax have an increased relative risk to develop lung cancer, especially among patients 35 to 49 years of age. The more frequent the occurrence of spontaneous pneumothorax, the greater the relative risk of lung cancer. If the spontaneous pneumothorax frequency was greater than 2 times per year, the increase in risk of lung cancer was more than 30-fold.
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Affiliation(s)
- Chien-Kuang Chen
- Division of Thoracic Surgery, Department of Surgery, China Medical University Hospital
- Graduate Institute of Clinical Medical Science, China Medical University
| | - Yen-Jung Chang
- Management Office for Health Data, China Medical University Hospital
| | - Hsin-Yuan Fang
- Division of Thoracic Surgery, Department of Surgery, China Medical University Hospital
- School of Medicine, China Medical University, Taichung, Taiwan
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Pleasants RA, Rivera MP, Tilley SL, Bhatt SP. Both Duration and Pack-Years of Tobacco Smoking Should Be Used for Clinical Practice and Research. Ann Am Thorac Soc 2020; 17:804-806. [PMID: 32348693 PMCID: PMC7405110 DOI: 10.1513/annalsats.202002-133vp] [Citation(s) in RCA: 41] [Impact Index Per Article: 8.2] [Reference Citation Analysis] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/13/2020] [Accepted: 04/29/2020] [Indexed: 11/20/2022] Open
Affiliation(s)
- Roy A. Pleasants
- Division of Pulmonary Diseases and Critical Care Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina
- North Carolina Thoracic Society, Chapel Hill, North Carolina; and
| | - M. Patricia Rivera
- Division of Pulmonary Diseases and Critical Care Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina
| | - Stephen L. Tilley
- Division of Pulmonary Diseases and Critical Care Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina
| | - Surya P. Bhatt
- Division of Pulmonary, Allergy, and Critical Care Medicine, University of Alabama at Birmingham, Birmingham, Alabama
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Haghani A, Arpawong TE, Kim JK, Lewinger JP, Finch CE, Crimmins E. Female vulnerability to the effects of smoking on health outcomes in older people. PLoS One 2020; 15:e0234015. [PMID: 32497122 PMCID: PMC7272024 DOI: 10.1371/journal.pone.0234015] [Citation(s) in RCA: 22] [Impact Index Per Article: 4.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/06/2020] [Accepted: 05/15/2020] [Indexed: 12/20/2022] Open
Abstract
Cigarette smoking is among the leading risk factors for mortality and morbidity. While men have a higher smoking prevalence, mechanistic experiments suggest that women are at higher risk for health problems due to smoking. Moreover, the comparison of smoking effects on multiple conditions and mortality for men and women has not yet been done in a population-based group with race/ethnic diversity. We used proportional hazards models and restricted mean survival time to assess differences in smoking effects by sex for multiple health outcomes using data from the U.S. Health and Retirement Study (HRS), a population-representative cohort of individuals aged 50+ (n = 22,708, 1992-2014). Men had experienced more smoking pack-years than women (22.0 vs 15.6 average pack-years). Age of death, onset of lung disorders, heart disease, stroke, and cancer showed dose-dependent effects of smoking for both sexes. Among heavy smokers (>28 pack-years) women had higher risk of earlier age of death (HR = 1.3, 95%CI:1.03-1.65) and stroke (HR = 1.37, 95%CI:1.02-1.83). Risk of cancer and heart disease did not differ by sex for smokers. Women had earlier age of onset for lung disorders (HR = 2.83, 95%CI:1.74-4.6), but men risk due to smoking were higher (Smoking-Sex interaction P<0.02) than women. Passive smoke exposure increased risk of earlier heart disease (HR = 1.33, 95%CI:1.07-1.65) and stroke (HR:1.54, 95%CI:1.07-2.22) for non-smokers, mainly in men. Smoking cessation after 15 years partially attenuated the deleterious smoking effects for all health outcomes. In sum, our results suggest that women are more vulnerable to ever smoking for earlier death and risk of stroke, but less vulnerable for lung disorders. From an epidemiological perspective, sex differences in smoking effects are important considerations that could underlie sex differences in health outcomes. These findings also encourage future mechanistic experiments to resolve potential mechanisms of sex-specific cigarette smoke toxicity.
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Affiliation(s)
- Amin Haghani
- Leonard Davis School of Gerontology, University of Southern California, Los Angeles, California, United States of America
| | - Thalida Em Arpawong
- Leonard Davis School of Gerontology, University of Southern California, Los Angeles, California, United States of America
| | - Jung Ki Kim
- Leonard Davis School of Gerontology, University of Southern California, Los Angeles, California, United States of America
| | - Juan Pablo Lewinger
- Department of Preventive Medicine, University of Southern California, Los Angeles, California, United States of America
| | - Caleb E. Finch
- Leonard Davis School of Gerontology, University of Southern California, Los Angeles, California, United States of America
| | - Eileen Crimmins
- Leonard Davis School of Gerontology, University of Southern California, Los Angeles, California, United States of America
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Inoue-Choi M, Christensen CH, Rostron BL, Cosgrove CM, Reyes-Guzman C, Apelberg B, Freedman ND. Dose-Response Association of Low-Intensity and Nondaily Smoking With Mortality in the United States. JAMA Netw Open 2020; 3:e206436. [PMID: 32492162 PMCID: PMC7272118 DOI: 10.1001/jamanetworkopen.2020.6436] [Citation(s) in RCA: 50] [Impact Index Per Article: 10.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/17/2022] Open
Abstract
IMPORTANCE An increasing proportion of US smokers smoke at low intensity and not every day. Some nondaily smokers have always had this pattern, whereas others previously smoked daily. The effect of reducing the level of smoking from daily to nondaily smoking and the dose response at low smoking levels are poorly understood. OBJECTIVE To evaluate risk of all-cause and cause-specific mortality among nondaily and daily cigarette smokers, by cigarettes per month, years after reducing from daily to nondaily smoking, and years since quitting. DESIGN, SETTING, AND PARTICIPANTS A prospective cohort study using harmonized data from multiple cycles of the Tobacco Use Supplements to the Current Population Survey (TUS-CPS), linked to the National Death Index, were analyzed during the period from 2018 to 2020. Adults completed the 1992-1993, 1995-1996, 1998-1999, 2000, 2001-2002, 2003, 2006-2007, or 2010-2011 TUS-CPS. Cigarette smokers were classified as daily or nondaily users; current nondaily smokers were further categorized by whether they previously smoked every day. MAIN OUTCOMES AND MEASURES Hazard ratios (HRs) and 95% CIs for risks of mortality vs never smoking. Age was the underlying time metric, adjusted for sex, race/ethnicity, education, survey year, and household income. RESULTS Among 505 500 participants (aged 18-103 years), approximately 47 000 deaths occurred. The median number of cigarettes smoked per month was 600 (interquartile range, 300-600) (20 cigarettes per day [interquartile range, 10-20 cigarettes per day]) for daily cigarette smokers and 40 (interquartile range, 15-90) for lifelong nondaily smokers. Nevertheless, both current daily (HR, 2.32; 95% CI, 2.25-2.38) and lifelong nondaily (HR, 1.82; 95% CI, 1.65-2.01) smokers had higher all-cause mortality risks than never smokers. Associations were observed for 6 to 10 cigarettes per month and increased with greater-intensity use. Nondaily smokers who previously smoked every day had lower mortality risks than daily smokers, with similar HRs after 10 or more years of nondaily smoking as lifelong nondaily smokers (HR vs never smokers, 1.73; 95% CI, 1.56-1.92). Yet, their risks were higher than former smokers who quit 10 or more years before (HR vs never smokers, 1.18; 95% CI, 1.15-1.22). CONCLUSIONS AND RELEVANCE Although reducing smoking from daily to nondaily was associated with decreased mortality risk, cessation was associated with far greater benefit. Lifelong nondaily smokers have higher mortality risks than never smokers, even among those smoking 6 to 10 cigarettes per month. Thus, all smokers should quit, regardless of how infrequently they smoke.
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Affiliation(s)
- Maki Inoue-Choi
- Metabolic Epidemiology Branch, Division of Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland
| | - Carol H. Christensen
- Office of Science, Center for Tobacco Products Food and Drug Administration, Silver Spring, Maryland
| | - Brian L. Rostron
- Office of Science, Center for Tobacco Products Food and Drug Administration, Silver Spring, Maryland
| | | | - Carolyn Reyes-Guzman
- Tobacco Control Research Branch, Behavioral Research Program, Division of Cancer Control and Population Sciences, National Cancer Institute, National Institutes of Health, Bethesda, Maryland
| | - Benjamin Apelberg
- Office of Science, Center for Tobacco Products Food and Drug Administration, Silver Spring, Maryland
| | - Neal D. Freedman
- Metabolic Epidemiology Branch, Division of Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland
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Effect of Smoking on Outcomes of Allogeneic Transplantation: A Single-Center Analysis. Biol Blood Marrow Transplant 2020; 26:1131-1136. [PMID: 32200122 DOI: 10.1016/j.bbmt.2020.03.015] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/11/2019] [Revised: 01/25/2020] [Accepted: 03/12/2020] [Indexed: 12/18/2022]
Abstract
Pulmonary complications are fatal adverse events after allogeneic hematopoietic cell transplantation (allo-HCT). On the other hand, smoking is a well-known risk factor for various pulmonary diseases and also increases the incidence of pulmonary complications and overall mortality in allo-HCT recipients. In this study, we retrospectively assessed the impact of smoking intensity on survival outcomes. This study included consecutive allo-HCT recipients at our center between June 2007 and May 2019 whose smoking profiles were available (n = 408); they were divided into high (pack-years >10, n = 171) and low (pack-years ≤10, n = 231) pack-years groups. In univariate analyses, nonrelapse mortality (NRM) and overall survival (OS) were significantly inferior in the high pack-years group (1-year NRM 26.6% versus 13.9%, P < .001; 1-year OS 58.4% versus 70.1%, P = .0067). However, this association was not observed in multivariate analyses. In subgroup analyses according to sex, the survival outcomes in the high pack-years group were significantly inferior in males (NRM hazard ratio [HR], 2.24 [95% confidence interval (CI), 1.23 to 4.07], P = .0082; OS HR, 1.54 [95% CI, 1.04 to 2.28], P = .031), but not in females (NRM HR, 0.587 [95% CI, 0.241 to 1.43], P = .24; OS HR, 0.689 [95% CI, 0.400 to 1.19], P = .18). In summary, high pack-years were associated with inferior survival of allo-HCT recipients, especially in males.
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Nilsson R, Tong J. Opinion on reconsideration of lung cancer risk from domestic radon exposure. RADIATION MEDICINE AND PROTECTION 2020. [DOI: 10.1016/j.radmp.2020.01.001] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/24/2022] Open
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Yoshida K, Gowers KHC, Lee-Six H, Chandrasekharan DP, Coorens T, Maughan EF, Beal K, Menzies A, Millar FR, Anderson E, Clarke SE, Pennycuick A, Thakrar RM, Butler CR, Kakiuchi N, Hirano T, Hynds RE, Stratton MR, Martincorena I, Janes SM, Campbell PJ. Tobacco smoking and somatic mutations in human bronchial epithelium. Nature 2020; 578:266-272. [PMID: 31996850 PMCID: PMC7021511 DOI: 10.1038/s41586-020-1961-1] [Citation(s) in RCA: 324] [Impact Index Per Article: 64.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/07/2019] [Accepted: 12/29/2019] [Indexed: 01/06/2023]
Abstract
Tobacco smoking causes lung cancer1-3, a process that is driven by more than 60 carcinogens in cigarette smoke that directly damage and mutate DNA4,5. The profound effects of tobacco on the genome of lung cancer cells are well-documented6-10, but equivalent data for normal bronchial cells are lacking. Here we sequenced whole genomes of 632 colonies derived from single bronchial epithelial cells across 16 subjects. Tobacco smoking was the major influence on mutational burden, typically adding from 1,000 to 10,000 mutations per cell; massively increasing the variance both within and between subjects; and generating several distinct mutational signatures of substitutions and of insertions and deletions. A population of cells in individuals with a history of smoking had mutational burdens that were equivalent to those expected for people who had never smoked: these cells had less damage from tobacco-specific mutational processes, were fourfold more frequent in ex-smokers than current smokers and had considerably longer telomeres than their more-mutated counterparts. Driver mutations increased in frequency with age, affecting 4-14% of cells in middle-aged subjects who had never smoked. In current smokers, at least 25% of cells carried driver mutations and 0-6% of cells had two or even three drivers. Thus, tobacco smoking increases mutational burden, cell-to-cell heterogeneity and driver mutations, but quitting promotes replenishment of the bronchial epithelium from mitotically quiescent cells that have avoided tobacco mutagenesis.
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Affiliation(s)
- Kenichi Yoshida
- Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton, UK
| | - Kate H C Gowers
- Lungs For Living Research Centre, UCL Respiratory, University College London, London, UK
| | - Henry Lee-Six
- Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton, UK
| | | | - Tim Coorens
- Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton, UK
| | - Elizabeth F Maughan
- Lungs For Living Research Centre, UCL Respiratory, University College London, London, UK
| | - Kathryn Beal
- Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton, UK
| | - Andrew Menzies
- Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton, UK
| | - Fraser R Millar
- Lungs For Living Research Centre, UCL Respiratory, University College London, London, UK
| | | | - Sarah E Clarke
- Lungs For Living Research Centre, UCL Respiratory, University College London, London, UK
| | - Adam Pennycuick
- Lungs For Living Research Centre, UCL Respiratory, University College London, London, UK
| | - Ricky M Thakrar
- Lungs For Living Research Centre, UCL Respiratory, University College London, London, UK
- Department of Thoracic Medicine, University College London Hospital, London, UK
| | - Colin R Butler
- Lungs For Living Research Centre, UCL Respiratory, University College London, London, UK
- Department of Thoracic Medicine, University College London Hospital, London, UK
| | - Nobuyuki Kakiuchi
- Department of Pathology and Tumor Biology, Kyoto University, Kyoto, Japan
| | - Tomonori Hirano
- Department of Pathology and Tumor Biology, Kyoto University, Kyoto, Japan
| | - Robert E Hynds
- Lungs For Living Research Centre, UCL Respiratory, University College London, London, UK
- CRUK Lung Cancer Centre of Excellence, UCL Cancer Institute, University College London, London, UK
| | | | | | - Sam M Janes
- Lungs For Living Research Centre, UCL Respiratory, University College London, London, UK.
- Department of Thoracic Medicine, University College London Hospital, London, UK.
| | - Peter J Campbell
- Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton, UK.
- Stem Cell Institute, University of Cambridge, Cambridge, UK.
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34
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Lipfert FW, Wyzga RE. Longitudinal relationships between lung cancer mortality rates, smoking, and ambient air quality: a comprehensive review and analysis. Crit Rev Toxicol 2020; 49:790-818. [DOI: 10.1080/10408444.2019.1700210] [Citation(s) in RCA: 13] [Impact Index Per Article: 2.6] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/07/2023]
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35
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Kilibarda B, Vuković D. Smoking prevention among youth. MEDICINSKI PODMLADAK 2020. [DOI: 10.5937/mp71-28273] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/02/2022] Open
Abstract
For majority of smokers, onset of smoking occurs during adolescence, period of intensive growth and development, and this early smoking initiation is associated with many adverse health effects. Smoking prevention measures include not only prevention of onset, but also prevention of transition from experimentation to chronic tobacco use and dependence and smoking cessation. Effective preventive measures should be based on relevant theory and scientific evidence on behavior determinants. In this review article, we present evidence from researches on effectiveness of school programs, community-based programs, media campaigns and stress the importance of considering new challenges in tobacco control and other promising strategies, as well as the need for early detection of nicotine dependence signs among adolescents. In practice, many preventive measures are not based on theory and some interventions can be contra productive. Regardless of type of intervention and setting in which is implemented, it is of importance to take into account context for its implementation.
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Craig DJ, Morrison T, Khuder SA, Crawford EL, Wu L, Xu J, Blomquist TM, Willey JC. Technical advance in targeted NGS analysis enables identification of lung cancer risk-associated low frequency TP53, PIK3CA, and BRAF mutations in airway epithelial cells. BMC Cancer 2019; 19:1081. [PMID: 31711466 PMCID: PMC6844032 DOI: 10.1186/s12885-019-6313-x] [Citation(s) in RCA: 9] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/05/2019] [Accepted: 10/30/2019] [Indexed: 12/14/2022] Open
Abstract
BACKGROUND Standardized Nucleic Acid Quantification for SEQuencing (SNAQ-SEQ) is a novel method that utilizes synthetic DNA internal standards spiked into each sample prior to next generation sequencing (NGS) library preparation. This method was applied to analysis of normal appearing airway epithelial cells (AEC) obtained by bronchoscopy in an effort to define a somatic mutation field effect associated with lung cancer risk. There is a need for biomarkers that reliably detect those at highest lung cancer risk, thereby enabling more effective screening by annual low dose CT. The purpose of this study was to test the hypothesis that lung cancer risk is characterized by increased prevalence of low variant allele frequency (VAF) somatic mutations in lung cancer driver genes in AEC. METHODS Synthetic DNA internal standards (IS) were prepared for 11 lung cancer driver genes and mixed with each AEC genomic (g) DNA specimen prior to competitive multiplex PCR amplicon NGS library preparation. A custom Perl script was developed to separate IS reads and respective specimen gDNA reads from each target into separate files for parallel variant frequency analysis. This approach identified nucleotide-specific sequencing error and enabled reliable detection of specimen mutations with VAF as low as 5 × 10- 4 (0.05%). This method was applied in a retrospective case-control study of AEC specimens collected by bronchoscopic brush biopsy from the normal airways of 19 subjects, including eleven lung cancer cases and eight non-cancer controls, and the association of lung cancer risk with AEC driver gene mutations was tested. RESULTS TP53 mutations with 0.05-1.0% VAF were more prevalent (p < 0.05) and also enriched for tobacco smoke and age-associated mutation signatures in normal AEC from lung cancer cases compared to non-cancer controls matched for smoking and age. Further, PIK3CA and BRAF mutations in this VAF range were identified in AEC from cases but not controls. CONCLUSIONS Application of SNAQ-SEQ to measure mutations in the 0.05-1.0% VAF range enabled identification of an AEC somatic mutation field of injury associated with lung cancer risk. A biomarker comprising TP53, PIK3CA, and BRAF somatic mutations may better stratify individuals for optimal lung cancer screening and prevention outcomes.
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Affiliation(s)
- Daniel J. Craig
- Department of Medicine, The University of Toledo College of Medicine, 3000 Arlington Avenue, Toledo, OH 43614 USA
| | - Thomas Morrison
- Accugenomics, Inc, 1410 Commonwealth Dr #105, Wilmington, NC 28403 USA
| | - Sadik A. Khuder
- Department of Medicine, The University of Toledo College of Medicine, 3000 Arlington Avenue, Toledo, OH 43614 USA
| | - Erin L. Crawford
- Department of Medicine, The University of Toledo College of Medicine, 3000 Arlington Avenue, Toledo, OH 43614 USA
| | - Leihong Wu
- National Center for Toxicological Research, U.S. Food & Drug Administration, Jefferson, AR USA
| | - Joshua Xu
- National Center for Toxicological Research, U.S. Food & Drug Administration, Jefferson, AR USA
| | - Thomas M. Blomquist
- Department of Pathology, The University of Toledo College of Medicine, 3000 Arlington Avenue, Toledo, OH 43614 USA
| | - James C. Willey
- Department of Medicine, The University of Toledo College of Medicine, 3000 Arlington Avenue, Toledo, OH 43614 USA
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Jackson SE, Hill E, Shahab L, Beard E, Michie S, Brown J. Prevalence and correlates of long-term e-cigarette and nicotine replacement therapy use: a prospective study in England. BMJ Open 2019; 9:e029252. [PMID: 31604784 PMCID: PMC6797372 DOI: 10.1136/bmjopen-2019-029252] [Citation(s) in RCA: 12] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/18/2019] [Revised: 08/29/2019] [Accepted: 09/23/2019] [Indexed: 11/07/2022] Open
Abstract
OBJECTIVES To examine the prevalence of, and sociodemographic and smoking-related characteristics associated with, long-term e-cigarette use compared with long-term nicotine replacement therapy (NRT) use. DESIGN Cross-sectional and prospective survey, the Smoking Toolkit Study, with baseline data collected between September 2014 and September 2016 and follow-ups at 6 and 12 months. SETTING England. PARTICIPANTS Population representative sample of 40 933 adults aged 16+ years. MAIN OUTCOME MEASURES Prevalence of long-term (≥12 months) use of e-cigarettes and NRT by retrospective self-report among baseline respondents (all adults, n=40 933; smokers, n=8406) and current use at baseline, 6 months and 12 months in a subsample of smokers who responded to follow-up (n=733). RESULTS Of baseline respondents, 1.5% (95% CI 1.4% to 1.6%, n=604) of adults and 3.9% (95% CI 3.5% to 4.3%, n=327) of smokers were long-term e-cigarette users and 0.5% (95% CI 0.4% to 0.6%, n=205) of adults and 1.3% (95% CI 1.1% to 1.5%, n=112) of smokers were long-term NRT users. Assessed prospectively, 13.4% (95% CI 10.9% to 15.9%, n=100) of smokers were long-term e-cigarette users and 1.9% (95% CI 0.9% to 2.9%, n=14) were long-term NRT users. Among all adults, long-term use by never smokers of either e-cigarettes (0.1%, n=27) or NRT (0.0%, n=7) was rare. Among past-year smokers, long-term e-cigarette and NRT use was higher among older smokers compared with those who were 16-34 years old (OR range=1.55-5.21). Long-term e-cigarette use only was lower in smokers who were less educated (OR=0.63, 95% CI 0.49 to 0.81), from social grades C2DE (OR=0.66, 95% CI 0.52 to 0.84) and with children in the household (OR=0.66, 95% CI 0.51 to 0.85). Long-term e-cigarette use and long-term NRT use were higher among smokers more motivated to quit (OR=2.05, 95% CI 1.63 to 2.60 and OR=2.33, 95% CI 1.57 to 3.46). CONCLUSIONS In the adult population in England, long-term use of e-cigarettes and long-term use of NRT are almost exclusively by current or ex-smokers. Only a minority of past-year smokers retrospectively report long-term e-cigarette or NRT use, but this figure may be an underestimate, especially for e-cigarette use, which is more than threefold higher when assessed prospectively.
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Affiliation(s)
- Sarah E Jackson
- Department of Behavioural Science and Health, University College London, London, United Kingdom
| | - Emily Hill
- Department of Behavioural Science and Health, University College London, London, United Kingdom
| | - Lion Shahab
- Department of Behavioural Science and Health, University College London, London, United Kingdom
| | - Emma Beard
- Department of Behavioural Science and Health, University College London, London, United Kingdom
| | - Susan Michie
- Department of Clinical, Educational and Health Psychology, University College London, London, United Kingdom
| | - Jamie Brown
- Department of Behavioural Science and Health, University College London, London, United Kingdom
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Paik SH, Yeo CD, Jeong JE, Kim JS, Lee SH, Kim SJ, Kim DJ. Prevalence and analysis of tobacco use disorder in patients diagnosed with lung cancer. PLoS One 2019; 14:e0220127. [PMID: 31490942 PMCID: PMC6730883 DOI: 10.1371/journal.pone.0220127] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/03/2019] [Accepted: 07/09/2019] [Indexed: 11/18/2022] Open
Abstract
INTRODUCTION Tobacco use disorder (TUD), previously known as nicotine dependence, was associated with increased risk of lung cancer. However, little is known about the prevalence of TUD and symptom manifestation in smokers with lung cancer. OBJECTIVES The aim of the present study was to investigate the prevalence of TUD using DSM-5 diagnostic criteria in patients diagnosed with lung cancer and analyze their tobacco use characteristics. METHODS A total of 200 histologically confirmed lung cancer patients who used tobacco within the prior 12-month period at the time of diagnosis were recruited for this study. Participants were assessed using interviewer-administered questionnaires to determine TUD symptoms and smoking-related behaviors, and self-administered Fagerstrom Test for Nicotine Dependence (FTND) was also administered. RESULTS The prevalence of DSM-5 TUD was 92.0% (n = 184). Of a total of 200 subjects, 23 (11.5%), 35 (17.5%), and 126 (63.0%) were classified into mild, moderate, and severe TUD categories, respectively. A total of 19 (81.3%) moderate TUD and 98 (77.8%) severe TUD patients had attempted smoking cessation. Of these subjects, 21 (21.4%) severe TUD and 12 (63.2%) moderate TUD patients tried more than three times. The number of satisfied criteria under DSM-5 TUD was positively correlated with FTND score, cumulative lifetime smoking amount, and daily smoking levels. CONCLUSIONS Smokers diagnosed with lung cancer showed a high prevalence of DSM-5 TUD. Their heavy and consistent tobacco use suggests reduced motivation to abstain from smoking.
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Affiliation(s)
- Soo-Hyun Paik
- Addiction Center, Keyo Hospital, Ojeon-ro, Uiwang-city, Gyeonggi-do, Republic of Korea
| | - Chang Dong Yeo
- Division of Pulmonology, Department of Internal Medicine, The Cancer Research Institute, College of Medicine, The Catholic University of Korea, Banpo-daero, Seocho-gu, Seoul, Republic of Korea
| | - Jo-Eun Jeong
- Department of Psychiatry, Seoul St. Mary’s Hospital, College of Medicine, The Catholic University of Korea, Banpo-daero, Seocho-gu, Seoul, Republic of Korea
| | - Ju Sang Kim
- Division of Pulmonology, Department of Internal Medicine, The Cancer Research Institute, College of Medicine, The Catholic University of Korea, Banpo-daero, Seocho-gu, Seoul, Republic of Korea
| | - Sang Haak Lee
- Division of Pulmonology, Department of Internal Medicine, The Cancer Research Institute, College of Medicine, The Catholic University of Korea, Banpo-daero, Seocho-gu, Seoul, Republic of Korea
| | - Seung Joon Kim
- Division of Pulmonology, Department of Internal Medicine, The Cancer Research Institute, College of Medicine, The Catholic University of Korea, Banpo-daero, Seocho-gu, Seoul, Republic of Korea
| | - Dai-Jin Kim
- Department of Psychiatry, Seoul St. Mary’s Hospital, College of Medicine, The Catholic University of Korea, Banpo-daero, Seocho-gu, Seoul, Republic of Korea
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Yu XQ, Luo Q, Hughes S, Wade S, Caruana M, Canfell K, O'Connell DL. Statistical projection methods for lung cancer incidence and mortality: a systematic review. BMJ Open 2019; 9:e028497. [PMID: 31462469 PMCID: PMC6720154 DOI: 10.1136/bmjopen-2018-028497] [Citation(s) in RCA: 16] [Impact Index Per Article: 2.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/14/2022] Open
Abstract
OBJECTIVES To identify and summarise all studies using statistical methods to project lung cancer incidence or mortality rates more than 5 years into the future. STUDY TYPE Systematic review. METHODS We performed a systematic literature search in multiple electronic databases to identify studies published from 1 January 1988 to 14 August 2018, which used statistical methods to project lung cancer incidence and/or mortality rates. Reference lists of relevant articles were checked for additional potentially relevant articles. We developed an organisational framework to classify methods into groups according to the type of data and the statistical models used. Included studies were critically appraised using prespecified criteria. RESULTS One hundred and one studies met the inclusion criteria; six studies used more than one statistical method. The number of studies reporting statistical projections for lung cancer increased substantially over time. Eighty-eight studies used projection methods, which did not incorporate data on smoking in the population, and 16 studies used a method which did incorporate data on smoking. Age-period-cohort models (44 studies) were the most commonly used methods, followed by other generalised linear models (35 studies). The majority of models were developed using observed rates for more than 10 years and used data that were considered to be good quality. A quarter of studies provided comparisons of fitted and observed rates. While validation by withholding the most recent observed data from the model and then comparing the projected and observed rates for the most recent period provides important information on the model's performance, only 12 studies reported doing this. CONCLUSION This systematic review provides an up-to-date summary of the statistical methods used in published lung cancer incidence or mortality projections. The assessment of the strengths of existing methods will help researchers to better apply and develop statistical methods for projecting lung cancer rates. Some of the common methods described in this review can be applied to the projection of rates for other cancer types or other non-infectious diseases.
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Affiliation(s)
- Xue Qin Yu
- Cancer Research Division, Cancer Council NSW, Sydney, New South Wales, Australia
- The University of Sydney School of Public Health, Faculty of Medicine and Health, The University of Sydney, Sydney, New South Wales, Australia
| | - Qingwei Luo
- Cancer Research Division, Cancer Council NSW, Sydney, New South Wales, Australia
| | - Suzanne Hughes
- Cancer Research Division, Cancer Council NSW, Sydney, New South Wales, Australia
| | - Stephen Wade
- Cancer Research Division, Cancer Council NSW, Sydney, New South Wales, Australia
| | - Michael Caruana
- Cancer Research Division, Cancer Council NSW, Sydney, New South Wales, Australia
| | - Karen Canfell
- Cancer Research Division, Cancer Council NSW, Sydney, New South Wales, Australia
- The University of Sydney School of Public Health, Faculty of Medicine and Health, The University of Sydney, Sydney, New South Wales, Australia
- Prince of Wales Clinical School, University of New South Wales, Sydney, New South Wales, Australia
| | - Dianne L O'Connell
- Cancer Research Division, Cancer Council NSW, Sydney, New South Wales, Australia
- The University of Sydney School of Public Health, Faculty of Medicine and Health, The University of Sydney, Sydney, New South Wales, Australia
- School of Medicine and Public Health, University of Newcastle, Newcastle, New South Wales, Australia
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Saccone NL, Emery LS, Sofer T, Gogarten SM, Becker DM, Bottinger EP, Chen LS, Culverhouse RC, Duan W, Hancock DB, Hosgood HD, Johnson EO, Loos RJF, Louie T, Papanicolaou G, Perreira KM, Rodriquez EJ, Schurmann C, Stilp AM, Szpiro AA, Talavera GA, Taylor KD, Thrasher JF, Yanek LR, Laurie CC, Pérez-Stable EJ, Bierut LJ, Kaplan RC. Genome-Wide Association Study of Heavy Smoking and Daily/Nondaily Smoking in the Hispanic Community Health Study/Study of Latinos (HCHS/SOL). Nicotine Tob Res 2019; 20:448-457. [PMID: 28520984 DOI: 10.1093/ntr/ntx107] [Citation(s) in RCA: 20] [Impact Index Per Article: 3.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/16/2016] [Accepted: 05/11/2017] [Indexed: 02/07/2023]
Abstract
Introduction Genetic variants associated with nicotine dependence have previously been identified, primarily in European-ancestry populations. No genome-wide association studies (GWAS) have been reported for smoking behaviors in Hispanics/Latinos in the United States and Latin America, who are of mixed ancestry with European, African, and American Indigenous components. Methods We examined genetic associations with smoking behaviors in the Hispanic Community Health Study/Study of Latinos (HCHS/SOL) (N = 12 741 with smoking data, 5119 ever-smokers), using ~2.3 million genotyped variants imputed to the 1000 Genomes Project phase 3. Mixed logistic regression models accounted for population structure, sampling, relatedness, sex, and age. Results The known region of CHRNA5, which encodes the α5 cholinergic nicotinic receptor subunit, was associated with heavy smoking at genome-wide significance (p ≤ 5 × 10-8) in a comparison of 1929 ever-smokers reporting cigarettes per day (CPD) > 10 versus 3156 reporting CPD ≤ 10. The functional variant rs16969968 in CHRNA5 had a p value of 2.20 × 10-7 and odds ratio (OR) of 1.32 for the minor allele (A); its minor allele frequency was 0.22 overall and similar across Hispanic/Latino background groups (Central American = 0.17; South American = 0.19; Mexican = 0.18; Puerto Rican = 0.22; Cuban = 0.29; Dominican = 0.19). CHRNA4 on chromosome 20 attained p < 10-4, supporting prior findings in non-Hispanics. For nondaily smoking, which is prevalent in Hispanic/Latino smokers, compared to daily smoking, loci on chromosomes 2 and 4 achieved genome-wide significance; replication attempts were limited by small Hispanic/Latino sample sizes. Conclusions Associations of nicotinic receptor gene variants with smoking, first reported in non-Hispanic European-ancestry populations, generalized to Hispanics/Latinos despite different patterns of smoking behavior. Implications We conducted the first large-scale genome-wide association study (GWAS) of smoking behavior in a US Hispanic/Latino cohort, and the first GWAS of daily/nondaily smoking in any population. Results show that the region of the nicotinic receptor subunit gene CHRNA5, which in non-Hispanic European-ancestry smokers has been associated with heavy smoking as well as cessation and treatment efficacy, is also significantly associated with heavy smoking in this Hispanic/Latino cohort. The results are an important addition to understanding the impact of genetic variants in understudied Hispanic/Latino smokers.
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Affiliation(s)
- Nancy L Saccone
- Department of Genetics, Washington University School of Medicine, St. Louis, MO
| | - Leslie S Emery
- Department of Biostatistics, University of Washington, Seattle, WA
| | - Tamar Sofer
- Department of Biostatistics, University of Washington, Seattle, WA
| | | | - Diane M Becker
- GeneSTAR Research Program, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD
| | - Erwin P Bottinger
- Charles Bronfman Institute for Personalized Medicine, Icahn School of Medicine at Mount Sinai, New York, NY
| | - Li-Shiun Chen
- Department of Psychiatry, Washington University School of Medicine, St. Louis, MO
| | | | - Weimin Duan
- Department of Genetics, Washington University School of Medicine, St. Louis, MO
| | - Dana B Hancock
- Behavioral and Urban Health Program, Behavioral Health and Criminal Justice Division, RTI International, Research Triangle Park, NC
| | - H Dean Hosgood
- Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, NY
| | - Eric O Johnson
- Fellow Program and Behavioral Health and Criminal Justice Division, RTI International, Research Triangle Park, NC
| | - Ruth J F Loos
- Charles Bronfman Institute for Personalized Medicine, Icahn School of Medicine at Mount Sinai, New York, NY
| | - Tin Louie
- Department of Biostatistics, University of Washington, Seattle, WA
| | - George Papanicolaou
- Division of Cardiovascular Sciences, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD
| | - Krista M Perreira
- Department of Public Policy, University of North Carolina at Chapel Hill, Chapel Hill, NC
| | - Erik J Rodriquez
- National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD.,Division of General Internal Medicine, University of California, San Francisco, San Francisco, CA
| | - Claudia Schurmann
- Charles Bronfman Institute for Personalized Medicine, Icahn School of Medicine at Mount Sinai, New York, NY
| | - Adrienne M Stilp
- Department of Biostatistics, University of Washington, Seattle, WA
| | - Adam A Szpiro
- Department of Biostatistics, University of Washington, Seattle, WA
| | - Gregory A Talavera
- Graduate School of Public Health, San Diego State University, San Diego, CA
| | - Kent D Taylor
- Institute for Translational Genomics and Population Sciences, Los Angeles Biomedical Research Institute and Department of Pediatrics, Harbor-UCLA Medical Center, Torrance, CA
| | - James F Thrasher
- Department of Health Promotion, Education and Behavior, University of South Carolina, Columbia, SC
| | - Lisa R Yanek
- GeneSTAR Research Program, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD
| | - Cathy C Laurie
- Department of Biostatistics, University of Washington, Seattle, WA
| | - Eliseo J Pérez-Stable
- National Institute on Minority Health and Health Disparities, National Institutes of Health, Bethesda, MD
| | - Laura J Bierut
- Department of Psychiatry, Washington University School of Medicine, St. Louis, MO
| | - Robert C Kaplan
- Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, NY
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Rostron BL, Corey CG, Chang JT, van Bemmel DM, Miller ME, Chang CM. Associations of Cigarettes Smoked Per Day with Biomarkers of Exposure Among U.S. Adult Cigarette Smokers in the Population Assessment of Tobacco and Health (PATH) Study Wave 1 (2013-2014). Cancer Epidemiol Biomarkers Prev 2019; 28:1443-1453. [PMID: 31239264 DOI: 10.1158/1055-9965.epi-19-0013] [Citation(s) in RCA: 22] [Impact Index Per Article: 3.7] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/03/2019] [Revised: 04/02/2019] [Accepted: 06/20/2019] [Indexed: 11/16/2022] Open
Abstract
BACKGROUND The dose-response relationships between number of cigarettes smoked per day (CPD) and health outcomes, such as cancer and heart disease, are well established, but much less is known about the relationships between CPD and biomarkers of exposure. METHODS We analyzed biomarker data by CPD from more than 2,700 adult daily cigarette smokers in Wave 1 of the Population Assessment of Tobacco and Health Study. Tobacco use categories consisted of exclusive cigarette smokers, dual cigarette and e-cigarette users, and dual cigarette and smokeless tobacco users. RESULTS Biomarker concentrations consistently increased with CPD for each tobacco user group, although concentrations tended to level off at high smoking levels, such as those at and above 20 CPD. Dual cigarette and e-cigarette users had higher levels of some biomarkers such as Total Nicotine Equivalents-2 (P = 0.0036) than exclusive cigarette smokers, and dual cigarette and smokeless tobacco users had higher levels of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (P < 0.0001) and N'-nitrosonornicotine (P = 0.0236) than exclusive cigarette smokers. CONCLUSIONS Among daily smokers, exposure to tobacco toxicants and constituents exhibits a dose-response relationship by number of cigarettes smoked, but the relationship is not necessarily linear in form. Dual users of cigarettes with either e-cigarettes or smokeless tobacco are exposed to higher levels of certain toxicants and carcinogens than exclusive cigarette smokers. IMPACT Availability of biomarker data by CPD may aid in comparisons between cigarette smoking and use of new and potentially reduced exposure tobacco products, which may result in different levels of constituent and toxicant exposure.
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Affiliation(s)
- Brian L Rostron
- Center for Tobacco Products, Food and Drug Administration, Silver Spring, Maryland.
| | - Catherine G Corey
- Center for Tobacco Products, Food and Drug Administration, Silver Spring, Maryland
| | - Joanne T Chang
- Center for Tobacco Products, Food and Drug Administration, Silver Spring, Maryland
| | - Dana M van Bemmel
- Center for Tobacco Products, Food and Drug Administration, Silver Spring, Maryland
| | - Mollie E Miller
- Center for Tobacco Products, Food and Drug Administration, Silver Spring, Maryland
| | - Cindy M Chang
- Center for Tobacco Products, Food and Drug Administration, Silver Spring, Maryland
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How do age and major risk factors for mortality interact over the life-course? Implications for health disparities research and public health policy. SSM Popul Health 2019; 8:100438. [PMID: 31321279 PMCID: PMC6612923 DOI: 10.1016/j.ssmph.2019.100438] [Citation(s) in RCA: 18] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/19/2019] [Revised: 06/20/2019] [Accepted: 06/23/2019] [Indexed: 12/30/2022] Open
Abstract
A critical question in life-course research is whether the relationship between a risk factor and mortality strengthens, weakens, or remains constant with age. The objective of this paper is to shed light on the importance of measurement scale in examining this question. Many studies address this question solely on the multiplicative (relative) scale and report that the hazard ratio of dying associated with a risk factor declines with age. A wide set of risk factors have been shown to conform to this pattern including those that are socioeconomic, behavioral, and physiological in nature. Drawing from well-known principles on interpreting statistical interactions, we show that evaluations on the additive (absolute) scale often lead to a different set of conclusions about how the association between a risk factor and mortality changes with age than interpretations on the multiplicative scale. We show that on the additive scale the excess death risks posed by key socio-demographic and behavioral risk factors increase with age. Studies have not generally recognized the additive interpretation, but it has relevancy for testing life-course theories and informing public health interventions. We discuss these implications and provide general guidance on choosing a scale. Data from the U.S. National Health Interview Survey are used to provide empirical support.
Studies often conclude that the effect of demographic and behavioral risk factors on mortality weakens with age. We show that this conclusion is premature as studies often fail to interpret their findings on the additive scale. We show empirically that on the additive scale the excess death risks posed by key risk factors strengthens with age. The general pattern of increasing susceptibility by age on the additive scale has not been previously recognized. We argue that the pattern has critical implications for sociological theory and public health policy.
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43
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Pujol JL, Bommart S, Pujol P. Response to comment on: 'Synchronous multiple non-small cell lung cancers in an allograft lung recipient'. Lung Cancer 2019; 131:155-156. [PMID: 30935718 DOI: 10.1016/j.lungcan.2019.03.027] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/14/2019] [Accepted: 03/25/2019] [Indexed: 10/27/2022]
Affiliation(s)
- Jean-Louis Pujol
- Thoracic Oncology, Centre Hospitalier Univesitaire de Montpellier, Hôpital Arnaud de Villeneuve, Avenue du Doyen Giraud, 34295, Montpellier CEDEX, France.
| | - Sébastien Bommart
- Department of Thoracic Radiology, Centre Hospitalier Univesitaire de Montpellier, Hôpital Arnaud de Villeneuve, Avenue du Doyen Giraud, 34295, Montpellier CEDEX, France
| | - Pascal Pujol
- Oncogenetics Department, Centre Hospitalier Univesitaire de Montpellier, Hôpital Arnaud de Villeneuve, Avenue du Doyen Giraud, 34295, Montpellier CEDEX, France
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Davis JS, Banfield E, Lee HY, Peng HL, Chang S, Wood AC. Lifestyle behavior patterns and mortality among adults in the NHANES 1988-1994 population: A latent profile analysis. Prev Med 2019; 120:131-139. [PMID: 30660707 DOI: 10.1016/j.ypmed.2019.01.012] [Citation(s) in RCA: 9] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/16/2018] [Revised: 12/04/2018] [Accepted: 01/15/2019] [Indexed: 10/27/2022]
Abstract
Evidence suggests interdependent associations of individual modifiable behaviors with health outcomes. However, such interrelations have not been accounted for in previous behavior-outcome associations. We conducted latent profile analysis (LPA) on self-reported levels of alcohol consumption, restaurant dining, vitamin/mineral supplement use, physical activity (PA) and smoke exposure (first- and second-hand smoke) separately for smokers (N = 4530) and non-smokers (N = 13,421) using data from the third National Health and Nutrition Examination Survey (NHANES III) to identify subgroups with similar levels within and across behaviors. Cox-proportional hazards models were used to compare mortality rates between subgroups from cancer, cardiovascular disease (CVD) and all-causes at an average of 16.4 (±6.1) years follow-up. Five behavioral typologies were identified in non-smokers ("Moderates", "Low Risk Factors", "Restaurant Diners", "Moderate Passive Smokers" and "Heavy Passive Smokers"), and four in smokers ("Moderates", "Low Risk Factors", "Heavy Smokers" and "Physically Active"). As a group, "Moderates" had levels of each behavior that were not significantly different from at least one other group. Compared to "Moderates", in non-smokers "Restaurant Diners" had lower hazard from all-cause (hazard ratio (HR):0.84, 95% CI:0.74-0.97) and CVD (HR:0.59, 0.43-0.82) mortality, while "Low Risk Factors" had higher cancer mortality (HR:1.38,1.03-1.84). In smokers, compared to "Moderates", higher hazards for mortality were found for "Heavy Smokers" (all cause: HR:1.34, 1.12-1.60; CVD: HR:1.52, 1.04-2.23; cancer: HR:1.41 1.02-1.96) and "Low Risk Factors" (all-cause: HR:1.58, 1.14-2.17). Taken together, when restaurant dining, PA and smoking exposures are grouped together, novel predictions for mortality occur, suggesting data on multiple behaviors may be informative for risk stratification.
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Affiliation(s)
- Jennifer S Davis
- Department of Epidemiology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
| | - Emilyn Banfield
- Department of Epidemiology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA; Division of Epidemiology, Human Genetics and Environmental Sciences, The University of Texas School of Public Health, Houston, TX, USA
| | - Hwa Young Lee
- Department of Epidemiology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
| | - Ho-Lan Peng
- Department of Management, Policy and Community Health, The University of Texas School of Public Health, Houston, TX, USA
| | - Shine Chang
- Department of Epidemiology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
| | - Alexis C Wood
- USDA/ARS Children's Nutrition Research Center, Baylor College of Medicine, Houston, TX, USA
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45
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Ryan BM. Lung cancer health disparities. Carcinogenesis 2019; 39:741-751. [PMID: 29547922 DOI: 10.1093/carcin/bgy047] [Citation(s) in RCA: 70] [Impact Index Per Article: 11.7] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/13/2017] [Accepted: 03/13/2018] [Indexed: 12/16/2022] Open
Abstract
Compared with all other racial and ethnic groups in the United States, African Americans are disproportionally affected by lung cancer, both in terms of incidence and survival. It is likely that smoking, as the main etiological factor associated with lung cancer, contributes to these disparities, but the precise mechanism is still unclear. This paper seeks to explore the history of lung cancer disparities and review to the literature regarding the various factors that contribute to them.
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Affiliation(s)
- Bríd M Ryan
- Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA
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46
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Inoue-Choi M, McNeel TS, Hartge P, Caporaso NE, Graubard BI, Freedman ND. Non-Daily Cigarette Smokers: Mortality Risks in the U.S. Am J Prev Med 2019; 56:27-37. [PMID: 30454906 PMCID: PMC7477821 DOI: 10.1016/j.amepre.2018.06.025] [Citation(s) in RCA: 48] [Impact Index Per Article: 8.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/05/2018] [Revised: 05/20/2018] [Accepted: 06/20/2018] [Indexed: 10/28/2022]
Abstract
INTRODUCTION Worldwide, an estimated 189 million adults smoke tobacco "occasionally" but not every day. Yet few studies have examined the health risks of non-daily smoking. METHODS Data from the 1991, 1992, and 1995 U.S. National Health Interview Surveys, a nationally representative sample of 70,913 U.S. adults (aged 18-95 years) were pooled. Hazard ratios and 95% CIs for death through 2011 were estimated from Cox proportional hazards regression using age as the underlying time metric and stratified by 5-year birth cohorts in 2017. RESULTS Non-daily smokers reported smoking a median of 15 days and 50 cigarettes per month in contrast to daily smokers who smoked a median of 600 cigarettes per month. Compared with never smokers, lifelong nondaily smokers who had never smoked daily had a 72% higher mortality risk (95% CI=1.36, 2.18): higher risks were observed for cancer, heart disease, and respiratory disease mortalities. Higher mortality risks were observed among lifelong non-daily smokers who reported 11-30 (hazard ratio=1.34, 95% CI=0.81, 2.20); 31-60 (hazard ratio=2.02, 95% CI=1.17, 3.29); and >60 cigarettes per month (hazard ratio=1.74, 95% CI=1.12, 2.72) than never smokers. Median life-expectancy was about 5 years shorter for lifelong non-daily smokers than never smokers. As expected, daily smokers had even higher mortality risks (hazard ratio=2.50, 95% CI=2.35, 2.66) and shorter survival (10 years less). CONCLUSIONS Although the mortality risks of non-daily smokers are lower than daily smokers, they are still substantial. Policies should be specifically directed at this growing group of smokers.
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Affiliation(s)
- Maki Inoue-Choi
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, Maryland.
| | | | - Patricia Hartge
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, Maryland
| | - Neil E Caporaso
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, Maryland
| | - Barry I Graubard
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, Maryland
| | - Neal D Freedman
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, Maryland
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Nichter M, Mini G, Thankappan K. Low- level smoking among diabetes patients in India: a smoking cessation challenge. CLINICAL EPIDEMIOLOGY AND GLOBAL HEALTH 2018. [DOI: 10.1016/j.cegh.2017.11.005] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/18/2022] Open
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48
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Luo Q, Yu XQ, Wade S, Caruana M, Pesola F, Canfell K, O'Connell DL. Lung cancer mortality in Australia: Projected outcomes to 2040. Lung Cancer 2018; 125:68-76. [PMID: 30429040 DOI: 10.1016/j.lungcan.2018.09.001] [Citation(s) in RCA: 18] [Impact Index Per Article: 2.6] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/05/2018] [Revised: 08/30/2018] [Accepted: 09/03/2018] [Indexed: 10/28/2022]
Abstract
OBJECTIVES The aim was to develop and validate a statistical model which uses past trends for lung cancer mortality and historical and current data on tobacco consumption to project lung cancer mortality rates into the future for Australia. METHODS We used generalized linear models (GLMs) with Poisson distribution including either age, birth cohort or period, and/or various measures of population tobacco exposure (considering cross-sectional smoking prevalence, cigarettes smoked and tar exposure per capita). Sex-specific models were fitted to data for 1956-2015 and age-standardized lung cancer mortality rates were projected forward to 2040. Possible lags of 20-30 years between tobacco exposure and lung cancer mortality were examined. The best model was selected using analysis of deviance. To validate the selected model, we temporarily re-fitted it to data for 1956-1990 and compared the projected rates to 2015 with the observed rates for 1991-2015. RESULTS The best fitting model used information on age, birth cohort and tar exposure per capita; close concordance with the observed data was achieved in the validation. The forward projections for lung cancer mortality using this model indicate that male and female age-standardized rates will decline over the period 2011-2015 to 2036-2040 from 27.2 to 15.1 per 100,000, and 15.8 to 11.8 per 100,000, respectively. However, due to population growth and ageing the number of deaths will increase by 7.9% for males and 57.9% for females; from 41,040 (24,831 males, 16,209 females) in 2011-2015 to 52,403 (26,805 males, 25,598 females) in 2036-2040. CONCLUSION In the context of the mature tobacco epidemic with past peaks in tobacco consumption for both males and females, lung cancer mortality rates are expected to continually decline over the next 25 years. However, the number of lung cancer deaths will continue to be substantial, and to increase, in Australia's ageing population.
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Affiliation(s)
- Qingwei Luo
- Cancer Research Division, Cancer Council NSW, Sydney, NSW, Australia; The University of Sydney School of Public Health, Faculty of Medicine and Health, The University of Sydney, Sydney, Australia.
| | - Xue Qin Yu
- Cancer Research Division, Cancer Council NSW, Sydney, NSW, Australia; The University of Sydney School of Public Health, Faculty of Medicine and Health, The University of Sydney, Sydney, Australia.
| | - Stephen Wade
- Cancer Research Division, Cancer Council NSW, Sydney, NSW, Australia.
| | - Michael Caruana
- Cancer Research Division, Cancer Council NSW, Sydney, NSW, Australia.
| | - Francesca Pesola
- Faculty of Life Sciences & Medicine, School of Cancer & Pharmaceutical Sciences, Innovation Hub, Guys Cancer Centre, Guys Hospital, King's College London, London, UK.
| | - Karen Canfell
- Cancer Research Division, Cancer Council NSW, Sydney, NSW, Australia; The University of Sydney School of Public Health, Faculty of Medicine and Health, The University of Sydney, Sydney, Australia.
| | - Dianne L O'Connell
- Cancer Research Division, Cancer Council NSW, Sydney, NSW, Australia; The University of Sydney School of Public Health, Faculty of Medicine and Health, The University of Sydney, Sydney, Australia; School of Medicine and Public Health, University of Newcastle, Newcastle, NSW, Australia.
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Glantz SA. PMI's own in vivo clinical data on biomarkers of potential harm in Americans show that IQOS is not detectably different from conventional cigarettes. Tob Control 2018; 27:s9-s12. [PMID: 30131374 PMCID: PMC6202159 DOI: 10.1136/tobaccocontrol-2018-054413] [Citation(s) in RCA: 45] [Impact Index Per Article: 6.4] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/04/2018] [Revised: 07/10/2018] [Accepted: 08/01/2018] [Indexed: 11/03/2022]
Abstract
INTRODUCTION New 'heated tobacco products' are being marketed in several countries with claims that they expose users to lower levels of toxins than conventional cigarettes which could be read as being less likely to cause health problems than conventional cigarettes. In the USA, Philip Morris International (PMI) has submitted an application to the Food and Drug Administration for permission to market its heated tobacco product, IQOS, with reduced exposure and reduced risk claims. METHODS Analysis of detailed results on 24 biomarkers of potential harm in PMI studies of humans using IQOS compared with humans using conventional cigarettes. RESULTS Among American adults, there is no statistically detectable difference between IQOS and conventional cigarette users for 23 of the 24 biomarkers of potential harm in PMI's studies. In Japan, there were no significant differences between people using IQOS and conventional cigarettes in 10 of 13 biomarkers of potential harm. It is likely that some of the significant differences are false positives. CONCLUSION Despite delivering lower levels of some toxins than conventional cigarettes, PMI's own data fail to show consistently lower risks of harm in humans using its heated tobacco product, IQOS, than conventional cigarettes.
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Affiliation(s)
- Stanton A Glantz
- Department of Medicine/Division of Cardiology, University of California San Francisco, San Francisco, CA 94143-1390, USA
- Center for Tobacco Control Research and Education, University of California San Francisco, San Francisco, CA 94143-1390, USA
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50
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Kobberø Lauridsen B, Stender S, Frikke-Schmidt R, Nordestgaard BG, Tybjærg-Hansen A. Using genetics to explore whether the cholesterol-lowering drug ezetimibe may cause an increased risk of cancer. Int J Epidemiol 2018; 46:1777-1785. [PMID: 29106532 DOI: 10.1093/ije/dyx096] [Citation(s) in RCA: 8] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Accepted: 05/13/2017] [Indexed: 11/13/2022] Open
Abstract
Background Results from randomized controlled trials (RCTs) have raised concern that the cholesterol-lowering drug ezetimibe might increase the risk of cancer. We tested the hypothesis that genetic variation in NPC1L1, mimicking treatment with ezetimibe, was associated with an increased risk of cancer. Methods We included 67 257 individuals from the general population. Of these, 8333 developed cancer and 2057 died of cancer from 1968 to 2011. To mimic the effect of ezetimibe, we calculated weighted allele scores based on the low-density lipoprotein (LDL) cholesterol-lowering(= NPC1L1-inhibitory) effect of each variant. We tested the associations of the NPC1L1 allele scores with LDL cholesterol and with risk of any cancer, death from any cancer and 27 site-specific cancers. As a positive control, we tested the association of the NPC1L1 allele scores with risk of ischaemic vascular disease (IVD). Results The NPC1L1 allele scores did not associate with risk of any cancer, death from any cancer or with any of 27 site-specific cancers. Hazard ratios (HRs) for a 1-unit increase in internally weighted allele scores were 1.00 (95% confidence interval: 0.98-1.02) for any cancer, and 1.02 (0.98-1.06) for cancer death. The corresponding HR for IVD was 0.97 (0.94-0.99). Results were similar for an externally weighted allele score and for a simple allele count. Finally, the null association with cancer was robust in sensitivity analyses. Conclusions Lifelong, genetic inhibition of NPC1L1, mimicking treatment with ezetimibe, does not associate with risk of cancer. These results suggest that long-term treatment with ezetimibe is unlikely to increase the risk of cancer, in agreement with the overall evidence from ezetimibe RCTs.
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Affiliation(s)
| | - Stefan Stender
- Department of Clinical Biochemistry, Rigshospitalet, Copenhagen, Denmark
| | - Ruth Frikke-Schmidt
- Department of Clinical Biochemistry, Rigshospitalet, Copenhagen, Denmark.,Copenhagen General Population Study, Herlev and Gentofte Hospital, Herlev, Denmark.,Copenhagen University Hospitals and Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
| | - Børge G Nordestgaard
- Copenhagen General Population Study, Herlev and Gentofte Hospital, Herlev, Denmark.,Copenhagen University Hospitals and Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.,Department of Clinical Biochemistry.,Copenhagen City Heart Study, Frederiksberg Hospital, Frederiksberg, Denmark
| | - Anne Tybjærg-Hansen
- Department of Clinical Biochemistry, Rigshospitalet, Copenhagen, Denmark.,Copenhagen General Population Study, Herlev and Gentofte Hospital, Herlev, Denmark.,Copenhagen University Hospitals and Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.,Copenhagen City Heart Study, Frederiksberg Hospital, Frederiksberg, Denmark
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