Alcohol Drinking in Never Users of Tobacco, Cigarette Smoking in Never Drinkers, and the Risk of Head and Neck Cancer: Pooled Analysis in the International Head and Neck Cancer Epidemiology Consortium
International Agency for Research on Cancer1, French Institute of Health and Medical Research2, Fred Hutchinson Cancer Research Center3, Universidade Federal do Rio Grande do Sul4, National Institutes of Health5, Oswaldo Cruz Foundation6, University of Milan7, Pennsylvania State University8, University of Lausanne9, University of Buenos Aires10, Universidade Federal de Pelotas11, University of São Paulo12, University of North Carolina at Chapel Hill13, University of Iowa14, University of Texas MD Anderson Cancer Center15, Nofer Institute of Occupational Medicine16, Russian Academy17, University of California, Los Angeles18
16 May 2007-Journal of the National Cancer Institute (Oxford University Press)-Vol. 99, Iss: 10, pp 777-789
TL;DR: The results represent the most precise estimates available of the independent association of each of the two main risk factors of head and neck cancer, and they exemplify the strengths of large-scale consortia in cancer epidemiology.
Abstract: Background At least 75% of head and neck cancers are attributable to a combination of cigarette smoking and alcohol drinking. A precise understanding of the independent association of each of these factors in the absence of the other with the risk of head and neck cancer is needed to elucidate mechanisms of head and neck carcinogenesis and to assess the efficacy of interventions aimed at controlling either risk factor. Methods We examined the extent to which head and neck cancer is associated with cigarette smoking among never drinkers and with alcohol drinking among never users of tobacco. We pooled individual-level data from 15 case – control studies that included 10 244 head and neck cancer case subjects and 15 227 control subjects, of whom 1072 case subjects and 5775 control subjects were never users of tobacco and 1598 case subjects and 4051 control subjects were never drinkers of alcohol. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using unconditional logistic regression models. All statistical tests were two-sided. Results Among never drinkers, cigarette smoking was associated with an increased risk of head and neck cancer (OR for ever versus never smoking = 2.13, 95% CI = 1.52 to 2.98), and there were clear dose – response relationships for the frequency, duration, and number of pack-years of cigarette smoking. Approximately 24% (95% CI = 16% to 31%) of head and neck cancer cases among nondrinkers in this study would have been prevented if these individuals had not smoked cigarettes. Among never users of tobacco, alcohol consumption was associated with an increased risk of head and neck cancer only when alcohol was consumed at high frequency (OR for three or more drinks per day versus never drinking = 2.04, 95% CI = 1.29 to 3.21). The association with high-frequency alcohol intake was limited to cancers of the oropharynx/hypopharynx and larynx. Conclusions Our results represent the most precise estimates available of the independent association of each of the two main risk factors of head and neck cancer, and they exemplify the strengths of large-scale consortia in cancer epidemiology. J Natl Cancer Inst 2007;99: 777 – 89
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TL;DR: The epidemiology, molecular pathogenesis, diagnosis and staging, and the latest multimodal management of squamous cell carcinoma of the head and neck are reviewed.
1,644 citations
26 Nov 2020
TL;DR: This Primer provides an overview of the epidemiology, pathogenesis and treatment of HNSCCs of different aetiologies and the effects of the cancer and its treatment on patient quality of life.
Abstract: Most head and neck cancers are derived from the mucosal epithelium in the oral cavity, pharynx and larynx and are known collectively as head and neck squamous cell carcinoma (HNSCC). Oral cavity and larynx cancers are generally associated with tobacco consumption, alcohol abuse or both, whereas pharynx cancers are increasingly attributed to infection with human papillomavirus (HPV), primarily HPV-16. Thus, HNSCC can be separated into HPV-negative and HPV-positive HNSCC. Despite evidence of histological progression from cellular atypia through various degrees of dysplasia, ultimately leading to invasive HNSCC, most patients are diagnosed with late-stage HNSCC without a clinically evident antecedent pre-malignant lesion. Traditional staging of HNSCC using the tumour–node–metastasis system has been supplemented by the 2017 AJCC/UICC staging system, which incorporates additional information relevant to HPV-positive disease. Treatment is generally multimodal, consisting of surgery followed by chemoradiotherapy (CRT) for oral cavity cancers and primary CRT for pharynx and larynx cancers. The EGFR monoclonal antibody cetuximab is generally used in combination with radiation in HPV-negative HNSCC where comorbidities prevent the use of cytotoxic chemotherapy. The FDA approved the immune checkpoint inhibitors pembrolizumab and nivolumab for treatment of recurrent or metastatic HNSCC and pembrolizumab as primary treatment for unresectable disease. Elucidation of the molecular genetic landscape of HNSCC over the past decade has revealed new opportunities for therapeutic intervention. Ongoing efforts aim to integrate our understanding of HNSCC biology and immunobiology to identify predictive biomarkers that will enable delivery of the most effective, least-toxic therapies. Head and neck squamous cell carcinomas (HNSCCs) originate from the mucosal epithelium in the oral cavity, pharynx and larynx and are commonly associated with viral infection and tobacco use. This Primer provides an overview of the epidemiology, pathogenesis and treatment of HNSCCs of different aetiologies and the effects of the cancer and its treatment on patient quality of life.
1,152 citations
TL;DR: OPC incidence significantly increased during 1983 to 2002 predominantly in developed countries and at younger ages, underscore a potential role for HPV infection on increasing OPC incidence, particularly among men.
Abstract: Purpose Human papillomavirus (HPV) has been identified as the cause of the increasing oropharyngeal cancer (OPC) incidence in some countries. To investigate whether this represents a global phenomenon, we evaluated incidence trends for OPCs and oral cavity cancers (OCCs) in 23 countries across four continents. Methods We used data from the Cancer Incidence in Five Continents database Volumes VI to IX (years 1983 to 2002). Using age-period-cohort modeling, incidence trends for OPCs were compared with those of OCCs and lung cancers to delineate the potential role of HPV vis-a-vis smoking on incidence trends. Analyses were country specific and sex specific. Results OPC incidence significantly increased during 1983 to 2002 predominantly in economically developed countries. Among men, OPC incidence significantly increased in the United States, Australia, Canada, Japan, and Slovakia, despite nonsignificant or significantly decreasing incidence of OCCs. In contrast, among women, in all countries with increasing ...
1,068 citations
TL;DR: Alcohol-related carcinogenesis may interact with other factors such as smoking, diet and comorbidities, and depends on genetic susceptibility.
Abstract: Approximately 3.6% of cancers worldwide derive from chronic alcohol drinking, including those of the upper aerodigestive tract, the liver, the colorectum and the breast. Although the mechanisms for alcohol-associated carcinogenesis are not completely understood, most recent research has focused on acetaldehyde, the first and most toxic ethanol metabolite, as a cancer-causing agent. Ethanol may also stimulate carcinogenesis by inhibiting DNA methylation and by interacting with retinoid metabolism. Alcohol-related carcinogenesis may interact with other factors such as smoking, diet and comorbidities, and depends on genetic susceptibility.
940 citations
International Agency for Research on Cancer1, Catholic University of the Sacred Heart2, Fred Hutchinson Cancer Research Center3, Universidade Federal do Rio Grande do Sul4, University of São Paulo5, National Institutes of Health6, Brown University7, Harvard University8, Oswaldo Cruz Foundation9, University of Milan10, Pennsylvania State University11, University of Lausanne12, University of Buenos Aires13, Universidade Federal de Pelotas14, Boston University15, University of North Carolina at Chapel Hill16, University of Iowa17, University of Texas MD Anderson Cancer Center18, Nofer Institute of Occupational Medicine19, Russian Academy20, Medical University of Warsaw21, University of California, Los Angeles22
TL;DR: It is confirmed that the joint effect between tobacco and alcohol use is greater than multiplicative on head and neck cancer risk, however, a substantial proportion of head and head cancers cannot be attributed to tobacco or alcohol use, particularly for oral cavity cancer and for head andneck cancer among women and among young-onset cases.
Abstract: Background: The magnitude of risk conferred by the interaction between tobacco and alcohol use on the risk of head and neck cancers is not clear because studies have used various methods to quantify the excess head and neck cancer burden. Methods: We analyzed individual-level pooled data from 17 European and American case-control studies (11,221 cases and 16,168 controls) participating in the International Head and Neck Cancer Epidemiology consortium. We estimated the multiplicative interaction parameter ( ψ ) and population attributable risks (PAR). Results: A greater than multiplicative joint effect between ever tobacco and alcohol use was observed for head and neck cancer risk ( ψ = 2.15; 95% confidence interval, 1.53-3.04). The PAR for tobacco or alcohol was 72% (95% confidence interval, 61-79%) for head and neck cancer, of which 4% was due to alcohol alone, 33% was due to tobacco alone, and 35% was due to tobacco and alcohol combined. The total PAR differed by subsite (64% for oral cavity cancer, 72% for pharyngeal cancer, 89% for laryngeal cancer), by sex (74% for men, 57% for women), by age (33% for cases 60 years), and by region (84% in Europe, 51% in North America, 83% in Latin America). Conclusions: Our results confirm that the joint effect between tobacco and alcohol use is greater than multiplicative on head and neck cancer risk. However, a substantial proportion of head and neck cancers cannot be attributed to tobacco or alcohol use, particularly for oral cavity cancer and for head and neck cancer among women and among young-onset cases. (Cancer Epidemiol Biomarkers Prev 2009;18(2):541–50)
858 citations
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TL;DR: This paper examines eight published reviews each reporting results from several related trials in order to evaluate the efficacy of a certain treatment for a specified medical condition and suggests a simple noniterative procedure for characterizing the distribution of treatment effects in a series of studies.
33,234 citations
Book•
01 Jan 1987
TL;DR: In this article, a survey of drinking behavior among men of retirement age was conducted and the results showed that the majority of the participants reported that they did not receive any benefits from the Social Security Administration.
Abstract: Tables and Figures. Glossary. 1. Introduction. 1.1 Overview. 1.2 Examples of Surveys with Nonresponse. 1.3 Properly Handling Nonresponse. 1.4 Single Imputation. 1.5 Multiple Imputation. 1.6 Numerical Example Using Multiple Imputation. 1.7 Guidance for the Reader. 2. Statistical Background. 2.1 Introduction. 2.2 Variables in the Finite Population. 2.3 Probability Distributions and Related Calculations. 2.4 Probability Specifications for Indicator Variables. 2.5 Probability Specifications for (X,Y). 2.6 Bayesian Inference for a Population Quality. 2.7 Interval Estimation. 2.8 Bayesian Procedures for Constructing Interval Estimates, Including Significance Levels and Point Estimates. 2.9 Evaluating the Performance of Procedures. 2.10 Similarity of Bayesian and Randomization--Based Inferences in Many Practical Cases. 3. Underlying Bayesian Theory. 3.1 Introduction and Summary of Repeated--Imputation Inferences. 3.2 Key Results for Analysis When the Multiple Imputations are Repeated Draws from the Posterior Distribution of the Missing Values. 3.3 Inference for Scalar Estimands from a Modest Number of Repeated Completed--Data Means and Variances. 3.4 Significance Levels for Multicomponent Estimands from a Modest Number of Repeated Completed--Data Means and Variance--Covariance Matrices. 3.5 Significance Levels from Repeated Completed--Data Significance Levels. 3.6 Relating the Completed--Data and Completed--Data Posterior Distributions When the Sampling Mechanism is Ignorable. 4. Randomization--Based Evaluations. 4.1 Introduction. 4.2 General Conditions for the Randomization--Validity of Infinite--m Repeated--Imputation Inferences. 4.3Examples of Proper and Improper Imputation Methods in a Simple Case with Ignorable Nonresponse. 4.4 Further Discussion of Proper Imputation Methods. 4.5 The Asymptotic Distibution of (Qm,Um,Bm) for Proper Imputation Methods. 4.6 Evaluations of Finite--m Inferences with Scalar Estimands. 4.7 Evaluation of Significance Levels from the Moment--Based Statistics Dm and Dm with Multicomponent Estimands. 4.8 Evaluation of Significance Levels Based on Repeated Significance Levels. 5. Procedures with Ignorable Nonresponse. 5.1 Introduction. 5.2 Creating Imputed Values under an Explicit Model. 5.3 Some Explicit Imputation Models with Univariate YI and Covariates. 5.4 Monotone Patterns of Missingness in Multivariate YI. 5.5 Missing Social Security Benefits in the Current Population Survey. 5.6 Beyond Monotone Missingness. 6. Procedures with Nonignorable Nonresponse. 6.1 Introduction. 6.2 Nonignorable Nonresponse with Univariate YI and No XI. 6.3 Formal Tasks with Nonignorable Nonresponse. 6.4 Illustrating Mixture Modeling Using Educational Testing Service Data. 6.5 Illustrating Selection Modeling Using CPS Data. 6.6 Extensions to Surveys with Follow--Ups. 6.7 Follow--Up Response in a Survey of Drinking Behavior Among Men of Retirement Age. References. Author Index. Subject Index. Appendix I. Report Written for the Social Security Administration in 1977. Appendix II. Report Written for the Census Bureau in 1983.
14,574 citations
TL;DR: This work focuses on the development of Imputation Models for Social Security Benefit Reconciliation in the context of a Finite Population and examines the role of Bayesian and Randomization--Based Inferences in these models.
Abstract: Tables and Figures. Glossary. 1. Introduction. 1.1 Overview. 1.2 Examples of Surveys with Nonresponse. 1.3 Properly Handling Nonresponse. 1.4 Single Imputation. 1.5 Multiple Imputation. 1.6 Numerical Example Using Multiple Imputation. 1.7 Guidance for the Reader. 2. Statistical Background. 2.1 Introduction. 2.2 Variables in the Finite Population. 2.3 Probability Distributions and Related Calculations. 2.4 Probability Specifications for Indicator Variables. 2.5 Probability Specifications for (X,Y). 2.6 Bayesian Inference for a Population Quality. 2.7 Interval Estimation. 2.8 Bayesian Procedures for Constructing Interval Estimates, Including Significance Levels and Point Estimates. 2.9 Evaluating the Performance of Procedures. 2.10 Similarity of Bayesian and Randomization--Based Inferences in Many Practical Cases. 3. Underlying Bayesian Theory. 3.1 Introduction and Summary of Repeated--Imputation Inferences. 3.2 Key Results for Analysis When the Multiple Imputations are Repeated Draws from the Posterior Distribution of the Missing Values. 3.3 Inference for Scalar Estimands from a Modest Number of Repeated Completed--Data Means and Variances. 3.4 Significance Levels for Multicomponent Estimands from a Modest Number of Repeated Completed--Data Means and Variance--Covariance Matrices. 3.5 Significance Levels from Repeated Completed--Data Significance Levels. 3.6 Relating the Completed--Data and Completed--Data Posterior Distributions When the Sampling Mechanism is Ignorable. 4. Randomization--Based Evaluations. 4.1 Introduction. 4.2 General Conditions for the Randomization--Validity of Infinite--m Repeated--Imputation Inferences. 4.3Examples of Proper and Improper Imputation Methods in a Simple Case with Ignorable Nonresponse. 4.4 Further Discussion of Proper Imputation Methods. 4.5 The Asymptotic Distibution of (Qm,Um,Bm) for Proper Imputation Methods. 4.6 Evaluations of Finite--m Inferences with Scalar Estimands. 4.7 Evaluation of Significance Levels from the Moment--Based Statistics Dm and Dm with Multicomponent Estimands. 4.8 Evaluation of Significance Levels Based on Repeated Significance Levels. 5. Procedures with Ignorable Nonresponse. 5.1 Introduction. 5.2 Creating Imputed Values under an Explicit Model. 5.3 Some Explicit Imputation Models with Univariate YI and Covariates. 5.4 Monotone Patterns of Missingness in Multivariate YI. 5.5 Missing Social Security Benefits in the Current Population Survey. 5.6 Beyond Monotone Missingness. 6. Procedures with Nonignorable Nonresponse. 6.1 Introduction. 6.2 Nonignorable Nonresponse with Univariate YI and No XI. 6.3 Formal Tasks with Nonignorable Nonresponse. 6.4 Illustrating Mixture Modeling Using Educational Testing Service Data. 6.5 Illustrating Selection Modeling Using CPS Data. 6.6 Extensions to Surveys with Follow--Ups. 6.7 Follow--Up Response in a Survey of Drinking Behavior Among Men of Retirement Age. References. Author Index. Subject Index. Appendix I. Report Written for the Social Security Administration in 1977. Appendix II. Report Written for the Census Bureau in 1983.
5,436 citations
Journal Article•
TL;DR: Risks of oropharyngeal cancer tended to combine more in a multiplicative than additive fashion and were increased more than 35-fold among those who consumed two or more packs of cigarettes and more than four alcoholic drinks/day.
Abstract: A case-control study of oral and pharyngeal cancer conducted in four areas of the United States provided information on the tobacco and alcohol use of 1114 patients and 1268 population-based controls. Because of the large study size, it could be shown that the risks of these cancers among nondrinkers increased with amount smoked, and conversely that the risks among nonsmokers increased with the level of alcohol intake. Among consumers of both products, risks of oropharyngeal cancer tended to combine more in a multiplicative than additive fashion and were increased more than 35-fold among those who consumed two or more packs of cigarettes and more than four alcoholic drinks/day. Cigarette, cigar, and pipe smoking were separately implicated, although it was shown for the first time that risk was not as high among male lifelong filter cigarette smokers. Cessation of smoking was associated with a sharply reduced risk of this cancer, with no excess detected among those having quit for 10 or more years, suggesting that smoking affects primarily a late stage in the process of oropharyngeal carcinogenesis. The risks varied by type of alcoholic beverage, being higher among those consuming hard liquor or beer than wine. The relative risk patterns were generally similar among whites and blacks, and among males and females, and showed little difference when oral and pharyngeal cancers were analyzed separately. From calculations of attributable risk, we estimate that tobacco smoking and alcohol drinking combine to account for approximately three-fourths of all oral and pharyngeal cancers in the United States.
1,894 citations