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      The precancer risk of betel quid chewing, tobacco use and alcohol consumption in oral leukoplakia and oral submucous fibrosis in southern Taiwan

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          Abstract

          In areas where the practise of betel quid chewing is widespread and the chewers also often smoke and drink alcohol, the relation between oral precancerous lesion and condition to the three habits is probably complex. To explore such association and their attributable effect on oral leukoplakia (OL) and oral submucous fibrosis (OSF), a gender–age-matched case–control study was conducted at Kaohsiung, southern Taiwan. This study included 219 patients with newly diagnosed and histologically confirmed OL or OSF, and 876 randomly selected community controls. All information was collected by a structured questionnaire through in-person interviews. A preponderance of younger patients had OSF, while a predominance of older patients had OL. Betel quid chewing was strongly associated with both these oral diseases, the attributable fraction of OL being 73.2% and of OSF 85.4%. While the heterogeneity in risk for areca nut chewing across the two diseases was not apparent, betel quid chewing patients with OSF experienced a higher risk at each exposure level of chewing duration, quantity and cumulative measure than those who had OL. Alcohol intake did not appear to be a risk factor. However, cigarette smoking had a significant contribution to the risk of OL, and modified the effect of chewing based on an additive interaction model. For the two oral premalignant diseases combined, 86.5% was attributable to chewing and smoking. Our results suggested that, although betel quid chewing was a major cause for both OL and OSF, its effect might be difference between the two diseases. Cigarette smoking has a modifying effect in the development of oral leukoplakia.

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          Most cited references25

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          Smoking and drinking in relation to oral and pharyngeal cancer.

          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.
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            Estimating the population attributable risk for multiple risk factors using case-control data.

            A straightforward and unified approach is presented for the calculation of the population attributable risk per cent (etiologic fraction) in the general multivariate setting, with emphasis on using data from case-control studies. The summary attributable risk for multiple factors can be estimated, with or without adjustment for other (confounding) risk factors. The relation of this approach to procedures in the literature is discussed. Given values of the relative risks for various combinations of factors, all that is required is the distribution of these factors among the cases only. The required information can often be estimated solely from case-control data, and in some situations relative risk estimates from one population can be applied to calculation of attributable risk for another population. The authors emphasize the benefits to be obtained from logistic regression models, so that risks need not be estimated separately in a large number of strata, some of which may contain inadequate numbers of individuals. This approach allows incorporation of important interactions between factors, but does not require that all possible interactions be included. The approach is illustrated with data on four risk factors from a pair-matched case-control study of participants in a multicenter breast cancer screening project.
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              Betel quid chewing, cigarette smoking and alcohol consumption related to oral cancer in Taiwan.

              A hospital-based case-control study of matched pairs was conducted to explore (a) the relationship between the use of betel quid chewing, cigarette smoking, alcohol drinking and oral cancer and (b) synergism between these factors. The case group consisted of 104 male and 3 female oral cancer patients and these were compared with 194 male and 6 female matched controls. We found by univariate analysis that alcohol consumption, smoking, betel quid chewing, educational level and occupation were associated with oral cancer. The adjusted odds ratios were to be found elevated in patients who were smoking and betel quid chewing. After adjusting for education and occupation covariates, the incidence of oral cancer was computed to be 123-fold higher in patients who smoked, drank alcohol and chewed betel quid than in abstainers. The synergistic effects of alcohol, tobacco smoke and betel quid in oral cancer were clearly demonstrated, but there was a statistically significant association between oral cancer and betel quid chewing alone. Swallowing betel quid juice (saliva extract of betel quid produced by chewing) or including unripened betel fruit in the quid both seemed to enhance the risks of contracting oral cancer.
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                Author and article information

                Journal
                Br J Cancer
                British Journal of Cancer
                Nature Publishing Group
                0007-0920
                1532-1827
                10 February 2003
                10 February 2003
                : 88
                : 3
                : 366-372
                Affiliations
                [1 ] 1Graduate Institute of Public Health, College of Health Science, Kaohsiung Medical University, Taiwan, ROC
                [2 ] 2Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Taiwan, ROC
                [3 ] 3Department of Nursing, Shu-Zen College of Medicine and Management, Taiwan, ROC
                [4 ] 4Graduate Institute of Dentistry, College of Dentistry, Kaohsiung Medical University, Taiwan, ROC
                [5 ] 5Graduate Institute of Oral Health Sciences, College of Dentistry, Kaohsiung Medical University, Taiwan, ROC
                Author notes
                [* ]Author for correspondence: ycko@ 123456kmu.edu.tw
                Article
                6600727
                10.1038/sj.bjc.6600727
                2747536
                12569378
                9958333c-01ad-4deb-b2b5-a53238f1f8be
                Copyright 2003, Cancer Research UK
                History
                : 02 August 2002
                : 21 October 2002
                : 25 October 2002
                Categories
                Epidemiology

                Oncology & Radiotherapy
                risk factors,smoking,oral leukoplakia,areca,alcohol drinking,oral submucous fibrosis

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