Risk factors for oral and pharyngeal cancer in never smokers

Fioretti, Francesca; Bosetti, Cristina; Tavani, Alessandra; Franceschi, Silvia; Vecchia, Carlo La

doi:10.1016/s1368-8375(98)00125-0

Cited by 84 publications

(44 citation statements)

References 19 publications

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“…This finding is in accordance with some studies (Fioretti et al, 1999;Turati et al, 2010), but this association is controversial (Goldstein et al, 2010). Additionally, taking the oxidative parameter analyses into account, it can be suggested that the damage in oral mucosa is cumulative and progressive.…”

Section: Ventral Tongue Mucosasupporting

confidence: 90%

“…Alcohol acts as an independent risk factor for oral cancer (Fioretti et al, 1999;Moreno-López et al, 2000;Bagnardi et al, 2001;Goldstein et al, 2010). Some studies demonstrated that there is a relation with dose et al., 1994;Maito et al, 2003;Carrard et al, 2004) and higher permeability to tobacco carcinogens (Squier et al, 1986;Du et al, 2000) have been demonstrated in oral mucosa after alcohol exposure.…”

Section: Introductionmentioning

confidence: 99%

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Exploring the mechanisms of alcohol-related damage in oral mucosa – is oxidative stress associated with the increase in cell proliferation in rat tongue epithelium?

Carrard

Pires

Mendez

et al. 2012

Pharmaceutical Biology

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Section: Ventral Tongue Mucosasupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Exploring the mechanisms of alcohol-related damage in oral mucosa – is oxidative stress associated with the increase in cell proliferation in rat tongue epithelium?

Carrard

Pires

Mendez

et al. 2012

Pharmaceutical Biology

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“…[41][42][43][44] Oral cancer risk significantly increased with both intensity (drinks per day) and duration of alcohol use and declined with cessation of use. 29 Alcohol consumption increased risk of oral cancer among never, 28,45 ever, 29 former, 46,47 and current smokers.…”

Section: Alcohol Consumption and Metabolismmentioning

confidence: 99%

Current topics in the epidemiology of oral cavity and oropharyngeal cancers

2007

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Oral cancer incidence rates rose dramatically during the twentieth century in the United States and Europe, especially among individuals under the age of 60 years. Although influenced by age, sex, and country of origin, incidence trends were most strongly affected by elevated risk among individuals born after approximately 1915. This cohort effect was indicative of strong behavioral influences on oral cancer risk. In this article, associations between oral cancer risk and established behavioral risk factors including alcohol and tobacco use are reviewed. Additionally, possible associations between oral cancer risk and oral hygiene, diet, nutritional status, and sexual behavior as well as the influence of genetic factors on oral cancer risk are considered. Special emphasis is placed on evaluating possible risk differences in individuals above and below the age of 45 and in users and nonusers of alcohol and tobacco. Oral squamous cell carcinomas arise from several anatomic sites within the oral cavity and oropharynx, but most commonly from the oral, mobile tongue.1 In the 1980s, 2 cancer centers in the United States (U.S.) reported an increase in the proportion of incident oral tongue cancers diagnosed in men younger 40 years.2,3 Although absolute numbers had increased, these reports provided no real evidence of rising incidence. Shortly thereafter, however, a significant 2-fold increase in oral tongue cancer mortality rates between 1950 and 1982 was reported in the U.S. for men younger than 30 years. 4 This finding was corroborated by a study in Scotland. 5 Further analysis of the Scottish data revealed that the increase in incidence was not restricted to those younger than 40 but extended to all age groups less than 65 years of age born after 1920-a strong ''cohort effect.'' The cohort effect was indicated by a strong effect of year of birth on oral cancer incidence rates. A flurry of research on global changes in oral cancer incidence was stimulated by these reports.

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“…Indeed, there is strong evidence that alcohol is an independent risk factor for oral cancer (4,(21)(22)(23)(24)(25)(26)(27). Conflicting results in case-control studies of alcohol and OPL may be the result of methodologic shortcomings, such as recall bias, insufficient control for tobacco, and selection bias.…”

Section: Introductionmentioning

confidence: 99%

Prospective Study of Alcohol Consumption and Risk of Oral Premalignant Lesions in Men

Maserejian

Joshipura

Rosner

et al. 2006

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Recent case-control studies indicate that alcohol increases the risk of oral premalignant lesions (OPL) among tobacco users, but the independent association between alcohol and OPL remains unclear. We prospectively evaluated the association between alcohol consumption and the incidence of OPL. Participants were 41,458 men in the Health Professionals Follow-up Study. Alcohol consumption was assessed every 4 years using validated food frequency questionnaires. We confirmed clinically or histopathologically diagnosed OPL events occurring between 1986 and 2002 by medical record review (193 cases). Multivariateadjusted relative risks of OPL were calculated from Cox proportional hazards models. With detailed control for tobacco and other variables, multivariate relative risks (95% confidence intervals) were 1.7 (0.9-3.2) for drinkers of 0.1 to 14.9 g/d, 2.9 (1.5-5.6) for 15 to 29.9 g/d, and 2.5 (1.3-5.1) for z30 g/d, compared with nondrinkers. Approximately one additional drink per day (12.5 g) was associated with a 22% increase in risk (P < 0.001). The associations did not vary by beverage type, frequency, or consumption with meals. Results were similar when restricted to cases of oral epithelial dysplasia. Alcohol increased OPL risk in neverusers of tobacco as well as in past or current users. An interaction between alcohol and tobacco was apparent by their more-than-additive joint effects. Alcohol is an independent risk factor for OPL, regardless of beverage type or drinking pattern. Recommendations to reduce alcohol intake have the potential to reduce incidence of OPL in nonsmokers and smokers alike.

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Risk factors for oral and pharyngeal cancer in never smokers

Cited by 84 publications

References 19 publications

Exploring the mechanisms of alcohol-related damage in oral mucosa – is oxidative stress associated with the increase in cell proliferation in rat tongue epithelium?

Exploring the mechanisms of alcohol-related damage in oral mucosa – is oxidative stress associated with the increase in cell proliferation in rat tongue epithelium?

Current topics in the epidemiology of oral cavity and oropharyngeal cancers

Prospective Study of Alcohol Consumption and Risk of Oral Premalignant Lesions in Men

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