Acrylamide exposure was investigated in subgroups of the EPIC study population (510 subjects from 9 European countries, randomly selected and stratified by age, gender, and smoking status) using hemoglobin adducts of acrylamide (HbAA) and its primary metabolite glycidamide (HbGA). Blood samples were analyzed for HbAA and HbGA by HPLC/MS/MS. Statistical models for HbAA and HbGA were developed including body mass index (BMI), educational level, and physical activity. A large variability in acrylamide exposure and metabolism between individuals and country groups was observed with HbAA and HbGA values ranging between 15-623 and 8-377 pmol/g of Hb, respectively. Both adducts differed significantly by country, sex, and smoking status. HbGA values were significantly lower in high alcohol consumers than in moderate consumers. With increasing BMI, HbGA in nonsmokers and HbAA in smokers decreased significantly. In the assessment of potential health effects related to acrylamide exposure, country of origin, BMI, alcohol consumption, sex, and smoking status should be considered.
The role of alcohol intake in the risk of Hodgkin lymphoma (HL) is still largely unclear. To summarize the evidence on the issue, we carried out a meta-analysis of the available studies. We identified eight case-control and two cohort studies, including a total of 1488 cases of HL. We derived meta-analytic estimates using random-effects models, taking into account the correlation between estimates, and carried out a dose-risk analysis using nonlinear random-effects metaregression models. Compared with nondrinkers, the relative risk for alcohol consumers was 0.70 [95% confidence interval (CI), 0.60-0.81] overall, 0.66 (95% CI, 0.56-0.78) among case-control, and 0.92 (95% CI, 0.63-1.33) among cohort studies. Compared with nondrinkers, the pooled relative risks were 0.71 (95% CI, 0.57-0.89) for light (i.e. 1 drink/day) alcohol drinking. This meta-analysis suggests a favourable effect of alcohol on HL, in the absence, however, of a dose-risk relationship. The inverse association was restricted to--or greater in--case-control as compared with cohort studies. This indicates caution in the interpretation of results.
OBJECTIVE: Alcohol consumption is a strong risk factor for oral cancer however; an ambiguous biphasic impact of moderate and excessive alcohol intake on the risk of upper aerodigestive tract cancers has also been published. The aim of the present study was to clarify the dose-related risk of alcohol consumption for oral cancer, in male and female cases.
MATERIALS AND METHODS: Six-hundred and eight non-smoker patients (466 males and 142 females) with squamous cell oral carcinomas (OCs) and 406 non-smoker tumor free controls (264 males and 142 females) were included into the study. Data of three groups; abstinent cases, moderate and excessive alcohol consumers were recorded according to the drinking habits of both OC cases and their controls. Blood glucose levels in male and female cases and menopausal state of women were also registered.
RESULTS: Mean age of female patients was significantly higher than of male cases (p<0.01). Excessive alcohol consumption was a strong risk factor for both sexes, however moderate alcohol intake proved to be an OC risk for men (OR: 1.4) and decreased the OC risk for women (OR: 0.7). Elevated blood glucose level proved to be an OC risk factor for the predominantly postmenopausal women (OR: 1.6), whereas did not affect the OC risk among men.
CONCLUSION: The presented findings are controversial to the hypothesis that women are more vulnerable to alcohol-induced carcinogenesis as compared with men. Increased insulin sensitivity and higher estrogen levels are advantageous systemic effects of moderate ethanol intake and they might reduce the risk for OC in postmenopausal women.
Because studies of the association between alcohol intake and the risk of primary liver cancer use varying cut-off points to classify alcohol intake, it is difficult to precisely quantify this association by meta-analysis of published data. Furthermore, there are limited data for women in prospective studies of the dose-specific relation of alcohol intake and the risk of primary liver cancer. We analyzed original data from 4 population-based prospective cohort studies encompassing 174,719 participants (89,863 men and 84,856 women). After adjustment for a common set of variables, we used Cox proportional hazards regression to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) of primary liver cancer incidence according to alcohol intake. We conducted a meta-analysis of the HRs derived from each study. During 1,964,136 person-years of follow-up, 804 primary liver cancer cases (605 men and 199 women) were identified. In male drinkers, the multivariate-adjusted HRs (95% CI) for alcohol intakes of 0.1-22.9, 23.0-45.9, 46.0-68.9, 69.0-91.9 and >/=92.0 g/day, as compared to occasional drinkers, were 0.88 (0.57-1.36), 1.06 (0.70-1.62), 1.07 (0.69-1.66), 1.76 (1.08-2.87) and 1.66 (0.98-2.82), respectively (p for trend = 0.015). In women, we observed a significantly increased risk among those who drank >/=23.0 g/day, as compared to occasional drinkers (HR: 3.60; 95% CI: 1.22-10.66). This pooled analysis of data from large prospective studies in Japan indicates that avoidance of (1) heavy alcohol drinking (>/=69.0 g alcohol/day) in men and (2) moderate drinking (>/=23.0 g alcohol/day) in women may reduce the risk of primary liver cancer.