• Energy Research

AbstractWe assessed hepatocellular carcinoma (HCC) risk associated with smoking and alcohol consumption and their interactions, using both questionnaire data and objective serum biomarkers. Information on smoking and alcohol consumption was collected at baseline from 450,112 participants of the EPIC cohort, among whom 255 developed HCC after a median follow‐up of 14 years. In a nested case–control subset of 108 HCC cases and 108 matched controls, known biomarkers of smoking (cotinine, nicotine) and habitual alcohol consumption (2‐hydroxy‐3‐methylbutyric acid) were annotated from untargeted metabolomics features. Multivariable‐adjusted hazard ratios (HRs) or odds ratios (ORs) with 95% confidence intervals (CIs) were computed, and multiplicative and additive interaction parameters were calculated. Compared to never smokers, current smokers had a higher HCC risk (HR = 2.46, 95% CI = 1.77–3.43) dose‐dependently with the number of cigarettes smoked per day (Ptrend <.001). Compared to light drinkers, HCC risk was higher in former (HR = 3.20, 95% CI = 1.70–6.03), periodically heavy (HR = 1.98, 95% CI = 1.11–3.54), and always heavy (HR = 5.51, 95% CI = 2.39–12.7) drinkers. Higher HCC risk was also observed in the highest versus the lowest tertiles of cotinine (OR = 4.88, 95% CI = 1.52–15.70), nicotine (OR = 5.80, 95% CI = 1.33–25.30) and 2‐hydroxy‐3‐methylbutyric acid (OR = 5.89, 95% CI = 1.33–26.12). Questionnaire‐assessed smoking and alcohol exposures did not demonstrate an HCC risk interaction at the multiplicative (MI = 0.88, 95% CI = 0.40–1.96) or additive (RERI = 0.71, 95% CI = −10.1 to 23.6; attributable proportion = 0.17, 95% CI = −0.52 to 1.16; synergy index = 1.27, 95% CI = 0.98–1.66) scales. Similar analyses with cotinine, nicotine, and 2‐hydroxy‐3‐methylbutyric acid also did not show interactions between smoking and alcohol consumption on HCC risk. Smoking and alcohol consumption are strong independent risk factors for HCC and do not appear to synergistically impact its risk, but larger studies are needed.

The present study estimated diet-related greenhouse gas emissions (GHGE) and land use (LU) in a sample of adults, examined main dietary contributors of GHGE, and evaluated socio demographic, lifestyle, and wellbeing factors as potential determinants of high environmental impact. A cross-sectional design based on data collected from the European Prospective Investigation into Cancer and Nutrition (EPIC)—Potsdam cohort (2010–2012) was used. Usual diet was assessed using food frequency questionnaires. Diet-related GHGE and LU were calculated using a European-average lifecycle analyses-food-item database (SHARP-ID). Information on potential determinants were collected using self-administered questionnaires. Men (n = 404) and women (n = 401) at an average age of 66.0 ± 8.4 years were included. Dietary-related energy-adjusted GHGE in men was 6.6 ± 0.9 and in women was 7.0 ± 1.1 kg CO2 eq per 2000 kcal. LU in men was 7.8 ± 1.2 and in women was 7.7 ± 1.2 m2/year per 2000 kcal. Food groups contributing to most GHGE included dairy, meat and non-alcoholic beverages. Among women, being single, having a job, being a smoker and having higher BMI were characteristics associated with higher GHGE, whereas for men these included being married, longer sleeping duration and higher BMI. Further studies are warranted to provide insights into population-specific determinants of sustainable dietary choices.