Since the first version of the dietary inflammatory index (DII®) developed in the past decade, several other versions have been developed. However, to date no study has attempted to compare these versions with respect to their associations with biomarkers of inflammation. We aimed to investigate the relationship between four dietary inflammatory scores [DII, two energy-adjusted derivatives (E-DII and E-DII_r), and the Inflammatory Score of the Diet (ISD)], and circulating levels of several inflammatory markers and adipokines. This study included 17 637 participants from the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort with at least one marker of inflammation measured in blood. Associations between the four scores and C-reactive protein (CRP), interleukin (IL)6, IL10, IL1RA, tumor necrosis factor-α (TNFα), soluble tumor necrosis factor receptor-1 (sTNFR1), sTNFR2, leptin, soluble leptin receptor (sLeptin R), adiponectin, and High Molecular Weight (HMW) adiponectin were evaluated using multivariable linear regressions adjusted for potential confounders. Positive associations were observed between the four dietary inflammatory scores and levels of CRP, IL6, sTNFR1, sTNFR2 and leptin. However, only the DII and the ISD were positively associated with IL1RA levels and only the DII and the E-DII_r were positively associated with TNFα levels. The proportion of variance of each biomarker explained by the scores was lower than 2%, which was equivalent to the variance explained by smoking status but much lower than that explained by body mass index. Our results suggest that the four dietary inflammatory scores were associated with some biomarkers of inflammation and could be used to assess the inflammatory potential of diet in European adults but are not sufficient to capture the inflammatory status of an individual. These findings can help to better understand the inflammatory potential of diet, but they need to be replicated in studies with repeated dietary measurements.

Mycotoxins have been hypothesized to contribute to a diversity of adverse health effects in humans, even at low concentrations. Certain mycotoxins are established human carcinogens, whereas for others research suggests potential carcinogenic effects. The aim of this study was to determine the association between dietary exposure to mycotoxins and hepatobiliary cancers in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. EPIC questionnaire data were matched to mycotoxin food occurrence data compiled by the European Food Safety Authority to assess long-term dietary mycotoxin exposure (expressed as μg/kg body weight/day) and then relate them to the risk of hepatocellular carcinoma (HCC) (n = 255) and biliary tract cancers (n = 273). Analyses were conducted using multivariable Cox proportional hazards regression models to compute hazard ratios (HR) and 95% confidence intervals (95% CI). Key food groups contributing to mycotoxin exposure were cereals and cereal-based products, vegetables, non-alcoholic beverages (including fruit juices) and fruits. Estimated intake of deoxynivalenol (DON) and its derivatives was positively associated with HCC risk (HR_T3vsT1: 1.90, 95% CI: 1.18–3.05, p-trend <0.01). No statistically significant associations were found for the other mycotoxins. Further research to confirm our observations and investigate potential underlying mechanisms of these compounds is warranted. These data may provide evidence of HCC risks associated with higher dietary intake levels of DON, which has not yet been classified as a human carcinogen.

While there is compelling evidence of the association between occupational exposure to polycyclic aromatic hydrocarbons (PAHs) and risk of breast cancer (BC), findings on PAH dietary exposure are less consistent. The present study aims to evaluate the association between PAH dietary intake and BC risk. The study included 67,879 women who completed a validated semi-quantitative dietary questionnaire (208 food items) from the E3N-Generations cohort study. PAH dietary intake was estimated by combining E3N food consumption data with food contamination levels obtained from the second French total diet study (TDS2). Cox regression was used to estimate adjusted hazard ratios (HRs) and 95 % confidence intervals (CIs) for the association between PAH dietary intake (sum of four PAHs (PAH₄) namely benzo[a]pyrene (BaP), chrysene (CHR), benzo[a]anthracene (BaA) and benzo[b]fluoranthene (BbF)) and BC risk. Additionally, BaP, a surrogate for total PAHs, was investigated as the second exposure variable. After an average follow-up of 17.6 years, 5,686 incident BC were diagnosed. Overall, the estimated HRs for the associations between each quintile of PAH₄ and BC risk, taking the first quintile as reference, were all greater than 1, but were statistically significant only for the third quintile (HR_{Q3 vs Q1} = 1.10; CI: 1.01-1.20). By estrogen (ER) and progesterone (PR) hormone receptor status, we observed a positive association between PAH₄ dietary intake and ER-PR- BC (HR_{Q4 vs Q1} = 1.34; CI: 1.01-1.76). Moreover, there was a borderline positive association with BaP, for the second (HR_{Q2 vs Q1} = 1.08; CI: 0.99-1.17) and third (HR_{Q3 vs Q1} = 1.07; CI: 0.98-1.16) quintiles. This study supports a relationship between PAH₄ dietary intake and BC risk, notably with a non-linear trend. A positive but marginal association was observed between BaP dietary intake and BC risk.