The association between renal cell cancer (RCC) and intake of fruit, vegetables and nutrients was examined in a population-based case–control study of 323 cases and 1827 controls; dietary intake was obtained using a mailed questionnaire. Cancer risks were estimated by OR and 95 % CI, adjusting for age, sex, smoking, obesity, hypertension, proxy status, alcohol consumption and dietary fat intake and energy. Intake of vegetables was associated with a decreased risk of RCC (OR 0·5; 95 % CI 0·3, 0·7; Ptrend = 0·002), (top compared to the bottom quartile of intake). When intake of individual nutrients was investigated, vegetable fibre intake was associated with decreased risks (OR 0·4; 95 % CI 0·2, 0·6; P < 0·001), but this was not the case with fruit fibre (OR 0·7; 95 % CI 0·4, 1·1) or grain fibre (OR 1·0; 95 % CI 0·6, 1·5). β-Cryptoxanthin and lycopene were also associated with decreased risks, but when both were included in a mutually adjusted backwards stepwise regression model, only β-cryptoxanthin remained significant (OR 0·5; 95 % CI 0·3, 0·8). When other micronutrients and types of fibre were investigated together, only vegetable fibre and β-cryptoxanthin had significant trends (P < 0·01) (OR 0·6; 95 % CI 0·3, 0·9) (OR 0·5; 95 % CI 0·3, 0·9), respectively. These findings were stronger in those aged over 65 years (Pinteraction = 0·001). Among non-smokers, low intake of cruciferous vegetables and fruit fibre was also associated with increased risk of RCC (Pinteraction = 0·03); similar inverse associations were found for β-cryptoxanthin, lycopene and vitamin C. When nutrients were mutually adjusted by backwards regression in these subgroups, only β-cryptoxanthin remained associated with lower RCC risk. These findings deserve further investigation in ongoing prospective studies when sample size becomes sufficient.

In contrast to some extensively examined food mutagens, for example, aflatoxins, N-nitrosamines and heterocyclic amines, some other food contaminants, in particular polycyclic aromatic hydrocarbons (PAH) and other aromatic compounds, have received less attention. Therefore, exploring the relationships between dietary habits and the levels of biomarkers related to exposure to aromatic compounds is highly relevant. We have investigated in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort the association between dietary items (food groups and nutrients) and aromatic DNA adducts and 4-aminobiphenyl-Hb adducts. Both types of adducts are biomarkers of carcinogen exposure and possibly of cancer risk, and were measured, respectively, in leucocytes and erythrocytes of 1086 (DNA adducts) and 190 (Hb adducts) non-smokers. An inverse, statistically significant, association has been found between DNA adduct levels and dietary fibre intake (P = 0·02), vitamin E (P = 0·04) and alcohol (P = 0·03) but not with other nutrients or food groups. Also, an inverse association between fibre and fruit intake, and BMI and 4-aminobiphenyl-Hb adducts (P = 0·03, 0·04, and 0·03 respectively) was observed. After multivariate regression analysis these inverse correlations remained statistically significant, except for the correlation adducts v. fruit intake. The present study suggests that fibre intake in the usual range can modify the level of DNA or Hb aromatic adducts, but such role seems to be quantitatively modest. Fibres could reduce the formation of DNA adducts in different manners, by diluting potential food mutagens and carcinogens in the gastrointestinal tract, by speeding their transit through the colon and by binding carcinogenic substances.

Nicotine has been shown to improve various aspects of cognitive processing such as attention and memory, however, its effects on lexical-semantic processing are relatively uncharted. Recent investigations of mnemonic processing in minimally deprived smokers suggest that nicotine might selectively modulate processes concerned with associative memory. This study investigated the effects of nicotine on lexical-semantic processing in non-smokers using a strategy-based lexical-decision priming paradigm. Transdermal nicotine patches (7 mg/24 h) were administered within a double-blind, placebo-controlled, cross-over design. Participants were trained to expect target words to come from a specified semantic category based on the prime word, although in some instances trained expectations were not met. Participants were presented with the stimuli at either a short or long stimulus onset asynchrony (SOA) to target automatic and attentional processing, respectively (n=12 and 17 for the short and long SOAs, respectively). Nicotine was found to selectively affect priming condition reaction times at the long SOA, indicating a nicotinic modulation of attentional mechanisms. Specifically, facilitation effects were dominant under placebo compared to a dominance of inhibition effects under nicotine. These results suggest that nicotine supports inhibitory attentional mechanisms in cognitively demanding semantic processing paradigms.