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Temme E.H.,The National Institute for Public Health and the Environment RIVM
Environmental health : a global access science source

Food choices influence health status, but also have a great impact on the environment. The production of animal-derived foods has a high environmental burden, whereas the burden of refined carbohydrates, vegetables and fruit is low. The aim of this study was to investigate the associations of greenhouse gas emission (GHGE) and land use of usual diet with mortality risk, and to estimate the effect of a modelled meat substitution scenario on health and the environment. The usual diet of 40011 subjects in the EPIC-NL cohort was assessed using a food frequency questionnaire. GHGE and land use of food products were based on life cycle analysis. Cox proportional hazard ratios (HR) were calculated to determine relative mortality risk. In the modelled meat-substitution scenario, one-third (35 gram) of the usual daily meat intake (105 gram) was substituted by other foods. During a follow-up of 15.9 years, 2563 deaths were registered. GHGE and land use of the usual diet were not associated with all-cause or with cause-specific mortality. Highest vs. lowest quartile of GHGE and land use adjusted hazard ratios for all-cause mortality were respectively 1.00 (95% CI: 0.86-1.17) and 1.05 (95% CI: 0.89-1.23). Modelled substitution of 35 g/d of meat with vegetables, fruit-nuts-seeds, pasta-rice-couscous, or fish significantly increased survival rates (6-19%), reduced GHGE (4-11%), and land use (10-12%). There were no significant associations observed between dietary-derived GHGE and land use and mortality in this Dutch cohort. However, the scenario-study showed that substitution of meat with other major food groups was associated with a lower mortality risk and a reduced environmental burden. Especially when vegetables, fruit-nuts-seeds, fish, or pasta-rice-couscous replaced meat. Source

Bayer C.,Robert Koch Institute | Bayer C.,U.S. Center for Disease Control and Prevention | Bernard H.,Robert Koch Institute | Prager R.,Robert Koch Institute | And 9 more authors.

The largest Salmonella enterica serovar Newport outbreak (n=106) ever reported in Germany occurred in October and November 2011. Twenty associated cases were reported in the Netherlands. The outbreak investigation included an analytical epidemiological study, molecular typing of human and food isolates and food traceback investigations. Unspecified Salmonella had been detected in samples of mung bean sprouts at a sprout producer (producer A) in the Netherlands and mung bean sprouts contaminated with S. Newport had been found during routine sampling at a sprout distributor in Germany. Therefore, we tested the hypothesis of sprouts being the infection vehicle. In a case-control study, we compared 50 notified adult S. Newport cases with 45 Salmonella enterica serovar Enteritidis cases regarding their food consumption in the three days before illness. In multivariable logistic regression analysis, only sprout consumption was significantly associated with S. Newport infection (odds ratio: 18.4; 95% confidence interval: 2.2-150.2). Molecular typing patterns of human isolates were indistinguishable from a mung bean sprouts isolate. Traceback of sprouts led to distributors and producer A in the Netherlands. Since sprouts are frequently contaminated with microorganisms, consumers need to be aware that consumption of raw or insufficiently cooked sprouts may pose a health risk. Source

Fredriksson L.,Leiden University | Wink S.,Leiden University | Herpers B.,Leiden University | Benedetti G.,Leiden University | And 8 more authors.
Toxicological Sciences

Drug-induced liver injury (DILI) is an important clinical problem. Here, we used a genomics approach to in detail investigate the hypothesis that critical drug-induced toxicity pathways act in synergy with the pro-inflammatory cytokine tumor necrosis factor α (TNFα) to cause cell death of liver HepG2 cells. Transcriptomics of the cell injury stress response pathways initiated by two hepatoxicants, diclofenac and carbamazepine, revealed the endoplasmic reticulum (ER) stress/translational initiation signaling and nuclear factor-erythroid 2 (NF-E2)-related factor 2 (Nrf2) antioxidant signaling as two major affected pathways, which was similar to that observed for the majority of ~80 DILI compounds in primary human hepatocytes. Compounds displaying weak or no TNFα synergism, namely ketoconazole, nefazodone, and methotrexate, failed to synchronously induce both pathways. The ER stress induced was primarily related to protein kinase R-like ER kinase (PERK) and activating transcription factor 4 (ATF4) activation and subsequent expression of C/EBP homologous protein (CHOP), which was all independent of TNFα signaling. Identical ATF4 dependent transcriptional programs were observed in primary human hepatocytes as well as primary precisioncut human liver slices. Targeted RNA interference studies revealed that whereas ER stress signaling through inositol-requiring enzyme 1α (IRE1α) and activating transcription factor 6 (ATF6) acted cytoprotective, activation of the ER stress protein kinase PERK and subsequent expression of CHOP was pivotal for the onset of drug/TNFα-induced apoptosis. Whereas inhibition of the Nrf2-dependent adaptive oxidative stress response enhanced the drug/TNFα cytotoxicity, Nrf2 signaling did not affect CHOP expression. Both hepatotoxic drugs enhanced expression of the translational initiation factor EIF4A1, which was essential for CHOP expression and drug/TNFα-mediated cell killing. Our data support a model in which enhanced drug-induced translation initiates PERK-mediated CHOP signaling in an EIF4A1 dependent manner, thereby sensitizing toward caspase-8-dependent TNFα- induced apoptosis. © The Author 2014. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. Source

Murphy N.,Imperial College London | Norat T.,Imperial College London | Ferrari P.,International Agency for Research on Cancer IARC WHO | Jenab M.,International Agency for Research on Cancer IARC WHO | And 52 more authors.

Background: Earlier analyses within the EPIC study showed that dietary fibre intake was inversely associated with colorectal cancer risk, but results from some large cohort studies do not support this finding. We explored whether the association remained after longer follow-up with a near threefold increase in colorectal cancer cases, and if the association varied by gender and tumour location. Methodology/Principal Findings: After a mean follow-up of 11.0 years, 4,517 incident cases of colorectal cancer were documented. Total, cereal, fruit, and vegetable fibre intakes were estimated from dietary questionnaires at baseline. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using Cox proportional hazards models stratified by age, sex, and centre, and adjusted for total energy intake, body mass index, physical activity, smoking, education, menopausal status, hormone replacement therapy, oral contraceptive use, and intakes of alcohol, folate, red and processed meats, and calcium. After multivariable adjustments, total dietary fibre was inversely associated with colorectal cancer (HR per 10 g/day increase in fibre 0.87, 95% CI: 0.79-0.96). Similar linear associations were observed for colon and rectal cancers. The association between total dietary fibre and risk of colorectal cancer risk did not differ by age, sex, or anthropometric, lifestyle, and dietary variables. Fibre from cereals and fibre from fruit and vegetables were similarly associated with colon cancer; but for rectal cancer, the inverse association was only evident for fibre from cereals. Conclusions/Significance: Our results strengthen the evidence for the role of high dietary fibre intake in colorectal cancer prevention. © 2012 Murphy et al. Source

Babisch W.,Federal Environment Agency | Pershagen G.,Karolinska Institutet | Selander J.,Karolinska Institutet | Houthuijs D.,The National Institute for Public Health and the Environment RIVM | And 9 more authors.
Science of the Total Environment

Objectives: The effect modifying impact of annoyance due to aircraft noise and road traffic noise on the relationships between the aircraft noise level and road traffic noise level on the prevalence of hypertension was investigated in 4861 subjects of the HYENA study (HYpertension and Exposure to Noise near Airports). Methods: Different models were investigated either including the noise level and noise annoyance variables separately, or simultaneously, or together with an interaction term referring to the same noise source for the noise level and the noise annoyance. Results: Significant effect modification was found with respect to the association between aircraft noise and hypertension. The association was stronger in more annoyed subjects. No clear interaction was found with respect to road traffic noise. The comparison of the magnitude of the main effects (per standard deviation or inter-quartile range) of noise level and noise annoyance variables revealed stronger associations with hypertension for the noise levels. Conclusion: There is some indication that the noise level has a stronger predictive meaning for the relationship between noise exposure and hypertension than the reported noise annoyance (main effects). The results from the Hyena study support the hypothesis that noise annoyance acts as an effect modifier of the relationship between the noise level and hypertension. © 2013 Elsevier B.V. Source

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