Arsenic in drinking water is a public health issue affecting hundreds of millions of people worldwide. This review summarizes 30 years of epidemiological studies on arsenic exposure in drinking water and the risk of bladder or kidney cancer, quantifying these risks using a meta-analytical framework. Forty studies met the selection criteria. Seventeen provided point estimates of arsenic concentrations in drinking water and were used in a meta-analysis of bladder cancer incidence (7 studies) and mortality (10 studies) and kidney cancer mortality (2 studies). Risk estimates for incidence and mortality were analyzed separately using Generalized Linear Models. Predicted risks for bladder cancer incidence were estimated at 10, 50 and 150 μg/L arsenic in drinking water. Bootstrap randomizations were used to assess robustness of effect size. Twenty-eight studies observed an association between arsenic in drinking water and bladder cancer. Ten studies showed an association with kidney cancer, although of lower magnitude than that for bladder cancer. The meta-analyses showed the predicted risks for bladder cancer incidence were 2.7 [1.2–4.1]; 4.2 [2.1–6.3] and; 5.8 [2.9–8.7] for drinking water arsenic levels of 10, 50, and 150 μg/L, respectively. Bootstrapped randomizations confirmed this increased risk, but, lowering the effect size to 1.4 [0.35–4.0], 2.3 [0.59–6.4], and 3.1 [0.80–8.9]. The latter suggests that with exposures to 50 μg/L, there was an 83% probability for elevated incidence of bladder cancer; and a 74% probability for elevated mortality. For both bladder and kidney cancers, mortality rates at 150 ug/L were about 30% greater than those at 10 μg/L. Arsenic in drinking water is associated with an increased risk of bladder and kidney cancers, although at lower levels (<150 μg/L), there is uncertainty due to the increased likelihood of exposure misclassification at the lower end of the exposure curve. Meta-analyses suggest exposure to 10 μg/L of arsenic in drinking water may double the risk of bladder cancer, or at the very least, increase it by about 40%. With the large number of people exposed to these arsenic concentrations worldwide the public health consequences of arsenic in drinking water are substantial.

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Arsenic in drinking water and urinary tract cancers: a systematic review of 30 years of epidemiological evidence.

Helicobacter pylori is a major human pathogen for which increasing antibiotic resistance constitutes a serious threat to human health. Molecular mechanisms underlying this resistance have been intensively studied and are discussed in this Review. Three profiles of resistance — single drug resistance, multidrug resistance and heteroresistance — seem to occur, probably with overlapping fundamental mechanisms and clinical implications. The mechanisms that have been most studied are related to mutational changes encoded chromosomally and disrupt the cellular activity of antibiotics through target-mediated mechanisms. Other biological attributes driving drug resistance in H. pylori have been less explored and this could imply more complex physiological changes (such as impaired regulation of drug uptake and/or efflux, or biofilm and coccoid formation) that remain largely elusive. Resistance-related attributes deployed by the pathogen cause treatment failures, diagnostic difficulties and ambiguity in clinical interpretation of therapeutic outcomes. Subsequent to the increasing antibiotic resistance, a substantial drop in H. pylori treatment efficacy has been noted globally. In the absence of an efficient vaccine, enhanced efforts are needed for setting new treatment strategies and for a better understanding of the emergence and spread of drug-resistant bacteria, as well as for improving diagnostic tools that can help optimize current antimicrobial regimens. Increasing levels of antibiotic resistance in Helicobacter pylori are a serious threat to human health globally. This Review discusses H. pylori infection and antibiotic resistance, and provides insights into the underlying mechanisms and clinical implications (including detection and management).

Helicobacter pylori infection and antibiotic resistance - from biology to clinical implications.

Following a request from the European Commission to EFSA, the EFSA Scientific Committee (SC) prepared a guidance for the risk assessment of substances present in food intended for infants below 16 weeks of age. In its approach to develop this guidance, the EFSA SC took into account, among others, (i) an exposure assessment based on infant formula as the only source of nutrition; (ii) knowledge of organ development in human infants, including the development of the gut, metabolic and excretory capacities, the brain and brain barriers, the immune system, the endocrine and reproductive systems; (iii) the overall toxicological profile of the substance identified through the standard toxicological tests, including critical effects; (iv) the relevance for the human infant of the neonatal experimental animal models used. The EFSA SC notes that during the period from birth up to 16 weeks, infants are expected to be exclusively fed on breast milk and/or infant formula. The EFSA SC views this period as the time where health-based guidance values for the general population do not apply without further considerations. High infant formula consumption per body weight is derived from 95th percentile consumption. The first weeks of life is the time of the highest relative consumption on a body weight basis. Therefore, when performing an exposure assessment, the EFSA SC proposes to use the high consumption value of 260 mL/kg bw per day. A decision tree approach is proposed that enables a risk assessment of substances present in food intended for infants below 16 weeks of age. The additional information needed when testing substances present in food for infants below 16 weeks of age and the approach to be taken for the risk assessment are on a case-by-case basis, depending on whether the substance is added intentionally to food and is systemically available.

https://efsa.onlinelibrary.wiley.com/doi/pdf/10.2903/j.efsa.2017.4849

Guidance on the risk assessment of substances present in food intended for infants below 16 weeks of age.

Acrylamide-forming potential of potatoes grown at different locations, and the ratio of free asparagine to reducing sugars at which free asparagine becomes a limiting factor for acrylamide formation.

The integration of terpyridyl and tricarboxylate functionality in a novel ligand allows concerted 3:1 stoichiometric assembly of size-and charge-complementary Zn2+/Tb3+ ions into a water-stable 3D luminescent framework (CTGU-8) capable of highly selective, sensitive, and recyclable of nitrofurans.

Ligand-Controlled Integration of Zn and Tb by Photoactive Terpyridyl-Functionalized Tricarboxylates as Highly Selective and Sensitive Sensors for Nitrofurans.

Nitrofurans are antimicrobial agents not authorised for use in food-producing animals in the European Union Nitrofurans are rapidly metabolised, occurring in animal tissues as protein-bound metabolites The European Commission requested EFSA to provide a scientific opinion on the risks to human health related to the presence of nitrofurans in food and whether a reference point for action (RPA) of 10 μg/kg for the marker metabolites is adequate to protect public health Data on occurrence of nitrofuran marker metabolites in food were extracted from the national residue monitoring plan results and from the Rapid Alert System for Food and Feed (RASFF) The CONTAM Panel concluded that these data were too limited to carry out a reliable human dietary exposure assessment Instead, human dietary exposure was calculated for a scenario in which a single nitrofuran marker metabolite is present at 10 μg/kg in foods of animal origin, excluding milk and dairy products The mean chronic dietary exposure for this worst-case scenario would range from 33 to 80 and 19 to 43 ng/kg bw per day for toddlers and adults, respectively Nitrofurans and their marker metabolites, generally, are genotoxic and carcinogenic and, also, have non-neoplastic effects in animals Margins of exposure (MOEs) were calculated at 20 × 105 or greater for carcinogenicity and at 25 × 103 or greater for non-neoplastic effects The CONTAM Panel concluded that it is unlikely that exposure to food contaminated with nitrofuran marker metabolites at or below 10 μg/kg is a health concern A scenario in which foods are considered to be contaminated with semicarbazide, from use of carrageenan as a food additive, at 1 μg/kg was used to assess whether it is appropriate to apply the RPA to foods of non-animal origin; MOEs of greater than 104 calculated for non-neoplastic effects do not indicate a health concern

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Efsa Contam Panel

Papers

Scientific Opinion on nitrofurans and their metabolites in food