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The European Commission asked EFSA for a risk assessment on complex organoarsenic species in food. They are typically found in marine foods and comprise mainly arsenobetaine (AsB), arsenosugars and arsenolipids. For AsB, no reference point (RP) could be derived because of insufficient toxicity data. AsB did not show adverse effects in the two available repeat dose toxicity tests in rodents. It has not shown genotoxicity in in vitro assays. There is no indication of an association with adverse outcomes in human studies. The highest 95th percentile exposure for AsB was observed in ‘Toddlers’ with an estimate of 12.5 μg As/kg bw per day (AsB expressed as elemental arsenic). There is sufficient evidence to conclude that AsB at current dietary exposure levels does not raise a health concern. For glycerol arsenosugar (AsSugOH) a RP of 0.85 mg As/kg bw per day was derived based on the BMDL10 values for cognitive and motor function in mice. A margin of exposure (MOE) of ≥ 1000 would not raise a health concern. The highest 95th percentile estimate of exposure for AsSugOH (for adult consumers of red seaweed Nori/Laver) was 0.71 μg As/kg bw per day (AsSugOH expressed as elemental arsenic), which results in an MOE > 1000, not raising a health concern. Based on qualitative consideration of all identified uncertainties, it is regarded likely that the dietary exposures to AsB and AsSugOH do not raise a health concern. No conclusions could be drawn regarding other arsenosugars. No risk characterisation could be conducted for arsenolipids, due to the lack of data.
The European Commission asked EFSA for a risk assessment on complex organoarsenic species in food. They are typically found in marine foods and comprise mainly arsenobetaine (AsB), arsenosugars and arsenolipids. For AsB, no reference point (RP) could be derived because of insufficient toxicity data. AsB did not show adverse effects in the two available repeat dose toxicity tests in rodents. It has not shown genotoxicity in in vitro assays. There is no indication of an association with adverse outcomes in human studies. The highest 95th percentile exposure for AsB was observed in ‘Toddlers’ with an estimate of 12.5 μg As/kg bw per day (AsB expressed as elemental arsenic). There is sufficient evidence to conclude that AsB at current dietary exposure levels does not raise a health concern. For glycerol arsenosugar (AsSugOH) a RP of 0.85 mg As/kg bw per day was derived based on the BMDL10 values for cognitive and motor function in mice. A margin of exposure (MOE) of ≥ 1000 would not raise a health concern. The highest 95th percentile estimate of exposure for AsSugOH (for adult consumers of red seaweed Nori/Laver) was 0.71 μg As/kg bw per day (AsSugOH expressed as elemental arsenic), which results in an MOE > 1000, not raising a health concern. Based on qualitative consideration of all identified uncertainties, it is regarded likely that the dietary exposures to AsB and AsSugOH do not raise a health concern. No conclusions could be drawn regarding other arsenosugars. No risk characterisation could be conducted for arsenolipids, due to the lack of data.
This risk profile identifies and characterises the primary hazards associated with shell eggs and egg products (EEPs) imported into the United Kingdom (UK) from domestic poultry species. The scope includes liquid, dry, cooked, and preserved egg products, excluding composite foods containing eggs or egg products. The document aims to provide essential background information on food safety concerns related to imported EEPs, support the assessment of market access requests for exporting EEPs to the UK, and assist in audit and assurance activities for EEP imports. A comprehensive literature review and analysis of incident and alert data identified over 100 potential hazards in eggs. Through expert judgement and inclusion criteria, 22 key hazards were shortlisted for characterisation. The microbiological hazards characterised include Campylobacter spp., Listeria monocytogenes, and non-typhoidal Salmonella (Salmonella Enteritidis and Salmonella Typhimurium), with Salmonella Enteritidis being the most frequently reported hazard. Chemical hazards characterised include agricultural contaminants (aflatoxins, ochratoxin A, pyrrolizidine alkaloids), biocides (fipronil, chlorate), environmental contaminants (persistent organic pollutants, melamine, metals), and various pesticides, veterinary medicinal products, and feed additives. Risk factors for microbiological hazards include hygiene and biosecurity failures, flock age and size, and environmental conditions. Chemical hazards are linked to environmental exposure and misuse of substances. Mitigation measures for microbiological hazards include eradication and vaccination programmes, while chemical hazard mitigation focuses on environmental controls and monitoring programmes. Regulatory measures in Great Britain and Northern Ireland are in place to control both chemical and microbiological hazards in eggs. This risk profile supports the Department for Environment, Food and Rural Affairs (DEFRA) and the Food Standards Agency (FSA) in ensuring the safety of imported EEPs and guiding market access and audit activities.
Introduction. Cyprodinil is a broad-spectrum systemic fungicide of the anilinopyrimidine class. Available literature data on the genotoxicity of this pesticide are contradictory. The aim of the work is to study the cytotoxic and genotoxic effects of ciprodinil. Material and methods. The mutation activity of cyprodinil was assessed in the Ames test. The level of DNA fragmentation in peripheral blood lymphocytes was determined by conducting alkaline gel electrophoresis of individual cells (DNA comet assay). Cell viability was assessed using a TC20 cell counter (BioRad). The ADAMII LS automated fluorescent cell analyzer (Nano Entek) was used to determine the pathways of cell death. Results. Cyprodinil has a cytotoxic effect on S. typhimurium bacterial cells starting from a concentration of 1.6 mg/ cup under metabolic activation conditions and at concentrations of 0.5 mg/cup and higher in the absence of the S9 mixture. No mutagenic effect was detected in the Ames test. The level of DNA breaks in peripheral blood lymphocytes (%, Tail Intensity) increased compared to the control after their cultivation in a medium with cyprodinil at a concentration of 100 μg/ml in the absence of metabolic activation. In this case, 70 to 95% of the cells died by apoptosis and necrosis. Limitations. The study is limited to in vitro cytotoxicity and genotoxicity assessment of cyprodinil only. Conclusion. Cyprodinil does not have a genotoxic effect. The observed increase in the level of DNA breaks in peripheral blood lymphocytes in vitro in the presence of cyprodinil is a consequence of the general toxic effect, which can lead to the destruction of cellular structures, the release of enzymes, including endonucleases, causing DNA breaks.
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