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Abstract The EFSA Panel on Contaminants in the Food Chain (CONTAM) reviewed new studies on nivalenol since the previous opinion on nivalenol published in 2013, but as no new relevant data were identified the tolerable daily intake (TDI) for nivalenol (NIV) of 1.2 μg/kg body weight (bw) established on bases of immuno‐ and haematotoxicity in rats was retained. An acute reference dose (ARfD) of 14 μg/kg bw was established based on acute emetic events in mink. The only phase I metabolite of NIV identified is de‐epoxy‐nivalenol (DE‐NIV) and the only phase II metabolite is nivalenol‐3‐glucoside (NIV3Glc). DE‐NIV is devoid of toxic activity and was thus not further considered. NIV3Glc can occur in cereals amounting up to about 50% of NIV. There are no toxicity data on NIV3Glc, but as it can be assumed that it is hydrolysed to NIV in the intestinal tract it should be included in a group TDI and in a group ARfD with NIV. The uncertainty associated with the present assessment is considered as high and it would rather overestimate than underestimate any risk.

The EFSA Panel on Contaminants in the Food Chain (CONTAM) reviewed new studies on nivalenol since the previous opinion on nivalenol published in 2013, but as no new relevant data were identified the tolerable daily intake (TDI) for nivalenol (NIV) of 1.2 lg/kg body weight (bw) established on bases of immuno- and haematotoxicity in rats was retained. An acute reference dose (ARfD) of 14 lg/kg bw was established based on acute emetic events in mink. The only phase I metabolite of NIV identified is de-epoxy-nivalenol (DE-NIV) and the only phase II metabolite is nivalenol-3-glucoside (NIV3Glc). DE-NIV is devoid of toxic activity and was thus not further considered. NIV3Glc can occur in cereals amounting up to about 50% of NIV. There are no toxicity data on NIV3Glc, but as it can be assumed that it is hydrolysed to NIV in the intestinal tract it should be included in a group TDI and in a group ARfD with NIV. The uncertainty associated with the present assessment is considered as high and it would rather overestimate than underestimate any risk. [ABSTRACT FROM AUTHOR]

Abstract Following a request from the European Commission, the risks to human and animal health related to modified forms of the Fusarium toxins zearalenone, nivalenol, T‐2 and HT‐2 toxins and fumonisins were evaluated. Modified (often called “masked”) mycotoxins are metabolites of the parent mycotoxin formed in the plant or fungus, e.g. by conjugation with polar compounds. Fumonisins, which are difficult to extract from the plant matrix, are also termed modified mycotoxins. The CONTAM Panel considered it appropriate to assess human exposure to modified forms of the various toxins in addition to the parent compounds, because many modified forms are hydrolysed into the parent compounds or released from the matrix during digestion. For modified forms of zearalenone, nivalenol, T‐2 and HT‐2 toxins and fumonisins, 100 %, 30 %, 10 % and 60 % were added, respectively based on reports on the relative contribution of modified forms. The same factors were used for animal exposure from feed. In the absence of specific toxicity data, toxicity equal to the parent compounds was assumed for modified mycotoxins. Risk characterization was done by comparing exposure scenarios with reference doses of the parent compounds. In humans, all lower bound (LB) and upper bound (UB) mean and 95th percentile exposures to the sum of modified and parent toxins were below the respective provisional maximum tolerable daily intakes (PMTDIs) and tolerable daily intakes (TDIs), with two exceptions: for zearalenone and modified zearalenone the UB 95th percentile exposure was up to 2.2‐fold the TDI. For fumonisins and modified fumonisins the exposure of toddlers and other children exceeded the PMTDI at both the LB and the UB estimates, which could be of concern. For farm animal species and pets the exposure to the sum of modified and parent toxins was in general not of concern. The risk in fish could not be addressed. The CONTAM Panel identified several uncertainties and data gaps for modified mycotoxins.

Nivalenol is a mycotoxin produced by various Fusarium species. The European Commission (EC) asked the European Food Safety Authority (EFSA) for a scientific opinion on the risk to human and animal health related to the presence of nivalenol in food and feed. A total of 13 164 results for nivalenol in food, feed and unprocessed grains, collected in 2001-2011 from 18 European countries, were available for the evaluation. The highest mean concentrations for nivalenol were observed in oats, maize, barley and wheat and products thereof. Grains and grain-based foods, in particular bread and rolls, grain milling products, pasta, fine bakery wares and breakfast cereals, made the largest contribution to nivalenol exposure for humans. Animal exposure to nivalenol is primarily from consuming cereal grains and cereal by-products. The available information on the toxicokinetics of nivalenol is incomplete. Evidence exists for metabolic de-epoxidation in some species. Based on the data available, the Panel on Contaminants in the Food Chain (CONTAM Panel) concluded that the overall weight of evidence is that nivalenol is unlikely to be genotoxic. Toxic effects of nivalenol include immunotoxicity and haematotoxicity. A reduction in white blood cell (WBC) counts in a 90-day rat study was identified as the critical effect for human risk assessment. Using these data and a benchmark dose analysis the CONTAM Panel established a tolerable daily intake (TDI) of 1.2 µg/kg b.w. per day. All chronic human dietary exposures to nivalenol estimated, based on the available occurrence data in food, are below the TDI, and are therefore not a health concern. No toxicity data were identified for ruminants, rabbits, fish and companion animals but lowest-observed-adverse-effect levels were identified in pigs and poultry. Based on estimates of exposure the risk of adverse health effects of feed containing nivalenol is low for both these species.

Following a request from the European Commission, the risks to human and animal health related to modified forms of the Fusarium toxins zearalenone, nivalenol, T-2 and HT-2 toxins and fumonisins were evaluated. Modified (often called 'masked') mycotoxins are metabolites of the parent mycotoxin formed in the plant or fungus, e.g. by conjugation with polar compounds. Fumonisins, which are difficult to extract from the plant matrix, are also termed modified mycotoxins. The CONTAM Panel considered it appropriate to assess human exposure to modified forms of the various toxins in addition to the parent compounds, because many modified forms are hydrolysed into the parent compounds or released from the matrix during digestion. For modified forms of zearalenone, nivalenol, T-2 and HT-2 toxins and fumonisins, 100 %, 30 %, 10 % and 60 % were added, respectively based on reports on the relative contribution of modified forms. The same factors were used for animal exposure from feed. In the absence of specific toxicity data, toxicity equal to the parent compounds was assumed for modified mycotoxins. Risk characterization was done by comparing exposure scenarios with reference doses of the parent compounds. In humans, all lower bound (LB) and upper bound (UB) mean and 95th percentile exposures to the sum of modified and parent toxins were below the respective provisional maximum tolerable daily intakes (PMTDIs) and tolerable daily intakes (TDIs), with two exceptions: for zearalenone and modified zearalenone the UB 95th percentile exposure was up to 2.2-fold the TDI. For fumonisins and modified fumonisins the exposure of toddlers and other children exceeded the PMTDI at both the LB and the UB estimates, which could be of concern. For farm animal species and pets the exposure to the sum of modified and parent toxins was in general not of concern. The risk in fish could not be addressed. The CONTAM Panel identified several uncertainties and data gaps for modified mycotoxins. [ABSTRACT FROM AUTHOR]

Nivalenol is a mycotoxin produced by various Fusarium species. The European Commission (EC) asked the European Food Safety Authority (EFSA) for a scientific opinion on the risk to human and animal health related to the presence of nivalenol in food and feed. A total of 13 164 results for nivalenol in food, feed and unprocessed grains, collected in 2001-2011 from 18 European countries, were available for the evaluation. The highest mean concentrations for nivalenol were observed in oats, maize, barley and wheat and products thereof. Grains and grain-based foods, in particular bread and rolls, grain milling products, pasta, fine bakery wares and breakfast cereals, made the largest contribution to nivalenol exposure for humans. Animal exposure to nivalenol is primarily from consuming cereal grains and cereal by-products. The available information on the toxicokinetics of nivalenol is incomplete. Evidence exists for metabolic de-epoxidation in some species. Based on the data available, the Panel on Contaminants in the Food Chain (CONTAM Panel) concluded that the overall weight of evidence is that nivalenol is unlikely to be genotoxic. Toxic effects of nivalenol include immunotoxicity and haematotoxicity. A reduction in white blood cell (WBC) counts in a 90-day rat study was identified as the critical effect for human risk assessment. Using these data and a benchmark dose analysis the CONTAM Panel established a tolerable daily intake (TDI) of 1.2 µg/kg b.w. per day. All chronic human dietary exposures to nivalenol estimated, based on the available occurrence data in food, are below the TDI, and are therefore not a health concern. No toxicity data were identified for ruminants, rabbits, fish and companion animals but lowest-observed-adverse-effect levels were identified in pigs and poultry. Based on estimates of exposure the risk of adverse health effects of feed containing nivalenol is low for both these species. [ABSTRACT FROM AUTHOR]