Search

This statement describes the approach followed by the EFSA Panel on Food Additives and Nutrient Sources added to Food (ANS) for performing refined exposure assessment in the framework of the re‐evaluation of already permitted food additives. Estimation of exposure is obtained through combination of different type of data originating from different sources: food additive concentration is obtained from information provided to EFSA on use levels and/or information obtained by means of analytical measurements. In recent years, the use of market research data has also been used. The statement provides also a description of the three different scenarios used for the exposure assessment of food additives under re‐evaluation, from the more conservative regulatory maximum level exposure assessment scenario to more refined ones. Lastly, a description is provided on the approach used for the uncertainty analysis which accompanies the exposure assessment. [ABSTRACT FROM AUTHOR]

Following a request from the European Commission, the EFSA Panel on Food Additives and Nutrient sources added to Food (ANS) was asked to deliver a scientific opinion on the re‐evaluation of 12 modified starches (E 1404, E 1410, E 1412, E 1413, E 1414, E 1420, E 1422, E 1440, E 1442, E 1450, E 1451 and E 1452) authorised as food additives in the EU in accordance with Regulation (EC) No 1333/2008 and previously evaluated by JECFA and the SCF. Both committees allocated an acceptable daily intake (ADI) ‘not specified’. In humans, modified starches are not absorbed intact but significantly hydrolysed by intestinal enzymes and then fermented by the intestinal microbiota. Using the read‐across approach, the Panel considered that adequate data on short‐ and long‐term toxicity and carcinogenicity, and reproductive toxicity are available. Based on in silico analyses, modified starches are considered not to be of genotoxic concern. No treatment‐related effects relevant for human risk assessment were observed in rats fed very high levels of modified starches (up to 31,000 mg/kg body weight (bw) per day). Modified starches (e.g. E 1450) were well tolerated in humans up to a single dose of 25,000 mg/person. Following the conceptual framework for the risk assessment of certain food additives, the Panel concluded that there is no safety concern for the use of modified starches as food additives at the reported uses and use levels for the general population and that there is no need for a numerical ADI. The combined exposure to E 1404–E 1451 at the 95th percentile of the refined (brand‐loyal) exposure assessment scenario for the general population was up to 3,053 mg/kg bw per day. Exposure to E 1452 for food supplement consumers only at the 95th percentile was up to 22.1 mg/kg bw per day. [ABSTRACT FROM AUTHOR]

Following a request from the European Commission, the EFSA Panel on Food Additives and Nutrient sources added to Food (ANS) was asked to deliver a scientific opinion on the re-evaluation of pectin (E 440i) and amidated pectin (E 440ii) as food additives. An acceptable daily intake (ADI) 'not specified' was allocated by the Scientific Committee for Food (SCF) for E 440i and E 440ii. Pectin and amidated pectin would not be absorbed intact, but extensively fermented by intestinal microbiota in animals and humans; products formed from pectins in the gastrointestinal tract are similar to manufactured pectin-derived acidic oligosaccharides (pAOS). There is no indication of genotoxicity for pectin and amidated pectin, although the available data were limited. No adverse effects were reported in a chronic toxicity study in rats at levels up to 5,000 mg pectin/kg bw per day, the highest dose tested. No treatment-related effects were observed in a dietary one-generation reproductive toxicity study with pAOS in rats at up to 6,200 mg/kg body weight (bw) per day, the highest dose tested. The Panel did not consider E 440i and E 440ii as having allergenic potential. A dose of 36 g/day (equivalent to 515 mg/kg bw per day) for 6 weeks in humans was without adverse effects. Exposure to pectins from their use as food additives ranged up to 442 mg/kg bw per day for toddlers at the 95th percentile (brand-loyal scenario). The Panel concluded that there is no safety concern for the use of pectin (E 440i) and amidated pectin (E 440ii) as food additives for the general population and that there is no need for a numerical ADI. [ABSTRACT FROM AUTHOR]

The Panel on Food Additives and Nutrient Sources added to Food (ANS) provides a scientific opinion re‐evaluating the safety of tara gum (E 417) as a food additive. Tara gum (E 417) has been evaluated by the EU Scientific Committee for Food (SCF,) and by the Joint FAO/WHO Expert Committee on Food Additives (JECFA,), who both allocated an acceptable daily intake (ADI) ‘not specified’ for this gum. Following the conceptual framework for the risk assessment of certain food additives, re‐evaluated under Commission Regulation (EU) No 257/2010, the Panel considered that adequate exposure and toxicity data were available for tara gum (E 417). Tara gum (E 417) is unlikely to be absorbed intact and is expected to be fermented by intestinal microbiota. No adverse effects were reported at the highest doses tested in subchronic, chronic and carcinogenicity studies and there is no concern with respect to the genotoxicity. The Panel concluded that there is no need for a numerical ADI for tara gum (E 417) and that there is no safety concern for the general population at the refined exposure assessment of tara gum (E 417) as a food additive at the reported uses and use levels. [ABSTRACT FROM AUTHOR]

The present opinion deals with the re‐evaluation of konjac (E 425), comprising konjac gum (E 425 i) and konjac glucomannan (E 425 ii) when used as food additives. Following the conceptual framework for the risk assessment of certain food additives re‐evaluated under Commission Regulation (EU) No 257/2010, the Panel considered that current use of konjac (E 425) was limited in all food categories to maximum permitted level (MPL) of 10 g/kg, and that the calculated indicative refined exposure assessment for all population groups was below 0.1 mg/kg body weight (bw) per day for the general population (mean and high level). Konjac gum and konjac glucomannan were unlikely to be absorbed intact and were significantly fermented by intestinal microbiota. The available database on toxicological studies was considered limited, however, no relevant adverse effects were seen in rats and dogs in 90‐day feeding studies according to the SCF, the no‐observed‐effect level (NOEL) in rats being 1,250 mg konjac glucomannan/kg bw per day. Konjac gum and konjac glucomannan were of no concern with respect to the genotoxicity. After a daily dosage of 3,000 mg in adults for 12 weeks, several individuals experienced abdominal discomfort including diarrhoea or constipation. The Panel concluded that there was no need for a numerical acceptable daily intake (ADI) and that there was no safety concern for the general population at the refined exposure assessment for the reported uses of konjac gum (E 425 i) and konjac glucomannan (E 425 ii) as food additives under the current conditions of use of 10 g/kg. The Panel agreed with the conclusions of the SCF () that the uses of konjac (E 425) as an additive at the levels up to 10 g/kg in food are acceptable, provided that the total intake from all sources stays below 3 g/day. [ABSTRACT FROM AUTHOR]

The Panel on Food Additives and Nutrient Sources added to Food (ANS) provides a scientific opinion re-evaluating the safety of tragacanth (E 413) as a food additive. In the EU, tragacanth (E 413) has been evaluated by the Scientific Committee for Food (SCF, 1989) and by the Joint FAO/WHO Expert Committee on Food Additives (JECFA, 1987), who both allocated an acceptable daily intake (ADI) 'not specified' for this gum. Following the conceptual framework for the risk assessment of certain food additives, re-evaluated under Commission Regulation (EU) No 257/2010, the Panel considered that adequate exposure and toxicity data were available. Tragacanth (E 413) is unlikely to be absorbed intact and is partially fermented by intestinal microbiota. No adverse effects were reported in carcinogenicity studies at the highest dose tested and there is no concern with respect to the genotoxicity. Oral daily intake of a large amount of tragacanth up to 9,900 mg tragacanth/person per day (approximately equivalent 141 mg tragacanth/kg body weight (bw) per day) for up to 21 days was well tolerated in humans. The Panel concluded that there is no need for a numerical ADI for tragacanth (E 413) and that there is no safety concern for the general population at the refined exposure assessment of tragacanth (E 413) as a food additive at the reported uses and use levels. [ABSTRACT FROM AUTHOR]

The Panel on Food Additives and Nutrient Sources added to Food (ANS) provided a scientific opinion re-evaluating the safety of sodium nitrate (E 251) and potassium nitrate (E 252) when used as food additives. The current acceptable daily intakes (ADIs) for nitrate of 3.7 mg/kg body weight (bw) per day were established by the SCF (1997) and JECFA (2002). The available data did not indicate genotoxic potential for sodium and potassium nitrate. The carcinogenicity studies in mice and rats were negative. The Panel considered the derivation of an ADI for nitrate based on the formation of methaemoglobin, following the conversion of nitrate, excreted in the saliva, to nitrite. However, there were large variations in the data on the nitrate-to-nitrite conversion in the saliva in humans. Therefore, the Panel considered that it was not possible to derive a single value of the ADI from the available data. The Panel noticed that even using the highest nitrate-to-nitrite conversion factor the methaemoglobin levels produced due to nitrite obtained from this conversion would not be clinically significant and would result to a theoretically estimated endogenous N-nitroso compounds (ENOC) production at levels which would be of low concern. Hence, and despite the uncertainty associated with the ADI established by the SCF, the Panel concluded that currently there was insufficient evidence to withdraw this ADI. The exposure to nitrate solely from its use as a food additive was estimated to be less than 5% of the overall exposure to nitrate in food based on a refined estimated exposure scenario. This exposure did not exceed the current ADI (SCF, 1997). However, if all sources of exposure to dietary nitrate are considered (food additive, natural presence and contamination), the ADI would be exceeded for all age groups at the mean and the highest exposure. [ABSTRACT FROM AUTHOR]

The European Commission asked EFSA to provide a scientific opinion on the request for a modification of the EU specifications for polyvinyl alcohol-polyethylene glycol-graft-co-polymer (PVA-PEG graft-co-polymer) (E 1209) and its possible impact on the safety. In accordance with Annex II to Regulation (EC) No 1333/2008, PVA-PEG graft-co-polymer (E 1209) has a single authorisation for use as a food additive in the EU, in the food category food supplements in solid form. According to the current EU specifications, ethylene glycol and diethylene glycol can be present as impurities in other food additives authorised in the EU, namely in polysorbates (E 432-436) and polyethylene glycol (E 1521). The exposure to ethylene glycol and diethylene glycol from their presence in E 1209 and in the other food additives was estimated considering the maximum limit permitted according to the EU specifications and the new proposed maximum limit in E 1209 of 620 mg/kg for the ethylene glycol individually or in combination with diethylene glycol in E 1209. This proposed request would result in a total exposure from food additive uses below the group tolerable daily intake (TDI) of 0.5 mg/kg body weight (bw) per day allocated by the Scientific Committee on Food (SCF) for these contaminants. Therefore, the Panel concluded that the requested amendment of the EU specifications for E 1209 would not result in a safety concern. The Panel noted that the analytical results provided were consistently and considerably lower (up to 360 mg/kg) than the proposed level of 620 mg/kg for ethylene glycol individually or in combination with diethylene glycol in the EU specifications for E 1209. [ABSTRACT FROM AUTHOR]

The Panel on Food Additives and Nutrient Sources added to Food (ANS) provided a scientific opinion re-evaluating the safety of potassium nitrite (E 249) and sodium nitrite (E 250) when used as food additives. The ADIs established by the SCF (1997) and by JECFA (2002) for nitrite were 0-0.06 and 0-0.07 mg/kg bw per day, respectively. The available information did not indicate in vivo genotoxic potential for sodium and potassium nitrite. Overall, an ADI for nitrite per se could be derived from the available repeated dose toxicity studies in animals, also considering the negative carcinogenicity results. The Panel concluded that an increased methaemoglobin level, observed in human and animals, was a relevant effect for the derivation of the ADI. The Panel, using a BMD approach, derived an ADI of 0.07 mg nitrite ion/kg bw per day. The exposure to nitrite resulting from its use as food additive did not exceed this ADI for the general population, except for a slight exceedance in children at the highest percentile. The Panel assessed the endogenous formation of nitrosamines from nitrites based on the theoretical calculation of the NDMA produced upon ingestion of nitrites at the ADI and estimated a MoE > 10,000. The Panel estimated the MoE to exogenous nitrosamines in meat products to be < 10,000 in all age groups at high level exposure. Based on the results of a systematic review, it was not possible to clearly discern nitrosamines produced from the nitrite added at the authorised levels, from those found in the food matrix without addition of external nitrite. In epidemiological studies there was some evidence to link (i) dietary nitrite and gastric cancers and (ii) the combination of nitrite plus nitrate from processed meat and colorectal cancers. There was evidence to link preformed NDMA and colorectal cancers. [ABSTRACT FROM AUTHOR]

The EFSA Panel on Food Additives and Nutrient Sources added to Food (ANS) provides a scientific opinion re-evaluating the safety of fatty acids (E 570) when used as a food additive. The food additive includes caprylic- (C8), capric- (C10), lauric- (C12), myristic- (C14), palmitic- (C16), stearic- (C18) and oleic acid (C18:1), present alone or in combination. In 1991, the Scientific Committee on Food (SCF) established a group acceptable daily intake (ADI) 'not specified' for the fatty acids (myristic, stearic, palmitic and oleic acid). The fatty acids (E 570) are absorbed in the same way as the free fatty acids from the regular diet. They show low acute toxicity. The available studies on subchronic toxicity were limited but there was no evidence for toxic effects at doses up to 10% in the diet (equivalent to 9,000 mg lauric acid/kg body weight (bw) per day). The Panel considered that the fatty acids (E 570) did not raise a concern for genotoxicity. Data on chronic toxicity, reproductive toxicity and developmental toxicity were too limited to reach a conclusion on these endpoints. The Panel noted that the contribution of fatty acids (E 570) represented on average only 1% of the overall exposure to saturated fatty acids from all dietary sources (food additive and regular diet). Based on the approach described in the conceptual framework for the risk assessment of certain food additives re-evaluated under Commission Regulation (EU) No 257/2010 and taking into account the considerations mentioned above, the Panel concluded that the food additive fatty acids (E 570) was of no safety concern at the reported uses and use levels. [ABSTRACT FROM AUTHOR]

The Panel on Food Additives and Nutrient Sources added to Food (ANS) provides a scientific opinion re-evaluating the safety of sorbitan monostearate (E 491), sorbitan tristearate (E 492), sorbitan monolaurate (E 493), sorbitan monooleate (E 494) and sorbitan monopalmitate (E 495) when used as food additives. The Scientific Committee on Food (SCF) allocated an acceptable daily intake (ADI) of 25 mg/kg body weight (bw) per day for E 491, E 492 and E 495 singly or in combination; and a separate group ADI for E 493 and E 494 singly or in combination of 5 mg/kg bw per day calculated as sorbitan monolaurate in 1974. The Panel noted that after oral administration sorbitan monostearate can be either hydrolysed to its fatty acid moiety and the corresponding anhydrides of sorbitol and excreted via urine or exhaled as CO2 or excreted intact in the faeces. The Panel considered that sorbitan esters did not raise concern for genotoxicity. Based on the no observed adverse effect level (NOAEL) of 2,600 mg sorbitan monostearate/kg bw per day, taking into account the ratio between the molecular weight of sorbitan monostearate (430.62 g/mol) and sorbitan (164.16 g/mol), and applying an uncertainty factor of 100, the Panel derived a group ADI of 10 mg/kg bw per day expressed as sorbitan for sorbitan esters (E 491-495) singly or in combination. This group ADI of 10 mg sorbitan/kg bw per day is equivalent to 26 mg sorbitan monostearate/kg bw per day. The Panel concluded that the exposure at the mean and the 95th percentile level, using non-brand-loyal scenario, did not exceed the ADI in any of the population groups. The Panel on the request for an amendment of specifications regarding the removal of 'congealing range' concluded that it could be eventually replaced by another identification parameter such as melting point. [ABSTRACT FROM AUTHOR]

The Panel on Food Additives and Nutrient Sources added tofood (ANS) provides a scientific opinion re-evaluating the safety of acacia gum (E 414) as a food additive. In the EU, acacia gum has not been formally evaluated by the Scientific Committee for Food (SCF), and therefore, no ADI has been allocated. However, it was accepted for use in weaning food (SCF, 1991). In 1999, the SCF considered 'that the use of acacia gum/gum arabic in coatings for nutrient preparations containing trace elements is acceptable provided carry-over levels in infant formulae, follow-on formulae or FSMP do not exceed 10 mg/kg'. Acacia gum was evaluated by JECFA in 1982 and 1990 and the specifications were amended in 1998. Based on the lack of adverse effects in the available toxicity studies, an ADI 'not specified' was allocated. Following the conceptual framework for the risk assessment of certain food additives re-evaluated under Commission Regulation (EU) No 257/2010, the Panel considered that adequate exposure and toxicity data were available. Acacia gum is unlikely to be absorbed intact and is slightly fermented by intestinal microbiota. No adverse effects were reported in subchronic and carcinogenicity studies at the highest dose tested and there is no concern with respect to the genotoxicity. Oral daily intake of a large amount of acacia gum up to 30,000 mg acacia gum/person per day (approximately equivalent 430 mg acacia gum/kg bw per day) for up to 18 days was well tolerated in adults but some individuals experienced flatulence which was considered by the Panel as undesirable but not adverse effect. The Panel concluded that there is no need for a numerical ADI for acacia gum (E 414), and there is no safety concern for the general population at the refined exposure assessment of acacia gum (E 414) as a food additive. [ABSTRACT FROM AUTHOR]

The present opinion deals with the re-evaluation of lecithins (E 322) when used as a food additive. Lecithins (E 322) is an authorised food additive in the EU according to Annex II and Annex III to Regulation (EC) No 1333/2008 on food additives, and have been previously evaluated by JECFA in 1973 and by the SCF in 1982. Among lecithins, phosphatidylcholine is hydrolysed in choline in the cytidine-5-diphosphate-choline pathway in all cells of the body. Following the conceptual framework for the risk assessment of certain food additives re-evaluated under Commission Regulation (EU) No 257/ 2010, the Panel concluded that there was no need for a numerical ADI for lecithins (E 322) and that there was no safety concern for the general population from more than 1 year of age at the refined exposure assessment for the reported uses of lecithins (E 322) as a food additive. The Panel further concluded that there is no safety concern for the exposure to the choline from lecithins (E 322) as a food additive at use and use levels reported by industry. For infants (from 12 weeks up to 11 months of age), the Panel concluded that there was no safety concern at the refined exposure assessment for the reported uses of lecithins (E 322) as a food additive and for the choline from lecithins (E 322) as a food additive at use and use levels reported by industry. For infants and young children consuming foods for special medical purposes, the Panel concluded that there was no safety concern with respect to the refined exposure assessment for the reported uses of lecithins (E 322) as a food additive and for exposure to choline resulting from these uses of lecithins (E 322). [ABSTRACT FROM AUTHOR]

Following a request from the European Commission, the EFSA Panel on Food Additives and Nutrient Sources added to Food (ANS) was asked to deliver a scientific opinion on the re-evaluation of soybean hemicellulose (E 426) as a food additive. Soybean hemicellulose is not absorbed intact, but is extensively fermented by the intestinal microflora in animals and humans. No adverse effects were reported in a 90-day dietary toxicity study in rats at the highest doses tested of 2,430 mg/kg body weight (bw) per day for males and 2,910 mg/kg bw per day for females. Furthermore, soybean hemicellulose is not of genotoxic concern. The highest exposure estimates calculated based on the maximum permitted levels were up to 191 mg/kg bw per day for children (95th percentile). Given the limited uses, if any, reported, the Panel considered it probable that the actual dietary exposure to soybean hemicellulose (E 426) would be negligible. Following the conceptual framework for the risk assessment of certain food additives, the Panel concluded that it is very unlikely that there is a safety concern from the current use of soybean hemicellulose (E 426) as a food additive, and that there is no need for a numerical acceptable daily intake (ADI). The Panel recommended that the amount of residual proteins in E 426 should be reduced as much as possible, and that consumers should be informed of the presence of potentially allergenic proteins in the food additive. © 2017 European Food Safety Authority. EFSA Journal published by John Wiley and Sons Ltd on behalf of European Food Safety Authority. [ABSTRACT FROM AUTHOR]

The Panel on Food Additives and Nutrient Sources added to Food (ANS) provides a scientific opinion re-evaluating the safety of polyglycerol polyricinoleate (PGPR, E 476) used as a food additive. In 1978, the Scientific Committee for Food (SCF) established an acceptable daily intake (ADI) of 7.5 mg/kg body weight (bw) per day for PGPR. PGPR is hydrolysed in the gut resulting in the liberation of free polyglycerols, polyricinoleic acid and ricinoleic acid. Di- and triglycerol are absorbed and excreted unchanged in the urine; long-chain polyglycerols show lower absorption and are mainly excreted unchanged in faeces. Acute oral toxicity of PGPR is low, and short-term and subchronic studies indicate PGPR is tolerated at high doses without adverse effects. PGPR (E 476) is not of concern with regard to genotoxicity or carcinogenicity. The single reproductive toxicity study with PGPR was limited and was not an appropriate study for deriving a health-based guidance value. Human studies with PGPR demonstrated that there is no indication of significant adverse effect. The Panel considered a 2-year combined chronic toxicity/carcinogenicity study for determining a reference point and derived a no observed adverse effect level (NOAEL) for PGPR (E 476) of 2,500 mg/kg bw per day, the only dose tested. Therefore, the Panel concluded that the present data set give reason to revise the ADI of 7.5 mg/kg bw per day allocated by SCF to 25 mg/kg bw per day. Exposure estimates did not exceed the ADI of 25 mg/kg bw per day and a proposed extension of use would not result in an exposure exceeding this ADI. The Panel recommended modification of the EU specifications for PGPR (E 476). [ABSTRACT FROM AUTHOR]

The ANS Panel provides a scientific opinion re-evaluating the safety of glycerol (E 422) used as a food additive. In 1981, the Scientific Committee on Food (SCF) endorsed the conclusion from the Joint FAO/ WHO Expert Committee on Food Additives (JECFA) in 1976 of 'acceptable daily intake (ADI) for man not specified'. The Panel concluded that glycerol has low acute toxicity and that local irritating effects of glycerol in the gastrointestinal tract reported in some gavage studies was likely due to hygroscopic and osmotic effects of glycerol. Glycerol did not raise concern with respect to genotoxicity and was of no concern with regard to carcinogenicity. Reproductive and prenatal developmental studies were limited to conclude on reproductive toxicity but no dose-related adverse effects were reported. None of the animal studies available identified an adverse effect for glycerol. The Panel conservatively estimated the lowest oral dose of glycerol required for therapeutic effect to be 125 mg/kg bw per hour and noted that infants and toddlers can be exposed to that dose by drinking less than the volume of one can (330 mL) of a flavoured drink. The Panel concluded that there is no need for a numerical ADI and no safety concern regarding the use of glycerol (E 422) as a food additive at the refined exposure assessment for the reported uses. The Panel also concluded that the manufacturing process of glycerol should not allow the production of a food additive, which contains genotoxic and carcinogenic residuals at a level which would result in a margin of exposure below 10,000. The Panel recommended modification of the EU specifications for E 422. The Panel also recommended that more information on uses and use levels and analytical data should be made available to the Panel. [ABSTRACT FROM AUTHOR]

The Panel on Food Additives and Nutrient Sources added to Food (ANS) provides a scientific opinion re‐evaluating the safety of guar gum (E 412) as a food additive. In the EU, guar gum was evaluated by the Joint FAO/WHO Expert Committee on Food Additives (JECFA) in 1970, 1974 and 1975, who allocated an acceptable daily intake (ADI) ‘not specified’. Guar gum has been also evaluated by the Scientific Committee for Food (SCF) in 1977 who endorsed the ADI ‘not specified’ allocated by JECFA. Following the conceptual framework for the risk assessment of certain food additives re‐evaluated under Commission Regulation (EU) No 257/2010, the Panel considered that adequate exposure and toxicity data were available. Guar gum is practically undigested, not absorbed intact, but significantly fermented by enteric bacteria in humans. No adverse effects were reported in subchronic and carcinogenicity studies at the highest dose tested; no concern with respect to the genotoxicity. Oral intake of guar gum was well tolerated in adults. The Panel concluded that there is no need for a numerical ADI for guar gum (E 412), and there is no safety concern for the general population at the refined exposure assessment of guar gum (E 412) as a food additive. The Panel considered that for uses of guar gum in foods intended for infants and young children the occurrence of abdominal discomfort should be monitored and if this effect is observed doses should be identified as a basis for further risk assessment. The Panel considered that no adequate specific studies addressing the safety of use of guar gum (E 412) in food categories 13.1.5.1 and 13.1.5.2 were available. Therefore, the Panel concluded that the available data do not allow an adequate assessment of the safety of guar gum (E 412) in infants and young children consuming these foods for special medical purposes. [ABSTRACT FROM AUTHOR]

Following a request from European Commission, the EFSA Panel on Food Additives and Nutrient Sources added to Food ( ANS) provides a scientific opinion re-evaluating the safety of locust bean gum (E 410) as a food additive. Locust bean gum (E 410) is an authorised food additive in the EU. Locust bean gum (E 410) as specified in the Commission Regulation ( EU) No 231/2012 is derived from the ground endosperm of the seeds of the strains of carob tree, Ceratonia siliqua (L.) Taub. (Family Leguminosae). An acceptable daily intake ( ADI) 'not specified' was allocated by the Joint Food and Agriculture Organization/World Health Organization Expert Committee on Food Additives ( JECFA) in 1981. Although not evaluated by the Scientific Committee for Food ( SCF), it was accepted by the SCF in 1991 for use in weaning food, and in 1994, in infant formulae for special medical purposes. Locust bean gum is practically undigested, not absorbed intact, but significantly fermented by enteric bacteria in humans. No adverse effects were reported in 90-day toxicity and carcinogenicity studies in rodents at the highest doses tested and there was no concern with respect to the genotoxicity and to reproductive and developmental toxicity of locust bean gum (E 410). The Panel concluded that there is no need for a numerical ADI for locust bean gum (E 410), and that there is no safety concern for the general population at the refined exposure assessment for its reported uses as a food additive. However, infants and young children consuming foods for special medical purposes may show a higher susceptibility to gastrointestinal effects of locust bean gum due to their underlying medical condition. The Panel concluded that the available data do not allow an adequate assessment of the safety of locust bean gum (E 410) in these foods for infants and young children. [ABSTRACT FROM AUTHOR]

The EFSA Panel on Food Additives and Nutrient Sources added to Food (ANS) provides a scientific opinion re-evaluating the safety of agar (E 406) as a food additive. In the European Union (EU), agar (E 406) has been evaluated by the Scientific Committee for Food (SCF) in 1989, who allocated to agar a not specified acceptable daily intake (ADI), and by the Joint FAO/WHO Expert Committee on Food Additives (JECFA) in 1974, who considered very few data to conclude to a not limited ADI. According to the conceptual framework for the risk assessment of certain food additives re-evaluated under Commission Regulation (EU) No 257/2010, the Panel considered that the safety assessment is limited to the use and use levels received from industry in 7 food categories for which data were considered in this opinion out of the 70 food categories in which agar (E 406) is authorised; an indicative high refined exposure assessment up to 26 mg/kg body weight (bw) per day has been calculated in toddlers at the 95th percentile (non-brand-loyal scenario); agar is unlikely to be absorbed unchanged and slightly fermented by intestinal microbiota; sufficient toxicity data were available; there was no concern with respect to the genotoxicity of agar; no carcinogenic effects were reported in carcinogenicity studies in mice and rats at the doses of 4,500 mg/kg bw per day and 2,500 mg/kg bw per day, respectively, the highest doses tested; oral intake of agar (4,500 mg/person corresponding to 64 mg/kg bw per day) was tolerated in humans for 12 weeks without noticeable side effects. Therefore, the Panel concluded that there is no need for a numerical ADI for agar and that there is no safety concern for the general population at the refined exposure assessment for the reported uses of agar as a food additive. [ABSTRACT FROM AUTHOR]

The EFSA Panel on Food Additives and Nutrient Sources added to Food (ANS) provides a scientific opinion re-evaluating the safety of β-cyclodextrin (E 459) as a food additive. β-Cyclodextrin is a non-reducing cyclic oligosaccharide consisting of seven α-1,4-linked D-glucopyranosyl units. The Scientific Committee on Food (SCF) allocated an acceptable daily intake (ADI) of 5 mg/kg body weight (bw) per day to b-cyclodextrin (E 459) in 1996. β-Cyclodextrin is poorly absorbed following oral administration in animals and humans. It is hydrolysed to maltose and glucose by the gut microflora and endogenous amylases in the colon; consequently, β-cyclodextrin levels in tissues and serum are low (< 1%). β-Cyclodextrin has a low acute oral toxicity. Short-term and subchronic toxicity studies were available in rats and dogs. In rats, the main reported effect was an adaptive enlargement of the caecum, resulting from consumption of poorly digestible carbohydrates. From a 6-month study in rats, a no observed adverse effect levels (NOAEL) of 600 mg/kg bw per day was identified and from a 52-week dogs study, the NOAEL was 466 and 476 mg/kg bw per day in males and females, respectively. The Panel considered that there was no indication for genotoxicity of β-cyclodextrin. From a chronic toxicity studies in rats, a NOAEL of 654 and 864 mg/kg bw per day in males and females, respectively, was identified. Carcinogenicity studies in mice and rats were available and no evidence for carcinogenicity was found. The Panel concluded that, based on the available toxicological database, there is no reason to revise the current ADI of 5 mg/kg bw per day for β-cyclodextrin. Based on the available reported use and use levels, the Panel also concluded that the ADI was exceeded in the refined brand-loyal scenario (considered the most relevant scenario) in all population groups except for infants at the mean and in all population groups at the 95th percentile. [ABSTRACT FROM AUTHOR]

Following a request from the European Commission, the EFSA Panel on Food Additives and Nutrient sources added to Food (ANS) was asked to deliver a scientific opinion on the re-evaluation of karaya gum (E 416) as a food additive. Karaya gum (E 416) is an authorised food additive in the EU. Karaya gum (E 416) as specified in the Commission Regulation (EU) No 231/2012 is derived from the exudates from the stems and branches of strains of Sterculia urens Roxburgh and other species of Sterculia (family Sterculiaceae) or from Cochlospermum gossypium A.P. De Candolle or other species of Cochlospermum (family Bixaceae). An acceptable daily intake (ADI) 'not specified' was allocated by the Joint Food and Agriculture Organization/World Health Organization Expert Committee on Food Additives (JECFA), whereas the Scientific Committee for Food (SCF) allocated an ADI of 12.5 mg/kg body weight (bw) per day. Karaya gum is practically undigested and not degraded by intestinal microflora and it is most probably not or only negligibly absorbed unchanged in humans. There is no concern with respect to the genotoxicity of karaya gum from Sterculia spp. Karaya gum (E 416) from Sterculia spp. did not induce toxic effects in animals at dose levels up to 1,250 mg/kg bw per day, the highest dose tested. Karaya gum from Sterculia spp. was well tolerated in humans at dose about 100 mg/kg bw per day for 4 weeks. The Panel concluded that there is no safety concern at the refined exposure assessment for the use of karaya gum as a food additive and that there is no need for a numerical ADI for karaya gum. The Panel further concluded that exposure to karaya gum by the use of this food additive should not exceed 7,000 mg/person per day in adults, the level at which some experienced abdominal discomfort. [ABSTRACT FROM AUTHOR]

The present scientific opinion deals with the safety of trimagnesium dicitrate anhydrous ( TMDC) when used as a stabiliser and anticaking agent in food supplements in solid and chewable forms. TMDC is a magnesium salt of citric acid in the anhydrous form. Following oral ingestion, TMDC is expected to fully and readily dissociate into magnesium and citrate ions. The toxicological data provided in support of the current application were not in accordance with the Tier 1 requirement of the 'Guidance for submission for food additive evaluations'; however, this was considered to be justified by the Panel given that both magnesium and citrate are natural constituents of the diet and also the human body. Exposure estimates to TMDC from its proposed use were calculated for both typical and maximum use levels alongside the resulting intake of magnesium and citrate. At the proposed typical level, the intake of magnesium resulting from the use of TMDC would be below the tolerable upper level ( UL) of 250 mg/day for supplemental magnesium. In the worst case scenario of high-level intakes of TMDC when used at the maximum proposed use level of 120,000 mg/kg, the maximum estimated intake of magnesium would be 311 mg/day per day in the elderly and 389 mg/day in adults, in both cases above the UL. The Panel noted that the intake of both magnesium and citrate resulting from the proposed use and use levels of TMDC appears to be within the normal dietary intake in the general population. The Panel concluded that there was no safety concern from the proposed typical use levels of TMDC as a stabiliser and anticaking agent in food supplements, whereas at the proposed maximum use levels, the resulting exposure to magnesium in adults and the elderly at the high-level would be above the UL. [ABSTRACT FROM AUTHOR]

The EFSA Panel on Food Additives and Nutrient Sources added to Food ( ANS) provides a scientific opinion re-evaluating the safety of ammonium phosphatides (E 442) as a food additive. The Scientific Committee on Food ( SCF) and the Joint FAO/ WHO Expert Committee on Food Additives ( JECFA) allocated an acceptable daily intake ( ADI) of 30 mg/kg body weight (bw) per day in 1978 and 1974, respectively. The Panel noted that after oral administration of E 442 ([32P] YN), a proportion of the radioactivity passed through the gastrointestinal tract and was excreted via faeces and also a quantity of radioactivity was absorbed rapidly after dosing as indicated by its presence in the skeletal tissue and liver. Acute oral toxicity of ammonium phosphatides is low and no adverse effects were observed in a 90-day rats study. The Panel considered that ammonium phosphatides did not raise concern for genotoxicity. The Panel identified no observed adverse effect levels ( NOAELs) of 8,500 and 3,000 mg/kg bw per day, the highest doses tested, from dietary chronic and carcinogenicity studies with ammonium phosphatides in mice and rats, respectively. No effects on reproduction and development were observed in a dietary two-generation reproductive toxicity study at the only dose tested of 3,000 mg/kg bw per day, and in addition, no maternal or developmental effects were recognised in a dietary prenatal developmental toxicity study up to a dose of 4,774 mg/kg bw per day. Based on the available toxicological database, the Panel concluded that there is no reason to revise the current ADI for ammonium phosphatides of 30 mg/kg bw per day. Considering that the ADI is not exceeded in any population group, the Panel also concluded that the use of ammonium phosphatides (E 442) as a food additive, at the permitted or reported use and use levels, would not be of safety concern. [ABSTRACT FROM AUTHOR]

With aim to provide information on chemical contaminants in byproducts in animal feed, the data from an official control by the Danish Plant Directorate during 1998–2009, were reviewed and several samples of citrus pulp and dried distillers grains with solubles (DDGS) were additionally collected for analysis and risk assessment. The levels of contaminants in the samples from the official control were below maximum limits from EU regulations with only a few exceptions in the following groups; dioxins and dioxin-like polychlorobiphenyls (PCBs) in fish-containing byproducts and dioxins in vegetable and animal fat, hydrogen cyanide in linseed, and cadmium in sunflowers. The levels of pesticides and mycotoxins in the additionally collected samples were below maximum limits. Enniatin B (ENN B) was present in all DDGS samples. The hypothetical cases of carry-over of contamination from these byproducts were designed assuming total absorption and accumulation of the ingested contaminant in meat and milk and high exposure (a byproduct formed 15–20% of the feed ration depending on the species). The risk assessment was refined based on literature data on metabolism in relevant animal species. Risk assessment of contaminants in byproducts is generally based on a worst-case approach, as data on carry-over of a contaminant are sparse. This may lead to erroneous estimation of health hazards. The presence of ENN B in all samples of DDGS indicates that potential impact of this emerging mycotoxin on feed and food safety deserves attention. A challenge for the future is to fill up gaps in toxicological databases and improve models for carry-over of contaminants. [ABSTRACT FROM AUTHOR]

Regular consumption of fruits and vegetables is associated with reduced risks of certain cancers and other diseases in observational studies and animal models of human diseases. The aim of the present study was to investigate whether feeding of rats with whole raw apple has potentially chemopreventive properties by affecting markers of colon cancer. The end-point was preneoplastic changes in the colon known as aberrant crypt foci (ACF). Rats initiated with the colon carcinogen 1,2-dimethylhydrazine dihydrochloride (DMH) were given 0, 5, or 10 g apple/day for 13 wk. The group fed 5 g apple but not 10 g had a significantly lower number of ACF (P = 0.009) compared to the initiated control. DNA damage evaluated by the comet assay was significantly increased in leucocytes of DMH-treated animals (P = 0.021). No antigenotoxic effect of apple feeding was apparent in the colon. Apple feeding tended to lower DNA damage in the liver (P = 0.136 in DMH-initiated and P = 0.284 in noninitiated rats). Liver alanine aminotransferase was significantly increased in rats fed apples (P = 0.008 in DMH-initiated and P = 0.019 in noninitiated rats). In conclusion, feeding whole fresh apple may affect the occurrence of preneoplastic changes in the rat colon, but the effect was not gradual. [ABSTRACT FROM AUTHOR]

Abstract: Objectives: To evaluate the effect of estrogen replacement therapy or soy isoflavones supplement on endothelium-dependent relaxation in vitro and gene expression of endothelial nitric oxide synthase (eNOS) in cerebral arteries in a rabbit model of human hypercholesterolemia. Study design: Thirty-six female ovariectomized Watanabe heritable hyperlipidemic (WHHL) rabbits were randomised to treatment with 17β-estradiol (17β-E2), SoyLife 150® or control for 16 weeks. Ring segments of basilar artery (BA) and posterior cerebral artery (PCA) were mounted in myographs for isometric tension recordings. Concentration response curves to carbamylcholine chloride, sodium nitroprusside (SNP) and l-NAME were evaluated after precontraction with potassium. Total RNA was extracted, reverse transcribed and eNOS quantitated by real-time polymerase chain reaction (real-time PCR). Results: Plasma cholesterol was significantly higher at termination in the SoyLife® group (P <0.0001), whereas low-density lipoprotein (LDL) cholesterol was comparable in all treatment groups. Neither treatment influenced the endothelium-dependent responses to carbamylcholine chloride or l-NAME or the endothelium-independent response to SNP in any of the arteries. Correspondingly, eNOS mRNA was similarly expressed in all treatment groups in both arteries. Conclusions: Improvement of cerebral endothelial function by estrogen or soy isoflavones in ovariectomized WHHL rabbits is not supported by the present data. The findings may be unique to the WHHL rabbit in which the hypocholesterolemic effect of estrogens mediated by upregulation of liver LDL receptors is excluded. [Copyright &y& Elsevier]

Sweeteners are substances with a sweet taste. Based on their relative sweetness compared to sucrose, sweeteners are divided into intense or bulk sweeteners. In the past, the Scientific Committee on Food was the scientific guarantor for the safety of food additives (including sweeteners) in use within the European Union (EU). At present, this responsibility lies with the European Food Safety Authority. Extensive scientific research has demonstrated the safety of all sweeteners permitted for food use in the EU. Their safety is documented by the results of several in vitro and in vivo animal studies, tests in humans, and in some cases epidemiological studies. Their safety has been evaluated through a risk assessment process covering hazard identification, hazard characterization, exposure assessment and risk characterization. Permitted sweeteners have been allocated an acceptable daily intake (ADI), which is the amount of a food additive, expressed as mg/kg body weight, that can be ingested daily over a lifetime without incurring any appreciable health risk. ADI “acceptable” means that the expected exposure to the substance used in foods at the levels necessary to achieve desired technological effects does not represent a hazard to health. The consumption of sweeteners in the quantities within the ADI does not constitute a health hazard to consumers. [ABSTRACT FROM AUTHOR]

Abstract: The toxicity and anti-diabetic properties of an aqueous plant extract made by boiling Rauwolfia vomitoria foilage and Citrus aurantium fruits were evaluated in mice. A single dosage corresponding to 70× the human-daily-dose was non-toxic when administered to 6-week-old NMRI lean mice or 6- or 11-week-old C57BL/6J lean mice. Daily treatment of 11-week-old C57BL/KsBom-db (db/db) genetic diabetic mice with a dose corresponding to 10× human-daily-dose for 6 weeks facilitated a significant weight loss as compared to the untreated controls. During treatment, the db/db mice were maintained on the carbohydrate-deficient Altromin C1009 diet. Although the food intake in the treated mice was not statistically significant from that in the controls, the treated animals had significantly higher serum triglyceride contents, suggesting that the treatment induced lipid mobilization from internal stores. Moreover, the fatty acid profile of the eyes from the treated animals showed a significant reduction in total fatty acid content accompanied by a 33% reduction in estimated Stearoyl-CoA desaturase activity (p =0.039) as compared with controls. The fatty acid mobilization and a protection of the brittle C57BL/KsBom-db pancreas were observed 5 weeks after cessation of treatment when the treated animals were maintained on the poorer Altromin C1009 diet. [Copyright &y& Elsevier]

Abstract: We investigated spontaneous mammary tumor development and mammary gland morphogenesis in female Tg.NK mice postnatally exposed to dietary soy isoflavones (0, 11, 39, and 130 mg aglycones/kg diet) added to a Western-style diet. Instead of preventing mammary tumorigenesis, the highest dose of isoflavones was associated with a small but significant increase in the number and size of tumors as compared to mice administered a Western-style control diet (P < 0.05). At postnatal Week 6, dynamic activity (measured as apoptotic density) at the highest dose and the degree of branching of the mammary tree in all isoflavone-exposed groups was increased as compared to controls (P < 0.05). At adulthood, the epithelium appeared more quiescent in the medium- and high-dose groups evident by reduced apoptotic density and a reduction in the percentage of terminal end buds (TEBs), respectively, as compared to controls (P < 0.05). The number of actively dividing cells within the TEBs was unaffected by isoflavone exposure as was the activity of drug-metabolizing and antioxidant enzymes. In conclusion, isoflavones may augment mammary gland and mammary tumor development. [ABSTRACT FROM AUTHOR]

The aim of the present study was to evaluate the impact of long-term estrogen replacement therapy (ERT) on the vasodilatory effect of the two peptides vasoactive intestinal polypeptide (VIP) and pituitary adenylate cyclase activating polypeptide (PACAP) in atherosclerotic coronary and cerebral arteries.Female ovariectomized homozygous Watanabe heritable hyperlipidemic rabbits were randomized to 16 weeks treatment with 17β-estradiol or placebo. The diet was semisynthetic, thereby avoiding the influence of phytoestrogens. Artery ring segments were mounted for isometric tension recordings in myographs. Following precontraction, the dose–response relationships for VIP and PACAP were evaluated.Treatment with 17β-estradiol significantly improved the maximum VIP-mediated vasodilation (Emax, percentage of precontraction) in proximal coronary arteries (45.8±9.6% vs. 24.1±3.7%, p<0.05). In the same artery segment, 17β-estradiol induced a significant decrease in the relative ratio between the repeated contractile response to potassium 30 and 120 mM (100±7% vs. 132±11%, p<0.05). For distal coronary arteries, there was a tendency to similar changes, but no statistical differences for the potassium or VIP responses in cerebral or distal coronary arteries were found between the two groups. 17β-estradiol induced no changes in the PACAP-mediated vasodilation.These results suggest that long-term treatment with 17β-estradiol improves the VIP-mediated but not the PACAP-mediated vasodilation in atherosclerotic proximal coronary arteries. [Copyright &y& Elsevier]

Phytoestrogens, like isoflavonoids and lignans, have been postulated as possible colorectal cancer protective constituents. To investigate this hypothesis, two high-fiber sources rich in lignan precursors, i.e., rye bran and flax-seed, were tested for their ability to modulate intestinal tumor development in Apc[SUPMin] mice. Test diets consisted of a control diet (a Western-style diet, adjusted for fiber and/or phytate content) supplemented with 5% flaxseed or 30% rye bran. Chemical analysis of diets and blood samples confirmed the enhanced systemic exposure of mice fed the test diets to the major lignan precursors, i.e., secoisolariciresinol and matairesinol. No statistically significant difference was observed in the incidence and multiplicity of small intestinal and colon tumors at terminal sacrifice between mice fed the control diet or the diet supplemented with 5% flaxseed. With the rye bran diet a statistically significant enhancement of the number of small intestinal tumors in female mice was observed. The number of colon tumors, however, was comparable between the control and rye bran-fed mice of either sex. Furthermore, no activating point mutations in the K-ras oncogene nor positive immunohistochemical staining for the p53 gene were observed in a set of 48 colon tumors. In conclusion, our results demonstrate that increased intake of lignan precursors from flaxseed or rye bran, administered in a Western-style diet, does not protect against intestinal tumor development in an appropriate animal model for intestinal neoplasia such as the Apc[SUPMin] mice. [ABSTRACT FROM AUTHOR]

The effect of a long-chained fructan Raftiline HP on spontaneous hypercholesterolemia and atherosclerosis was studied in 40 LDLR-/- male mice receiving isocaloric, balanced in fat content, purified diets with 0 or 10% Raftiline HP, for 16 weeks. The feed intake was comparable (3.9 v. 3.8 g/day) but the terminal body weight was lower in the Raftiline HP group (36 v. 32g, p<0.01). After 3 weeks of treatment, and throughout the study, mice receiving Raftiline HP had statistically significantly lower plasma cholesterol (9.12 v. 6.41 mmol/l, at termination) and its concentrations in LDL (2.36 v. 1.7 mmol/l), IDL (1.27 v. 0.77 mmol/l) and VLDL (1.53 v. 0.96 mmol/l) but not in HDL (1.13 v. 1.11). Plasma triglycerides were comparable between the groups (1.14 v. 1.04 mmol/l, at termination). The ratio intima/media was 15% lower (0.089 v. 0.076), although not statistically significantly different. In conclusion, the findings of this study emphasize the cholesterol lowering potential of inulin. [Copyright &y& Elsevier]

The potential of Xpa[sup -/-] and Xpa[sup -/-]/p[sup 53+/-] mice for short-term carcinogenicity assays was evaluated with di(2-ethylhexyl)phthalate (DEHP). Groups of 15 male and female Xpa[sup -/-] mice, received diets containing 0, 1,500, 3,000, or 6,000 ppm DEHP,and wild-type (WT) and Xpa[sup -/-]/p[sup 53+/-] mice 0 or 6,000 ppm DEHP for 39 weeks. Xpa[sup -/-], Xpa[sup -/-]/p[sup 53+/-], and WT males, fed 2,500 ppm p-cresidine, served as a positive control. In all models, the survival was not altered by DEHP. Increased incidences of nonneoplastic lesions were recorded in testes and kidneys with no apparent difference between the models. The only liver tumors in all models were adenomas in males with no statistically significantly increased incidence. For p-cresidine, the survival was decreased (p < 0.05) only in transgenic models. Statistically significantly increased incidences of nonneoplastic lesions were recorded in the liver, urinary bladder, and nasal cavity in all models, and in kidneys in transgenic models. The only tumors with statistically significantly increased incidence were liver adenomas in transgenic models (XPA: 1 vs 7; 'XPA/p53': 0 vs 12; WT: 0 vs 5, p = 0.053) and urinary bladder carcinomas in XPA/p53 model (0 vs 7). The negative carcinogenic response to DEHP and the positive response to p-cresidine support the expected sensitivity to genotoxic carcinogens in these transgenic models. [ABSTRACT FROM AUTHOR]

The food enzyme with phospholipase A1 (phosphatidycholine 1‐acylhydrolase, EC 3.1.1.32) and lysophospholipase (2‐lysophosphatidylcholine acylhydrolase, EC 3.1.1.5) activities is produced with the genetically modified Aspergillus niger strain PLN by DSM. The genetic modifications do not give rise to safety concerns. The food enzyme is free from viable cells of the production organism and its DNA. It is intended to be used for the production of refined edible fats and oils by degumming. Since residual amounts of total organic solids are removed during this process, dietary exposure was not calculated and toxicological studies were considered unnecessary for the assessment of this food enzyme. A search for the similarity of the amino acid sequence of the food enzyme to known allergens was made and no matches were found. The Panel considered that the risk of allergic reactions upon dietary exposure cannot be excluded, but the likelihood is low. Based on the data provided, the Panel concluded that this food enzyme does not give rise to safety concerns, under the intended conditions of use. [ABSTRACT FROM AUTHOR]

The food enzyme α‐amylase (4‐α‐d‐glucan glucanohydrolase; EC 3.2.1.1) is produced with the non‐genetically modified microorganism Bacillus licheniformis strain AE‐TA by Amano Enzyme Inc. The food enzyme is intended to be used in eight food manufacturing processes. Since residual amounts of food enzyme‐total organic solids (TOS) are removed in two food manufacturing processes, dietary exposure was calculated only for the remaining six processes. It was estimated to be up to 0.056 mg TOS/kg body weight per day in European populations. The production strain of the food enzyme fulfils the requirements for the qualified presumption of safety approach to safety assessment. Consequently, in the absence of other concerns, the Panel considered that toxicological studies were not needed for the safety assessment of this food enzyme. A search for the similarity of the amino acid sequence of the food enzyme to known allergens was made and two matches with respiratory allergens were found. The Panel considered that the risk of allergic reactions upon dietary exposure to this food enzyme cannot be excluded (except for the production of distilled alcohol), but the likelihood is low. Based on the data provided, the Panel concluded that this food enzyme does not give rise to safety concerns under the intended conditions of use. [ABSTRACT FROM AUTHOR]

The food enzyme with two declared activities, bacillolysin (EC 3.4.24.28) and subtilisin (EC 3.4.21.62), is produced with the non‐genetically modified Bacillus amyloliquefaciens strain AR‐383 by AB Enzymes GmbH. The food enzyme is intended to be used in nine food manufacturing processes. Since residual amounts of total organic solids (TOS) are removed in the production of distilled alcohol, dietary exposure was calculated only for the remaining eight food manufacturing processes. Exposure was estimated to be up to 1.958 mg TOS/kg body weight per day in European populations. As the production strain qualifies for the qualified presumption of safety approach to safety assessment and no issues of concern arising from the production process of the food enzyme were identified, the Panel considered that no toxicological studies other than the assessment of allergenicity were necessary. A search for the similarity of the amino acid sequence of the food enzyme to known allergens was made, and 30 matches were found, including one food allergen (melon). The Panel considered that, under the intended conditions of use, the risk of allergic reactions by dietary exposure to this food enzyme cannot be excluded, but for individuals sensitised to melon, this would not exceed the risk of consuming melon. Based on the data provided, the Panel concluded that this food enzyme does not give rise to safety concerns under the intended conditions of use. [ABSTRACT FROM AUTHOR]

The food enzyme laccase (benzenediol:oxygen oxidoreductase; EC 1.10.3.2) is produced with the non‐genetically modified Trametes hirsuta strain AE‐OR by Amano Enzyme Inc. The food enzyme is free from viable cells of the production organism. It is intended to be used in six food manufacturing processes. Dietary exposure to the food enzyme–total organic solids (TOS) was estimated to be up to 0.026 mg TOS/kg body weight (bw) per day in European populations. Genotoxicity tests did not raise a safety concern. The systemic toxicity was assessed by means of a repeated dose 90‐day oral toxicity study in rats. The Panel identified a no observed adverse effect level of 862 mg TOS/kg bw per day, the highest dose tested, which when compared with the estimated dietary exposure, resulted in a margin of exposure of at least 33,154. A search for the similarity of the amino acid sequence of the food enzyme to known allergens was made and no match was found. The Panel considered that a risk of allergic reactions by dietary exposure cannot be excluded, but the likelihood is low. Based on the data provided, the Panel concluded that this food enzyme does not give rise to safety concerns under the intended conditions of use. [ABSTRACT FROM AUTHOR]

The food enzyme carboxypeptidase D (EC 3.4.16.6) is produced with the genetically modified Aspergillus oryzae strain NZYM‐MK by Novozymes A/S. It is free from viable cells of the production organism and its DNA. The genetic modifications do not give rise to safety concerns. The food enzyme is intended to be used in five food manufacturing processes. Dietary exposure to the food enzyme‐total organic solids (TOS) was estimated to be up to 0.908 mg TOS/kg body weight (bw) per day in European populations. Genotoxicity tests did not indicate a safety concern. The systemic toxicity was assessed by means of a repeated dose 90‐day oral toxicity study in rats. The Panel identified a no observed adverse effect level of 2220 mg TOS/kg bw per day, the highest dose tested, which, when compared with the estimated dietary exposure, resulted in a margin of exposure of at least 2445. A search for the similarity of the amino acid sequence of the food enzyme to known allergens was made and two matches were found, one with a food allergen (wheat). The Panel considered that a risk of allergic reactions upon dietary exposure to this food enzyme, particularly in individuals sensitised to wheat, cannot be excluded, but will not exceed that of wheat consumption. Based on the data provided, the Panel concluded that this food enzyme does not give rise to safety concerns under the intended conditions of use. [ABSTRACT FROM AUTHOR]

The food enzyme sucrose phosphorylase (sucrose: phosphate α‐d‐glucosyltransferase; EC 2.4.1.7) is produced with the genetically modified Escherichia coli strain LE1B109‐pPB129 by c‐LEcta GmbH. The genetic modifications do not give rise to safety concerns. The food enzyme was free from viable cells of the production organism. It is intended to be used in combination with a cellobiose phosphorylase in the production of the specialty carbohydrate cellobiose. Since residual amounts of food enzyme–total organic solids are removed by the downstream purification steps, the Panel considered that toxicological studies other than assessment of allergenicity were unnecessary and a dietary exposure was not estimated. A search for the similarity of the amino acid sequence of the food enzyme to known allergens was made and no match was found. The Panel considered that the risk of allergic reactions upon dietary exposure cannot be excluded, but the likelihood is low. Based on the data provided, the Panel concluded that this food enzyme does not give rise to safety concerns under the intended conditions of use. [ABSTRACT FROM AUTHOR]

The food enzyme cellobiose phosphorylase (cellobiose: phosphate α‐d‐glucosyltransferase; EC 2.4.1.20) is produced with the genetically modified Escherichia coli strain LE1B109‐pPB130 by c‐LEcta GmbH. The genetic modifications do not give rise to safety concerns. The food enzyme is considered free from viable cells of the production organism and its DNA. It is intended to be used in combination with a sucrose phosphorylase in the production of the specialty carbohydrate cellobiose. Since residual amounts of total organic solids are removed by downstream purification steps, the Panel considered that toxicological studies other than assessment of allergenicity were unnecessary and a dietary exposure was not estimated. A search for similarity of the amino acid sequence of the food enzyme to known allergens was made and no match was found. The Panel considered that, under the intended conditions of use, the risk of allergic reactions upon dietary exposure cannot be excluded, but the likelihood is low. Based on the data provided, the Panel concluded that this food enzyme does not give rise to safety concerns under the intended conditions of use. [ABSTRACT FROM AUTHOR]

The food enzyme glucan 1,4‐α‐glucosidase (4‐α‐d‐glucan glucohydrolase; EC 3.2.1.3) is produced with the non‐genetically modified Rhizopus arrhizus strain AE‐G by Amano Enzyme Inc. A safety evaluation of this food enzyme was made previously, in which EFSA concluded that this food enzyme did not give rise to safety concerns when used in one food manufacturing process. Subsequently, the applicant requested to extend its use to nine additional processes and revised the use levels. In this assessment, EFSA updated the safety evaluation of this food enzyme for uses in a total of 10 food manufacturing processes. As the food enzyme–total organic solids (TOS) is removed from the final foods in two food manufacturing processes, the dietary exposure to the food enzyme–TOS was estimated only for the remaining eight processes. Dietary exposure was up to 0.424 mg TOS/kg body weight (bw) per day in European populations. When combined with the no observed adverse effect level previously reported (1868 mg TOS/kg bw per day, the highest dose tested), the Panel derived a margin of exposure of at least 4406. Based on the data provided for the previous evaluation and the margin of exposure revised in the present evaluation, the Panel concluded that this food enzyme does not give rise to safety concerns under the revised intended conditions of use. [ABSTRACT FROM AUTHOR]

The food enzyme β‐amylase (4‐α‐d‐glucan maltohydrolase, EC 3.2.1.2) is produced with the non‐genetically modified Bacillus flexus strain AE‐BAF by Amano Enzyme Inc. A safety evaluation of this food enzyme was made previously, in which EFSA concluded that this food enzyme did not give rise to safety concerns when used in three food manufacturing processes. Subsequently, the applicant requested to extend its use to four additional processes and revised the use levels. In this assessment, EFSA updated the safety evaluation of this food enzyme for use in a total of seven food manufacturing processes. As the food enzyme‐total organic solids (TOS) are removed from the final foods in one food manufacturing process, the dietary exposure to the food enzyme‐TOS was estimated only for the remaining six processes. The dietary exposure was estimated to be up to 0.247 mg TOS/kg body weight per day in European populations. Based on the data provided for the previous evaluation and the dietary exposure revised in the present evaluation, the Panel concluded that this food enzyme does not give rise to safety concerns under the revised intended conditions of use. [ABSTRACT FROM AUTHOR]

The food enzyme inulinase (1‐β‐d‐fructan fructanohydrolase; EC 3.2.1.7) is produced with the non‐genetically modified Aspergillus welwitschiae strain NZYM‐KF by Novozymes A/S. The food enzyme is free from viable cells of the production organism. It is intended to be used in the processing of fructo‐polysaccharides for the production of fructo‐oligosaccharides. Since residual amounts of total organic solids (TOS) are removed during the food manufacturing process, toxicological studies other than allergenicity were considered unnecessary and dietary exposure was not calculated. A search for the similarity of the amino acid sequence of the food enzyme to known allergens was made and two matches with tomato allergens were found. The Panel considered that the risk of allergic reactions upon dietary exposure to this food enzyme, particularly in individuals sensitised to tomato, cannot be excluded, but is expected not to exceed that of tomato. As the prevalence of allergic reactions to tomato is low, also the likelihood of such reactions to occur to the food enzyme is low. Based on the data provided, the Panel concluded that this food enzyme does not give rise to safety concerns, under the intended conditions of use. [ABSTRACT FROM AUTHOR]

Bacillus paralicheniformis, a species known to produce the antimicrobial bacitracin, could be misidentified as Bacillus licheniformis, depending on the identification method used. For this reason, the European Commission requested EFSA to review the taxonomic identification of formerly assessed B. licheniformis production strains. Following this request, EFSA retrieved the raw data from 27 technical dossiers submitted and found that the taxonomic identification was established by 16S rRNA gene analyses for 15 strains and by whole genome sequence analysis for 12 strains. As a conclusion, only these 12 strains could be unambiguously identified as B. licheniformis. [ABSTRACT FROM AUTHOR]

The EFSA Panel on Food Contact Materials, Enzymes and Processing Aids (CEP) assessed the safety of amines, di‐C14‐C18‐alkyl, oxidised, renamed by the Panel as amines, di‐C14‐C20‐alkyl, oxidised, from hydrogenated vegetable oil. The substance amines, bis(hydrogenated tallow alkyl) oxidised, consisting of the same components, but originating from tallow, is currently authorised as FCM substance No 768. The vegetable‐sourced substance is intended to be used at up to 0.1% w/w as antioxidant and/or stabiliser in the manufacture of polyolefin food contact materials (FCM) and articles intended for contact with dry, aqueous and acidic foods. The substance is a mixture consisting of linear N,N‐dialkyl hydroxylamines and their corresponding amine, nitrone and oxime derivatives, as well as further components: tert‐N‐oxides, secondary amides and carboxylic acids. Specific migration was tested from polyethylene samples in 10% ethanol and 3% acetic acid for 2 h at 100°C followed by 10 days at 60°C. None of the non‐authorised components were detected to migrate at detection limits (LoD) in the range 0.003–0.029 mg/kg. The LoD of authorised carboxylic acids was 0.35 mg/kg. The Panel reassessed the genotoxicity studies carried out on FCM No 768 and evaluated two new bacterial reverse mutation tests on the nitrone and oxime derivatives as well as new (qualitative/quantitative) structure–activity relationship (Q)SAR analyses on other components. The Panel concluded that the substance did not raise a concern for genotoxicity. The Panel concluded that the substance is not of safety concern for the consumers if it is used as an additive at 0.1% w/w in the manufacture of polyolefin FCM intended to be in contact with foods simulated by food simulants A, B, C and E, except for infant formula and human milk, for storage above 6 months at room temperature and below, including hot‐fill conditions and heating up to 100°C for 2 h. [ABSTRACT FROM AUTHOR]

Guar gum (E 412) was re‐evaluated in 2017 by the former EFSA Panel on Food Additives and Nutrient sources added to Food (ANS). As a follow‐up to this assessment, the Panel on Food Additives and Flavourings (FAF) was requested to assess the safety of guar gum (E 412) for its uses as food additive in food for infants below 16 weeks of age belonging to food categories 13.1.1 (Infant formulae) and 13.1.5.1 (Dietary foods for infants for special medical purposes and special formulae for infants). In addition, the FAF Panel was requested to address the issues already identified during the re‐evaluation of the food additive when used in food for the general population. The process involved the publication of a call for data to allow the interested business operators to provide the requested information to complete the risk assessment. In the response to EFSA requests, one IBO stated that E 412 is not used in food categories 13.1.1 and 13.1.5.1, but it is present in products under food category 13.1.5.2. The Panel concluded that the submitted data are not sufficient to support the safe use of guar gum (E 412) in food for infants (below and above 16 weeks of age) and young children under FC 13.1.1, 13.1.5.1 and 13.1.5.2. Additionally, the Panel concluded that the technical data provided by the IBO support further amendments of the specifications for E 412 laid down in Commission Regulation (EU) No 231/2012. [ABSTRACT FROM AUTHOR]

The food enzyme subtilisin (EC 3.4.21.62) is produced with the genetically modified Bacillus licheniformis strain NZYM‐CB by Novozymes A/S. The genetic modifications do not give rise to safety concerns. The food enzyme is considered free from viable cells of the production organism and its DNA. It is intended to be used in six food manufacturing processes. The dietary exposure to the food enzyme‐TOS was estimated to be up to 0.722 mg TOS/kg body weight (bw) per day in European populations. The production strain of the food enzyme fulfils the requirements for the qualified presumption of safety approach to safety assessment. As no other concerns arising from the manufacturing process were identified, the Panel considered that toxicological tests were not required for the assessment of this food enzyme. A search for the similarity of the amino acid sequence of the food enzyme to known allergens was made and 20 matches were found, including two food allergens (melon and pomegranate). The Panel considered that the risk of allergic reactions by dietary exposure cannot be excluded, particularly in individuals sensitised to melon and pomegranate, but would not exceed the risk from consumption of melon or pomegranate. Based on the data provided, the Panel concluded that this food enzyme does not give rise to safety concerns under the intended conditions of use. [ABSTRACT FROM AUTHOR]

The food enzyme phosphodiesterase I (oligonucleotide 5′‐nucleotidohydrolase; EC 3.1.4.1) is produced with the non‐genetically modified Leptographium procerum strain FDA by DSM Food Specialties B.V. The food enzyme is free from viable cells of the production organism. It is intended to be used in the processing of yeast and yeast products. Dietary exposure to the food enzyme‐total organic solids (TOS) was estimated to be up to 0.171 mg TOS/kg body weight (bw) per day in European populations. Genotoxicity tests did not indicate a safety concern. The systemic toxicity was assessed by means of a repeated dose 90‐day oral toxicity study in rats. The Panel identified a no observed adverse effect level of 1000 mg TOS/kg bw per day, the highest dose tested, which, when compared with the estimated dietary exposure, resulted in a margin of exposure of at least 5848. A search for the similarity of the amino acid sequence of the food enzyme to known allergens was made and no match was found. The Panel considered that the risk of allergic reactions by dietary exposure cannot be excluded, but the likelihood is low. Based on the data provided, the Panel concluded that this food enzyme does not give rise to safety concerns under the intended conditions of use. [ABSTRACT FROM AUTHOR]