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This opinion deals with the re‐evaluation of polydextrose (E 1200) when used as a food additive. The Panel followed the conceptual framework for the risk assessment of certain additives and considered that: adequate exposure estimates were available; the margin of safety (MOS)/margin of exposure (MOE) for arsenic was between 0.5‐14 and 8.5 for lead; the exhaustions of the tolerable weekly intake (TWI) for cadmium would be 165%, 10% for mercury, whereas the exhaustion of the tolerable daily intake (TDI) for nickel would be 9%; the absorption is limited and part of polydextrose is fermented in the large intestine into short‐chain fatty acids (SCFA); adequate toxicity data were available; there is no concern with respect to genotoxicity; no adverse effects were reported in subchronic studies in rats, dogs or monkeys nor in chronic or carcinogenicity studies in mice and rats at the highest doses tested of up 12,500 mg/kg body weight (bw) per day and 15,000 mg/kg bw per day, respectively; the nephrocalcinosis in dogs given high doses of polydextrose was considered to be a treatment‐related but a secondary effect related to diarrhoea, and hence not relevant for the risk assessment; no adverse effects were reported in reproductive or developmental toxicity studies in rats administered up to 10,000 mg polydextrose/kg bw per day, or in a developmental toxicity study in rabbits up to 1,818 mg/kg bw per day (the highest dose tested). Therefore, the Panel concluded that there is no need for numerical acceptable daily intake (ADI) for polydextrose (E 1200), and that there is no safety concern for the reported uses and use levels of polydextrose as a food additive. The Panel recommended that European Commission considers to lower the maximum limit for lead and to introduce limits for arsenic, cadmium and mercury in the EU specifications for polydextrose (E 1200), and to verify that polydextrose‐N as a food additive (E 1200) is no longer marketed in the EU.

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.

The Panel on Food Additives and Nutrient Sources added to Food (ANS) provides a scientific opinion re‐evaluating the safety of xanthan gum (E 415) as food additive. 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. Based on the reported use levels, a refined exposure of up to 64 mg/kg bw per day in children for the general population, 38 mg/kg bw per day for children consumers only of food supplements at the high level exposure and 115 mg/kg bw per day for infants consuming foods for special medical purposes and special formulae (FSMPs), were estimated. Xanthan gum (E 415) 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 chronic and carcinogenicity studies and there is no concern with respect to the genotoxicity. Repeated oral intake by adults of xanthan gum up to 214 mg/kg bw per day for ten days was well tolerated, but some individuals experienced abdominal discomfort, an undesirable but not adverse effect. The Panel concluded that there is no need for a numerical ADI for xanthan gum (E 415), and that there is no safety concern for the general population at the refined exposure assessment of xanthan gum (E 415) as food additive. Considering the outcome of clinical studies and post‐marketing surveillance, the Panel concluded that there is no safety concern from the use of xanthan gum (E 415) in FSMPs for infants and young children at concentrations reported by the food industry. The current re‐evaluation of xanthan gum (E 415) as a food additive is not considered to be applicable for infants under the age of 12 weeks.

The EFSA Panel on Food Additives and Nutrient Sources added to Food (ANS) provides a scientific opinion re‐evaluating the safety of glutamic acid–glutamates (E 620–625) when used as food additives. Glutamate is absorbed in the intestine and it is presystemically metabolised in the gut wall. No adverse effects were observed in the available short‐term, subchronic, chronic, reproductive and developmental studies. The only effect observed was increased kidney weight and increased spleen weight; however, the increase in organ weight was not accompanied by adverse histopathological findings and, therefore, the increase in organ weight was not considered as an adverse effect. The Panel considered that glutamic acid–glutamates (E 620–625) did not raise concern with regards to genotoxicity. From a neurodevelopmental toxicity study, a no observed adverse effect level (NOAEL) of 3,200 mg monosodium glutamate/kg body weight (bw) per day could be identified. The Panel assessed the suitability of human data to be used for the derivation of a health‐based guidance value. Although effects on humans were identified human data were not suitable due to the lack of dose–response data from which a dose without effect could be identified. Based on the NOAEL of 3,200 mg monosodium glutamate/kg bw per day from the neurodevelopmental toxicity study and applying the default uncertainty factor of 100, the Panel derived a group acceptable daily intake (ADI) of 30 mg/kg bw per day, expressed as glutamic acid, for glutamic acid and glutamates (E 620–625). The Panel noted that the exposure to glutamic acid and glutamates (E 620–625) exceeded not only the proposed ADI, but also doses associated with adverse effects in humans for some population groups.

Background: Endometriosis is a common gynecologic disease characterized by the ectopic growth of endometrial tissue. In industrialized countries, it affects approximately 10% of women of reproductive age. Its etiology is unclear, but a multifactorial origin is considered to be most plausible. Environmental organochlorinated persistent pollutants, in particular dioxins and polychlorinated biphenyls (PCBs), have been hypothesized to play a role in the disease etiopathogenesis. However, results of studies carried out on humans are conflicting. Objective: We evaluated the exposure to organochlorinated persistent pollutants as a risk factor for endometriosis. Methods: We conducted a case-control study in Rome on 158 women comprising 80 cases and 78 controls. In all women, serum concentrations of selected non-dioxin-like PCBs (NDL-PCBs) and dioxin-like PCBs (DL-PCBs), 1,1-dichloro-2,2,-bis(4-chlorophenyl)-ethene (p,p'-DDE), and hexachlorobenzene (HCB) were determined by ion-trap mass spectrometry. DR-CALUX bioassay was employed to assess the 2,3,7,8-tetrachlorodibenzo-p-dioxin toxicity equivalent (TEQ) concentrations of polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), and DL-PCBs. Results: We found an increased risk of endometriosis for DL-PCB-118 [odds ratio (OR) = 3.79; 95% confidence interval (CI), 1.61-8.91], NDL-PCB-138 (OR = 3.78; 95% CI, 1.60-8.94), NDL-PCB-153 (OR = 4.88; 95% CI, 2.01-11.0), NDL-PCB-170 (OR = 3.52; 95% CI, 1.41-8.79), and the sum of DL-PCBs and NDL-PCBs (OR = 5.63; 95% CI, 2.25-14.10). No significant associations were observed with respect to HCB or to the sum of PCDDs, PCDFs, and DL-PCBs given as total TEQs. Conclusions: The results of this study show that an association exists between increased PCB and p,p'-DDE serum concentrations and the risk of endometriosis.

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.

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 re‐evaluating the safety of microcrystalline cellulose (E 460(i)), powdered cellulose (E 460(ii)), methyl cellulose (E 461), ethyl cellulose (E 462), hydroxypropyl cellulose (E 463), hydroxypropyl methyl cellulose (E 464), ethyl methyl cellulose (E 465), sodium carboxy methyl cellulose (E 466), enzymatically hydrolysed carboxy methyl cellulose (E 469) and cross‐linked carboxy methyl cellulose (E 468) as food additives. The Joint FAO/WHO Expert Committee on Food Additives (JECFA) and the Scientific Committee on Food (SCF) established an acceptable daily intake (ADI) ‘not specified’ for unmodified and modified celluloses. Celluloses are not absorbed and are excreted intact in the faeces; in addition, microcrystalline cellulose, powdered and modified celluloses could be fermented by the intestinal flora in animals and humans. Specific toxicity data were not always available for all the celluloses evaluated in the present opinion and for all endpoints. Given their structural, physicochemical and biological similarities, the Panel considered it possible to read‐across between all the celluloses. The acute toxicity of celluloses was low and there was no genotoxic concern. Short‐term and subchronic dietary toxicity studies performed with E 460(i), E 461, E 462, E 463, E 464, E 466 and E 469 at levels up to 10% did not indicate specific treatment related adverse effects. In chronic toxicity studies performed with E 460(i), E 461, E 463, E 464, E 465 and E 466, the no observed adverse effect level (NOAEL) values reported ranged up to 9,000 mg/kg body weight (bw) per day. No carcinogenic properties were detected for microcrystalline cellulose and modified celluloses. Adverse effects on reproductive performance or developmental effects were not observed with celluloses at doses greater than 1,000 mg/kg bw by gavage (often the highest dose tested). The combined exposure to celluloses (E 460–466, E 468 and E 469) at 95th percentile of the refined (brand‐loyal) exposure assessment for the general population was up to 506 mg/kg bw per day. The Panel concluded that there was no need for a numerical ADI and that there would be no safety concern at the reported uses and use levels for the unmodified and modified celluloses (E 460(i); E 460(ii); E 461–466; E 468 and E 469). The Panel considered an indicative total exposure of around 660–900 mg/kg bw per day for microcrystalline, powdered and modified celluloses.

The present opinion deals with the re‐evaluation of shellac (E 904) when used as a food additive and with the new application on the extension of use of shellac (E 904) in dietary foods for special medical purposes. The Panel derived an acceptable daily intake (ADI) of 4 mg/kg body weight (bw) per day for wax‐free shellac (E 904) produced by physical decolouring, based on a NOAEL of 400 mg/kg bw per day and applying an uncertainty factor of 100. The Panel concluded that the ADI of 4 mg/kg bw per day should be considered temporary for wax‐free shellac (E 904) produced by chemical bleaching, while new data are generated on the identity and levels of the organochlorine impurities in E 904. This ADI is not applicable for wax‐containing shellac as a food additive. For several age groups, the ADI was exceeded at the 95th percentile in the non‐brand‐loyal exposure assessment scenario and maximum level exposure assessment scenario. Considering the low exceedance and the fact that both the exposure estimation and the toxicological evaluation of shellac were conservative, the panel concluded that the calculated exceedance of the ADI does not indicate a safety concern. The Panel recommended to the European Commission separating specifications for E 904 depending on the manufacturing process, chemical bleaching and physical decolouring, because they result in different impurities; revising the definition of the food additive to include a description of each manufacturing process; deleting information on wax‐containing shellac from the EU specifications; revising the acid value for wax‐free shellac produced by chemical bleaching; lowering the maximum limit for lead; to consider introducing limits for other toxic elements potentially present in shellac; including a maximum limit for chloroform and total inorganic chloride in the EU specification for shellac produced by chemical bleaching.

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.

The present opinion deals with the re‐evaluation of polyvinylpyrrolidone (E 1201, PVP) and polyvinylpolypyrrolidone (E 1202, PVPP) when used as food additives. One request for extension of use of PVP (E 1201) in foods for special medical purposes was also considered in this assessment. The Panel followed the conceptual framework under Commission Regulation (EU) No 257/2010 and considered that: the exposure assessment was based on the reported use and use levels (one food category out of the two food categories in which PVP and PVPP are authorised); the 95th percentile of exposure to PVP and PVPP of maximally 23.7 and 25 mg/kg body weight (bw) per day in children, respectively, was overestimated, because it was assumed that 100% of the food supplements consumed contained PVP or PVPP at the maximum reported use levels; the extension of use of PVP (E 1201) to foods for special medical purposes (FC 13.2) would result in an exposure of PVP of 4.3 mg/kg bw per day for children; the absorption of PVP and PVPP is very low; sufficient toxicity data were available for PVP; there is no concern with respect to the genotoxicity of PVP and PVPP; no carcinogenic effects were reported in carcinogenicity studies in rats at a dose of 2,500 mg PVP/kg bw per day, the highest dose tested; there is no need for chronic toxicity/carcinogenicity data for PVPP for the safety assessment of PVPP given the chemical similarity between PVP and PVPP, and the lack of adverse effects in the available repeated dose toxicity studies. Therefore, the Panel concluded that there is no need for numerical acceptable daily intakes (ADIs) for PVP and PVPP, and that there is no safety concern for the reported uses and use levels of PVP and PVPP as food additives. The Panel further concluded that the proposed extension of use is not expected to be of safety concern at the proposed maximum permitted level (MPL) and recommended consumption level.