Based on the analytical feasibility to measure the chemical compounds routinely in accredited laboratories, the production volumes, the occurrence of the chemical compounds in food and feed, their persistence in the environment and their toxicity, the inclusion of the following compounds in the core group of brominated flame retardants (BFRs) in a European monitoring programme for feed and food is recommended:polybrominated diphenyl ethers (PBDEs): BDE congeners #28, 47, 99, 100, 153, 154, 183 and 209.hexabromocyclododecane (HBCD): total amount (isomer specific analysis of a limited number of samples and/or pools in case of significantly elevated levels or increasing trends).polybrominated biphenyls (PBBs): BB congener #153.Optionally, the following BFRs could be included in this monitoring programme:additional PBDE congenersdecabromodiphenyl ethanehexabromobenzenebis (2,4,6-tribromophenoxy)ethane

Ochratoxin A (OTA) is a mycotoxin produced by several fungal species of the genera Penicillium and Aspergillus. Contamination of food commodities, including cereals and cereal products, pulses, coffee, beer, grape juice, dry vine fruits and wine as well as cacao products, nuts and spices, has been reported from all over the world. In addition, contamination of animal feeds with OTA may result in the presence of residues in edible offal and blood serum, whereas the OTA contamination in meat, milk and eggs is negligible. Despite efforts to reduce the amount of this mycotoxin in foods as consumed, a certain degree of contamination seems unavoidable at present.Some early epidemiological data had suggested that OTA might be involved in the pathogenesis of distinct renal diseases and otherwise rare tumours of the kidneys in certain endemic regions of the Balkan Peninsula. However, these epidemiological data are incomplete and do not justify the classification of OTA as a human renal carcinogen. OTA has been found to be a potent renal toxin in all of the animal species tested. It induces a typical karyomegaly and a progressive nephropathy. The extent of renal injury is dose-dependent, but also associated with the duration of exposure, as OTA accumulates in renal tissue. Previous National Toxicology Program (NTP) studies in United States showed that OTA can induce renal tumours in rodents at high dosages.Recent scientific evidence indicates that the site-specific renal toxicity as well as the DNA damage and genotoxic effects of OTA, measured in various in vivo and in vitro studies, are most likely attributable to cellular oxidative damage. Furthermore, advanced chemical analytical procedures failed to demonstrate the existence of specific OTA-DNA adducts. Considering the lack of evidence for the existence of OTA-DNA adducts, the Panel used a threshold-based approach in its risk assessment of OTA. On the basis of the lowest observed adverse effect level (LOAEL) of 8 mu g/kg body weight (b.w.) per day for early markers of renal toxicity in pigs (the most sensitive animal species), and applying a composite uncertainty factor of 450 for the uncertainties in the extrapolation of experimental data derived from animals to humans as well as for intra-species variability, a Tolerable Weekly Intake (TWI) of 120 ng/kg b.w. was derived for OTA.Recent analyses of the dietary exposure of adult European consumers to OTA revealed that at present the weekly exposure ranges from 15 to 60 ng OTA per kg bodyweight per week, including high consumers of foods containing OTA. This rate of exposure is below the TWI value of 120 ng/kg b.w. as derived by the Panel. However, as current EFSA consumption databases do not include infants and children, the CONTAM Panel concluded that more data would be needed to assess exposure rates of this segment of consumers, taking into account their dietary preferences.

Arsenic is a naturally occurring element, present in soil, ground water and plants. Regions with high geological occurrence of inorganic arsenic have been identified in particular in Asia and other non-European countries. In Europe, environmental arsenic levels are rather low, with the exception of distinct geological or industrial areas. Arsenic is a metalloid, displaying different valences (-3, 0, +3, +5) resulting in a broad variety of arsenic compounds with diverse chemical characteristics. Inorganic and organic forms of arsenic also differ significantly in their toxicity, the organic arsenic compounds exhibiting a very low toxic potential. Consequently, the potential adverse effects of arsenic to animal (and human) health are determined by the inorganic fraction in a given feed (or food) product, and data reporting only total arsenic in food materials are difficult to interpret in terms of the ability to induce adverse effects. Drinking water many contain significant amounts of inorganic arsenic and upper limits have been set in most countries. Seafood and fish have been identified as major source of arsenic in the human diet, and in animal feed materials that contain products derived from fish or other marine organisms. In seafood and fish, arsenic is present predominantly in the organic forms of arsenobetaine and arsenocholine, which are virtually non-toxic. Analytical data from the Member States on total arsenic in feed materials do not indicate arsenic levels of concern in materials others than fish-derived products, for which further data on chemical speciation are needed, to identify the actual levels of inorganic arsenic. As the carry-over of arsenic in its inorganic form into edible tissue of mammals and poultry is low, food derived from terrestrial animals contributes only insignificantly to human exposure.

Polychlorinated biphenyls (PCB) cover a group of 209 different PCB congeners which can be divided into two groups according to their toxicological properties. One group, consisting of 12 congeners, show toxicological properties similar to dioxins, is therefore termed "dioxin-like PCB" (DL-PCB), and these have been included in the "Risk Assessment of Dioxins and Dioxin-Like PCBs in Food" performed by the EU Scientific Committee on Food (SCF). The other PCB, referred to as "non dioxin-like PCB" (NDL-PCB), have not been previously evaluated by the SCF or EFSA. Both groups of PCB, NDL-PCB as well DL-PCB, are usually found in feed and food.PCB were widely used in a number of industrial and commercial applications. It is estimated that more than 1 million tons of technical PCB mixtures were produced world-wide since their first commercial use in the late 1920s. Although produced by comparable production processes, technical PCB mixtures contain both DL and NDL-PCB and may vary considerably with respect to their congener composition due to differences in the amount of chlorine and the reaction conditions applied. Moreover, technical PCB mixtures contain other dioxin-like compounds as impurities, such as polychlorinated dibenzofurans (PCDF). The different compositions as well as the presence of toxicologically relevant impurities may have a significant impact on the results of toxicological studies with technical PCB mixtures.Although the manufacture, processing and distribution of PCB has been prohibited in almost all industrial countries since the late 1980s, their entry into the environment still occurs, especially due to improper disposal practices or leaks in electrical equipment and hydraulic systems still in use. PCB are highly persistent and are globally circulated by atmospheric transport and thus are present in all environmental media.Data on the occurrence of NDL-PCB in food and feed have been reported in different ways for example as the sum of three PCB congeners (PCB 138, 153 and 180), as the sum of six PCB congeners (PCB 28, 52, 101, 138, 153, 180) often referred to as indicator PCB or as the sum of seven (sum of six indicator PCB plus PCB 118). This lack of consistency often hampers a direct comparison of occurrence data. The Panel decided to use the sum of the six indicator PCB as the basis for the evaluation in this opinion, because these congeners are appropriate indicators for different PCB patterns in various sample matrices and are most suitable for a risk assessment of NDL-PCB on the basis of the available data. The Panel noted that the sum of the six indicator PCB represents about 50% of total NDL-PCB in food.Following exposure of farm animals, NDL-PCB will accumulate in meat, liver and particularly in fat tissues. In addition, NDL-PCB will be transferred into milk and eggs, and levels in these products will reach a steady state following exposure over a period of several weeks. PCB 138 and 153, both with six chlorine atoms, show the highest carry-over into milk and eggs, in the order of 50-60%. After cessation of exposure, levels in eggs and milk initially decrease rapidly to about 50%, followed by a slower elimination phase. In fattened animals like calves, piglets, and poultry, and also farmed fish, no steady state is obtained, due to the fact that these animals are slaughtered at a young age.For risk assessment of domestic animals, the Panel compared the effect concentrations in the experimental diet with the NDL-PCB concentration in animal feed. Following a conservative approach, the 90th percentile of the sum of six NDL-PCB in compound feed, 0.02 mg/kg feed was taken as the point of comparison. This figure corresponds to about 0.04 mg total NDL-PCB, which is more than two orders of magnitude below the concentrations causing effects in most domestic animals studied. Mink are usually given feed based on fish. The 90th percentile of the sum of the six NDL-PCB in fish and fish products is 0.067 mg/kg corresponding to 0.13 mg/kg total NDL-PCB. This is only about five times below the concentration of PCB in feed that produced pronounced effects on reproduction in mink. The Panel therefore concluded that current background levels of NDL-PCB in animal feed are of no health concern for most domestic animals, with the possible exception of mink.Congener patterns in feed, particularly that of plant origin and in edible tissue may differ considerably. Due to the different sources of contamination, different origins of the feed and of food commodities, there is generally no correlation between the concentrations of NDL-PCB and DL-PCB Toxic Equivalents (TEQ) or the total TEQ (polychlorinated dibenzo-p-dioxins (PCDD), polychlorinated dibenzofurans (PCDF) and DL-PCB) with the exception of samples where the circumstances of contamination are known.More than 90% of the NDL-PCB exposure in the general population is via food. Average daily dietary intakes of total NDL-PCB can be estimated to be in the range of 10-45 ng/kg body weight (b.w.) per day. Limited exposure data for young children, up to six years of age, indicates that the average intake (breastfeeding excluded) of total NDL-PCB is about 27-50 ng/kg b.w. per day. However, where data on both adults and children within a specific population were available, in general children had exposure levels 2.5 fold higher than adults. In specific subpopulations with high dietary PCB exposure such as Baltic Sea fishermen the daily intake from fish of the sum of the six NDL-PCB could be about 40 ng/kg b.w., corresponding to an intake of total NDL-PCB of 80 ng/kg b.w. per day before taking into account the rest of the diet. Breastfed infants are a group of high NDL-PCB intake which might be two orders of magnitude higher than adult exposure.Other routes of exposure such as ambient and indoor air, dust and soil, do not usually contribute significantly to the body burden of the general population. However, there are situations in which contribution from contaminated indoor air could be considerable.Technical PCB mixtures used in toxicity studies contain both NDL-PCB and dioxin-like compounds such as DL-PCB. These mixtures exert a variety of toxicological effects such as effects on liver, thyroid, immune function, reproduction and behaviour as well as carcinogenicity. The adverse effects reported in laboratory animals following exposure to individual NDL-PCB were effects on the thyroid, liver and brain biochemistry, as well as immunotoxicity, oestrogenicity, and reproductive and neurodevelopmental effects. The latter effects are particularly found in the offspring of rodents following in utero exposure. However, these effects are not all specific for NDL-PCB but are also to be seen following exposure to polychlorinated dibenzo-p-dioxins, polychlorinated dibenzofurans, and DL-PCB.Several NDL-PCB congeners are metabolised to hydroxy-PCB and/or methylsulfonyl-PCB. Some of these metabolites may contribute to hormone-like effects seen with PCB.Results of in vitro and in vivo genotoxicity studies indicate that PCB are not mutagenic at the gene or chromosome level. Some NDL-PCB, in particular the lower chlorinated congeners, caused DNA damage, probably resulting from the formation of reactive oxygen species. In two-stage initiation-promotion studies, technical PCB mixtures containing NDL-PCB as well as DL-PCB promote liver carcinogenesis in rats, following initiation with genotoxic carcinogens. Data from animal experiments with several technical mixtures (Aroclor 1016, 1242, 1254 and 1260) indicate that PCB can cause liver and thyroid neoplasms in rats. The International Agency for Research on Cancer (IARC) classified PCB in Group 2A (probably carcinogenic to humans), based on limited evidence in humans and sufficient evidence in animals. Evaluation of the cancer studies in rats with technical PCB mixtures, and comparison with data obtained with TCDD, indicate that the dioxin-like components in technical PCB mixtures are likely to be responsible for the carcinogenic response of these mixtures. No peer reviewed data are available on the carcinogenicity of individual NDL-PCB congeners.Occupational exposures to PCB have been reported to be associated with an increased risk of cancer of the digestive system and possibly other sites. Some studies suggest that environmental PCB exposure may be linked to the development of breast cancer, although perhaps only in certain vulnerable sub-groups. Among non-cancer effects reported to be associated with environmental PCB exposure, adverse reproductive outcomes, delayed neurodevelopment and impairment of the immune system during development are considered to be the most important. The epidemiological studies however do not allow an estimation of the toxicity that may specifically be attributed to the NDL-PCB.Benchmark dose calculations have been based on human studies on developmental neurotoxicity and immunotoxicity after perinatal exposure to total DL and NDL-PCB. The 95% lower confidence limit of benchmark dose (BMDL) of approximately 1 mu g PCB/g lipid is only about four times higher than the current median concentration in human milk.The Panel noted that the comprehensive toxicological database on health effects of technical PCB mixtures was not suitable for the separate assessment of NDL-PCB, and that the human data on exposure to environmental mixtures containing PCB could not differentiate between the effects of NDL-PCB and DL-PCB and polychlorinated dibenzo-p-dioxins/polychlorinated dibenzofurans. Therefore, in its assessment the Panel concentrated on the toxicological information available for individual NDL-PCB congeners. Although the absence of mutagenicity indicates that a threshold approach is appropriate for the hazard characterisation, the toxicological database however, was considered to be too limited to allow the establishment of a health based guidance value for NDL-PCB. The Panel therefore decided to perform its health risk characterisation on the basis of a margin of exposure approach.The most sensitive effects seen in studies with individual NDL-PCB congeners in experimental animals were liver and thyroid toxicity. The NOAELs for these effects in 90-day rat studies with the individual NDL-PCB congeners PCB 28, 128, and 153 were in the range of 30-40 mu g/kg b.w. per day. For compounds that accumulate in the body, such as NDL-PCB, evaluations based on body burden (BB) calculations are considered more appropriate than evaluations based on the external dose. The Panel therefore applied a body burden approach to the results of the 90-day rat studies, and estimated body burdens at the "no observed adverse effect level" (NOAEL) of 400, 800, and 1,200 mu g/kg b.w. for PCB 28, 128, and 153, respectively. The Panel compared estimated body burdens at the NOAEL for different effects in animals with the estimated median human body burden derived from the analyses of human milk. The "margin of body burdens" at the NOAEL (NOAEL MoBB) were calculated by dividing the estimated animal body burden with the estimated median human body burden.NOAEL MoBBs of 900, 6,300, and 85 were obtained for the effects on liver and/or thyroid of PCB 28, 128, and 153, respectively. Although PCB 28, 128, and 153 showed similar potencies in the 90-day toxicity studies, PCB 153 had the lowest NOAEL MoBB due to its abundance in human tissues. Application of the same approach to experimental animal studies on reproductive and developmental effects, oestrogenicity, thyroid effects and effects on the immune system and the developing nervous system, revealed NOAEL MoBBs that were higher than 1,600.In order to evaluate the impact of exposure to total NDL-PCB, the Panel noted that the available toxicological database on NDL-PCB covered a number of congeners present in food and human tissues. Considering that the "lowest observed adverse effect level" BB for the most sensitive effects (liver, thyroid) were 10 times higher than the NOAEL BB (400, 800, and 1,200 mu g /kg b.w. for PCB 28, 128, and 153, respectively), the Panel chose an overall body burden of 500 mu g /kg b.w. as a representative conservative body burden at the NOAEL (NOAEL BB) for all individual NDL-PCB and for the sum of NDL-PCB occurring in human tissues. Based on the median total concentration of all NDL-PCB measured in human milk sampled in European countries of about 240 ng/g fat, and assuming 20% fat content in the human body, a median human body burden of about 50 mu g/kg b.w. was estimated. Consequently the overall NOAEL MoBB is about 10.Although this margin appears rather small, it should be stressed that the endpoints considered in the evaluation of the individual NDL-PCB congeners, can also be observed after treatment with polychlorinated dibenzo-p-dioxins, polychlorinated dibenzofurans, or DL-PCB. Since a number of these latter compounds have relatively high potencies for these effects in rats, minor contamination (in the range of 0.1%) of the NDL-PCB congeners studied with potent dioxin-like compounds might be sufficient to explain the effects observed. Thus, any estimate of a NOAEL for NDL-PCB is hampered by the uncertainty in the extent to which NDL-PCB congeners might have been contaminated with polychlorinated dibenzofurans and/or DL-PCB. Therefore the "true" NOAEL MoBB for NDL-PCB might be larger. On the other hand, the MoBB was calculated on the basis of the median concentrations of NDL-PCB in human milk, and some populations in Europe may have considerably higher body burdens.During the nursing period, breastfed infants may have daily intakes, on a body weight basis, of NDL-PCB estimated to be about two orders of magnitude higher than the average adult intake. This elevated intake by the infants is related to the mother's long-term intake of NDL-PCB with food. However, the subtle neurodevelopmental effects that were reported in some studies of human infants were mainly associated with exposure to a mixture of NDL-PCB, DL-PCB, and polychlorinated dibenzo-p-dioxins/polychlorinated dibenzofurans, and any causal role of NDL-PCB is unclear. The Panel noted that in many other studies of infants, breastfeeding was associated with beneficial effects, in spite of the contaminants present in human milk.In conclusion, no health based guidance value for humans can be established for NDL-PCB because simultaneous exposure to NDL-PCB and dioxin-like compounds hampers the interpretation of the results of the toxicological and epidemiological studies, and the database on effects of individual NDL-PCB congeners is rather limited. There are however indications that subtle developmental effects, being caused by NDL-PCB, DL-PCB, or polychlorinated dibenzo-p-dioxins/polychlorinated dibenzofurans alone, or in combination, may occur at maternal body burdens that are only slightly higher than those expected from the average daily intake in European countries. Because some individuals and some European (sub)-populations may be exposed to considerably higher average intakes, a continued effort to lower the levels of NDL-PCB in food is warranted.

Aldrin and dieldrin (a metabolite of aldrin as well as a marketed pesticide) are both fat soluble persistent and bio-accumulating organochlorine insecticides. Commercial manufacture began in 1950. They have been widely used in the past, but are now banned in most countries world wide and are included in the Stockholm convention on persistent organic pollutants (POPs) and the United Nations Economic Commission for Europe (UNECE) Convention on long-range transboundary air pollution protocol on POPs. There are still residues of dieldrin in the environment and in human tissues, but the levels have been declining during the last 30 years.In both animals and humans, aldrin and dieldrin are readily absorbed via the gastrointestinal tract. The conversion of aldrin to dieldrin occurs much more rapidly than the subsequent biotransformation and elimination of dieldrin, resulting in the accumulation of dieldrin in lipid rich tissues. The dominant toxic effects are in the nervous system and the liver, the latter mainly following chronic exposure. Aldrin and dieldrin are approximately equally toxic. They are not genotoxic or teratogenic.The transfer rates from feed to milk, eggs and adipose tissue are among the highest found for chlorinated pesticides, making aldrin, and especially dieldrin, highly accumulative compounds. Dieldrin rather than aldrin predominates in feed materials of animal origin. Due to a high level of bioaccumulation in the aquatic food chain, fish derived products, particularly fish oil, were identified to contain the highest levels of dieldrin. The majority of fish oil samples contained dieldrin at levels below 50 mu g/kg. Other fish derived feed material contained dieldrin at levels ten fold lower. Feed products of plant origin occasionally show levels of aldrin and dieldrin above the limit of detection which is mostly in the range of 1 to 10 mu g/kg. The levels found in feed are much lower than the levels which would induce toxicity in farmed animals and pets.Due to the ban on aldrin and dieldrin in the EU, and in most other countries world-wide, human exposure to these two pesticides is steadily decreasing. The levels in samples taken recently are below 10 % of those in samples taken 20 years ago. The daily intake from food for adults and children seems to be in the range of 1 to 10 ng/kg b. w. Thus, the dietary intake is substantially below the provisional tolerable daily intake (PTDI) of 100 ng/kg b.w. established by the JMPR (FAO/WHO Joint Meeting on Pesticide Residues).

Technical hexachlorocyclohexane (HCH) is a mixture of various HCH isomers; alpha (alpha), beta (beta), delta (delta) and gamma (gamma) (also known as lindane). Both technical HCH and gamma-HCH have been globally used as insecticides, and gamma-HCH also for medical treatment in humans and animals. The insecticidal activity can be almost exclusively attributed to the gamma-isomer. In some areas in the world these compounds are still in use. Because of the lipophilic properties and persistence in the environment, beta-HCH followed by alpha-HCH and to a less extent gamma-HCH may give rise to bioaccumulation and biomagnification through the food chain.HCHs are rapidly absorbed from the gastrointestinal tract, pass the placenta and are transferred into milk. The toxicity of the isomers varies, gamma-HCH being the most acutely neurotoxic followed by alpha-HCH beta-HCH penetrates less readily into the central nervous system, is more persistent and tends to accumulate in the body over time. All isomers cause liver hyperplasia and/or liver tumours. Except for experimental animals there are relatively few data on toxicity in other animal species. Neurotoxicity and liver effects have been reported in fish and ruminants. There is a lack of data on dose-effect relationship, particularly for fish and ruminants beta-HCH has weak estrogenic activity. alpha- and beta-HCH are tumour promoters in rat liver. HCHs were classified by IARC in group 2B (possibly carcinogenic) on the basis of inadequate evidence for carcinogenicity to humans, sufficient (for technical grade and the alpha-isomer) and limited evidence for carcinogenicity to animals (for beta- and gamma-HCHs).Data on occurrence in various feed categories including fish feed indicate levels in the mu g/kg range of alpha-, beta- and gamma-HCH. Accumulation data in fish exposed through feed is lacking. The contamination route of HCHs into feed is not clear. However, the global trade of feedingstuffs and feed ingredients from regions with ongoing or recent use of HCHs may be a major source. A European reporting system, allowing for exposure assessment of undesirable substances in feed is missing.Recent assessments of human dietary exposure to HCHs in Europe are scarce. Considering the available intake data from Czech Republic, Canada and USA and taking into account the decreasing concentration of HCHs in breast milk (about 80 % since the eighties in Germany), current exposure through food is likely to be very low. beta-HCH is usually still present but aand gamma-HCH are only occasionally found in human milk samples from European Countries, which banned the production and use of technical HCH in the late 1970s. Some East European and developing countries with a longer use of technical HCH show higher contamination levels in breast milk.

Fumonisins are a distinct group of mycotoxins produced by several field fungi, including Fusarium verticillioides and Fusarium proliferatum. Fumonisins are occurring particularly in maize and maize-based products. Co-occurrence with other Fusarium toxins, such as zearalenone and deoxynivalenol, is regularly observed. Fumonisin B-1 is considered to be the most prevalent and most toxic derivative within the group of fumonisins. It is a prototypic inhibitor of cellular sphingosine (sphinganine) N-acetyltransferase. Inhibition of this enzyme is followed by an accumulation of sphinganine (Sa) and sometimes also sphingosine (So) and a depletion of complex sphingolipids in eukaryotic cells, which in turn results in impairment of cell cycle regulation and cellular differentiation, and in oxidative stress as well as apoptosis and necrosis. Fumonisin B-1 is carcinogenic in rodents, but it is devoid of significant genotoxic activity. In vivo rodent experiments suggest that fumonisins are tumour promoters. The increased Sa: So ratio in body fluids and tissues serves as a sensitive biomarker of exposure to fumonisins. Equidae and porcine species are considered to be the most sensitive animal species to fumonisins, developing species-specific clinical syndromes such as equine leukoencephalomalacia and porcine pulmonary oedema. Ruminants and poultry show a low responsiveness to fumonisins. Few data are available on the effects of fumonisins on farmed fish and on minor species, such as rabbits, goats and minks. The available data on animal exposure via feedingstuffs are limited and monitoring of feed materials is needed to improve exposure assessment. Available data on carry-over of fumonisins from animal feeds into edible tissues, including milk and eggs, indicate that transfer is limited, and thus residues in animal tissues contribute insignificantly to total human exposure.

Camphechlor is a non-systemic insecticide with some acaricidal action and was used on crops and animals. It has been the most heavily applied pesticide in many parts of the world and replaced DDT in the early 1970s. The use of camphechlor is now phased out in most of the world. Technical camphechlor mixtures show a complex composition, with at least 202 different compounds identified. Due to its persistence and chemical properties it has found a widespread distribution. Environmental biotransformation and accumulation in the aquatic environment has led to relatively high levels of certain camphechlor congeners in fish, marine mammals and sea birds while other congeners rapidly degrade.Camphechlor is readily absorbed from the gastrointestinal tract and distributed to the lipid portion of the organism. It passes the placenta and transfer to milk has been shown in animals and humans. Neurotoxicity has been reported in fish, birds and mammals. Other toxic effects occur in the liver, thyroid and immune system.Fish oil and fish meal are the main sources of camphechlor exposure of farmed animals, particularly fish. Human dietary exposure is mainly from fatty fish, which is estimated to be between 1 and 25 ng/kg b.w./day. High fish consumers may have intakes of about 60 ng/kg b.w./day, which is still considered to remain without health effects, based on a NOAEL of 100 mu g/kg b.w. for immunotoxicity, the most sensitive endpoint, from a 33 week study in macaque.The congeners CHB 26, 50 and 62, which accumulate in the food chain, can serve as indicators of camphechlor contamination. Moreover, congeners CHB 40, 41, 42 and 44, should also be included in analytical studies as they are also found in fish samples and as CHB 42 appears to be one of the most toxic congeners. Furthermore, CHB 32 should be included as an indicator for a recent contamination.There are substantial data gaps for camphechlor. Detailed occurrence data for camphechlor in feedingstuffs and food of animal (other than fish) and plant origin are lacking. There is also a general lack of congener specific toxicity data as well as data on oral toxicity for farmed fish.

The Panel has been asked to advise on maximum concentrations of boron and fluoride in natural mineral waters that will not pose a health risk to consumers. The Scientific Panel on Dietetic Products, Nutrition, and Allergies (NDA) recently issued two opinions on the tolerable upper intake level (UL) for boron and fluoride. The CONTAM Panel based its advice on these UL values and did not re-evaluate these.High consumption of mineral water ranges from 0.5 up to about 2 litres per day, based on data from 3 EU countries. The CONTAM Panel noted that for mineral water, brand loyalty of consumers is a key element to be taken into consideration and it has to be assumed that always the same brand is consumed by the same individual. Therefore, even when a brand represents a limited percentage of the market share, this brand may be consumed by a limited number of consumers that will include individuals with a high intake according to the distribution of intake seen for mineral water generally.Taking into account the UL values of 10 mg boron per day for adults and 3, 4, 5, 7 and 9 mg boron per day for children aged 1-3, 4-6, 7-10 11-14 and 15-17 years, respectively, the CONTAM Panel concluded that it is very unlikely that intake by the general population including children older than 14 years would exceed these levels even at the highest reported levels in bottled water. For children from 1 to 14 years of age, a maximum limit of 1.5 mg boron/l in bottled water would protect these children from exceeding the UL.Calculating the dietary exposure of fluoride by combining a realistic high intake of mineral water of 1 litre/day with the maximum reported fluoride concentration (8 mg/l), the CONTAM Panel noted that the estimated exposure would exceed the UL for adults of 7 mg/person. The UL for a child of 1 to 3 years of age (1.4 mg/day) would be reached with the consumption of 200 ml of mineral water containing 8 mg/l. The Panel described scenarios for maximum limits for fluoride in mineral water. When a maximum limit of 1 mg/l is chosen, exposure to fluoride from bottled water in the whole population including young children would be unlikely to reach the UL values. When 5 mg/l is chosen as a maximum limit for fluoride, only the population of 15 years and older would be protected from exceeding the UL and only if exposure from other sources for this population would be negligible.

Endrin is a fat soluble organochlorine insecticide. Commercial manufacture and use began in the early 1950s. It has been banned in most countries world wide during the last 25 years. Endrin is included in the Stockholm convention on persistent organic pollutants (POPs) and the United Nations Economic Commission for Europe (UNECE) Convention on long-range transboundary air pollution on POPs. Endrin is partly transformed in the environment into delta-ketoendrin.In both animals and humans, endrin is readily absorbed via the gastrointestinal tract. Compared to lower organisms which show some bioaccumulation, endrin is rapidly biotransformed in mammals and therefore does not bioaccumulate significantly. The dominant effects are neurotoxicity and liver toxicity, the latter seen following chronic exposure. Endrin is neither genotoxic nor teratogenic, but foetal toxicity can occur.Fish derived products, particularly fish oil, contained the highest levels of endrin. The majority of fish oil samples contained endrin at levels between 1 and 10 mu g/kg. Feed products of plant origin seldom show detectable levels of endrin. However, the limit of detection was often higher (1-10 mu g/kg) than that for fish oil. The levels found in feed are usually much lower than the levels which induce toxicity in farmed animals and pets.Due to the low production of endrin, its ban in the EU and most other countries world-wide and its rather low tendency to bioaccumulate in the environment, human daily intake for adults and children of this pesticide seems to be below 1 ng/kg b.w. Thus, human exposure is far below the provisional tolerable daily intake (PTDI) of 200 ng/kg b.w. established by JMPR (FAO/WHO Joint Meeting on Pesticide Residues).

The CONTAM Panel noted the use of the MOE approach that incorporated data from European countries, including information gathered under collaborative initiatives between the Commission and EFSA. The Panel agrees with the principal conclusions and recommendations of the JECFA and concludes that at present an additional evaluation by EFSA is not necessary.