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This study summarises the results of the levels of 21 perfluoroalkyl substances (PFASs) in 50 selected pooled samples representing 15 food commodities with the special focus on those of animal origin, as meat, seafood, fish, milk, dairy products and hen eggs, which are commonly consumed in various European markets, e.g. Czech, Italian, Belgian and Norwegian. A new, rapid sample preparation approach based on the QuEChERS extraction procedure was applied. Ultra-performance liquid chromatography (UHPLC) coupled to tandem mass spectrometry (MS/MS) employing electrospray ionisation (ESI) in negative mode was used for the quantification of target analytes. Method quantification limits (MQLs) were in the range of 1-10 ng kg(-1) (ng l(-1)) for fish, meat, hen eggs, cheese and milk, and in the range of 2.5-125 ng kg(-1) for butter. Only 16 of the group of 21 PFASs were found in at least one analysed sample. From 16 PFASs, perfluorooctane sulfonate (PFOS) was the most frequently detected analyte present in approximately 50% of samples (in the range of 0.98-2600 ng kg(-1)). PFCAs with C8-C14 carbon chain were presented in approximately 20% of samples. The concentration ranges of individual compounds in the respective groups of PFASs were: 2.33-76.3 ng kg(-1) for PFSAs (without PFOS), 4.99-961 ng kg(-1) for PFCAs, 10.6-95.4 ng kg(-1) for PFPAs, and 1.61-519 ng kg(-1) for FOSA. The contamination level in the analysed food commodities decreased in the following order: seafood > pig/bovine liver >> freshwater/marine fish > hen egg > meat >> butter. When comparing the total contamination and profiles of PFASs in food commodities that originated from various sampling countries, differences were identified, and the contents decreased as follows: Belgium >> Norway, Italy > Czech Republic.

Human exposure to brominated flame retardants (BFRs) varies widely throughout the world as it depends on country-related usage, production and legislation of these chemicals. US and UK exposure assessments show very diverse levels and patterns which in turn, are likely to differ from those in background exposed countries such as Belgium, where levels tend to be about an order of magnitude lower. The current study assessed human exposure to BFRs through the indoor and outdoor environment (e.g. dust, soil, and air) and food for all age groups in Flanders, Belgium. Most relevant food groups were identified based on a national food consumption survey and food items with Flemish origin were collected. Dust samples were collected using a standardized protocol in 43 homes and 10 offices throughout Flanders. Food, human milk and dust samples were analysed for their polybrominated diphenylethers (PBDE) and hexabromocyclodecane (HBCD) content using GC/MS and LC/MS-MS. An exposure model was developed including all analysed data, complemented with literature data. The model covered human exposure of infants, children and adults through human milk, food, dust/soil ingestion and air inhalation. Total human exposure was compared to the existing toxicological criteria and previous exposure estimates. In general, the exposure levels through human milk are consistent with those of a background exposed European population, whereas dust and food intake are at the low end of what has been reported in previous European intake assessments. Total average intake of SigmaHBCD and SigmaBDE(5) at 50th percentile (P50) levels by newborns equals 3.1 and 12.0ng/kg body weight (bw) day, respectively. This intake increases to 15.2 and 20.9ng/kgbwday for SigmaHBCD and SigmaBDE(5), for higher exposed newborns (95th percentile=P95 levels). Due to the limited database on health-based limit values for PBDEs and HBCD, it is difficult to assess the immediate health concern for any of the age groups, although the higher intake of newborns indicates the need for ongoing monitoring. For median exposed individuals, the average SigmaHBCD intake peaked at the age 3 to 6years with an intake of 6.59ng/kgbwday and declines to approximately 1ng/kgbwday at later age. SigmaBDE(5) intake exhibited a different profile compared to SigmaHBCD with maximal levels for newborns and a decline to approximately 0.7ng/kgbwday at adulthood.

The widespread distribution and degradation of PFCs in the environment results in a very complex exposure pattern, which makes it difficult to define the relative contribution to human exposure from different exposure pathways. The present review is designed to provide an overview of the existing data on levels of PFCs measured in the human diet and in drinking water. Data on levels of PFCs in the human diet are rather scarce, but the level in the fish appear to be well documented. Among PFCs, PFOS and PFOA are the best studied compounds in fish from both experimental and monitoring studies. Recently, the number of publications that address other PFCs has increased, but the total number available is still limited. In general, we discovered that care should be exercised when using the reviewed data, because, in the majority of publications, quality control and/or details on analysis are, at least partly, lacking. It has been well documented that PFOA and PFOS have the potential to accumulate in fish and concentrations up to 7 and 170 ng/g wwt, respectively in edible fish species have been found. PFOS is the most crucial and prominent compound identified, followed by the PFOA. Also, in aquatic invertebrate such as shrimps, mussels, clams, and oysters, high PFOS levels have been reported (up to 387 ng/g wwt). However in most publications PFC level reported in molluscs were less than 1 ng/g wwt. Positive correlations were found between PFC body burden and self reported fish consumption. In recognition of the potential for human exposure to PFCs via fish consumption, the Minnesota Department of Health has recently issued fish consumption advisories for contaminated sections of the Mississippi River. It is interesting to note that 79% of the reviewed publications on PFCs in the whole fish homogenates exceed the that threshold. Moreover, five of the PFC concentration reported in muscles tissue exceeded the advisory level of 38 ng/g wwt. Even though several authors concluded that consumption of contaminated food and drinking water constitutes the major exposure pathway for humans, only a few reports on PFCs in composite food exist. Food can be contaminated in an indirect way, because PFCs are widely used in food-packaging coatings and cooking materials. On the other hand, PFCs can also enter food organisms via environmental routes such as inhalation or adsorption from air. In a few studies, composite samples, duplicate diet samples, or other food items were analyzed for several PFCs, PFOS and PFOA, PFHpA, PFHxA, and PFHxS were meAsured and displayed concentrations ranging from-detected up to 15 ng/g wwt. In one study, a very high PFOA concentration of 118 ng/g were reported, but overall, PFC levels are below 10 ng/g wwt. It is important to note that, among all studies reviewed, PFCs were found in a maximum of 50% of the analyzed samples and generally only in 10% or less of samples analyzed. In contrast to what is observed in fish and other food items PFOA levels in drinking water (ND - 50 ng/L) and other PFCs (1-3 ng/L). In one study, extremely high values (519 ng/L) were measured in drinking water of a contaminated area in the Ruhr region. In Spain, bottled water was analyzed and four PFCs (PFOA, PFNA,PFDA and PFHpA) were found at low levels (<1 ng/L). Because of higher levels found in drinking water at several locations, some provisional drinking water guideline values for PFOS and PFOA have already been established, e.g., in the UK, Bavaria, and Minnesota. Since PFCs are present both in food and drinking water, Tolerable Daily Intake values for PFOS and PFOA have also been proposed by several institutes in Europe and in the USA. The ingestion of dust through hand-to-mouth transfer from indoor house dust can also be a potential source of PFC exposure, especially for toddlers and children. In publications on PFCs in indoor dust, the mean PFOS and PFOA levels varied between 39 and 1,200 ng/g and between 11 and 220 ng/g, respectively. Overall, it is clear that there is still lack of PFC exposure data for food and beverages, which renders the assessment of the contribution of the diet to total human PFC exposure uncertain. It is, therefore, appropriate that several scientific projects have recently been launched that addresses the assessment of human exposure to PFCs and related compounds from dietary sources.

The human diet is recognised as one possible major exposure route to the overall perfluorinated alkylated substances (PFAS) burden of the human population, resulting directly from contamination of dietary food items, as well as migration of PFAS from food packaging or cookware. Most European countries carry out national monitoring programs (food basket studies) to monitor contamination with pollutants. Usually, for PFASs, non-coordinated approaches are used in Europe, since food basket studies are mainly carried out by national authorities following national requirements and questions, making comparisons between different countries difficult. A harmonised sampling campaign collecting similar food items in a uniform procedure enabling direct comparison between different regions in Europe was designed. We selected four countries (Belgium, Czech Republic, Italy and Norway), representing the four regions of Europe: West, East, South and North. In spring 2010 and 2011, 20 different types of vegetables were sampled in Belgium, Czech Republic, Italy and Norway. Perfluorinated carboxylic acids (PFCAs) were the main group of detected PFASs, with perfluorinated octanoic acid (PFOA) as the most abundant PFCA (with exception of samples from Czech Republic), followed by perfluorinated hexanoic acid and perfluorinated nonanoic acid. Dietary intake estimates for PFOA show only low human exposure due to vegetable consumption for adults and children, mostly governed by high intake of potatoes. [ABSTRACT FROM AUTHOR]