We report here the first confirmation of the recent Swedish findings of acrylamide in heated foods. The verification exercise used an LC-MS/MS method developed for the purpose as well as an established GCMS method for acrylamide analysis. LC-MS/MS was suitable for the direct determination of acrylamide in aqueous extracts of foods by isotope dilution mass spectrometry (IDMS) using triply deuterated acrylamide. Some food matrices were not suited to the new method and mixed-mode solid-phase extraction (SPE) was used to clean these extracts. The foods tested included UK versions of some of the key food groups analysed in Sweden. Also tested were some foods heated under home-cooking conditions. There was good agreement between the LC-MS/MS results and the GC-MS results and the levels of acrylamide found here were similar to those reported for the corresponding foods analysed in the Swedish study. The analyses confirmed that acrylamide is absent from the raw or boiled foods but present at significant levels in fried, grilled, baked and toasted foods. The highest result was 12000 microg kg(-1) acrylamide in overcooked oil-fried chips.

The volatile compounds released by orthodox (desiccation-tolerant) seeds during ageing can be analysed using gas chromatography–mass spectrometry (GC-MS). Comparison of three legume species (Pisum sativum, Lathyrus pratensis, and Cytisus scoparius) during artificial ageing at 60% relative humidity and 50 °C revealed variation in the seed volatile fingerprint between species, although in all species the overall volatile concentration increased with storage period, and changes could be detected prior to the onset of viability loss. The volatile compounds are proposed to derive from three main sources: alcoholic fermentation, lipid peroxidation, and Maillard reactions. Lipid peroxidation was confirmed in P. sativum seeds through analysis of malondialdehyde and 4-hydroxynonenal. Volatile production by ageing orthodox seeds was compared with that of recalcitrant (desiccation-sensitive) seeds of Quercus robur during desiccation. Many of the volatiles were common to both ageing orthodox seeds and desiccating recalcitrant seeds, with alcoholic fermentation forming the major source of volatiles. Finally, comparison was made between two methods of analysis; the first used a Tenax adsorbent to trap volatiles, whilst the second used solid phase microextraction to extract volatiles from the headspace of vials containing powdered seeds. Solid phase microextraction was found to be more sensitive, detecting a far greater number of compounds. Seed volatile analysis provides a non-invasive means of characterizing the processes involved in seed deterioration, and potentially identifying volatile marker compounds for the diagnosis of seed viability loss.

Our results demonstrate that masked trichothecenes will reach the colon intact to be released as parent mycotoxins by gut microbiota, hence contributing to mycotoxin exposure. Masked zearalenone compounds are metabolized by gut microbiota and epithelial cells and the identity and toxicity of metabolites remain to be determined.

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Although interindividual variation in isoflavone metabolism was high, intraindividual variation was low. Only concentrations of O-DMA in plasma and urine appeared to be influenced by sex. Chronic soy consumption does not appear to induce many significant changes to the gut metabolism of isoflavones other than higher beta-glucosidase activity.

The urinary excretion of soya isoflavones and gut microflora metabolites was investigated in infants and children who had been fed soyabased infant formulas in early infancy. These infants and children were compared with cows'-milk formula-fed controls, to determine at what age gut microflora metabolism of daidzein to equol and/or O-desmethylangolensin (O-DMA) was established, and whether exposure to isoflavones in early infancy influences their metabolism at a later stage of development. Sixty infants and children (aged 4 months -7 years) participated in the study; thirty in each of the soya and control groups. There were four age groups. These were: 4 -6 months (seven in the soya group and seven in the control group); 7 -12 months (seven in the soya group and nine in the control group); 1 -3 years (six in the soya group and eight in the control group); 3 -7 years (ten in the soya group and six in the control group). Urine samples were collected to measure isoflavonoids by MS, and faecal samples were collected to measure gut-health-related bacterial composition, by fluorescent in situ hybridisation with oligonucleotide probes, and metabolic activity. A soya challenge (typically a soya yoghurt alternative product containing 4·8 g soya protein and on average 22 mg total isoflavones) was given to control-group infants (. 6 months) and children, and also to soya-group children that were no longer consuming soya, to determine their ability to produce equol and/or O-DMA. Urinary genistein, daidzein and glycitein were detected in all infants (4 -6 months) fed soya-based infant formula; O-DMA was detected in 75 % of infants but equol was detected in only 25 %. In the controls (4 -6 months), urinary isoflavonoids were very low or not detected. In the older age groups (7 months -7 years), O-DMA was found in the urine samples of 75 % of the soya group and 50 % of the controls, after the soya challenge. Equol excretion was detected in 19 % of the soya-group infants and children, and in only 5 % of the controls. However, in the oldest (3 -7 years) children, the proportion excreting O-DMA and equol was similar in both groups. Faecal bacterial numbers for bifidobacteria (P, 0·001), bacteroides and clostridia (P, 0·05) were significantly lower for the soya group compared with the control group. There appears to be no lasting effect of early-life isoflavone exposure on isoflavone metabolism. Soya isoflavone metabolism: Equol: Soya-based infant formula: Gut bacterial microflora

The analysis of 252 food samples (UK-produced and imported) purchased from a variety of retail outlets in the UK was undertaken for the presence of perfluorooctanesulphonic acid (PFOS), perfluorooctanoic acid (PFOA) and nine other perfluorocompounds (PFCs). A limit of quantification (LOQ) of 1 microg/kg was achieved for all target analytes, in all samples. Standard addition was used for quantification of PFC levels. All 11 of the targeted PFCs were detected in 75 individual food items. In 70% of the samples, including all meat other than offal, none of the analytes were present above the LOD. The highest levels found were 59 microg/kg perfluorooctanesulphonic acid (PFOS) and 63 microg/kg total PFCs (SigmaPFCs) in an eel sample, and 40 microg/kg PFOS (62 microg/kg SigmaPFCs) in a whitebait sample. The highest level in an offal sample was 10 microg/kg, in a wild roe deer liver. There were six samples with SigmaPFCs >15 microg/kg (fish, shellfish, crustaceans), a further seven samples with SigmaPFCs ranging 11-15 microg/kg (including a liver), nine with SigmaPFCs ranging 6-10 microg/kg (fish and livers), 31 with SigmaPFCs in the range 2-5 microg/kg (including kidneys, popcorn and processed peas) and a further 22 with SigmaPFCs close to the LOD of 1 microg/kg (including eggs and potatoes). These concentrations indicate that UK consumers are being exposed to a low level of PFC contamination from food. The estimated upper bound dietary intake of 10 ng/kg bodyweight (bw)/day of PFOS for average adult consumers is well below the 0.15 microg (150 ng)/kg bw tolerable daily intake (TDI) set by the European Food Safety Authority. The lower bound adult dietary intake estimate of 1 ng/kg bw/day is similar to estimates undertaken and reported in countries such as Canada, Germany and Spain.

No abstract