Exposure assessment of process-related contaminants in food by biomarker monitoring.

Exposure assessment is a fundamental part of the risk assessment paradigm, but can often present a number of challenges and uncertainties. This is especially the case for process contaminants formed during the processing, e.g. heating of food, since they are in part highly reactive and/or volatile, thus making exposure assessment by analysing contents in food unreliable. New approaches are therefore required to accurately assess consumer exposure and thus better inform the risk assessment. Such novel approaches may include the use of biomarkers, physiologically based kinetic (PBK) modelling-facilitated reverse dosimetry, and/or duplicate diet studies. This review focuses on the state of the art with respect to the use of biomarkers of exposure for the process contaminants acrylamide, 3-MCPD esters, glycidyl esters, furan and acrolein. From the overview presented, it becomes clear that the field of assessing human exposure to process-related contaminants in food by biomarker monitoring is promising and strongly developing. The current state of the art as well as the existing data gaps and challenges for the future were defined. They include (1) using PBK modelling and duplicate diet studies to establish, preferably in humans, correlations between external exposure and biomarkers; (2) elucidation of the possible endogenous formation of the process-related contaminants and the resulting biomarker levels; (3) the influence of inter-individual variations and how to include that in the biomarker-based exposure predictions; (4) the correction for confounding factors; (5) the value of the different biomarkers in relation to exposure scenario's and risk assessment, and (6) the possibilities of novel methodologies. In spite of these challenges it can be concluded that biomarker-based exposure assessment provides a unique opportunity to more accurately assess consumer exposure to process-related contaminants in food and thus to better inform risk assessment.

Urinary concentrations of acrylamide (AA) and N-acetyl-S-(2-carbamoylethyl)-cysteine (AAMA) and associations with demographic factors in the South Korean population.

Acrylamide (AA) and N-acetyl-S-(2-carbamoylethyl)-cysteine (AAMA) are important urinary biomarkers of acrylamide exposure in human biomonitoring, because AA is classified as a probable carcinogen in humans. In this study, urinary AA and AAMA were assessed in the South Korean adult population aged 18-69, based on the Korean National Human Biomonitoring Survey conducted in 2009. Urinary metabolites in samples were analyzed with LC-MS/MS system. Relying on data from 1873 representative South Korean adults, the population-weighted geometric means of urinary AA and AAMA concentrations were 6.8 ng/ml (95% CI: 6.4-7.3), and 30.0 ng/ml (95% confidence interval (CI): 28.2-31.8), respectively. The creatinine-adjusted geometric means of AA and AAMA were 6.2 µg/g creatinine (95% CI: 5.8-6.7) and 26.4µg/g creatinine (95% CI: 24.9-28.0), respectively. When covariates for predictors of urinary metabolites were adjusted simultaneously in a log-linear multiple regressions, the strongest predictors of urinary AA were education (OR=1.08-1.28; 95% CI: 1.11-1.48; p=0.0024) and age (OR=0.66-0.84; 95% CI: 0.54-0.97; p=0.0003), and those of urinary AAMA were smoking status (OR=1.16-2.63; 95% CI: 0.98-3.08; p=0.001) and education (OR=1.12-1.19; 95% CI: 1.02-1.38; p=0.0425). The ratio of current/never smokers for urinary AA was 1.3, whereas the same ratio for urinary AAMA was 3.0. These findings suggested that most South Koreans had detectable levels of AA and AAMA (98.7% and 99.4%, respectively) in their urine and that the body burden of AA and AAMA varied according to demographic, geographic, and lifestyle (smoking) factors.

Acrylamide in children--exposure assessment via urinary acrylamide metabolites as biomarkers.

UNLABELLED: Acrylamide (AA), a substance classified as probably carcinogenic to humans, was detected for the first time in food products in 2002. AA can be primarily found in foods containing carbohydrates and proteins, where it is formed during the heating process. Exposure assessment based on food consumption data revealed an average daily intake of AA between 0.3 and 0.8 microg/kg BW/day. These data have been confirmed by human biomonitoring using haemoglobin adducts of AA in blood or the specific mercapturic acids in urine. However, human biomonitoring data on the internal exposure of children were only sporadically available. Especially data about the excretion of both relevant mercapturic acids were missing. The mercapturic acids other than the haemoglobin adducts give the recent AA exposure of the last 24h. In this study, we quantify the internal exposure of AA and the genotoxic metabolite glycidamide (GA) in 110 children with regard to their exposure through diet and/or environmental tobacco smoke. MATERIAL AND METHODS: Hundred and ten 5-6-year-old children were randomly selected. Their dietary habits as well as their exposure to the environmental tobacco smoke were assessed by means of a questionnaire. By means of spot urine samples, mercapturic acids of acrylamide (AAMA) and mercapturic acids of glycidamide (GAMA) were analysed with LC-ESI-MS/MS. RESULTS: Median (95th percentile) urinary levels were 36.0 (152.7) microg AAMA/l and 13.4 (55.9) microg GAMA/l. Based on the metabolite levels, the median uptake of acrylamide was calculated to be 0.54 microg/kg BW/d. A number of associations with the consumption of French fries, various potato products, as well as fried cereals could be found. Significant results were found for French fries. No correlations between the exposure to environmental smoke and cotinine levels in urine were found. CONCLUSION: This is the first study to show the presence of AAMA and GAMA in urine specimens of 110 children, thus providing evidence for a background exposure by nutrition. Median (95th percentile) uptake of AA in children was 0.54 (1.91) microg/kg bodyweight and day, exceeding exposure in adults by 50%. These findings support the efforts to minimize AA formation and contamination in food. Comparing our findings with that of other human studies, there are hints that children have a higher AA intake than adults and that children more effectively oxidize AA. Both findings indicate that children might be the most vulnerable group of the population.