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Drinking water intake of arsenic (As) from private wells may represent a significant exposure pathway and induce oxidative DNA damage. We measured total As concentrations in hair and nails, and concentrations of the different species of As and its metabolites as well as 8-OHdG in urine of 110 non-smoking adults living in a rural region of the Province of Quebec, Canada. Significant differences in exposure biomarker levels were observed between individuals consuming drinking water with As levels of≤1.0,>1.0 -≤10 and>10 μg/l. Multivariate linear regression analysis also showed a significant relationship between estimated daily drinking water intakes of As and biomarker levels. Conversely, 8-OHdG levels were not significantly related to daily drinking water intakes of As or to hair, nail or urinary exposure biomarker levels, according to multivariate linear regression analysis. Even at the relatively low levels of As found in well water of our participants, water consumption significantly increases their body load of As, as confirmed by multiple matrix measurements, which reflected exposure over different time frames. However, this increased internal As dose was not associated with higher oxidative damage to DNA as reflected by urinary 8-OHdG levels. [ABSTRACT FROM AUTHOR]

Acrylamide (AA) is a probable human carcinogen found in several foods. Little information is available regarding exposure of adolescents, a subgroup potentially consuming more AA-rich foods. We investigated the relationship between dietary AA intake and levels of biomarkers of exposure (urinary metabolites and hemoglobin adducts) in 195 non-smoking teenagers of Montreal Island aged 10-17 years. Dietary habits and personal characteristics were documented by questionnaire. AA and its metabolites were quantified in 12-h urine collections by LC-MS/MS. Hemoglobin adducts from 165 blood samples were also analyzed by LC-MS/MS. Most prevalent urinary metabolites were NACP and NACP-S, with respective geometric mean concentrations of 31.2 and 14.2 μmol/mol creatinine. Geometric mean concentrations of AAVal and GAVal (hemoglobin adducts of AA and glycidamide (GA) with N-terminal valine residues) were 45.4 and 45.6 pmol/g globin, respectively. AA intake during the 2 days before urine collection was a significant predictor of NACP+NACP-S urinary concentrations (P<0.0001). AA intakes during the month before blood collection (P<0.0001) and passive smoking (P<0.05) were associated with adduct levels. Levels of hemoglobin adducts were above biomonitoring equivalent values corresponding to a 1 × 10−4 excess cancer risk, which may indicate the need to reduce AA exposure in the population. [ABSTRACT FROM AUTHOR]

Methylmercury (MeHg) is a neurotoxic contaminant and one of the main sources of exposure in humans is seafood consumption. It is thus of interest to assess precisely MeHg exposure. The objective of this study was to estimate MeHg daily intake in exposed individuals using two different approaches, a food questionnaire and toxicokinetic modeling, and compare the complementary and use of each method. For this purpose, a group of 23 fishermen from northern Quebec provided blood and hair samples and answered a standard food questionnaire focusing on seafood consumption. A published and validated toxicokinetic model was then used to reconstruct MeHg daily intakes from mercury (Hg) measurements in biological samples. These intakes were compared to those estimated using a standard food questionnaire on seafood consumption. Daily intakes of MeHg from seafood (mean/median (range)) estimated from hair concentrations with the toxicokinetic-based approach were 6.1/5.2 (0.0-19) μg/day. These intake values were on average six times lower than those estimated using a food questionnaire, that is, 49/32 (7.2-163) μg/day. No correlation was found between the toxicokinetic-based and the questionnaire estimates of MeHg daily intakes. Most of the MeHg intakes estimated with the food questionnaire (21/23) exceeded the US EPA RfD of 0.1 μg/kg bw/day, whereas only a small proportion (6/23) of modeled estimates exceeded the RfD. This study shows that human health risk estimates strongly depend on the chosen approach. [ABSTRACT FROM AUTHOR]

Significant amounts of methylmercury (MeHg) can bioaccumulate in fish and sea mammals. To monitor MeHg exposure in individuals, organic and inorganic mercury are often measured in blood samples or in hair strands, the latter being by far the best integrator of past exposure. With knowledge of the MeHg kinetics in humans, the levels of both biomarkers can be related to MeHg body burden and intakes. In the present study, we use the toxicokinetic model of Carrier et al. (2001) describing the distribution and excretion of MeHg in humans, to reconstruct the history of MeHg intakes of indigenous women of the Inuvik region in Canada starting from total mercury concentrations in hair segments. From these reconstructed MeHg intakes, the corresponding simulated mercury blood concentrations are found to be good predictors of the concentrations actually measured in blood samples. An important conclusion of this study is that, for almost all subjects, the reconstructed history of their MeHg intakes provides much lower intake values than intakes estimated from questionnaires on food consumption and estimated MeHg levels in these foods; the mean value of the reconstructed MeHg intakes is 0.03 μg/kg/day compared with the mean value of 0.20 μg/kg/day obtained from questionnaires. The model was also used to back-calculate the MeHg intakes from concentrations in hair strands collected from aboriginals of the Amazon region in Brazil, a population significantly more exposed than the population of the Inuvik region. [ABSTRACT FROM AUTHOR]