Seasonal variations in exposure to methylmercury and its dietary sources among pregnant Inuit women in Nunavik, Canada.

Among populations living in close connection with the sea, rivers and lakes for subsistence, diet varies according to local monthly wildlife species availability and food preferences. This may lead to variations in methylmercury (MeHg) exposure over a year, although no biomonitoring studies have documented this issue in Circumpolar populations, the most exposed to international Hg emissions. Our aim was to characterize seasonal variations in MeHg exposure among pregnant Inuit women from Nunavik and to identify country foods responsible for these variations. Between October 2016 and March 2017, 97 participants were recruited. Blood mercury (Hg) was tested and hair Hg was measured by centimeter as a surrogate for monthly MeHg exposure over the past year. Latent class growth analysis was conducted to identify groups of pregnant women with similar hair Hg monthly trajectories. Country foods consumption was documented by season. Seasonal daily intakes of MeHg were estimated based on concentrations in country foods. Retrospective monthly hair Hg analyses revealed that MeHg exposure was lowest in winter, and highest in summer and early fall months. Three latent classes (groups) of pregnant women with similar trajectories of monthly hair Hg variations were identified: high (n = 20, 21%), moderate (n = 38, 41%) and low variation (n = 35, 38%). Beluga meat was the country food contributing to most of daily MeHg intake, primarily during summer and fall, and was the only one associated with the odds of being classified into moderate and high variation groups (OR 95% CI: 1.19 [1.01-1.39] and 1.25 [1.04-1.50]). These findings underscore the importance of monthly variations in exposure to MeHg due to the seasonality of local foods consumed and responsible for elevated MeHg exposure. Further studies critically need to understand local diet fluctuations over a year to adequately assess MeHg exposure, adopt timely preventive interventions and evaluate the effectiveness of the Minamata Convention.

Exposure to ambient air pollutants and the onset of dementia in Québec, Canada.

BACKGROUND: Effects of air pollutants are related to oxidative stress which is also linked to the pathogenesis of dementia including Alzheimer's and related diseases. OBJECTIVE: We assessed associations between exposure to air pollutants and the onset of dementia; the association with the distance between residence and major roads was also assessed for the island of Montreal. METHODS: We created an open cohort of adults aged 65 years and older starting in 2000 and ending in 2012 in the province of Québec, Canada using linked medico-administrative databases. New cases of dementia were defined based on a validated algorithm. Annual residential levels of nitrogen dioxide (NO2) and fine particles (PM2.5) at residential levels were estimated for each year of follow up using estimates based on satellite images and ground air monitoring data. Hazard ratios (HRs) were assessed with Extended (time dependent exposure) Cox models with age as the time axis and stratified for sex, for the annual exposure level at each residential address. Models were adjusted for the calendar year, area-wide social and material deprivation indexes and for NO2 or PM2.5; they were also indirectly adjusted for smoking. RESULTS: 1,807,133 persons (13,242,270 person-years) were followed and 199,826 developed dementia. From models (adjusted for calendar year, social and material deprivation indexes), HRs for an interquartile range (IQR) increase in time-varying exposure to NO2 (IQR 13.26 ppb), PM2.5 (IQR 3.90 µg/m³), and distance to major roads (IQR 150 m, in Montreal only), were 1.005 (CI 95% 0.994-1.017), 1.016 (CI 95% 1.003-1.028) and 0.969 (CI 95% 0.958-0.980), respectively. CONCLUSIONS: Results suggest that the onset of dementia may be related to residential exposure to PM2.5, NO2, and distance to major roads.

Methylmercury exposure, PON1 gene variants and serum paraoxonase activity in Eastern James Bay Cree adults.

There is growing evidence that cardiovascular health can be affected by exposure to methylmercury (MeHg), by a mechanism involving oxidative stress. Paraoxonase 1 (PON1) is a high-density lipoprotein-bound enzyme that hydrolyzes toxic oxidized lipids and protects against cardiovascular diseases. Evidence from in vitro studies indicates that MeHg can inhibit PON1 activity but little is known regarding this effect in humans. We investigated whether increased blood mercury levels are associated with decreased serum PON1 activity in Cree people who are exposed to MeHg by fish consumption. We conducted a multi-community study of 881 Cree adults living in Eastern James Bay communities (Canada). Multivariate analyses considered sociodemographic, anthropometric, clinical, dietary and lifestyle variables and six PON1 gene variants (rs705379 (-108C/T), rs662 (Q192R), rs854560 (L55M), rs854572 (-909C/G), rs854571 (-832C/T) and rs705381 (-162C/T)). In a multiple regression model adjusted for all potential confounding factors and the rs854560 PON1 variant, a statistically significant MeHg*rs705379 interaction was observed. Blood mercury levels were inversely associated with serum PON1 activities in individual homozygous for the -108T allele (P=0.009). Our results suggest a gene-environment interaction between the rs705379 polymorphism and MeHg exposure on PON1 activity levels in this aboriginal population. This finding will need to be replicated in other population studies.

Relation between methylmercury exposure and plasma paraoxonase activity in inuit adults from Nunavik.

BACKGROUND: Methylmercury (MeHg) exposure has been linked to an increased risk of coronary heart disease (CHD). Paraoxonase 1 (PON1), an enzyme located in the high-density-lipoprotein (HDL) fraction of blood lipids, may protect against CHD by metabolizing toxic oxidized lipids associated with low-density liproprotein and HDL. MeHg has been shown to inhibit PON1 activity in vitro, but this effect has not been studied in human populations. OBJECTIVES: This study was conducted to determine whether blood mercury levels are linked to decreased plasma PON1 activities in Inuit people who are highly exposed to MeHg through their seafood-based diet. METHODS: We measured plasma PON1 activity using a fluorogenic substrate and blood concentrations of mercury and selenium by inductively coupled plasma mass spectrometry in 896 Inuit adults. Sociodemographic, anthropometric, clinical, dietary, and lifestyle variables as well as PON1 gene variants (rs705379, rs662, rs854560) were considered as possible confounders or modifiers of the mercury-PON1 relation in multivariate analyses. RESULTS: In a multiple regression model adjusted for age, HDL cholesterol levels, omega-3 fatty acid content of erythrocyte membranes, and PON1 variants, blood mercury concentrations were inversely associated with PON1 activities [ß-coefficient = -0.063; 95% confidence interval (CI), -0.091 to -0.035; p < 0.001], whereas blood selenium concentrations were positively associated with PON1 activities (ß-coefficient = 0.067; 95% CI, 0.045-0.088; p < 0.001). We found no interaction between blood mercury levels and PON1 genotypes. CONCLUSIONS: Our results suggest that MeHg exposure exerts an inhibitory effect on PON1 activity, which seems to be offset by selenium intake.