Methylmercury Exposure Research Articles

Latent alterations in swimming behavior by developmental methylmercury exposure are modulated by the homolog of tyrosine hydroxylase in Caenorhabditis elegans

Methylmercury (MeHg) is a persistent environmental neurotoxicant that may cause adverse neurodevelopmental effects. Previous studies showed that developmental MeHg exposure caused damage to brain functions that were unmasked after a silent period of years or decades. However, the underlying mechanisms of the latent neurotoxicity associated with MeHg exposure from earlier developmental stages have yet to be fully understood. Herein, we established a Caenorhabditis elegans (C. elegans) model of developmental MeHg latent toxicity. Synchronized L1 stage worms were exposed to MeHg (0, 0.05, 0.5 and 5 μM) for 48 h. Swimming moving speeds at adulthood were analyzed in worms exposed to MeHg exposure at early larvae stages. Worms developmentally exposed to MeHg had a significant decline in swimming moving speed on day 10 adult stage, but not on day 1 or 5 adult stage, even though the mercury level in the worms exposed to 0.05 or 0.5 μM MeHg were below the quantification limit on day 10 adult. Day 10 adult worms treated with MeHg showed a significant decrease in bending angle and bending frequency during swimming. Furthermore, their reduced moving speeds tended to increase during the 300-s swimming experiment. Dopamine signaling is known to be involved in the regulation of worms' moving speed. Accordingly, the moving speed of worms with cat-2 (mammalian tyrosine hydroxylase homolog) mutation or dat-1 deletion were assayed on day 10 adult. The cat-2 mutant worms did not show a decline in moving speeds, body bends or bending angles during swimming on day 10 adult stage. Analyses of moving speeds of worms with dat-1 deletion showed that the moving speeds were further reduced after MeHg exposure. However, the effects of MeHg and dat-1 deletion were not synergistic, as the interaction between these parameters did not attain statistical significance. Altogether, our results suggest that developmental MeHg exposure reduced moving speed, and this latent toxicity was less pronounced in the context of deficient production of dopamine synthesis. Tyrosine hydroxylase plays an important role in regulating dopamine-mediated modulation of neurobehavioral functions. These findings uncovered a pivotal role of dopamine and its metabolism in the latent neurotoxic effects of MeHg.

Impact of Methylmercury and Other Heavy Metals Exposure on Neurocognitive Function in Children Aged 7 Years: Study Protocol of the Follow-up.

BackgroundThe extent to which prenatal low-level mercury (Hg) exposure through maternal fish intake and heavy metals exposure affect children’s neurodevelopment is controversial and may appear in the long term. In 2007, a prospective cohort, the Northern Adriatic Cohort II (NAC-II), was established to investigate the association between prenatal Hg exposure from maternal fish consumption and child neurodevelopment. The study enrolled 900 pregnant women, and 632 and 470 children underwent neurodevelopmental evaluation at 18 and 40 months of age, respectively. The NAC-II cohort is a part of the Mediterranean cohort in the “Public health impact of long-term, low-level, mixed element exposure in susceptible population strata” project.MethodsThis protocol describes the follow-up assessment of the effects of prenatal low level Hg and other heavy metals exposure on the developing nervous system of the children born within the NAC-II who reached the age of 7 years. Child diet components are estimated through a Diet Diary. Child hair and urine are collected for determination of Hg level. In addition, levels of other potentially neurotoxic metals, namely Manganese, Cadmium, Lead, Arsenic, and Selenium, are also measured in the same matrices.DiscussionThis protocol extends to the first years of schooling age the evaluation of the neurotoxicant effect of Mercury and of the other heavy metals on children’s neurodevelopment, adjusting for the potential confounders, such as the lifestyles and social economic status of children’s families. Longitudinal analysis of neurodevelopment, assessed in different ages (18 months, 40 months, and 7 years), are performed.

Impacts of climate change on methylmercury formation and bioaccumulation in the 21st century ocean

Impacts of climate change on methylmercury formation and bioaccumulation in the 21st century ocean

Associations of prenatal methylmercury exposure and maternal polyunsaturated fatty acid status with neurodevelopmental outcomes at 7 years of age: results from the Seychelles Child Development Study Nutrition Cohort 2

Fish is a primary source of protein and n-3 PUFA but also contains methylmercury (MeHg), a naturally occurring neurotoxicant to which, at sufficient exposure levels, the developing fetal brain is particularly sensitive. To examine the association between prenatal MeHg and maternal status of n-3 and n-6 PUFA with neurodevelopment, and to determine whether PUFA might modify prenatal MeHg associations with neurodevelopment. We examined the Seychelles Child Development Study Nutrition Cohort 2 (NC2) at age 7 y. We used a sophisticated and extensive neurodevelopmental test battery that addressed 17 specific outcomes in multiple neurodevelopmental domains: cognition, executive and psychomotor function, language development, behavior, scholastic achievement, and social communication. Analyses were undertaken on 1237 mother-child pairs with complete covariate data (after exclusions) and a measure of at least 1 outcome. We examined the main and interactive associations of prenatal MeHg exposure (measured as maternal hair mercury) and prenatal PUFA status (measured in maternal serum at 28 weeks' gestation) on child neurodevelopmental outcomes using linear regression models. We applied the Bonferroni correction to account for multiple comparisons and considered P values<0.0029 to be statistically significant. Prenatal MeHg exposure and maternal DHA and arachidonic acid (20:4n-6) (AA) status were not significantly associated with any neurodevelopmental outcomes. Findings for 4 outcomes encompassing executive function, cognition, and linguistic skills suggested better performance with an increasing maternal n-6:n-3 PUFA ratio (P values ranging from 0.004 to 0.05), but none of these associations were significant after adjusting for multiple comparisons. No significant interaction between MeHg exposure and PUFA status was present. Our findings do not support an association between prenatal MeHg exposure or maternal DHA and AA status with neurodevelopmental outcomes at age 7 y. The roles of n-6 and n-3 PUFA in child neurodevelopment need further research.

Increased expression of TCF3, transcription factor 3, is a defense response against methylmercury toxicity in mouse neuronal C17.2 cells.

Methylmercury is an environmental pollutant that induces potent neurotoxicity. We previously identified transcription factor 3 (TCF3) as a transcription factor that is activated in the brains of mice treated with methylmercury, and reported that methylmercury sensitivity was increased in cells in which TCF3 expression was suppressed. However, the mechanisms involved in the activation of TCF3 by methylmercury and in the reduction of methylmercury toxicity by TCF3 remained unclear. We found that treatment of mouse neuronal C17.2 cells with methylmercury increased TCF3 protein levels and promoted the binding of TCF3 to DNA consensus sequences. In cells treated with actinomycin D, a transcription inhibitor, an increase in TCF3 protein levels was also observed under methylmercury exposure. However, in the presence of cycloheximide, a translation inhibitor, methylmercury delayed the degradation of TCF3 protein. In addition, treatment with MG132, a proteasome inhibitor, increased TCF3 protein levels, and there was not significant increase in TCF3 protein levels by methylmercury under these conditions. These results suggest that methylmercury may activate TCF3 by increasing its levels through inhibition of TCF3 degradation by the proteasome. It has been previously reported that the induction of apoptosis in neurons is involved in methylmercury-induced neuronal damage in the brain. Although apoptosis was induced in C17.2 cells treated with methylmercury, this induction was largely suppressed by overexpression of TCF3. These results indicate that TCF3, which is increased in the brain upon exposure to methylmercury, may be a novel defense factor against methylmercury-induced neurotoxicity.

Reflections about three influential Ambio articles impacting environmental biogeochemistry research and knowledge : This article belongs to Ambio's 50th Anniversary Collection. Theme: Environmental contaminants.

Reflections about three influential environmental contaminants papers published in Ambio are presented. The PCB Story by Jensen in (1972) had a very important influence on environmental chemistry. This is captured by way of comments and personal anecdotes. Wania's and MacKay's (1993) paper highlights the physical chemistry underlying transport of PCBs and organochlorine pesticides from temperate zone ecosystems to Polar Regions. Their paper exemplifies how principles of chemistry and environmental processes informed understanding the biogeochemical cycles of chemicals of environmental concern (CEC). Mergler et al.'s (2007) paper reviews knowledge of methyl mercury exposure and impacts in humans and served as an example of how to approach exposure and human health concerns for all CECs. All great progress. Then, the question: "How we missed for two decades the importance of plastics in the environment identified in a paper published the same year as The PCB Story? Are we missing yet another important environmental contaminant now?

DNA methyltransferase- and histone deacetylase-mediated epigenetic alterations induced by low-level methylmercury exposure disrupt neuronal development.

Methylmercury (MeHg) is a chemical substance that causes adverse effects on fetal development. However, the molecular mechanisms by which environmental MeHg affects fetal development have not been clarified. Recently, it has been suggested that the toxic effects of chemicals on fetal development are related alterations in epigenetics, such as DNA methylation and histone modification. In order to analyze the epigenetic effects of low-level MeHg exposure on neuronal development, we evaluated neuronal development both in vivo and in vitro. Pregnant mice (C57BL/6J) were orally administrated 3mg/kg of MeHg once daily from embryonic day 12-14. Fetuses were removed on embryonic day 19 and brain tissues were collected. LUHMES cells were treated with 1nM of MeHg for 6days and collected on the last day of treatment. In both in vivo and in vitro samples, MeHg significantly suppressed neurite outgrowth. Decreased acetylated histone H3 (AcH3) levels and increased histone deacetylase (HDAC) 3 and HDAC6 levels were observed in response to MeHg treatment in both in vivo and in vitro experiments. In addition, increased DNA methylation and DNA methyltransferase 1 (DNMT1) levels were observed in both in vivo and in vitro experiments. The inhibition of neurite outgrowth resulting from MeHg exposure was restored by co-treatment with DNMT inhibitor or HDAC inhibitors. Our results suggest that neurological effects such as reduced neurite outgrowth due to low-level MeHg exposure result from epigenetic changes, including a decrease in AcH3 via increased HDAC levels and an increase in DNA methylation via increased DNMT1 levels.

The Effect of Methylmercury Exposure on Astrocyte of Cerebellar Cortex of White Rats (Rattus novergicus)

The aim of this research was to investigate the effect of different dose methylmercury (II) chloride on astrocyte in cerebellar cortex of white rat (Rattus norvegicus) exposed. This study used randomized control design using 15 adult female Wistar rats weight 180-200 g of body weight. Before treatment the white rats was adapted in a week, then randomly divided into 3 groups each consist of 5 rats. P0 as control were given 0.5 ml aquades, P1 and P2 were given 0.1 and 0.2 mg/kg/day respectively. All groups were given treatment per oral in 30 days with sonde. The data was analyzed by ANOVA, Duncan's multiple range (Duncan's Multiple Range Test). White rats exposed by methylmercury (II) chloride, had a significant differences in the percentage of necrotic astrocyte (p&lt;0.05). Methylmercury chloride exposure increases the number of necrotic astrocytes on white rat.

Combined Effect of Weathered Coal Based Amendments and Soil Water Management on Methylmercury Accumulation in Paddy Soil and Rice Grains

A pot experiment and field experiment were designed to study the changes in the grain methyl mercury content in paddy soil and rice yield by sowing soil amendments that contained weathered coal, CaCO3, and Na2SeO3 as the main raw materials, combined with water management in a paddy field (80% field capacity after the heading and flowering periods). The results showed that:① In pot experiment, the content of methylmercury in rice rhizosphere soil decreased by 86.6% and the content of methylmercury in the rice grains decreased by 65.2% compared with that of the control. In field experiment, the content of methylmercury in rice rhizosphere soil decreased by 77.4% and the content of methylmercury in rice grains decreased by 60.6% upon adding the amendment+water management compared with that of CK. ② The soil pH increased by more than 0.3 in the pot experiment and 0.2 in the field experiment compared with that of the control. Furthermore, rice yield and plant biomass did not decrease in the two parts of the experiment. It can be inferred that the soil amendment and agronomic regulation measures (water management) used in this study have the advantages of quick effects, convenient use, and remarkable control effects and without secondary pollution. More, they can effectively reduce the risk of rice methylmercury exposure.

Community-driven research in the canadian arctic: dietary exposure to methylmercury and gastric health outcomes

ABSTRACT Indigenous Arctic Canadians have a higher prevalence of gastric neoplasms relative to North Americans of European ancestry. We investigated the hypothesis that low-dose methylmercury exposure from eating fish/whale increases the risk of gastric cancer in Arctic communities. We used intermediate endpoints from an established model of gastric carcinogenesis: intestinal metaplasia, atrophy, and severe chronic gastritis. During 2008–2012, we obtained gastric biopsies from participants of community-driven projects in 3 communities. In 2016, we collected hair samples to measure methylmercury levels and interviewed them about diet. In cross-sectional analysis, logistic regression estimated odds ratios for the estimated effect of hair-methylmercury concentration on the prevalence of each pathology outcome stratified by selenium intake. Among 80 participants, prevalence of intestinal metaplasia, atrophy and severe chronic gastritis was 17, 29 and 38%, respectively. Adjusted Odds of severe chronic gastritis and atrophy were highest at hair-methylmercury concentrations ≥1μg/g when estimated selenium intake was 0, and approached 0 for all methylmercury levels as estimated selenium intake increased. Gastric pathology increased with methylmercury exposure when selenium intake was low. Though limited by small numbers, these findings suggest selenium ingested by eating fish/whale may counter harmful effects of methylmercury exposure in Arctic populations.

Implications and Significance of Methyl Mercury Toxicity and Exposure in Riceand Fish

Rice and fish are staple food items in many cultures and are particularly vulnerable to the accumulation of heavy metals, specifically mercury, when exposed to agricultural contamination via agricultural soils and water sources. These contaminated foods are then consumed by higher organisms up in the food chain, leading to further accumulation of the mercury, a process known as bio-amplification. Mercury is considered to be the most toxic heavy metal due to the fact that it causes significant systemic toxic effects. This commentary discusses the implications and significance of mercury in rice and fish and illustrates the necessity for further research to demonstrate the importance for public awareness and education for prevention of exposure to mercury via fish and rice ingestion.

Prenatal methylmercury exposure and DNA methylation in seven-year-old children in the Seychelles Child Development Study

BackgroundMethylmercury (MeHg) is present in fish and is a neurotoxicant at sufficiently high levels. One potential mechanism of MeHg toxicity early in life is epigenetic dysregulation that may affect long-term neurodevelopment. Altered DNA methylation of nervous system-related genes has been associated with adult mental health outcomes. ObjectiveTo assess associations between prenatal MeHg exposure and DNA methylation (at the cytosine of CG dinucleotides, CpGs) in three nervous system-related genes, encoding brain-derived neurotropic factor (BDNF), glutamate receptor subunit NR2B (GRIN2B), and the glucocorticoid receptor (NR3C1), in children who were exposed to MeHg in utero. MethodsWe tested 406 seven-year-old Seychellois children participating in the Seychelles Child Development Study (Nutrition Cohort 2), who were prenatally exposed to MeHg from maternal fish consumption. Total mercury in maternal hair (prenatal MeHg exposure measure) collected during pregnancy was measured using atomic absorption spectroscopy. Methylation in DNA from the children’s saliva was measured by pyrosequencing. To assess associations between prenatal MeHg exposure and CpG methylation at seven years of age, we used multivariable linear regression models adjusted for covariates. ResultsWe identified associations with prenatal MeHg exposure for DNA methylation of one GRIN2B CpG and two NR3C1 CpGs out of 12 total CpG sites. Higher prenatal MeHg was associated with higher methylation for each CpG site. For example, NR3C1 CpG3 had an expected increase of 0.03-fold for each additional 1 ppm of prenatal MeHg (B = 0.030, 95% CI 0.001, 0.059; p = 0.047). Several CpG sites associated with MeHg are located in transcription factor binding sites and the observed methylation changes are predicted to lead to lower gene expression. ConclusionsIn a population of people who consume large amounts of fish, we showed that higher prenatal MeHg exposure was associated with differential DNA methylation at seven years of age at specific CpG sites that may influence neurodevelopment and mental health.

China's retrofitting measures in coal-fired power plants bring significant mercury-related health benefits

Summary China has implemented retrofitting measures in coal-fired power plants (CFPPs) to reduce air pollution through small unit shutdown, the installation of air pollution control devices (APCDs), and power generation efficiency improvement. The reductions in highly toxic Hg emissions and their related health impacts by these measures remain poorly understood. Here, we evaluated the health benefits of reduced Hg emissions via retrofitting measures during China's 12th Five-Year Plan (2011–2015) by combining plant-level Hg emission inventories with the China Hg Risk-Source-Tracking Model. We found that the measures reduced Hg emissions by 23.5 tons (approximately 1/5 of that from CFPPs in 2010), preventing 30,484.77 total points of intelligence quotient decrement and 114 deaths between 2011 and 2015. These benefits were dominated by CFPP shutdowns and APCD installations, and nearly 50% of provincial health benefits were attributable to Hg reductions in other regions. We suggest that Hg control strategies should consider various factors, such as CFPP location, population density, and trade-offs between reductions in total Hg and in Hg2+.

Mercury bioaccumulation pathways in tusk (Brosme brosme) from Sognefjord, Norway: Insights from C and N isotopes.

Seafood is the main source of methylmercury (MeHg) exposure for humans and elevated total mercury (Hg) concentrations have been reported in marine fish from Norwegian fjords compared with offshore areas. Hg in tusk fillets (n=201) and liver samples (n=177) were measured in individuals from different habitats including offshore, coastal area, outer and inner Sognefjord. Specifically, the effects of habitat, energy sources and trophic complexity on Hg bioaccumulation pathways in tusk (Brosme brosme) were investigated using stable isotopes of carbon (δ13C) and nitrogen (δ15N). The concentrations of Hg in tusk increased from offshore towards inner Sognefjord. While Hg concentrations in sediment were at background levels, tusk fillet samples from 7 of 8 sites in Sognefjord had higher Hg levels than the maximum level set by European Union. Based on these findings, human consumption advice for tusk from Sognefjord was issued by the Norwegian Food Safety Authority. δ13C values in tusk successfully discriminated individuals from different habitats and were positively correlated to Hg concentrations in tusk across individuals, sites and habitats, outlining the potential importance of terrestrial carbon and most likely the atmospheric deposition of Hg from the catchment to the overall Hg bioaccumulation and exposure regime in tusk. Additionally, we postulate that the effects of terrestrial carbon sources increased towards inner Sognefjord and likely influenced Hg bioavailability throughout the food web. In contrast, δ15N values were patchy throughout the fjord system and although trophic position explained some of the Hg variation between individual fish, it was not correlated with Hg variation across sites and habitats. Our results suggest that tusk can accumulate high levels of Hg in fjord ecosystems and that catchment runoff is likely an important driver of Hg bioaccumulation in this species.

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.

Methylmercury cytotoxicity and possible mechanisms in human trophoblastic HTR-8/SVneo cells

Methylmercury (MeHg) exposure during pregnancy can lead to adverse outcomes, including miscarriage and intrauterine growth retardation. In this study, MeHg cytotoxicity and its mechanisms in HTR-8/SVneo cells were investigated. MeHg inhibited HTR-8/SVneo cell viability and severely disrupted the cellular submicrostructure, showing a time-dose effect relationship. After MeHg treatment, the reactive oxygen species levels, malondialdehyde content, and superoxide dismutase (SOD) and catalase activities in the HTR-8/SVneo cells increased significantly with increased MeHg concentration (P<0.05). Similarly, MeHg also induced HTR-8/SVneo cell apoptosis in a dose-dependent manner. The proportion of cells in G1 phase decreased with increasing MeHg concentration, while that in the S and G2/M phases gradually increased. Moreover, cell migration and invasion capacities gradually decreased with increasing MeHg concentration, showing a significant difference between the MeHg-treated and control groups. Genes related to oxidative stress (HSPA6, HSPA1A, Nrf2, SOD1, HO-1, NQO1, OSGIN1, and gPX1), cell cycle (P21 and CDC25A), apoptosis (CYCS and AIFM2), and migration and invasion (CXCL8, CXCL3, CLU, IL24, COL3A1, MAPT, and ITGA7) were differentially expressed in the MeHg-treated group, indicating MeHg toxicity and mechanism of action. This study will provide insights into the prevention and treatment of pregnancy-related diseases caused by MeHg.

Associations of Prenatal Methylmercury Exposure, Maternal PUFA Status and Neurodevelopment

Associations of Prenatal Methylmercury Exposure, Maternal PUFA Status and Neurodevelopment

Monthly variations in mercury exposure of school children and adults in an industrial area of southwestern China

Recent studies have shown that rice consumption can be the major pathway for human methylmercury (MeHg) exposure in inland China. However, few studies have considered the susceptible population of school children's exposure through rice ingestion. In this study, monthly variations in total Hg (THg)/MeHg concentrations in rice, fish, hair, and urine samples were studied to evaluate the Hg (both THg and MeHg) exposure in Guiyang, a typical industrial area with high anthropogenic emission of Hg. A total of 17 primary school (school A) students, 29 middle school (school B) students, and 46 guardians participated in this study for one year. Hair THg, hair MeHg, and urine THg concentrations ranged from 355–413 ng g−1, 213–236 ng g−1, and 469–518 ng g−1 Creatinine (ng·g−1 Cr), respectively, and no significant differences were observed between different genders and age groups. Hair and urine Hg concentrations showed slightly higher values in the cold season (October to February) than the hot season (March to September), but without significant difference. High monthly variability of individual hair and urine Hg concentrations suggested that long-term study could effectively decrease the uncertainty. The school students showed significantly higher urine THg concentrations than adults due to children's unique physiological structure and behaviors. Probable daily intake (PDI) of MeHg via rice and fish ingestion averaged at 0.0091, 0.0090, and 0.0079 μg kg−1 d−1 for school A students, school B students, and their guardians, respectively, which means that 86%, 84%, and 87% of the PDI were originated from rice ingestion, respectively. Therefore, more attention should be paid to children as a susceptible population. The results indicated low risk of Hg exposure via rice and fish consumption for urban residents in a Chinese industrial city.

Contrasting Spatial and Seasonal Trends of Methylmercury Exposure Pathways of Arctic Seabirds: Combination of Large-Scale Tracking and Stable Isotopic Approaches.

Despite the limited direct anthropogenic mercury (Hg) inputs in the circumpolar Arctic, elevated concentrations of methylmercury (MeHg) are accumulated in Arctic marine biota. However, the MeHg production and bioaccumulation pathways in these ecosystems have not been completely unraveled. We measured Hg concentrations and stable isotope ratios of Hg, carbon, and nitrogen in the feathers and blood of geolocator-tracked little auk Alle alle from five Arctic breeding colonies. The wide-range spatial mobility and tissue-specific Hg integration times of this planktivorous seabird allowed the exploration of their spatial (wintering quarters/breeding grounds) and seasonal (nonbreeding/breeding periods) MeHg exposures. An east-to-west increase of head feather Hg concentrations (1.74-3.48 μg·g-1) was accompanied by significant spatial trends of Hg isotope (particularly Δ199Hg: 0.96-1.13‰) and carbon isotope (δ13C: -20.6 to -19.4‰) ratios. These trends suggest a distinct mixing/proportion of MeHg sources between western North Atlantic and eastern Arctic regions. Higher Δ199Hg values (+0.4‰) in northern colonies indicate an accumulation of more photochemically impacted MeHg, supporting shallow MeHg production and bioaccumulation in high Arctic waters. The combination of seabird tissue isotopic analysis and spatial tracking helps in tracing the MeHg sources at various spatio-temporal scales.

Prenatal low-level methyl mercury exposure and child development in an Italian coastal area

Environmental studies have identified mercury pollution in the Northern Adriatic Sea (Italy). High- level methyl mercury exposure is a known cause of neurodevelopmental disorders. However, the exposure-effect relation at levels <10ppm is controversial. To assess the possible health effects of prenatal methyl mercury exposure through maternal fish consumption, we conducted an epidemiologic cohort study in a mercury polluted area of the Adriatic Sea. We identified all the children born between 1999 and 2001 to women who were resident in two coastal fishing towns. A comparison group was identified inland. A total of 243 children were enrolled. Their mothers were interviewed approximately two months after delivery to determine a variety of covariates and the type, quantity and origin of fish consumed during pregnancy. Total mercury (THg) and methyl mercury (MeHg) were assessed in maternal hair and breast milk and in the child's hair. The children were evaluated after age 18 months with a physical examination and the Denver Developmental Screening Test II (DDST II). Statistical analyses matched by residential area are not presented since they were not associated with fresh fish consumption, THg or MeHg exposure level or neurodevelopmental outcomes. To date 52 children have been evaluated. After adjustment for a number of potential confounders, preliminary results indicate that the fine motor adaptive score on the Denver Developmental test is inversely related to maternal hair THg. These pilot findings are suggestive of an association between children's fine motor skills and their prenatal methyl mercury exposure from maternal fish consumption. However, only a small number of the cohort have been tested and more extensive testing with more sensitive and specific tests is needed to determine if these findings persist.