Prenatal Mercury Research Articles

Prenatal mercury exposure and the secondary sex ratio: The Japan Environment and Children's Study

Prior research into the association between prenatal mercury (Hg) exposure and the secondary sex ratio has yielded inconclusive and conflicting results. Notably, no study has used cord blood Hg measurement in this context. Also, the differences in Hg species and the potential modifying role of selenium (Se) on this association remain unexplored. Using data from the Japan Environment and Children's Study, we analyzed mother–child pairs with available data for concentrations of total mercury (THg) and Se in maternal blood during late pregnancy, and THg, inorganic mercury (IHg), methylmercury (MeHg), and Se in cord blood. Logistic regression models were employed to examine the association between Hg and Se biomarkers and the secondary sex ratio. Out of the total sample of 3698 children, 1877 (50.8 %) were male, corresponding to an overall secondary sex ratio of 1.03. After adjusting for maternal age and parity, no significant associations were observed between THg concentrations of maternal blood and the secondary sex ratio. Nevertheless, we identified that two-fold increases in THg, IHg, and MeHg concentrations in cord blood were positively associated with increased odds of having a male child, yielding adjusted odds ratios of 1.13 (95 %CI: 1.04, 1.22), 1.12 (1.03, 1.21), and 1.12 (1.03, 1.22), respectively. When stratified by the median Se concentrations, no apparent differences were detected in the associations between Hg concentrations and the secondary sex ratio. In summary, elevated Hg concentrations in cord blood, but not maternal blood, were associated with an increased probability of male births.

Integrating Multi-Omics with environmental data for precision health: A novel analytic framework and case study on prenatal mercury induced childhood fatty liver disease

BackgroundPrecision Health aims to revolutionize disease prevention by leveraging information across multiple omic datasets (multi-omics). However, existing methods generally do not consider personalized environmental risk factors (e.g., environmental pollutants). ObjectiveTo develop and apply a precision health framework which combines multiomic integration (including early, intermediate, and late integration, representing sequential stages at which omics layers are combined for modeling) with mediation approaches (including high-dimensional mediation to identify biomarkers, mediation with latent factors to identify pathways, and integrated/quasi-mediation to identify high-risk subpopulations) to identify novel biomarkers of prenatal mercury induced metabolic dysfunction-associated fatty liver disease (MAFLD), elucidate molecular pathways linking prenatal mercury with MAFLD in children, and identify high-risk children based on integrated exposure and multiomics data. MethodsThis prospective cohort study used data from 420 mother–child pairs from the Human Early Life Exposome (HELIX) project. Mercury concentrations were determined in maternal or cord blood from pregnancy. Cytokeratin 18 (CK-18; a MAFLD biomarker) and five omics layers (DNA Methylation, gene transcription, microRNA, proteins, and metabolites) were measured in blood in childhood (age 6–10 years). ResultsEach standard deviation increase in prenatal mercury was associated with a 0.11 [95% confidence interval: 0.02–0.21] standard deviation increase in CK-18. High dimensional mediation analysis identified 10 biomarkers linking prenatal mercury and CK-18, including six CpG sites and four transcripts. Mediation with latent factors identified molecular pathways linking mercury and MAFLD, including altered cytokine signaling and hepatic stellate cell activation. Integrated/quasi-mediation identified high risk subgroups of children based on unique combinations of exposure levels, omics profiles (driven by epigenetic markers), and MAFLD. ConclusionsPrenatal mercury exposure is associated with elevated liver enzymes in childhood, likely through alterations in DNA methylation and gene expression. Our analytic framework can be applied across many different fields and serve as a resource to help guide future precision health investigations.

Early life exposure to mercury and relationships with telomere length and mitochondrial DNA content in European children

BackgroundTelomere length (TL) and mitochondrial function expressed as mitochondrial DNA copy number (mtDNAcn) are biomarkers of aging and oxidative stress and inflammation, respectively. Methylmercury (MeHg), a common pollutant in fish, induces oxidative stress. We hypothesized that elevated oxidative stress from exposure to MeHg decreases mtDNAcn and shortens TL. MethodsStudy participants are 6–11-year-old children from the HELIX multi-center birth cohort study, comprising six European countries. Prenatal and postnatal total mercury (THg) concentrations were measured in blood samples, TL and mtDNAcn were determined in child DNA. Covariates and confounders were obtained by questionnaires. Robust regression models were run, considering sociodemographic and lifestyle covariates, as well as fish consumption. Sex, ethnicity, and fish consumption interaction models were also run. ResultsWe found longer TL with higher pre- and postnatal THg blood concentrations, even at low-level THg exposure according to the RfD proposed by the US EPA. The prenatal association showed a significant linear relationship with a 3.46 % increase in TL for each unit increased THg. The postnatal association followed an inverted U-shaped marginal non-linear relationship with 1.38 % an increase in TL for each unit increased THg until reaching a cut-point at 0.96 μg/L blood THg, from which TL attrition was observed. Higher pre- and postnatal blood THg concentrations were consistently related to longer TL among cohorts and no modification effect of fish consumption nor children's sex was observed. No association between THg exposure and mtDNAcn was found. DiscussionWe found evidence that THg is associated with TL but the associations seem to be time- and concentration-dependent. Further studies are needed to clarify the mechanism behind the telomere changes of THg and related health effects.

The impact of prenatal mercury on neurobehavioral functioning longitudinally assessed from a young age to pre-adolescence in a Spanish birth cohort

The objective is to investigate the relation between cord blood mercury concentrations and child neurobehavioural functioning assessed longitudinally during childhood until pre-adolescence. MethodsThe study involves mothers and their offspring engaged in the Spanish INMA birth cohort (n = 1147). Total mercury (THg) was determined in cord blood. Behavioural problems were assessed several times during childhood using the ADHD-DSM-IV at age 4, SDQ at ages 7 and 11, CPRS-R:S and the CBCL at ages 7, 9 and 11. Covariates were obtained through questionnaires during the whole period. Multivariate generalised negative binomial (MGNB) models or mixed-effects MGNB (for those tests with information at one or more time points, respectively) were used to investigate the relation between cord blood THg and the children's punctuations. Models were adjusted for prenatal fish intake. Effect modification by sex, prenatal and postnatal fish intake, prenatal fruit and vegetable intake, and maternal polychlorinated biphenyl concentrations (PCBs) was assessed by interaction terms. ResultsThe geometric mean ± standard deviation of cord blood THg was 8.22 ± 2.19 μg/L. Despite adjusting for fish consumption, our results did not show any statistically significant relationship between prenatal Hg and the children's performance on behavioural tests conducted between the ages of 4 and 11. Upon assessing the impact of various factors, we observed no statistically significant interaction. ConclusionDespite elevated prenatal THg exposure, no association was found with children's behavioural functioning assessed from early childhood to pre-adolescence. The nutrients in fish could offset the potential neurotoxic impact of Hg. Further birth cohort studies with longitudinal data are warranted.

Infantile allergic diseases: a cohort study prenatal fish intake and mercury exposure context

BackgroundAllergic diseases (ADs) have been increasingly reported in infants and children over the last decade. Diet, especially the inclusion of fish intake, may help to lower the risk of ADs. However, fish also, can bioaccumulate environmental contaminants such as mercury. Hence, our study aims to determine what effects the type and frequency of fish intake have on ADs in six-month-old infants, independently and jointly with mercury exposure.MethodsThis study is part of the prospective birth cohort: Mothers and Children’s Environmental Health (MOCEH) study in South Korea. Data was collected on prenatal fish intake, prenatal mercury concentration and ADs for infants aged six months for 590 eligible mother-infant pairs. Logistic regression analysis was conducted to evaluate the risk of prenatal fish intake and mercury concentration on ADs in infants. Finally, interaction between fish intake and mercury concentration affecting ADs in infants was evaluated. Hazard ratios of prenatal fish intake on ADs in 6 month old infants were calculated by prenatal mercury exposure.ResultsLogistic regression analysis showed that white fish (OR: 0.53; 95% CI 0.30–0.94; P < 0.05) intake frequency, once a week significantly decreased the risk of ADs in infants. Stratification analysis showed that consuming white fish once a week significantly reduced the hazard of ADs (HR: 0.44; 95% CI 0.21–0.92; P < 0.05) in infants in the high-mercury (≥ 50th percentile) exposure group.ConclusionThe result indicates that prenatal white fish intake at least once a week reduces the risk of ADs in infants, especially in the group with high prenatal mercury exposure.

Early exposure to mercury and cardiovascular function of seven-year old children in Guadeloupe (French West Indies)

BackgroundThe cardiotoxicity of prenatal exposure to mercury has been suggested in populations having regular contaminated seafood intake, though replications in the literature are inconsistent. MethodsThe Timoun Mother-Child Cohort Study was set up in Guadeloupe, an island in the Caribbean Sea where seafood consumption is regular. At seven years of age, 592 children underwent a medical examination, including cardiac function assessment. Blood pressure (BP) was taken using an automated blood pressure monitor, heart rate variability (HRV, 9 parameters) and electrocardiogram (ECG) characteristics (QT, T-wave parameters) were measured using Holter cardiac monitoring during the examination. Total mercury concentrations were measured in cord blood at birth (median = 6.6 μg/L, N = 399) and in the children's blood at age 7 (median = 1.7 μg/L, N = 310). Adjusted linear and non-linear modelling was used to study the association of each cardiac parameter with prenatal and childhood exposures. Sensitivity analyses included co-exposures to lead and cadmium, adjustment for maternal seafood consumption, selenium and polyunsaturated fatty acids (n3-PUFAs), and for sporting activity. ResultsHigher prenatal mercury was associated with higher systolic BP at 7 years of age (βlog2 = 1.02; 95% Confidence Interval (CI) = 0.10, 1.19). In boys, intermediate prenatal exposure was associated with reduced overall HRV and parasympathetic activity, and longer QT was observed with increasing prenatal mercury (βlog2 = 4.02; CI = 0.48, 7.56). In girls, HRV tended to increase linearly with prenatal exposure, and no association was observed with QT-wave related parameters. Mercury exposure at 7 years was associated with decreased BP in girls (βlog2 = −1.13; CI = −2.22, −0.004 for diastolic BP). In boys, the low/high-frequency (LF/HF) ratio increased for intermediate levels of exposure. ConclusionOur study suggests sex-specific and non-monotonic modifications in some cardiac health parameters following prenatal exposure to mercury in pre-pubertal children from an insular fish-consuming population.

Prenatal arsenic and mercury levels among women practicing geophagy in areas with artisanal and small-scale gold mining activities, Northwestern Tanzania

BackgroundArtisanal and small-scale gold mining (ASGM) areas potentially pose increased exposure to arsenic and mercury through community contamination, occupations at gold mines, and/or geophagy when soil is locally sourced. This study examined the effects of geophagy, a deliberate soil eating practice, along with community and occupational exposures in ASGM areas on urinary arsenic and blood mercury levels among pregnant women in the Mining and Health Longitudinal Cohort in northwestern Tanzania.MethodsData on maternal arsenic and mercury levels were captured for 1056 pregnant women using an unprovoked morning urine samples and dried blood spots respectively. We used a step-wise generalized linear regression model to retain the most relevant covariates for the model. A generalized linear regression model with identity link function was used to predict the effect of geophagy practices on arsenic and mercury levels separately. The model was adjusted using sociodemographic correlates, including maternal age, education level, whether respondents lived in mining or non-mining area, years of residence, marital status, maternal occupation, individual partner’s education, and occupational, and socioeconomic status.ResultsIn the adjusted regression model, eating soil during pregnancy increased arsenic concentration by almost 23% (β = 1.229, 95% CI: 1.094, 1.38, p < 0.001) and living in mining areas had a 21.2% (β = 1.212; 95% CI: 1.039,1.414, p = 0.014) increased risk. Geophagy significantly increased mercury levels by 13.3% (β = 1.133, 95% CI: 1.022, 1.257, p = 0.018). Living in areas with ASGM activities was associated with a 142% (β = 2.422, 95% CI: 2.111, 2.776, p < 0.0001) increase in blood mercury.ConclusionGeophagy practices increased urinary arsenic and blood mercury levels in pregnant women, which was especially true for arsenic when living in areas with ASGM activities. Working in mining = increased risk for blood mercury levels. Community-based environmental health policies should address reductions in occupational and community exposures, along with strategic geophagy reduction interventions.

KEAP1 polymorphisms and neurodevelopmental outcomes in children with exposure to prenatal MeHg from the Seychelles Child Development Study Nutrition Cohort 2

BackgroundHumans differ in the metabolism of the neurotoxicant methyl mercury (MeHg). This variation may be partially due to variation in genes encoding the transcription factor Nuclear factor E2-related factor 2 (NRF2) and its negative regulator Kelch-like ECH-Associated Protein 1 (KEAP1), which regulate glutathione and related transporter and antioxidant proteins that play a role in the metabolism and neurotoxicity of MeHg. AimTo elucidate a potential risk from genetic variation in NFE2L2 (encoding NRF2) and KEAP1 toward prenatal mercury exposure and child neurodevelopmental outcomes at 20 months and 7 years of age in a population with variable prenatal exposure to MeHg from maternal fish consumption. Material and MethodsNutrition Cohort 2 is a mother–child cohort in the Republic of Seychelles. Children were genotyped for NFE2L2 (rs2364723, rs13001694) and KEAP1 (rs8113472, rs9676881) polymorphisms (N = 1285 after removing siblings). Total mercury (Hg) was measured in cord blood as a biomarker for prenatal MeHg exposure. Child neurodevelopmental outcomes included the Bayley Scales of Infant Development II administered at 20 months of age, and outcomes across multiple neurodevelopmental domains from 14 tests administered in children and 3 instruments completed by parents when children were 7 years of age. ResultsThe mean cord blood MeHg concentration was 34 (95% CI 11, 75) µg/L. None of the four polymorphisms had a significant association (p < 0.05) with either cord MeHg or neurodevelopmental test results at 20 months. There were no significant associations between either NFE2L2 polymorphism and any developmental test scores. At 7 years, children carrying KEAP1 rs8113472 CA showed significantly worse performance on psychomotor function than children with the CC variant (finger tapping, dominant hand: β − 1.19, SE 0.34; finger tapping, non-dominant hand: β − 0.92, SE 0.31) and worse social communication (SCQ Total: β 0.65, SE 0.27). Children carrying rs8113472 AA, versus children with CC, showed significantly better performance on social communication (SRS Total: β − 8.88, SE 3.60). Children carrying KEAP1 rs9676881 AG, versus children with GG, showed significantly worse performance on psychomotor function (trailmaking A time: β 8.66, SE 3.37) and cognition (KBIT Matrices: β − 0.96, SE 0.36). ConclusionNo associations between NFE2L2 and KEAP1 polymorphisms and MeHg concentration were identified. However, at 7 years, KEAP1 polymorphisms were associated with differences in neurodevelopmental outcomes in children from a population with high fish intake.

Prenatal exposure to selenium, mercury, and manganese during pregnancy and allergic diseases in early childhood: The Japan Environment and Children's study

BackgroundPrenatal exposure to metallic elements may adversely affect early childhood health. However, more evidence is needed as population-based cohort studies are currently limited. ObjectivesWe aimed to examine the associations between prenatal metallic (mercury, selenium, and manganese) exposure and the risk of allergic diseases in early childhood until three years of age. MethodsThe data from 94,794 mother-infant pairs, who participated in the Japan Environment and Children’s study, were used in this study. Prenatal metallic element exposure was measured in maternal blood collected during mid-pregnancy. The incidence of atopic dermatitis, food allergies, asthma, and allergic rhinitis during the first three years of life was prospectively investigated using self-reports of physician-diagnosed allergies. A multivariable modified Poisson regression model was used to estimate the cumulative incidence ratio and their 95% confidence intervals of allergic diseases associated with prenatal exposure to mercury, selenium, and manganese. We further evaluated the interaction between mercury and selenium exposures in this association. ResultsWe confirmed 26,238 cases of childhood allergic diseases: atopic dermatitis, food allergies, asthma, and allergic rhinitis in 9,715 (10.3%), 10,897 (11.5%), and 9,857 (10.4%), 4,630 (4.9%), respectively. No association was found between prenatal mercury or manganese exposure and the risk of allergic diseases. Prenatal selenium exposure was inversely associated with atopic dermatitis, food allergies, allergic rhinitis, and any allergic diseases, but not with asthma. These inverse associations were more pronounced for lower mercury exposures than for higher exposures. ConclusionsOur findings suggest that prenatal exposure to selenium may be beneficial for reducing the risk of atopic dermatitis, food allergies, allergic rhinitis, and any allergic diseases in early childhood, especially with lower prenatal mercury exposure.

Prenatal and concurrent blood mercury concentrations and associations with IQ in canadian preschool children

BackgroundPrenatal and childhood mercury (Hg) exposures have been associated with negative impacts on child neurodevelopment. It is unclear if associations persist at the low Hg exposures typical in Western countries. ObjectiveTo examine associations between prenatal/childhood blood Hg concentrations and child IQ in Canadian male and female children while considering the potential modifying role of prenatal fish consumption. MethodsWe analyzed data from the Maternal-Infant Research on Environmental Chemicals study. Hg was measured in first trimester (n = 527), cord (n = 430), and child (at 3–4 years of age, n = 355) blood and examined sex-stratified associations between blood Hg and children's Full Scale IQ (FSIQ), Verbal IQ (VIQ), Performance IQ (PIQ), and General Language Composite (GLC) scores (assessed with WPPSI-III). Prenatal Hg analyses were further stratified by prenatal fish consumption (low: 0–2, moderate: 3–7, or high: ≥8 times/month). ResultsHigher cord blood Hg concentrations were associated with lower PIQ (ß = −3.27; 95%CI: 6.44, −0.09) in male children with the lowest prenatal fish consumption. Progressively stronger positive associations were observed with PIQ in male children for moderate (ß = 1.08; 95%CI: 0.10, 2.26) and high (ß = 3.07; 95%CI: 1.95, 4.19) prenatal fish consumption. Cord blood Hg concentrations were positively associated with female children's FSIQ (ß = 1.29; 95% CI: 0.77, 1.81) and PIQ (ß = 2.01; 95% CI: 1.19, 2.83); however, when stratified only in the highest fish consumption subgroup. Among female children, higher child blood Hg concentrations were associated with an approximately 1-point increase in FSIQ, VIQ, and GLC. ConclusionsPrenatal exposure to low levels of Hg was associated with lower PIQ scores in male children with low prenatal fish intake. Positive associations between cord and child blood Hg concentrations and IQ were primarily observed in female children and may be due to beneficial effects of prenatal fish intake.

Prenatal Mercury Exposure and Infant Weight Trajectories in a UK Observational Birth Cohort.

Mercury is highly toxic metal found in trace quantities in common foods. There is concern that exposure during pregnancy could impair infant development. Epidemiological evidence is mixed, but few studies have examined postnatal growth. Differences in nutrition, exposures, and the living environment after birth may make it easier to detect a negative impact from mercury toxicity on infant growth. This study includes 544 mother-child pairs from the Avon Longitudinal Study of Parents and Children. Blood mercury was measured in early pregnancy and infant weight at 10 intervals between 4 and 61 months. Mixed-effect models were used to estimate the change in infant weight associated with prenatal mercury exposure. The estimated difference in monthly weight gain was -0.02 kg per 1 standard deviation increase in Hg (95% confidence intervals: -0.10 to 0.06 kg). When restricted to the 10th decile of Hg, the association with weight at each age level was consistently negative but with wide confidence intervals. The lack of evidence for an association may indicate that at Hg levels in this cohort (median 1.9 µg/L) there is minimal biological impact, and the effect is too small to be either clinically relevant or detectable.

Prenatal mercury exposure, fish intake and child emotional behavioural regulation in the Norwegian Mother, Father and Child Cohort Study

ObjectiveWhile maternal fish consumption in pregnancy has consistently been linked to better cognitive and emotional outcomes in children, fish is also a primary source of exposure to methyl mercury (MeHg),...

Occupational and environmental mercury exposure and human reproductive health - a review.

Mercury is a toxic heavy metal. Humans are exposed to mercury through several sources including environmental, occupational, contaminated food and water and from mercury-containing dental amalgam. Mercury exposure is known to harm the nervous system profoundly, and have a negative impact on digestive and immune systems, and other organs. To review and discuss the effect of mercury exposure through environmental or occupational routes on human reproduction, pregnancy, and its outcome. Published information about the potential toxic effects of mercury on human reproduction were collected and summarized. Literature was identified by systematic search using relevant keywords. Literature review revealed a number of negative impacts of mercury on human reproduction. These included effects on semen quality, including reduced sperm count, motility, and changes in morphology that may reduce fertility potential. There may also be an effect in changing reproductive hormone levels. Mercury exposure might also affect pregnancy but the data concerning mercury effects on female reproduction are limited except for some data about mercury exposure and poor pregnancy outcomes. Available data indicate that mercury exposure may have a toxicity effect on reproductive potential, especially in males. Prenatal mercury exposure may affect pregnancy or its outcome and this appears to be dependent upon dose, duration, and timing of exposure. Nutritional status of exposed individual might also influence the impact of mercury.

Pre and postnatal exposure to mercury and sexual development in 9-year-old children in Spain: The role of brain-derived neurotrophic factor

Early exposure to mercury has been related to endocrine disruption. Steroid hormones play a crucial role in neural cell migration, differentiation, etc., as well as protecting against several neurotoxic compounds.We investigate the relation between mercury exposure and children's sexual development, and we evaluate the possible influence of different brain-derived neurotrophic factor (BDNF) polymorphisms on this association.Our study sample comprised 412 9-year-old children participating in the INMA cohort (2004–2015). Mercury concentrations were measured at birth (cord blood) and at 4 and 9 years of age (hair). Sexual development was assessed by levels of sex steroid hormones (estradiol and testosterone) in saliva and the Tanner stages of sex development at 9 years (categorized as 1: prepuberty and >1: pubertal onset). Covariates and confounders were collected through questionnaires during pregnancy and childhood. Polymorphisms in the BDNF gene were genotyped in cord blood DNA. Multivariate linear regression analyses were performed between mercury levels and children's sexual development by sex. Effect modification by genetic polymorphisms and fish intake was assessed.We found marginally significant inverse associations between postnatal exposure to mercury (at 9 years) and testosterone levels (β[95%CI] = -0.16[-0.33,0.001], and −0.20[-0.42,0.03], for boys and girls, respectively). Additionally, we found that prenatal mercury was negatively associated with Tanner stage >1 in boys. Finally, we found significant genetic interactions for some single nucleotide polymorphisms in the BDNF gene.In conclusion, pre and postnatal exposure to mercury seems to affect children's sexual development and BDNF may play a role in this association, but further research would be needed.

DNA methylation changes associated with prenatal mercury exposure: A meta-analysis of prospective cohort studies from PACE consortium.

Mercury (Hg) is a ubiquitous heavy metal that originates from both natural and anthropogenic sources and is transformed in the environment to its most toxicant form, methylmercury (MeHg). Recent studies suggest that MeHg exposure can alter epigenetic modifications during embryogenesis. In this study, we examined associations between prenatal MeHg exposure and levels of cord blood DNA methylation (DNAm) by meta-analysis in up to seven independent studies (n=1462) as well as persistence of those relationships in blood from 7 to 8 year-old children (n=794). In cord blood, we found limited evidence of differential DNAm at cg24184221 in MED31 (β=2.28×10-4, p-value=5.87×10-5) in relation to prenatal MeHg exposure. In child blood, we identified differential DNAm at cg15288800 (β=0.004, p-value=4.97×10-5), also located in MED31. This repeated link to MED31, a gene involved in lipid metabolism and RNA Polymerase II transcription function, may suggest a DNAm perturbation related to MeHg exposure that persists into early childhood. Further, we found evidence for association between prenatal MeHg exposure and child blood DNAm levels at two additional CpGs: cg12204245 (β=0.002, p-value=4.81×10-7) in GRK1 and cg02212000 (β=-0.001, p-value=8.13×10-7) in GGH. Prenatal MeHg exposure was associated with DNAm modifications that may influence health outcomes, such as cognitive or anthropometric development, in different populations.

Prenatal Mercury Exposure and Neurodevelopment up to the Age of 5 Years: A Systematic Review.

Neurodevelopmental delays can interfere with children’s engagement with the world and further development, and may have negative consequences into adulthood. Mercury is highly toxic and may negatively influence neurodevelopment because it can freely cross the placenta and accumulate in the fetal brain. We searched four publication databases (Embase, PsycINFO, PubMed/MEDLINE, Scopus) for studies examining the relationship between early life mercury exposure and scores on neurodevelopmental performance measures in children aged 0 to 5 years old. Study quality was assessed using the National Institutes of Health (NIH) Quality Assessment Tool. Thirty-two prospective studies were included in the review. Neurodevelopmental performance was measured using 23 different scales, most commonly the Bayley Scales of Infant and Toddler Development (BSID). In most cases, the evidence for an association between mercury and neurodevelopment was weak. There did not appear to be exceptions for particular childhood ages, outcome scales, or mercury levels. The small number of results to the contrary were more likely to be studies which did not meet our high-quality criteria, and could be a consequence of multiple testing, selection bias, or incomplete confounder adjustment. Based on current evidence, dietary mercury exposure during pregnancy is unlikely to be a risk factor for low neurodevelopmental functioning in early childhood.

Atopic dermatitis in infants: The role of prenatal fish intake and mercury exposure

BACKGROUND AND AIM: Incidence of atopic dermatitis (AD) are increasing in infants and children over the last decade. Diet plays an important role in connection with allergic diseases. Especially fish intake, lower the risk of AD and other allergic diseases. But, fish bio accumulates environmental contaminants, such as mercury. Thus, the objective of our study to evaluate the effect of maternal fish intake: type and frequency on AD in six-month-old infants concerning mercury exposure. METHODS: Five hundred sixty-five eligible mother-infant pairs from the Mother and Children’s environmental health study in South Korea were selected. Data was collected on prenatal fish intake, prenatal mercury concentration, and AD in infants at six months of age. A joint logistic regression analysis was conducted to evaluate the risk of prenatal fish intake and prenatal mercury concentration on AD in infants at six months of age. We explored multiplicative and additive interaction between fish intake and mercury concentration affecting AD in infants. RESULTS:Total fish (odds ratio: 0.68,95% CI 0.46 to 0.99; P 0.05) and white fish (odds ratio: 0.49.95% CI 0.27 to 0.89; P0.05) intake frequency 1 time per week significantly decreased the risk of AD in infants at six months. Stratified analysis by prenatal mercury exposure showed that consuming fish 1 time per week reduced the risk of AD in six-month-old infants in the high-mercury (25th percentile) exposure group significantly in comparison with low-mercury exposure group. CONCLUSIONS:Our results show that prenatal white fish intake 1 time per week reduces the AD risk in infants with high prenatal mercury exposure. KEYWORDS: atopic dermatitis, fish, pregnancy, mercury

Early pregnancy exposure to metals and maternal depressive symptom trajectories in Project Viva

BACKGROUND AND AIM: Exposure to neurotoxicant metals, hypothesized to alter dopaminergic function, have not been sufficiently explored as a risk factor for maternal depression. We evaluated the extent to which early pregnancy blood levels of essential and non-essential metals were prospectively associated with depressive symptom trajectories from mid-pregnancy to 7-years postpartum. METHODS: Participants were 872 women in Project Viva, a longitudinal Boston-area cohort recruited during pregnancy (1999-2002). We measured levels of 11 metal(loid)s (arsenic, barium, cadmium, cesium, copper, mercury, magnesium, manganese, lead, selenium, zinc) in maternal first trimester erythrocytes. We assessed depressive symptoms via the Edinburgh Postnatal Depression Scale at mid-pregnancy and four postpartum timepoints (6 months, 1, 3, 7 years). Utilizing latent class mixed modeling, we identified three depressive symptom trajectories: stable low (86%); elevated perinatal symptoms, then decreasing (9%); and moderate perinatal symptoms, then increasing (5%), among women with ≥3 repeat measures. Adjusting for maternal sociodemographics and dietary intake, we used multinomial logistic regression to test associations of individual metal levels with odds of having an increasing or decreasing trajectory. RESULTS:In our cohort of moderately high socioeconomic status participants (e.g., 75% college graduate), correlations between metal levels were mostly positive (Spearman: 0.01-0.60), except for negative correlations between barium and all other elements. Compared to having a stable low trajectory, a doubling of blood arsenic was associated with 1.27 (95% confidence interval: 1.01, 1.59) odds of an increasing depressive trajectory. Greater prenatal mercury blood level was associated with lower odds of having a decreasing trajectory [0.88 (95% confidence interval: 0.77, 1.00)]. All other first trimester metal levels were not associated with depressive symptom trajectory. CONCLUSIONS:In our study investigating associations of several early pregnancy metals with maternal depressive symptom trajectories, we did not observe strong evidence of associations. Residual confounding or multiple testing may explain observed associations with arsenic and mercury. KEYWORDS: Mental health outcomes, heavy metals, chemical exposures, female

Mercury and Prenatal Growth: A Systematic Review.

The intrauterine environment is critical for healthy prenatal growth and affects neonatal survival and later health. Mercury is a toxic metal which can freely cross the placenta and disrupt a wide range of cellular processes. Many observational studies have investigated mercury exposure and prenatal growth, but no prior review has synthesised this evidence. Four relevant publication databases (Embase, MEDLINE/PubMed, PsycINFO, and Scopus) were systematically searched to identify studies of prenatal mercury exposure and birth weight, birth length, or head circumference. Study quality was assessed using the NIH Quality Assessment Tool, and results synthesised in a narrative review. Twenty-seven studies met the review criteria, these were in 17 countries and used 8 types of mercury biomarker. Studies of birth weight (total = 27) involving populations with high levels of mercury exposure, non-linear methods, or identified as high quality were more likely to report an association with mercury, but overall results were inconsistent. Most studies reported no strong evidence of association between mercury and birth length (n = 14) or head circumference (n = 14). Overall, our review did not identify strong evidence that mercury exposure leads to impaired prenatal growth, although there was some evidence of a negative association of mercury with birth weight.

Maternal gestational mercury exposure in relation to cord blood T cell alterations and placental gene expression signatures

The immunotoxic impacts of mercury during early life is poorly understood. We investigated the associations between gestational mercury exposure and frequency of cord blood T cells as well as placental gene expression. Frequency of natural Treg cells was positively associated with prenatal and postpartum mercury toenail concentrations. Frequency of NKT and activated naïve Th cells was positively associated with prenatal toenail mercury concentrations and number of maternal silver-mercury dental amalgams, respectively. Placental gene expression analyses revealed distinct gene signatures associated with mercury exposure. Decreased placental expression of a histone demethylase, KDM4DL, was associated with both higher prenatal and postpartum maternal toenail mercury levels among male infants and remained statistically significant after adjustment for fish and seafood consumption. The results suggest that gestational exposure to mercury concentrations contribute to alterations in both T cells and gene expression in placenta at birth. These alterations may inform mechanisms of mercury immunotoxicity.