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Mercury poisoning still occurs as a result of accidental and occupational exposure. For the general population, however, the main concern is the possible adverse effect of exposure to mercury through fish consumption and the receipt of dental amalgams and thimerosal, a preservative used in vaccines. This review summarizes both the facts and the controversies surrounding exposure to methyl mercury, mercury vapor, and the ethyl mercury in thimerosal. Mercury has been used commercially and medically for centuries. In the past it was a common constituent of many medications. It is still used in hospitals in thermometers and blood-pressure cuffs and commercially in batteries, switches, and fluorescent light bulbs. Large quantities of metallic mercury are employed as electrodes in the electrolytic production of chlorine and sodium hydroxide from saline. These uses still give rise to accidental and occupational exposures. 1 Today, however, exposure of the general population comes from three major sources: fish consumption, dental amalgams, and vaccines. Each has its own characteristic form of mercury and distinctive toxicologic profile . . .

Exposure to methylmercury (MeHg) before birth can adversely affect children's neurodevelopment. The most common form of prenatal exposure is aternal fish consumption, but whether such exposure harms the fetus is unknown. We aimed to identify adverse neurodevelopmental effects in a fish-consuming population. We investigated 779 mother-infant pairs residing in the Republic of Seychelles. Mothers reported consuming fish on average 12 meals per week. Fish in Seychelles contain much the same concentrations of MeHg as commercial ocean fish elsewhere. Prenatal MeHg exposure was determined from maternal hair growing during pregnancy. We assessed neurocognitive, language, memory, motor, perceptual-motor, and behavioural functions in children at age 9 years. The ssociation between prenatal MeHg exposure and the primary endpoints was investigated with multiple linear regression with adjustment for covariates that affect child development. Mean prenatal MeHg exposure was 6·9 parts per million (SD 4·5ppm). Only two endpoints were associated with prenatal MeHg exposure. Increased exposure as associated with decreased performance in the grooved pegboard using the non-dominant hand in males and improved scores in the hyperactivity index of the Conner's teacher rating scale. Covariates affecting child development were appropriately associated with endpoints. These data do not support the hypothesis that there is a neurodevelopmental risk from prenatal MeHg exposure resulting solely from ocean fish consumption.

Background: There continues to be public concern that mercury exposure and autism spectrum disorder (ASD) may be associated. The primary source of exposure to organic mercury in humans is to methylmercury from fish consumption. We evaluated the association between prenatal methylmercury exposure and ASD phenotype in children and adolescents in the Republic of Seychelles, where fish consumption is high. Methods: We administered the Social Communication Questionnaire to parents of a cohort of 1784 children, adolescents, and young adults. The Social Responsiveness Scale was administered to teachers of 537 cohort subjects at about 10 years of age. Prenatal exposure to methylmercury was measured in maternal hair samples collected at or near the time of birth. Multivariable regression models evaluated the relationship between prenatal methylmercury exposure and ASD phenotypic scores, adjusting for relevant covariates. Results: The mean prenatal methylmercury exposure for subjects in the analysis was 8.4 ppm (standard deviation [SD] = 5.7). The mean Social Communication Questionnaire score was 8.0 (SD = 4.4). The mean prenatal methylmercury exposure for subjects with Social Responsiveness Scale scores was 6.7 ppm (SD = 4.4) and the mean Social Responsiveness Scale score was 57.6 (SD = 26.8). No consistent association between prenatal methylmercury exposure and ASD screening instrument was found, using linear and nonlinear regression analyses. Conclusions: Prenatal exposure to methylmercury was not associated with ASD phenotypic behaviors in our cohort of high fish consumers. Our findings contribute to the growing literature suggesting that exposure to methylmercury does not play an important role in the development of ASD phenotypic behavior.

[...]the authors review the evidence for exposure above the reference value.

Telomere length (TL) and mitochondrial DNA copy number (mtDNAcn) variations are linked to age-related diseases and are associated with environmental exposure and nutritional status. Limited data, however, exist on the associations with mercury exposure, particularly early in life. We examined the association between prenatal mercury (Hg) exposure and TL and mtDNAcn in 1,145 Seychelles children, characterized by a fish-rich diet. Total mercury (THg) was determined in maternal hair at delivery and cord blood. TL and mtDNAcn were determined relative to a single-copy hemoglobin beta gene in the saliva of 7-y-old children. Linear regression models assessed associations between THg and relative TL (rTL) and relative mtDNAcn (rmtDNAcn) while controlling for maternal and cord serum polyunsaturated fatty acid (PUFA) status and sociodemographic factors. Interactions between THg and child sex, PUFA, and telomerase genotypes were evaluated for rTL and rmtDNAcn. Higher THg concentrations in maternal hair and cord blood were associated with longer rTL [ ; 95% confidence interval (CI): 0.002, 0.016 and ; 95% CI: 0.001, 0.003, respectively], irrespective of sex, PUFA, or telomerase genotypes. Maternal serum n-6 PUFA and n-6/n-3 ratio were associated with shorter [ ; 95% CI: , and ; 95% CI: , , respectively] and PUFA with longer ( ; 95% CI: 0.032, 0.65) rTL. Cord blood n-6 PUFA was associated with longer ( ; 95% CI: 0.050, 0.26) rTL. Further analyses revealed linoleic acid in maternal blood and arachidonic acid in cord blood as the main drivers of the n-6 PUFA associations. No associations were observed for THg and PUFA with rmtDNAcn. Our results indicate that prenatal THg exposure and PUFA status are associated with rTL later in childhood, although not consistently aligned with our initial hypothesis. Subsequent research is needed to confirm this finding, further evaluate the potential confounding of fish intake, and investigate the underlying molecular mechanisms to verify the use of rTL as a true biomarker of THg exposure. https://doi.org/10.1289/EHP14776.

Maternal thyroid hormones facilitate optimal foetal neurodevelopment; however, the exact role of the thyroid hormones on specific cognitive outcomes is unknown. The present study aimed to investigate associations between maternal thyroid function and neurodevelopmental outcomes in the Seychelles Child Development Study (SCDS) Nutrition 2 cohort (n 1328). Maternal free thyroid hormones (fT3, fT4 and fTSH) were assessed at 28 weeks’ gestation with a range of child cognitive outcomes analysed at 20 months. Dietary iodine intake was analysed for a subset of women through a Food Frequency Questionnaire. Linear regression analysis was used to test associations between serum concentrations of maternal thyroid hormones and child neurodevelopment outcomes. Thyroid hormones were analysed as continuous data and categorised as quintiles. 95% of mothers had optimal thyroid function based on fTSH concentrations. Overall, the present study shows that maternal thyroid function is not associated with neurodevelopmental outcomes in this high fish-eating population. However, a positive association, using quintiles for fT3, was reported for the Mental Developmental Index, between Q3 v. Q4 (β 0⋅073; P 0⋅043) and for Q3 v. Q5 (β value 0⋅086; P 0⋅018). To conclude, mothers in our cohort, who largely have optimal thyroid function and iodine intakes, appear able to regulate thyroid function throughout pregnancy to meet neurodevelopmental needs. However, it is possible that minor imbalances of fT3, as indicated from our secondary analysis, may impact offspring neurodevelopment. Further investigation of the relationship between maternal thyroid function and infant neurodevelopment is warranted, particularly in populations with different dietary patterns and thereby iodine intakes.

Maternal fish consumption exposes the fetus to beneficial nutrients and potentially adverse neurotoxicants. The current study investigated associations between maternal fish consumption and child neurodevelopmental outcomes. Maternal fish consumption was assessed in the Seychelles Child Development Study Nutrition Cohort 1 (n 229) using 4-day food diaries. Neurodevelopment was evaluated at 9 and 30 months, and 5 and 9 years with test batteries assessing twenty-six endpoints and covering multiple neurodevelopmental domains. Analyses used multiple linear regression with adjustment for covariates known to influence child neurodevelopment. This cohort consumed an average of 8 fish meals/week and the total fish intake during pregnancy was 106·8 (sd 61·9) g/d. Among the twenty-six endpoints evaluated in the primary analysis there was one beneficial association. Children whose mothers consumed larger quantities of fish performed marginally better on the Kaufman Brief Intelligence Test (a test of nonverbal intelligence) at age 5 years (β 0·003, 95 % CI (0, 0·005)). A secondary analysis dividing fish consumption into tertiles found no significant associations when comparing the highest and lowest consumption groups. In this cohort, where fish consumption is substantially higher than current global recommendations, maternal fish consumption during pregnancy was not beneficially or adversely associated with children’s neurodevelopmental outcomes.

Findings from animal models suggest early exposure to polyunsaturated fatty acids (PUFAs) during pregnancy may influence developmental plasticity including adiposity(1). Birth cohort studies examining associations between offspring weight and maternal n-3 PUFA status or maternal fish intakes, the richest dietary source of n-3 PUFAs have been few and have yielded inconsistent findings. Some have reported lower weight at birth and throughout childhood with increasing maternal fish intakes and n-3 PUFA status(2), whilst others have observed positive or null associations(3,4). These have focused on the first few years of life and have been conducted within low fish-consuming populations. Our study provides novel data by examining associations between maternal fish consumption and prenatal PUFA (n-3 & n-6) status and offspring weight at birth and throughout childhood (7 & 13 years) in a high fish-eating population. Pregnant women were enrolled in the Seychelles Child Development Study Nutrition Cohort 2 between 2008-2011. Serum PUFAs were quantified in maternal blood collected at 28-weeks’ gestation and in cord blood collected at delivery using gas-chromatography tandem mass spectrometry. Maternal fish consumption was assessed at 28-weeks’ gestation using a Fish Use Questionnaire. Childbirth weight (kg) was measured at delivery and classified according to WHO growth standards(5) (n = 1185). Child height (m), weight (kg), waist and hip circumference (cm) were recorded at 7 (n = 1167) and 13 (n = 878) years. Statistical analysis was conducted using logistic and multiple linear regression adjusting for child sex, gestational age, maternal age, BMI, alcohol use, socioeconomic status, and parity. Models at 7 & 13 years were additionally adjusted for child height and fish intakes. Women were consuming on average 8.49 ± 4.51 fish meals/week during pregnancy. No significant associations were found between maternal fish intakes and anthropometric outcomes at birth, 7 & 13 years. No significant associations were observed between maternal PUFAs and offspring weight at birth. At both 7 & 13 years, however, higher maternal total n-6 PUFAs were associated with increased child weight [7yr; β = 0.070, p = 0.003, 13yr; β = 0.097, p = 0.004], waist circumference [7yr; β = 0.086, p = 0.003, 13yr; β = 0.105, p = 0.004], and hip circumference [7yr; β = 0.062, p = 0.027, 13yr; β = 0.090, p = 0.013]. No significant associations were found between cord n-6 PUFAs and birth weight. In quartile analysis, cord docosahexaenoic acid (DHA; C22:6n-3) concentrations <0.071mg/ml were associated with a higher risk of large for gestational age (LGA; >90th percentile) when compared to cord DHA concentrations >0.129mg/ml [OR 4.17, p = 0.017]. There were no significant associations between cord PUFAs and anthropometric outcomes at 7 & 13 years. These findings suggest lower cord DHA, an n-3 PUFA, may be associated with higher risk of LGA at birth whilst higher n-6 PUFAs during pregnancy may be associated with adiposity development throughout childhood. Future work is needed to determine the potential long-term metabolic consequences of such associations.

This multicenter trial showed no significant differences in the composite outcome of death or neurodevelopmental impairment among extremely preterm infants randomly assigned to early CPAP or early surfactant and to lower or higher oxygen saturation. Extremely premature infants are at high risk for death and neurosensory or developmental impairment in early childhood. 1 – 3 The risk of neurodevelopmental impairment increases with decreasing gestational age and greater severity of illness. Neurodevelopmental impairment is often a consequence of neonatal complications. 4 – 12 Although surfactant administration decreases the risk of death and bronchopulmonary dysplasia, randomized, controlled trials of various respiratory interventions have not shown significant reductions in mortality and morbidity or improvement in developmental outcomes. 13 – 17 We previously reported results of the multicenter, randomized, controlled Surfactant, Positive Pressure, and Pulse Oximetry Randomized Trial (SUPPORT), which involved extremely premature infants (from . . .