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Prenatal exposure to mercury, a known neurotoxic metal, is associated with lower cognitive performance during childhood. Disruption of fetal epigenetic programming could explain mercury’s neurodevelopmental effects. We screened for epigenome-wide methylation differences associated with maternal prenatal blood mercury levels in 321 cord blood DNA samples and examined the persistence of these alterations during early (n = 75; 2.9–4.9 years) and mid-childhood (n = 291; 6.7–10.5 years). Among males, prenatal mercury levels were associated with lower regional cord blood DNA methylation at the Paraoxonase 1 gene ( PON1 ) that persisted in early childhood and was attenuated in mid-childhood blood. Cord blood methylation at the PON1 locus predicted lower cognitive test scores measured during early childhood. Methylation at the PON1 locus was associated with PON1 expression in an independent set of cord blood samples. The observed persistent epigenetic disruption of the PON1 gene may modulate mercury toxicity in humans and might serve as a biomarker of exposure and disease susceptibility.

Background: Manganese is both an essential element and a known neurotoxicant to children. High manganese exposures have been associated with negative reproductive outcomes in animals, but few epidemiologic studies have examined the effects of human fetal manganese exposure. Methods: We studied the association between maternal and umbilical cord blood manganese levels and birth weight in a cohort of 470 mother-infant pairs born at term (≥37 weeks gestation) in Ottawa County, Oklahoma. Nonlinear spline and quadratic regression models were used to test the hypothesis of an inverted U-shaped relationship between manganese levels and birth weight. Results: Mean (standard deviation) concentration of manganese was 2.4 (0.95) μg/dL in the maternal blood and 4.2 (1.6) μg/dL in the cord blood. Umbilical cord manganese was not associated with birth weight. A nonlinear relationship was observed between maternal manganese and birth weight after adjusting for potential confounders. Birth weight increased with manganese levels up to 3.1 μg/L, and then a slight reduction in weight was observed at higher levels. Compared with the 3.1-μg/L point of inflection, birth weight estimates at the 5th (1.3 μg/L) and 95th (4.0 μg/L) percentiles of exposure were - 160 g (95% confidence interval = -286 to -33) and -46 g (-38 to 131), respectively. Conclusions: Maternal blood manganese levels during pregnancy are associated with birth weight in a nonlinear pattern in full-term infants. These findings suggest that manganese may affect fetal growth. Possible detrimental effects of elevated manganese levels on the fetus should be further examined in more highly exposed populations.

Fish and other seafood may contain organic mercury but also beneficial nutrients such as n-3 polyunsaturated fatty acids. We endeavored to study whether maternal fish consumption during pregnancy harms or benefits fetal brain development. We examined associations of maternal fish intake during pregnancy and maternal hair mercury at delivery with infant cognition among 135 mother-infant pairs in Project Viva, a prospective U.S. pregnancy and child cohort study. We assessed infant cognition by the percent novelty preference on visual recognition memory (VRM) testing at 6 months of age. Mothers consumed an average of 1.2 fish servings per week during the second trimester. Mean maternal hair mercury was 0.55 ppm, with 10% of samples > 1.2 ppm. Mean VRM score was 59.8 (range, 10.9-92.5). After adjusting for participant characteristics using linear regression, higher fish intake was associated with higher infant cognition. This association strengthened after adjustment for hair mercury level: For each additional weekly fish serving, offspring VRM score was 4.0 points higher [95% confidence interval (CI), 1.3 to 6.7]. However, an increase of 1 ppm in mercury was associated with a decrement in VRM score of 7.5 (95% CI, -13.7 to -1.2) points. VRM scores were highest among infants of women who consumed > 2 weekly fish servings but had mercury levels ≤ 1.2 ppm. Higher fish consumption in pregnancy was associated with better infant cognition, but higher mercury levels were associated with lower cognition. Women should continue to eat fish during pregnancy but choose varieties with lower mercury contamination.

Human milk is a potential source of lead exposure. Yet lactational transfer of lead from maternal blood into breast milk and its contribution to infant lead burden remains poorly understood. We explored the dose-response relationships between maternal blood, plasma, and breast milk to better understand lactational transfer of lead from blood and plasma into milk and, ultimately, to the breastfeeding infant. We measured lead in 81 maternal blood, plasma, and breast milk samples at 1 month postpartum and in 60 infant blood samples at 3 months of age. Milk-to-plasma (M/P) lead ratios were calculated. Multivariate linear, piecewise, and generalized additive models were used to examine dose-response relationships between blood, plasma, and milk lead levels. Maternal lead levels (mean±SD) were as follows: blood: 7.7±4.0 μg/dL; plasma: 0.1±0.1 μg/L; milk: 0.8±0.7 μg/L. The average M/P lead ratio was 7.7 (range, 0.6-39.8) with 97% of the ratios being >1. The dose-response relationship between plasma lead and M/P ratio was nonlinear (empirical distribution function=6.5, p=0.0006) with the M/P ratio decreasing by 16.6 and 0.6 per 0.1 μg/L of plasma lead, respectively, below and above 0.1 μg/L plasma lead. Infant blood lead level (3.4±2.2 μg/dL) increased by 1.8 μg/dL per 1 μg/L milk lead (p<0.0001, R2=0.3). The M/P ratio for lead in humans is substantially higher than previously reported, and transfer of lead from plasma to milk may be higher at lower levels of plasma lead. Breast milk is an important determinant of lead burden among breastfeeding infants.

Polychlorinated biphenyls (PCBs), organochlorine pesticides, and methylmercury (MeHg) are environmentally persistent with adverse effects on neurodevelopment. However, especially among populations with commonly experienced low levels of exposure, research on neurodevelopmental effects of these toxicants has produced conflicting results. We assessed the association of low-level prenatal exposure to these contaminants with memory and learning. We studied 393 children, born between 1993 and 1998 to mothers residing near a PCB-contaminated harbor in New Bedford, Massachusetts. Cord serum PCB, DDE (dichlorodiphenyldichloroethylene), and maternal peripartum hair mercury (Hg) levels were measured to estimate prenatal exposure. Memory and learning were assessed at 8 years of age (range, 7-11 years) using the Wide Range Assessment of Memory and Learning (WRAML), age-standardized to a mean ± SD of 100 ± 15. Associations with each WRAML index-Visual Memory, Verbal Memory, and Learning-were examined with multivariable linear regression, controlling for potential confounders. Although cord serum PCB levels were low (sum of four PCBs: mean, 0.3 ng/g serum; range, 0.01-4.4), hair Hg levels were typical of the U.S. fish-eating population (mean, 0.6 μg/g; range, 0.3-5.1). In multivariable models, each microgram per gram increase in hair Hg was associated with, on average, decrements of -2.8 on Visual Memory (95% CI: -5.0, -0.6, p = 0.01), -2.2 on Learning (95% CI: -4.6, 0.2, p = 0.08), and -1.7 on Verbal Memory (95% CI: -3.9, 0.6, p = 0.14). There were no significant adverse associations of PCBs or DDE with WRAML indices. These results support an adverse relationship between low-level prenatal MeHg exposure and childhood memory and learning, particularly visual memory.

Mercury is a global pollutant, and prenatal exposure is associated with adverse health effects. To date, no studies have evaluated the association between prenatal mercury exposure and DNA hydroxymethylation, an epigenetic modification important for tissue differentiation and embryonic development. We sought to evaluate the association between prenatal mercury exposure and offspring global DNA methylation and hydroxymethylation at birth and test for persistence of the association in childhood. Within Project Viva, a U.S. prebirth cohort, we examined associations of maternal second trimester red blood cell mercury (RBC-Hg) concentrations with global 5-hydroxymethylcytosine (%-5hmC) and 5-methylcytosine (%-5mC) DNA content in blood collected at birth ( =306), early childhood ( =68; 2.9 to 4.9 y), and midchildhood ( =260; 6.7 to 10.5 y). Median prenatal RBC-Hg concentration was 3.23μg/g [interquartile range (IQR)=3.29]. At birth, median cord blood %-5mC, %-5hmC, and their ratio were 4.95%, 0.22%, and 24.37, respectively. The mean adjusted difference [95% confidence interval (CI)] of blood %-5hmC for a doubling in prenatal RBC-Hg concentration was -0.013% (-0.029, 0.002), -0.031% (-0.056, -0.006), and 0.005% (-0.007, 0.018) at birth, early, and midchildhood, respectively. The corresponding relative adjusted change in the genomic ratio of %-5mC to %-5hmC for a doubling in prenatal RBC-Hg concentration was 4.70% (0.04, 9.58), 22.42% (7.73, 39.11), and 0.73% (-4.18, 5.88) at birth, early, and midchildhood, respectively. No associations were present between prenatal maternal RBC-Hg and %-5mC at any time point. Prenatal mercury exposure was associated with lower %-5hmC genomic content and a corresponding increase in the ratio of %-5mC to %-5hmC in cord blood. This association was persistent in early but not midchildhood blood. Our results demonstrate the potential malleability of epigenetic modifications associated with mercury exposure . https://doi.org/10.1289/EHP1467.

BACKGROUND: Accumulating evidence has shown an increased risk of type 2 diabetes in general populations exposed to arsenic, but little is known about exposures during pregnancy and the association with gestational diabetes (GD). OBJECTIVES: We studied 532 women living proximate to the Tar Creek Superfund Site to investigate whether arsenic exposure is associated with impaired glucose tolerance during pregnancy. METHODS: Blood glucose was measured between 24 and 28 weeks gestation after a 1-hr oral glucose tolerance test (GTT) as part of routine prenatal care. Blood and hair were collected at delivery and analyzed for arsenic using inductively coupled plasma mass spectrometry with dynamic reaction cell. RESULTS: Arsenic concentrations ranged from 0.2 to 24.1 microg/L (ppb) (mean +/- SD, 1.7 +/-1.5) and 1.1 to 724.4 ng/g (ppb) (mean +/- SD, 27.4 +/- 61.6) in blood and hair, respectively. One-hour glucose levels ranged from 40 to 284 mg/dL (mean +/- SD, 108.7 +/- 29.5); impaired glucose tolerance was observed in 11.9% of women when using standard screening criterion ( 140 mg/dL). Adjusting for age, Native-American race, prepregnancy body mass index, Medicaid use, and marital status, women in the highest quartile of blood arsenic exposure had 2.8 higher odds of impaired GTT than women in the lowest quartile of exposure (95% confidence interval, 1.1-6.9) (p-trend = 0.008). CONCLUSIONS: Among this population of pregnant women, arsenic exposure was associated with increased risk of impaired GTT at 24-28 weeks gestation and therefore may be associated with increased risk of GD.

Background: Accumulating evidence has shown an increased risk of type 2 diabetes in general populations exposed to arsenic, but little is known about exposures during pregnancy and the association with gestational diabetes (GD). Objectives: We studied 532 women living proximate to the Tar Creek Superfund Site to investigate whether arsenic exposure is associated with impaired glucose tolerance during pregnancy. Methods: Blood glucose was measured between 24 and 28 weeks gestation after a 1-hr oral glucose tolerance test (GTT) as part of routine prenatal care. Blood and hair were collected at delivery and analyzed for arsenic using inductively coupled plasma mass spectrometry with dynamic reaction cell. Results: Arsenic concentrations ranged from 0.2 to 24.1 μg/L (ppb) (mean ± SD, 1.7 ±1.5) and 1.1 to 724.4 ng/g (ppb) (mean ± SD, 27.4 ± 61.6) in blood and hair, respectively. One-hour glucose levels ranged from 40 to 284 mg/dL (mean ± SD, 108.7 ± 29.5); impaired glucose tolerance was observed in 11.9% of women when using standard screening criterion (> 140 mg/dL). Adjusting for age, Native-American race, prepregnancy body mass index, Medicaid use, and marital status, women in the highest quartile of blood arsenic exposure had 2.8 higher odds of impaired GTT than women in the lowest quartile of exposure (95% confidence interval, 1.1-6.9) (p-trend = 0.008). Conclusions: Among this population of pregnant women, arsenic exposure was associated with increased risk of impaired GTT at 24-28 weeks gestation and therefore may be associated with increased risk of GD.

Infant exposures to metals are a concern for mining-impacted communities, although limited information is available to assess residential exposures over the first year of life. We measured lead (Pb), manganese, arsenic, and cadmium in indoor air, house dust, yard soil, and tap water from 53 infants’ homes near the Tar Creek Superfund Site (Oklahoma, USA) at two time points representing developmental stages before and during initial ambulation (age 0–6 and 6–12 months). We measured infant metal biomarkers in: umbilical cord blood ( n =53); 12- ( n =43) and 24- ( n =22) month blood; and hair at age 12 months ( n =39). We evaluated cross-sectional and longitudinal associations between infant residential and biomarker concentrations. A doubling of mean dust Pb concentration was consistently associated with 36–49% higher 12-month blood Pb adjusting for cord blood Pb ( P ⩽0.05). Adjusted dust concentration explained 29–35% of blood Pb variance, and consistent associations with other media were not observed. Although concentrations in dust and blood were generally low, strong and consistent associations between dust and body burden suggest that house dust in mining-impacted communities may impact children’s health. These relationships were observed at a young age, typically before blood Pb levels peak and when children’s development may be particularly vulnerable to toxic insult.

Fish consumption influences a number of health outcomes. Few studies have directly compared dietary assessment methods to determine the best approach to estimating intakes of fish and its component nutrients, including DHA, and toxicants, including methylmercury. Our objective was to compare three methods of assessing fish intake. We assessed 30 d fish intake using three approaches: (i) a single question on total fish consumption; (ii) a brief comprehensive FFQ that included four questions about fish; and (iii) a focused FFQ with thirty-six questions about different finfish and shellfish. Obstetrics practices in Boston, MA, USA. Fifty-nine pregnant women who consumed ≤2 monthly fish servings. Estimated intakes of fish, DHA and Hg were lowest with the one-question screener and highest with the thirty-six-item fish questionnaire. Estimated intake of DHA with the thirty-six-item questionnaire was 4·4-fold higher (97 v. 22 mg/d), and intake of Hg was 3·8-fold higher (1·6 v. 0·42 μg/d), compared with the one-question screener. Plasma DHA concentration was correlated with fish intake assessed with the one-question screener (Spearman r = 0·27, P = 0·04), but not with the four-item FFQ (r = 0·08, P = 0·54) or the thirty-six-item fish questionnaire (r = 0·01, P = 0·93). In contrast, blood and hair Hg concentrations were similarly correlated with fish and Hg intakes regardless of the assessment method (r = 0·35 to 0·52). A longer questionnaire provides no advantage over shorter questionnaires in ranking intakes of fish, DHA and Hg compared with biomarkers, but estimates of absolute intakes can vary by as much as fourfold across methods.