Maternal Lead Exposure Research Articles

Maternal lead exposure during lactation persistently impairs testicular development and steroidogenesis in male offspring

Lead (Pb) is a testicular toxicant. In the present study, we investigated the effects of maternal Pb exposure during lactation on testicular development and steroidogenesis in male offspring. Maternal mice were exposed to different concentration of lead acetate (200 or 2000 ppm) through drinking water from postnatal day (PND) 0 to PND21. As expected, a high concentration of Pb was measured in the kidneys and liver of pups whose mothers were exposed to Pb during lactation. In addition, maternal Pb exposure during lactation elevated, to a less extent, Pb content in testes of weaning pups. Testis weight in weaning pups was significantly decreased when maternal mice were exposed to Pb during lactation. The level of serum and testicular T was reduced in Pb-exposed pups. The expression of P450scc, P450(17α) and 17β-HSD, key enzymes for T synthesis, was down-regulated in testes of weaning pups whose mothers were exposed to Pb during lactation. Interestingly, the level of serum and testicular T remained decreased in adult offspring whose mothers were exposed to Pb during lactation. Importantly, the number of spermatozoa was significantly reduced in Pb-exposed male offspring. Taken together, these results suggest that Pb could be transported from dams to pups through milk. Maternal Pb exposure during lactation persistently disrupts testicular development and steroidogenesis in male offspring.

Detrimental Effects of Maternal Lead Exposure during Pregnancy and Lactation on Molar Development in the Young Rat

The purpose of this animal study was to investigate the influence of maternal lead exposure during pregnancy and lactation on molar development in the offspring. Scanning electron microscopy revealed no significant differences in the molar morphology among the groups. However, in all the experimental groups, deep, wide cracks were found in the occlusal enamel. Further, the experimental groups had smaller molar diameters than the control group, lead exposure during lactation had a greater influence on the molar size in the offspring, and the groups with the higher dose of lead exposure during pregnancy and lactation had significantly smaller molar sizes than the groups that received the lower dose. The mesiodistal and buccolingual diameters of molars were measured as 3.10 ± 0.07 and 1.95 ± 0.04 mm for control group, 2.97 ± 0.08 and 1.94 ± 0.01 mm for lactation group of low dose, 2.96 ± 0.05 and 1.84 ± 0.02 mm for lactation group of high dose, 3.09 ± 0.06 and 1.94 ± 0.04 mm for pregnancy group of low dose, and 3.02 ± 0.06 and 1.85 ± 0.06 mm for pregnancy group of high dose, respectively.

Ascorbic acid ameliorates oxidative damage induced by maternal low-level lead exposure in the hippocampus of rat pups during gestation and lactation

This study was to investigate the effects of ascorbic acid on the hippocampus of suckling rats in the presence of lead (Pb)-induced oxidative stress. Pregnant Sprague–Dawley rats received treatment with drinking water, divided into three groups, as follows: (1) distilled water; (2) 0.2% Pb; (3) 0.2% Pb+ascorbic acid (100mg/kg/day). Rat pups were euthanized at the age of 21days and their brain tissue was examined using light microscopy. Protein levels of Cu/Zn superoxide dismutase (Cu/Zn SOD), manganese superoxide dismutase (Mn SOD), and catalase (CAT) in the hippocampus were determined by Western blotting. We found a significant decrease in levels of Cu/Zn SOD and Mn SOD among Pb-exposed pups. Ascorbic acid supplementation appeared to negate the decrease in protein levels for Cu/Zn SOD and Mn SOD. In the case of CAT, there was no effect from Pb administration alone and Pb plus ascorbic acid appeared to increase the levels. In histopathology, ascorbic acid decreased the number of damaged cells in cornu ammonis areas CA1, CA3, and the dentate gyrus (DG) in hippocampus. Our results showed that administration of ascorbic acid during pregnancy and lactation could ameliorate some of the oxidative damage induced by Pb exposure in the developing rat hippocampus.

Lead impairs ability of learning and memory and affects expression of synaptosomal-associated protein-25 in hippocampus of offspring

To find the effects of lead taken by pregnant mice on learning and memory and the expression of synaptosomal-associated protein (SNAP)-25 mRNA and protein, in order to reveal the mechanism of neurotoxicity induced by lead. Lead exposure was conducted through freely drinking the corresponding lead acetate solutions with dosages of 0.3, 1.0, 3.0 g/L respectively. Each group was composed of 10 mice. 7, 14 and 21 days after their birth. The lead contents in blood and hippocampus of the offspring were determined. At the 21st day the expression of SNAP-25 mRNA and protein in hippocampus of all the offspring in various dosages groups were determined by RT-PCR and immunohistochemistry assay. The lead contents in blood and hippocampus of various lead exposed groups were significantly higher than those of the control group (P < 0.05). The lead levels in blood and hippocampus changed accordingly to the days of growth. In Water Morris Maze experiment, the result of 0.3 g/L group was not significantly different from that of the control group (P > 0.05), however, the results of 1.0, 3.0 g/L groups (5.89 ± 0.54, 9.53 ± 1.03) were significantly different from those of the control group (1.73 ± 0.07) (P < 0.05, P < 0.01). The expression of SNAP-25 mRNA and protein was lower in lead exposed groups than that of the control group (P < 0.05). Maternal lead exposure may induce the damage in the ability of learning and memory of the offspring. The neurotoxicity of lead may be induced by decreasing the expression of SNAP-25 mRNA and protein so as to affect the release of neurotransmitter from presynaptic terminal resulted in nerve damages.

Maternal MTHFR genotype and haplotype predict deficits in early cognitive development in a lead-exposed birth cohort in Mexico City

Maternal folate nutritional status and prenatal lead exposure can influence fetal development and subsequent health. The methylenetetrahydrofolate reductase (MTHFR) gene is important for folate metabolism, and 2 common polymorphisms, C677T and A1298C, reduce enzymatic activity; C677T is present at high penetrance in Mexican populations. The objective of this study was to examine potential links between maternal and child MTHFR polymorphisms and child neurodevelopment in a lead-exposed population. Data regarding MTHFR polymorphisms C677T and A1298C, peri- and postnatal lead measures, and Bayley Mental Development Index at 24 mo of age (MDI-24) scores were available for 255 mother-child pairs who participated in the ELEMENT (Early Life Exposures in Mexico to Environmental Toxicants) study during 1994-1995. In covariate-adjusted regression models, maternal MTHFR 677 genotype predicted MDI-24 scores, in which each copy of the maternal MTHFR 677T variant allele was associated with lower MDI-24 scores (beta = -3.52; 95% CI: -6.12, -0.93; P = 0.004). Maternal MTHFR haplotype also predicted MDI-24 scores (mean +/- SE: 93.3 +/- 1.2 for 677C-1298A compared with 89.9 +/- 0.8 for 677T-1298A; P < 0.05). MDI-24 scores were not associated with maternal MTHFR 1298 genotype or child MTHFR genotypes. We did not observe significant MTHFR genotype x lead interactions with respect to any of the subject biomarkers of lead exposure. The maternal MTHFR 677T allele is an independent predictor of poorer child neurodevelopment at 24 mo. These results suggest that maternal genetic variations in folate metabolism during pregnancy may program offspring neurodevelopment trajectories. Further research is warranted to determine the generalizability of these results across other populations.

Maternal Low-Level Lead Exposure and Fetal Growth

BackgroundLimited epidemiologic studies have examined the association between maternal low-level lead exposure [blood lead (PbB) < 10 μg/dL] and fetal growth.ObjectiveWe examined whether maternal low-level lead exposure is associated with decreased fetal growth.MethodsWe linked New York State Heavy Metals Registry records of women who had PbB measurements with birth certificates to identify 43,288 mother–infant pairs in upstate New York in a retrospective cohort study from 2003 through 2005. We used multiple linear regression with fractional polynomials and logistic regression to relate birth weight, preterm delivery, and small for gestational age to PbB levels, adjusting for potential confounders. We used a closed-test procedure to identify the best fractional polynomials for PbB among 44 combinations.ResultsWe found a statistically significant association between PbB (square root transformed) and birth weight. Relative to 0 μg/dL, PbBs of 5 and 10 μg/dL were associated with an average of 61-g and 87-g decrease in birth weight, respectively. The adjusted odds ratio for PbBs between 3.1 and 9.9 μg/dL (highest quartile) was 1.04 [95% confidence interval (CI), 0.89–1.22] for preterm delivery and 1.07 (95% CI, 0.93–1.23) for small for gestational age, relative to PbBs ≤ 1 μg/dL (lowest quartile). No clear dose–response trends were evident when all of the quartiles were assessed.ConclusionsLow-level PbB was associated with a small risk of decreased birth weight with a supralinear dose–response relationship, but was not related to preterm birth or small for gestational age. The results have important implications regarding maternal PbB.

Increased tau phosphorylation and beta amyloid in the hipocampus of mouse pups by early life lead exposure

The aim of this study was to investigate the effects of maternal lead exposure on the learning and memory ability and expression of tau protein phosphorylation (P-tau) and beta amyloid protein (Abeta) in hippocampus of mice offspring. Pb exposure initiated from beginning of gestation to weaning. Pb acetate administered in drinking solutions was dissolved in distilled deionized water at the concentrations of 0.1%, 0.5% and 1% groups. On the 21 th of postnatal day, the learning and memory ability of the mouse pups was tested by Water Maze test and the Pb levels in blood and hippocampus of the offspring were also determined. The expression of P-tau and Abeta in hippocampus was measured by immunohistochemistry and Western blotting. The Pb levels in blood and hippocampus of all exposure groups were significantly higher than that of the control group ( P < 0.05). In Water Maze test, the performances of 0.5% and 1% groups were worse than that of the control group ( P < 0.05). The expression of P-tau and Abeta was increased in Pb exposed groups than that of the control group ( P < 0.05). Tau hyper-phosphorylation and Abeta increase in the hippocampus of pups may contribute to the impairment of learning and memory associated with maternal Pb exposure.

Early-Life Lead Exposure Affects the Activity of TNF-α and Expression of SNARE Complex in Hippocampus of Mouse Pups

This study aims to investigate the effects of maternal lead exposure on learning and memory ability and the protein expression of TNF-alpha and SNARE complex (SNAP-25, VAMP-2, and Syntaxin 1A) in hippocampus of mice offspring. Pb exposure was initiated from beginning of gestation to weaning. Pb acetate administered in drinking solutions was dissolved in distilled deionized water at 0.1%, 0.5%, and 1% groups, respectively. On the PND21, the learning and memory ability of mouse pups was tested by water maze test, and the Pb levels in their blood and hippocampus were also determined. The protein expression of TNF-alpha and SNARE complex in hippocampus was measured by immunohistochemistry and Western blotting. The Pb levels in blood and hippocampus of all exposure groups were significantly higher than control group (P < 0.05). In the water maze test, the performances of 0.5% and 1% groups were worse than that of control group (P < 0.05). The expression of TNF-alpha, Syntaxin 1A, and VAMP-2 was increased in Pb-exposed groups comparing control group (P < 0.05), but the expression of SNAP-25 was decreased (P < 0.05). Up-regulation of TNF-alpha and disturbance of SNARE expression in the hippocampus of pups may contribute to impairment of learning and memory ability associated with maternal Pb exposure.

The Impact of Maternal MTHFR677 Genotype and Lead Exposure on Infant Genomic DNA Methylation

ISEE-0828 Background and Objective: Previous studies have indicated that genetic variations in methylenetetrahydrofolate reductase (MTHFR), a key regulatory enzyme of the one-carbon metabolic pathway, influence genomic DNA methylation levels. However, little is know about the transgenerational influence of the major variant of MTHFR, C677T, on genomic DNA methylation levels. Our objective was to evaluate the impact of maternal MTHFR C677T genotype on cord blood genomic DNA methylation levels and to determine if this association was influenced by maternal lead exposures. Methods: Our subject population consisted of 97 maternal-infant pairs for which DNA methylation and MTHFR genotype data were available from the Early Life Exposures in Mexico to Environmental Toxicants (ELEMENT) study. Genomic DNA methylation, prenatal lead exposure and MTHFR genotyping were assessed by LINE-1 Pyrosequencing, maternal patella bone lead levels using a spot source 109Cd K-XRF instrument and TaqMan technology, respectively. Results: Maternal MTHFR C677T genotype influenced infant LINE-1 DNA methylation levels (CC = 79.86% ± 0.5; CT = 79.83% ± 0.3; and TT = 78.90% ± 0.36; P for trend = 0.07). Furthermore, once stratified by median maternal patella lead exposure, the association between maternal MTHFR C677T genotype and infant LINE-1 DNA methylation was only apparent among mothers with high lead exposure (CC = 80.0% ± 0.93; CT = 79.32% ± 0.48; and TT = 78.35% ± 0.54; P for trend = 0.09); vs. mothers with low lead exposure (CC = 79.79 ± 0.60; CT = 80.39 ± 0.4; and TT = 79.45 ± 0.47; P for trend = 0.51). No significant associations were found among infants MTHFR C677T genotype and DNA methylation. Conclusion: Data from this study suggest that genetic variants of MTHFR C677T among pregnant women are associated with a decrease in genomic DNA methylation in their offspring. Maternal genotype along with environmental exposures may play a large role in epigenetic programming.

Effect of Maternal Lead Exposure on Craniofacial Ossification in Rat Fetuses and the Role of Antioxidant Therapy

Lead exposure during intrauterine life was found to result in reduced birth weight, impaired skeletal development and post-natal neurotoxic effects. In this study, the effect of pre-natal exposure to different doses of lead on the development of craniofacial skeleton in rat fetuses was investigated. Vitamin E was tested as a concomitant treatment, aiming to improve the fetotoxic effects of lead. Positively pregnant female rats were randomly divided into four groups; groups I and II (L250 and L500), exposed to lead acetate in doses of 250 and 500 mg/l respectively, group III (L500 + E), exposed to lead acetate (500 mg/l) wit concomitant vitamin E and group IV (Control) which was given sodium acetate only. All the treatments started from the first day of gestation till the 20th day, where all rats were sacrificed and the fetuses were recovered. Fetuses were processed to alizarin red staining for ossified components. Twenty-seven bones of the craniofacial skeleton were studied in each fetus where the ossification was scored as being complete, delayed or absent. In all studied fetuses from all groups, changes were found only in eight bones while the remaining craniofacial bones were normally ossified. In affected bones there was a significant decrease in the number of completely ossified bones; associated with a significant increase of both partially ossified and absent bones in L(250) and L(500) treated groups when compared to the control group. These differences were more significant in the L(500) treated group. Giving vitamin E improved the percentage of completely ossified craniofacial bones and decreased the percentage of both partially ossified and absent bones. The most affected bone was presphenoid, then to a lesser extent supraoccipital, squamosal, parietal, interparietal and frontal bone respectively. In conclusion, lead exposure to rats during pregnancy led to varying degrees of fetal growth retardation as well as delayed ossification of some craniofacial bones which were dose dependent and the concomitant supplementation with vitamin E greatly improved the deleterious effect of lead.

The role of metabotropic glutamate receptor 5 in developmental lead neurotoxicity

A complete explanation of the mechanisms of lead-induced developmental neurotoxicity remains unknown. The glutamate receptor is one of the most important targets of lead. More recently, metabotropic glutamate receptor 5 (mGluR5) has been shown to have a functional relationship with learning and memory. We investigated the impact of developmental lead exposure on hippocampal mGluR5 expression and its potential role in lead neurotoxicity. Both in vitro model of lead exposure with Pb2+ concentrations of 0, 10nM, 1μM, and 100μM in cultured rat embryonic hippocampal neurons, and the in vivo model of rat maternal lead exposure involving both gestational and lactational exposure with 0, 0.05%, 0.2%, and 0.5% lead acetate were utilized. Immunoperoxidase and immunofluorescent analyses, quantitative PCR and western blotting were used. In vitro studies revealed that expression of mGluR5 mRNA and protein was decreased dose-dependently after lead exposure, which was further confirmed by the results of in vivo studies. These data suggest that mGluR5 might be involved in lead-induced neurotoxicity by disturbing mGluR5-induced long-term depression and decreasing N-methyl-d-aspartic acid receptor (NMDAR)-dependent or protein synthesis-dependent long-term potentiation. These results might improve the understanding of the mechanism and potential treatments for moderate to severe lead poisoning in children.

Maternal low-level lead exposure reduces the expression of PSA-NCAM and the activity of sialyltransferase in the hippocampi of neonatal rat pups

Highly polysialylated neural cell adhesion molecule (PSA-NCAM) is transiently expressed specifically in newly generated cells, and is important for cell migration and neurite outgrowth. Developmental lead (Pb) exposure has been considered to affect the expression of PSA-NCAM, which contributes to the neurotoxicity of Pb exposure. However, the effect of maternal low-level Pb exposure on the expression of PSA-NCAM in neonatal rat pups has not been reported. In the present study, female Wistar rats were exposed to vehicle or different dosages of lead chloride (0.5–4 mM PbCl 2) 2 weeks before and during pregnancy. This exposure protocol resulted in neonatal rat pups blood Pb levels up to 12.12 ± 0.38 μg/dl, and hippocampal Pb levels up to 9.22 ± 0.81 μg/g at postnatal day 1 (PND 1). Immunohistochemistry analysis and Western blot analysis revealed that the expressions of PSA-NCAM and NCAM in the hippocampi of neonatal rat pups at PND 1 were significantly reduced by the maternal low-level Pb exposures. Furthermore, the mRNA levels of NCAM and polysialyltransferases (STX and PST), measured by the fluorescent real-time quantitative RT-PCR, dosage-dependently and significantly decreased by 13.26–37.62%, 25.17–59.67%, and 10.78–47.81%, respectively. In addition, the sialyltransferase activity in neonatal rat pups was significantly reduced by 6.23–32.50% in the presence of the low-level Pb exposure, too. Taken together, these results suggest that maternal low-level Pb exposure reduces the expression of PSA-NCAM, NCAM, and the activity of sialyltransferase in the hippocampi of neonatal rat pups, which might contribute to the learning and memory impairments in the developmental pups following maternal low-level Pb exposure.

Early Umbilical Cord Clamping Contributes to Elevated Blood Lead Levels among Infants with Higher Lead Exposure

To investigate whether infant iron status, modified by umbilical cord clamping time and infant feeding mode, affected infant blood lead concentration at 6 months of age. Participants were a subset of women and their infants randomized to receive early (10 seconds) or delayed (2 minutes) umbilical cord clamping and were monitored to 6 months postpartum in Mexico City. Iron and lead status was analyzed in maternal, placental, and 6-month infant blood samples. Baseline maternal lead exposure data and infant feeding data at 2, 4, and 6 months were collected. In the total sample, maternal blood lead concentration, infant ferritin, and breast-feeding practices predicted infant blood lead concentration. Among infants with higher placental blood lead concentration and breast-fed infants not receiving any iron-fortified formula or milk at 6 months, early clamping increased infant blood lead concentration, an effect mediated in part via decreased infant iron status. Early cord clamping, by decreasing infant iron status, contributes to higher blood lead concentrations at 6 months of age among infants at high risk.

The Association Between Maternal Tibia Lead, Folate Intake, and MTHFR Genotype, and Child Birth Weight

ISEE-644 Objective: Maternal lead exposure, folate intake, and mutations in methylenetetrahydrofolate (MTHFR) gene are known to affect birthweight (BW), but have not been investigated together. Materials and Methods: Our study sample consisted of Mexico City women (n = 487) with complete data on tibia lead (TPb), folate intake, MTHFR (C594T, C677T, A1298C), their child's BW, and covariates. Bone lead was measured using K-x-ray fluorescence; folate intake assessed with semiquantitative FFQ. We assumed autosomal dominant effect for MTHFR genotype. Associations of TPb, folate intake, and MTHFR genotypes with BW were analyzed, adjusting for covariates. Interactions between TPb, folate intake, and MTHFR genotype in predicting BW were investigated. Results: Mean TPb was 9.9 ± 9.8 μg/g bone; birth weight was 3166 ± 415 g; folate intake was 867 ± 891 μg/day. Allele frequencies were 3.9% (C594T), 59.1% (C677T), 10.9% (A1298C). All variants were in Hardy-Weinberg equilibrium. There was no main effect of folate or MTHFR genotype on BW. Each 1 μg/g increase in TPB was associated with a 4 g decrease in BW (P = 0.01); women with TPb >9.5 μg/g (median) had neonates 90 g lighter than those of women with TPb ≤9.5 μg/g. The associations between TPb and BW were as follows: by MTHFR genotype: 594CC (β = −5.0*), 594CT/TT (β = 8.9, interaction term for TPb*MTHFRP = 0.22); 677CC (β = −14.1*), 677CT/TT (β = −3.6*, interaction term P = 0.20); 1298AA (β = −6.1**), 1298AC/CC (β = 2.6, interaction term P = 0.20). Estimates for relationship between folate and BW did not differ by MTHFR genotype. Conclusions: We did not find 677CT/TT genotype or other MTHFR polymorphisms to be risk factors for lower BW. TPb consistently predicted lower BW in women. The relationship between TPb and BW appeared stronger in women with wild type MTHFR but was diminished in women who were variant carriers.

Maternal lead exposure, secondary sex ratio and dose-exposure fallacy

Maternal lead exposure, secondary sex ratio and dose-exposure fallacy

Reply: Maternal lead exposure, secondary sex ratio and dose-exposure fallacy

Reply: Maternal lead exposure, secondary sex ratio and dose-exposure fallacy

Specific factors for prenatal lead exposure in the border area of China

The objectives of this study are to examine the prevalence of increased blood lead concentrations in mothers and their umbilical cords, and to identify risk factors for prenatal lead exposure in Kunming city, Yunnan province, China. The study was conducted at two obstetrics departments, and 100 peripartum women were enrolled. The mean blood lead concentrations of the mothers and the umbilical cords were 67.3 μg/l and 53.1 μg/l, respectively. In multiple linear regression analysis, maternal occupational exposure, maternal consumption of homemade dehydrated vegetables and maternal habitation period in Kunming city were significantly associated with an increase of umbilical cord blood lead concentration. In addition, logistic regression analysis was used to assess the association of umbilical cord blood lead concentrations that possibly have adverse effects on brain development of newborns with each potential risk factor. Maternal frequent use of tableware with color patterns inside was significantly associated with higher cord blood lead concentration in addition to the three items in the multiple linear regression analysis. These points should be considered as specific recommendations for maternal and fetal lead exposure in this city.

Maternal lead exposure and the secondary sex ratio

A reduction in the secondary sex ratio may be associated with exposure to environmental toxicants. Little data exists relating this outcome to lead exposure, a well-known reproductive toxicant. We studied 1980 women having singleton births from 1994 to 1995 and from 1997 to 2001 who participated in a cohort study of lead exposure and infant outcomes in Mexico City. Levels of lead were measured in maternal and cord blood using graphite furnace atomic absorption spectroscopy, and levels of lead in maternal patella and tibia bone (a reflection of cumulative exposure) were measured using noninvasive K-X-ray fluorescence measurements. Using logistic regression models, we evaluated the relations of these measures to secondary sex ratio in the offspring, adjusting for maternal age, parity and year of infants' birth. We found no consistent association between any of the lead measures and secondary sex ratio. Results were unchanged when we adjusted for infants' year of birth, maternal age and parity. Despite a large sample size and the use of sensitive biomarkers, we did not find evidence that maternal and fetal lead exposure is associated with a lower secondary sex ratio among newborns.

Permanent alterations in stress responsivity in female offspring subjected to combined maternal lead exposure and/or stress

Elevated lead (Pb) exposures preferentially impact low socioeconomic status (SES) populations, the same groups thought to sustain the highest levels of environmental stress. As co-occurring risk factors, therefore, Pb and stress could interact, a possibility further supported by the fact that both act on mesocorticolimbic dopamine systems of the brain. We recently demonstrated in rats that maternal Pb exposure could permanently increase basal corticosterone levels of offspring consistent with altered hypothalamic pituitary adrenal (HPA) axis function. The current study was thus designed to test the hypothesis that stress responsivity of offspring should likewise be altered, with the outcome differing in response to Pb, stress or Pb + stress. The impact of intermittent variable stress challenges (restraint, novelty, cold) on behavior sensitive to Pb exposure (fixed interval (FI) schedule-controlled responding) and on stress-induced corticosterone changes were evaluated in adult female offspring of dams that had been exposed to Pb (150 ppm) in drinking water from 2 months prior to breeding through lactation with or without maternal restraint stress on days 16 and 17 of gestation. This design yielded four treatment groups: (NS/0, no maternal Pb, no maternal stress; S/0, no maternal Pb, maternal stress; NS/150, maternal Pb, no maternal stress; and S/150, maternal Pb exposure and maternal stress). While maternal Pb alone and stress alone each altered components of stress responsivity, the greatest number of effects was seen in response to Pb + stress. This included alterations in FI performance following both restraint and cold stress and in the corticosterone response to cold stress. Collectively, these studies reveal that maternal Pb exposure alone can permanently alter stress responsivity and that the profile of effects produced by maternal Pb differ from those produced by maternal Pb in conjunction with stress, findings which have both mechanistic and risk assessment significance.

133: Maternal Thyroid Function and Lead Exposure During Pregnancy and Childhood IQ

133: Maternal Thyroid Function and Lead Exposure During Pregnancy and Childhood IQ