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Determining prenatal, early childhood and cumulative long-term lead exposure using micro-spatial deciduous dentine levels.

ABSTRACT: The aim of this study was to assess the validity of micro-spatial dentine lead (Pb) levels as a biomarker for accurately estimating exposure timing over the prenatal and early childhood periods and long-term cumulative exposure to Pb. In a prospective pregnancy cohort sub-sample of 85 subjects, we compared dentine Pb levels measured using laser ablation-inductively coupled plasma mass spectrometry with Pb concentrations in maternal blood collected in the second and third trimesters, maternal bone, umbilical cord blood, and childhood serial blood samples collected from the ages of 3 months to ?6 years. We found that Pb levels (as 208Pb:43Ca) in dentine formed at birth were significantly associated with cord blood Pb (Spearman ??=?0.69; n?=?27; p<0.0001). The association of prenatal dentine Pb with maternal patella Pb (Spearman ??=?0.48; n?=?59; p<0.0001) was stronger than that observed for tibia Pb levels (Spearman ??=?0.35; n?=?41; p<0.03). When assessing postnatal exposure, we found that Pb levels in dentine formed at 3 months were significantly associated with Pb concentrations in children's blood collected concurrently (Spearman ??=?0.64; n?=?55; p<0.0001). We also found that mean Pb concentrations in secondary dentine (that is formed from root completion to tooth shedding) correlated positively with cumulative blood lead index (Spearman ??=?0.38; n?=?75; p<0.0007). Overall, our results support that micro-spatial measurements of Pb in dentine can be reliably used to reconstruct Pb exposure timing over the prenatal and early childhood periods, and secondary dentine holds the potential to estimate long-term exposure up to the time the tooth is shed.

SUBMITTER: Arora M

PROVIDER: S-EPMC4026445 | biostudies-literature | 2014

REPOSITORIES: biostudies-literature

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Determining prenatal, early childhood and cumulative long-term lead exposure using micro-spatial deciduous dentine levels.

Arora Manish M Austin Christine C Sarrafpour Babak B Hernández-Ávila Mauricio M Hu Howard H Wright Robert O RO Tellez-Rojo Martha Maria MM

PloS one 20140519 5

The aim of this study was to assess the validity of micro-spatial dentine lead (Pb) levels as a biomarker for accurately estimating exposure timing over the prenatal and early childhood periods and long-term cumulative exposure to Pb. In a prospective pregnancy cohort sub-sample of 85 subjects, we compared dentine Pb levels measured using laser ablation-inductively coupled plasma mass spectrometry with Pb concentrations in maternal blood collected in the second and third trimesters, maternal bon ...[more]

PMID: 24841926

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Project description:BACKGROUND:Lead is an established neurotoxicant and early life exposure to lead is associated with detrimental impacts on IQ and several neurobehavioral domains. Less is known, however, about effects of prenatal lead exposure below 5??g/dL on executive function and on social, emotional and self-regulatory behaviors in childhood. OBJECTIVES:To examine the association between prenatal lead exposure and childhood executive function and social, emotional and self-regulatory behaviors. METHODS:We included 1006 mother-child pairs from the Project Viva prospective pre-birth cohort. We measured prenatal maternal lead in second-trimester erythrocytes. In mid-childhood (median 7.7?years), parents and teachers rated executive function related behaviors using the Behavior Rating Inventory of Executive Function (BRIEF) and behavioral difficulties using the Strengths and Difficulties Questionnaire (SDQ). We used multivariable linear regression models adjusted for maternal, paternal, and child characteristics and metal co-exposures. RESULTS:Mean maternal erythrocyte lead concentration was 1.2??g/dL (interquartile range [IQR] 0.8-1.5??g /dL), equivalent to approximately 0.4??g/dL in whole blood. In adjusted models, associations with parent and teacher-rated scales were largely null, although effect estimates were consistently positive, suggesting worse scores with increasing lead levels. For an IQR increase in lead, BRIEF Global Executive Composite (GEC) was 0.73 (95% CI: -0.06, 1.52) points higher for parent-rated scores and 0.42 (95% CI: -0.39, 1.23) points higher for teacher-rated scores. Associations were strongest for parent-rated BRIEF plan/organize (??=?0.85; 95% CI: 0.12, 1.59) and shift (??=?0.88; 95% CI: 0.01, 1.75) subscales, as well as the SDQ emotional problems subscale (??=?0.18; 95% CI: 0.03, 0.33). DISCUSSION:In this cohort with lead levels commonly experienced by U.S. women, there were few statistically significant associations with childhood executive function and behavior. However, there was a trend of worse neurobehavioral scores with increasing prenatal lead concentrations, in particular for childhood emotional problems and capacity to plan/organize and shift. Our results highlight the importance of continuing efforts to eliminate lead exposure in the general population.

Project description:Background: Exposure to lead (Pb) during the early life stages has been associated with the development of metabolic syndrome (MetS). Longitudinal studies of Pb exposure in critical developmental windows in children are limited. Methods: Our study included 601 mother-child dyads from the PROGRESS (Programming Research in Obesity, Growth, Environment and Social Stressors) birth cohort. Blood lead levels (BLLs) were assessed during the second and third gestational trimesters, in cord blood at delivery, and at ages 1, 2, and 4 years. Bone lead levels in the patella and tibia were assessed at 1 month postpartum and evaluated in separate models. To account for cumulative exposure (prenatal, postnatal, and cumulative), we dichotomized the BLLs at each stage visit and determined the following: "higher" if a BLL was at least once above the median (HPb) and "lower" if all BLLs were below the median (LPb). We analyzed fasting glucose, HbA1c, triglycerides (TGs), total cholesterol (TC), high-density lipoprotein cholesterol (cHDL), low-density lipoprotein cholesterol (cLDL), body mass index, waist circumference (WC), body fat percentage, and systolic (SBP) and diastolic blood pressure (DBP) at two study visits between 6 and 12 years of age and created cutoff points based on the clinical guidelines for each indicator. Mixed effects models were used to analyze each outcome longitudinally for each BLL score, adjusting for child's sex, size for gestational age, child's age, maternal parity, mother's age, and socioeconomic status. Results: We observed associations for HPb exposure and TC in all stages (OR = 0.53, 95%CI = 0.32-0.86) and postnatally (OR = 0.59, 95%CI = 0.36-0.94) and for prenatal HPb and TGs (OR = 0.65, 95%CI = 0.44-0.95). HPb at all stages was associated with WC (OR = 0.27, 95%CI = 0.08-0.86), BMI (OR = 0.33, 95%CI = 0.11-0.99), SBP (OR = 0.53, 95%CI = 0.32-0.85), and DBP (OR = 0.57, 95%CI = 0.34-0.95). Pb levels in the patella were associated with cHDL (OR = 1.03, 95%CI = 1.00-1.07) and those in the tibia with TGs (OR = 0.95, 95%CI = 0.91-0.99). Conclusion: Early life exposure to Pb may alter early indicators of MetS. A follow-up of these children will allow for more definition on the impact of longer-term exposures.

Project description:Background: How prenatal smoke exposure affects DNA methylation leading to atopic disorders remains to be addressed. Epigenetic biomarkers informative of prenatal smoke exposure and atopic disorders are wanting. Since most children suffering from atopic dermatitis (AD) continue to develop asthma later in life, we explored whether prenatal smoke exposure e induces DNA methylation and searched for predictive epigenetic biomarkers for smoke related atopic disorders. Methods: Methylation differences associated with smoke exposure were screened by Illumina methylation panel for children from the Taiwan birth panel study cohort initially. Information about development of atopic dermatitis (AD) and risk factors were collected. Cord blood cotinine levels were measured to represent prenatal smoke exposure. CpG loci that demonstrated a statistically significant difference in methylation were validated by methylation-dependent fragment separation (MDFS). Differential methylation in three genes (TSLP, GSTT1, and CYB5R3) was identified through the screen and their functions were investigated. Results: Among these, only thymic stromal lymphopoietin (TSLP) gene displayed significant difference in promoter methylation percentage after being validated by MDFS (p=0.029). TSLP gene was further investigated in a larger sample of 92 children from the cohort. Methylation status of the TSLP 5′-CpG island (CGI) was found to be significantly associated with prenatal smoke exposure (OR=3.59, 95%CI=1.49-8.64; cotinine level 0.10 ng/ml, sensitivity= 77%; specificity = 61%) and with AD (OR=4.77, 95%CI=1.47-15.53). The degree of TSLP 5′CGI methylation inversely correlated with TSLP protein expression levels (per unit: β=－6.69 ng/ml; 95% CIs, －12.80~－0.59; p=0.032). Conclusions: The effect of prenatal tobacco smoke exposure on the risk for AD may be mediated through DNA methylation. Cord blood methylated TSLP 5′CGI may be a potential epigenetic biomarker for environmentally-related atopic disorders. The buffy coat and plasma samples were separated and stored at −80°C. DNA (100 ng-500 ng) was extracted from cord white blood cells. Microarrays have been performed to investigate fourteen samples, which were classified as two groups according to cotinine exposure dosage (7 versus 7 : high exposure verses low exposure).

Project description:Growing evidence suggests that environmental exposures can influence blood pressure over the course of a lifetime. Exposure to toxic metals, such as lead (Pb) and arsenic (As), has been associated with increased blood pressure in adults, but few studies have examined the impacts of in utero and early life toxic metals exposure on blood pressure in childhood. As subclinical vascular changes are thought to begin early in life, it is possible that in utero toxic metals exposure may play a role in blood pressure homeostasis. In the ongoing New Hampshire Birth Cohort Study, we investigated whether in utero exposure to Pb and As was associated with measures of blood pressure in a total of 323 young children (mean age 5.5 years, SD 0.4). Pb and As were measured in maternal toenail samples collected at ~28 weeks gestation (n = 257) and/or 6 weeks postpartum (n = 285), which represent exposures ~6 to 12 months prior to collection and therefore reflect the early prenatal and late prenatal exposures, respectively. Five measurements of systolic blood pressure (SBP) and diastolic blood pressure (DBP) were averaged for each child using a standardized technique. In linear regression analyses, where log2-transformed prenatal toenail Pb and As were modeled jointly and adjusted for child age, sex, height, weight and maternal smoking during pregnancy, we observed that a doubling of maternal prenatal toenail Pb was associated with statistically significant increases in child SBP (β: 0.58 mm Hg, 95% CI: 0.05, 1.11). We did not observe any association of prenatal or postpartum As, or postpartum Pb, with SBP or DBP. Exploratory sex-stratified analyses suggest that associations of prenatal Pb with BP may be stronger among boys (SBP β: 0.72 mm Hg: 95% CI: -0.01, 1.44; DBP β: 0.37; 95% CI: -0.09, 0.84), compared to girls (SBP β: 0.48 mm Hg: 95% CI: -0.31, 1.26; DBP β: -0.05; 95% CI: -0.52, 0.41), though tests for interaction did not reach statistical significance (p-interaction SBP = 0.059; DBP = 0.057). Our preliminary results suggest that in utero toxic metals exposures may be associated with early life increases in blood pressure in children, which could have consequences for long-term health.

Dataset Information

Determining prenatal, early childhood and cumulative long-term lead exposure using micro-spatial deciduous dentine levels.

Publications

Determining prenatal, early childhood and cumulative long-term lead exposure using micro-spatial deciduous dentine levels.

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