39 research outputs found

    The Case of Deborah Rice: Who Is the Environmental Protection Agency Protecting?

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    Why did the EPA dismiss a highly respected neurotoxicologist as chair of its external review panel on the fire retardant deca? Pioneering lead researcher Herbert Needleman, MD, argues that the answer has little to do with science

    Prenatal Lead Levels, Plasma Amyloid β Levels, and Gene Expression in Young Adulthood

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    Background: Animal studies suggest that early-life lead exposure influences gene expression and production of proteins associated with Alzheimer’s disease (AD)

    Low-level environmental lead exposure in childhood and adult intellectual function: a follow-up study

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    <p>Abstract</p> <p>Background</p> <p>Early life lead exposure might be a risk factor for neurocognitive impairment in adulthood.</p> <p>Objectives</p> <p>We sought to assess the relationship between early life environmental lead exposure and intellectual function in adulthood. We also attempted to identify which time period blood-lead concentrations are most predictive of adult outcome.</p> <p>Methods</p> <p>We recruited adults in the Boston area who had participated as newborns and young children in a prospective cohort study that examined the relationship between lead exposure and childhood intellectual function. IQ was measured using the Wechsler Abbreviated Scale of Intelligence (WASI). The association between lead concentrations and IQ scores was examined using linear regression.</p> <p>Results</p> <p>Forty-three adults participated in neuropsychological testing. Childhood blood-lead concentration (mean of the blood-lead concentrations at ages 4 and 10 years) had the strongest relationship with Full-Scale IQ (β = -1.89 ± 0.70, p = 0.01). Full-scale IQ was also significantly related to blood-lead concentration at age 6 months (β = -1.66 ± 0.75, p = 0.03), 4 years (β = -0.90 ± 0.41, p = 0.03) and 10 years (β = -1.95 ± 0.80, p = 0.02). Adjusting for maternal IQ altered the significance of the regression coefficient.</p> <p>Conclusions</p> <p>Our study suggests that lead exposure in childhood predicts intellectual functioning in young adulthood. Our results also suggest that school-age lead exposure may represent a period of increased susceptibility. Given the small sample size, however, the potentially confounding effects of maternal IQ cannot be excluded and should be evaluated in a larger study.</p

    Low-level environmental lead exposure in childhood and adult intellectual function: a follow-up study

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    <p>Abstract</p> <p>Background</p> <p>Early life lead exposure might be a risk factor for neurocognitive impairment in adulthood.</p> <p>Objectives</p> <p>We sought to assess the relationship between early life environmental lead exposure and intellectual function in adulthood. We also attempted to identify which time period blood-lead concentrations are most predictive of adult outcome.</p> <p>Methods</p> <p>We recruited adults in the Boston area who had participated as newborns and young children in a prospective cohort study that examined the relationship between lead exposure and childhood intellectual function. IQ was measured using the Wechsler Abbreviated Scale of Intelligence (WASI). The association between lead concentrations and IQ scores was examined using linear regression.</p> <p>Results</p> <p>Forty-three adults participated in neuropsychological testing. Childhood blood-lead concentration (mean of the blood-lead concentrations at ages 4 and 10 years) had the strongest relationship with Full-Scale IQ (β = -1.89 ± 0.70, p = 0.01). Full-scale IQ was also significantly related to blood-lead concentration at age 6 months (β = -1.66 ± 0.75, p = 0.03), 4 years (β = -0.90 ± 0.41, p = 0.03) and 10 years (β = -1.95 ± 0.80, p = 0.02). Adjusting for maternal IQ altered the significance of the regression coefficient.</p> <p>Conclusions</p> <p>Our study suggests that lead exposure in childhood predicts intellectual functioning in young adulthood. Our results also suggest that school-age lead exposure may represent a period of increased susceptibility. Given the small sample size, however, the potentially confounding effects of maternal IQ cannot be excluded and should be evaluated in a larger study.</p

    Low-Level Environmental Lead Exposure and Children’s Intellectual Function: An International Pooled Analysis

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    Lead is a confirmed neurotoxin, but questions remain about lead-associated intellectual deficits at blood lead levels < 10 μg/dL and whether lower exposures are, for a given change in exposure, associated with greater deficits. The objective of this study was to examine the association of intelligence test scores and blood lead concentration, especially for children who had maximal measured blood lead levels < 10 μg/dL. We examined data collected from 1,333 children who participated in seven international population-based longitudinal cohort studies, followed from birth or infancy until 5–10 years of age. The full-scale IQ score was the primary outcome measure. The geometric mean blood lead concentration of the children peaked at 17.8 μg/dL and declined to 9.4 μg/dL by 5–7 years of age; 244 (18%) children had a maximal blood lead concentration < 10 μg/dL, and 103 (8%) had a maximal blood lead concentration < 7.5 μg/dL. After adjustment for covariates, we found an inverse relationship between blood lead concentration and IQ score. Using a log-linear model, we found a 6.9 IQ point decrement [95% confidence interval (CI), 4.2–9.4] associated with an increase in concurrent blood lead levels from 2.4 to 30 μg/dL. The estimated IQ point decrements associated with an increase in blood lead from 2.4 to 10 μg/dL, 10 to 20 μg/dL, and 20 to 30 μg/dL were 3.9 (95% CI, 2.4–5.3), 1.9 (95% CI, 1.2–2.6), and 1.1 (95% CI, 0.7–1.5), respectively. For a given increase in blood lead, the lead-associated intellectual decrement for children with a maximal blood lead level < 7.5 μg/dL was significantly greater than that observed for those with a maximal blood lead level ≥7.5 μg/dL (p = 0.015). We conclude that environmental lead exposure in children who have maximal blood lead levels < 7.5 μg/dL is associated with intellectual deficits

    Regular breakfast and blood lead levels among preschool children

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    Background: Previous studies have shown that fasting increases lead absorption in the gastrointestinal tract of adults. Regular meals/snacks are recommended as a nutritional intervention for lead poisoning in children, but epidemiological evidence of links between fasting and blood lead levels (B-Pb) is rare. The purpose of this study was to examine the association between eating a regular breakfast and B-Pb among children using data from the China Jintan Child Cohort Study. Methods. Parents completed a questionnaire regarding children's breakfast-eating habit (regular or not), demographics, and food frequency. Whole blood samples were collected from 1,344 children for the measurements of B-Pb and micronutrients (iron, copper, zinc, calcium, and magnesium). B-Pb and other measures were compared between children with and without regular breakfast. Linear regression modeling was used to evaluate the association between regular breakfast and log-transformed B-Pb. The association between regular breakfast and risk of lead poisoning (B-Pb10 g/dL) was examined using logistic regression modeling. Results: Median B-Pb among children who ate breakfast regularly and those who did not eat breakfast regularly were 6.1 g/dL and 7.2 g/dL, respectively. Eating breakfast was also associated with greater zinc blood levels. Adjusting for other relevant factors, the linear regression model revealed that eating breakfast regularly was significantly associated with lower B-Pb (beta = -0.10 units of log-transformed B-Pb compared with children who did not eat breakfast regularly, p = 0.02). Conclusion: The present study provides some initial human data supporting the notion that eating a regular breakfast might reduce B-Pb in young children. To our knowledge, this is the first human study exploring the association between breakfast frequency and B-Pb in young children. © 2011 Liu et al; licensee BioMed Central Ltd
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