Literature DB >> 28886415

Burden of higher lead exposure in African-Americans starts in utero and persists into childhood.

Andrea E Cassidy-Bushrow1, Alexandra R Sitarik2, Suzanne Havstad2, Sung Kyun Park3, Lawrence F Bielak4, Christine Austin5, Christine Cole Johnson2, Manish Arora6.   

Abstract

BACKGROUND: Recent public health lead crises in urban areas emphasize the need to better understand exposure to environmental toxicants, particularly in higher risk groups. Although African-American children have the highest prevalence of elevated blood lead levels in the United States, little is known about when this trajectory of disproportionate burden of lead exposure first emerges.
OBJECTIVES: Using tooth-matrix biomarkers that directly measure fetal and early childhood metal levels, the primary goal of this study was to determine if there were racial disparities in lead levels during fetal development and early childhood. Manganese, an essential nutrient that modifies the neurotoxic effects of lead, was also measured.
METHODS: Pregnant women served by the Henry Ford Health System and living in a predefined geographic area in and around Detroit, Michigan, were recruited during the second trimester or later into the Wayne County Health, Environment, Allergy and Asthma Longitudinal Study (WHEALS), a population-based birth cohort. Offspring born between September 2003 and December 2007 were studied in childhood. Child race was parent-reported. Lead and manganese during the second and third trimesters, early postnatal life (birth through age 1year) and early childhood (age 1 through time of tooth shedding, which ranges from 6 to 12years) were measured via high-resolution microspatial mapping of dentin growth rings, a validated biomarker for prenatal and childhood metal exposure.
RESULTS: African-American children (N=71) had 2.2 times higher lead levels in the second and third trimesters (both p<0.001) and 1.9 times higher lead levels postnatally in the first year of life (p=0.003) compared to white children (N=51). Lead levels in African-American children were also higher during childhood, but this effect was only marginally significant (p=0.066) and was attenuated after covariate adjustment. Additionally, we observed that African-American children had lower tooth‑manganese levels during the third trimester (p=0.063) and postnatally (p=0.043), however these differences were attenuated after covariate adjustment.
CONCLUSION: The disproportionate burden of lead exposure is vertically transmitted (i.e., mother-to-child) to African-American children before they are born and persists into early childhood. Our results suggest that testing women for lead during pregnancy (or in pre-conception planning), may be needed to identify the risk to their future offspring, particularly for African-American women.
Copyright © 2017 Elsevier Ltd. All rights reserved.

Entities:  

Keywords:  Birth cohort; Environmental injustice; Lead; Manganese; Racial disparity

Mesh:

Substances:

Year:  2017        PMID: 28886415      PMCID: PMC5623116          DOI: 10.1016/j.envint.2017.08.021

Source DB:  PubMed          Journal:  Environ Int        ISSN: 0160-4120            Impact factor:   9.621


  41 in total

1.  Patterns of blood lead levels in US black and white women of childbearing age.

Authors:  A T Geronimus; M M Hillemeier
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2.  Lead-contaminated house dust and urban children's blood lead levels.

Authors:  B P Lanphear; M Weitzman; N L Winter; S Eberly; B Yakir; M Tanner; M Emond; T D Matte
Journal:  Am J Public Health       Date:  1996-10       Impact factor: 9.308

3.  Longitudinal data analysis for discrete and continuous outcomes.

Authors:  S L Zeger; K Y Liang
Journal:  Biometrics       Date:  1986-03       Impact factor: 2.571

4.  Subclinical lead exposure in philadelphia schoolchildren. Identification by dentine lead analysis.

Authors:  H L Needleman; I Davidson; E M Sewell; I M Shapiro
Journal:  N Engl J Med       Date:  1974-01-31       Impact factor: 91.245

Review 5.  Manganese deficiency and toxicity: are high or low dietary amounts of manganese cause for concern?

Authors:  J W Finley; C D Davis
Journal:  Biofactors       Date:  1999       Impact factor: 6.113

6.  Combined effects of prenatal medication use and delivery type are associated with eczema at age 2 years.

Authors:  G Wegienka; S Havstad; E M Zoratti; H Kim; D R Ownby; C C Johnson
Journal:  Clin Exp Allergy       Date:  2015-03       Impact factor: 5.018

Review 7.  Lead in bone: implications for toxicology during pregnancy and lactation.

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Journal:  Environ Health Perspect       Date:  1991-02       Impact factor: 9.031

8.  Manganese Exposure and Neurocognitive Outcomes in Rural School-Age Children: The Communities Actively Researching Exposure Study (Ohio, USA).

Authors:  Erin N Haynes; Heidi Sucharew; Pierce Kuhnell; Jody Alden; Mary Barnas; Robert O Wright; Patrick J Parsons; Kenneth M Aldous; Meredith L Praamsma; Caroline Beidler; Kim N Dietrich
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9.  Vitamin D receptor Fok1 polymorphism and blood lead concentration in children.

Authors:  Erin N Haynes; Heidi J Kalkwarf; Richard Hornung; Richard Wenstrup; Kim Dietrich; Bruce P Lanphear
Journal:  Environ Health Perspect       Date:  2003-10       Impact factor: 9.031

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Authors: 
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2.  In utero metal exposures measured in deciduous teeth and birth outcomes in a racially-diverse urban cohort.

Authors:  Andrea E Cassidy-Bushrow; Kuan-Han Hank Wu; Alexandra R Sitarik; Sung Kyun Park; Lawrence F Bielak; Christine Austin; Chris Gennings; Paul Curtin; Christine Cole Johnson; Manish Arora
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7.  Fetal and early postnatal lead exposure measured in teeth associates with infant gut microbiota.

Authors:  Alexandra R Sitarik; Manish Arora; Christine Austin; Lawrence F Bielak; Shoshannah Eggers; Christine C Johnson; Susan V Lynch; Sung Kyun Park; Kuan-Han Hank Wu; Germaine J M Yong; Andrea E Cassidy-Bushrow
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8.  The impact of childhood lead exposure on adult personality: Evidence from the United States, Europe, and a large-scale natural experiment.

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9.  Chronic developmental lead exposure increases μ-opiate receptor levels in the adolescent rat brain.

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