Format

Send to

Choose Destination
Environ Int. 2017 Nov;108:221-227. doi: 10.1016/j.envint.2017.08.021. Epub 2017 Sep 5.

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

Author information

1
Department of Public Health Sciences, Henry Ford Hospital, One Ford Place, Detroit, MI, USA; Center for Allergy, Asthma and Immunology Research, Henry Ford Hospital, Detroit, MI, USA. Electronic address: acassid1@hfhs.org.
2
Department of Public Health Sciences, Henry Ford Hospital, One Ford Place, Detroit, MI, USA; Center for Allergy, Asthma and Immunology Research, Henry Ford Hospital, Detroit, MI, USA.
3
Department of Epidemiology, University of Michigan, Ann Arbor, MI, USA; Department of Environmental Health Sciences, University of Michigan, Ann Arbor, MI, USA.
4
Department of Epidemiology, University of Michigan, Ann Arbor, MI, USA.
5
Senator Frank R Lautenberg Environmental Health Sciences Laboratory, Department of Environmental Medicine and Public Health, Division of Environmental Health, Icahn School of Medicine at Mount Sinai, New York City, NY, USA.
6
Senator Frank R Lautenberg Environmental Health Sciences Laboratory, Department of Environmental Medicine and Public Health, Division of Environmental Health, Icahn School of Medicine at Mount Sinai, New York City, NY, USA. Electronic address: manish.arora@mssm.edu.

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.

KEYWORDS:

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

PMID:
28886415
PMCID:
PMC5623116
DOI:
10.1016/j.envint.2017.08.021
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Elsevier Science Icon for PubMed Central
Loading ...
Support Center