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Environ Health Perspect. 2011 Oct;119(10):1429-35. doi: 10.1289/ehp.1003172. Epub 2011 Jun 30.

Thyroid dysfunction as a mediator of organochlorine neurotoxicity in preschool children.

Author information

1
Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts, USA. jjulvez@hsph.harvard.edu

Abstract

BACKGROUND:

Exposure to organochlorine compounds (OCs) can alter thyroid function in humans, and hypothyroidism during early life can adversely affect a child's neurodevelopment.

OBJECTIVES:

In this study we aimed to assess the relationship between developmental organochlorine exposures and thyroid function and the relationship between thyroid function and subsequent neurodevelopment.

METHODS:

A population-based birth cohort of 182 children was followed annually up to 5.5 years of age. The assessments included OC concentrations in maternal pregnancy serum and milk, clinical thyroid parameters in maternal and cord serum, and subsequent neuropsychological outcomes of the child, along with sociodemographic cofactors. Resin triiodothyronine uptake ratio (T3RU) was also assessed as an estimate of the amount of thyroxine-binding globulin (TBG) sites unsaturated by thyroxine. The T3RU is high in hyperthyroidism and low in hypothyroidism.

RESULTS:

The findings showed consistent inverse and monotonic associations between organochlorine exposure and T3RU after covariate adjustments. We observed no associations with other thyroid parameters. T3RU was positively associated with improved performance on most of the neuropsychological tests. For other thyroid parameters, the findings were less consistent.

CONCLUSIONS:

The results suggest that OC exposures may decrease the T3RU during early life, which is a proxy measure of the binding capacity of TBG. In addition, minor decreases of the thyroid function may be inversely associated with a child's neurodevelopment.

PMID:
21719373
PMCID:
PMC3230434
DOI:
10.1289/ehp.1003172
[Indexed for MEDLINE]
Free PMC Article
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