Relationship of Thyroid Hormone Levels to Levels of Polychlorinated Biphenyls, Lead, p,p′ - DDE, and Other Toxicants in Akwesasne Mohawk Youth

Abstract

Background

It is well documented that acute exposure to high levels of persistent organic pollutants, such as polychlorinated biphenyls (PCBs), p,p′ -dichlorophenyldichloroethylene ( p,p′ -DDE), and hexachlorobenzene (HCB), can affect human health including thyroid function. Chronic exposure to multiple toxicants is common but difficult to analyze, and most prior studies have focused on adults or newborns, creating a gap in our understanding of multitoxicant effects among adolescents.

Objective

We investigated whether levels of PCBs, p,p′ -DDE, HCB, mirex, lead, and mercury reflecting past chronic exposure are associated with alterations in levels of thyroid-stimulating hormone (TSH), triiodothyronine (T ₃), total thyroxine (TT ₄), and free thyroxine (FT ₄) among older children and adolescents.

Methods

The sample consists of youth from the Akwesasne Mohawk Nation ( n = 232) who reside in proximity to several industries that have contaminated the local environment. We used multiple regression analysis to examine the effect of PCB groupings, p,p′ -DDE, HCB, lead, and mercury on thyroid hormones after adjusting for sociodemographic covariates and controlling for all other toxicants.

Results

Exposure to PCBs affects the thyroid hormone profile in adolescents. The group of persistent PCBs was positively associated with TSH but inversely related to FT ₄. Nonpersistent PCBs were significantly and negatively related to FT ₄ only. HCB was negatively associated with T ₄, and lead was positively associated with T ₃. Breast-fed adolescents had higher levels of persistent PCBs and p,p′ -DDE but not of nonpersistent PCBs or any other toxicant when compared with non-breast-fed adolescents. Though having lower levels of persistent PCBs and p,p′ -DDE, non-breast-fed adolescents exhibited significant relationships between persistent PCBs and TSH and FT ₄, but breast-fed adolescents did not. It appears that PCBs from breast milk obscure the relationship between prenatal PCB exposure and thyroid function by adding random variation in PCB levels.

Conclusion

Our results demonstrate a reduction in thyroid function in adolescents in relation to their current serum levels of PCBs. These observations are consistent with the hypothesis that pre-natal exposure to PCBs alters thyroid function in a long-lasting manner but does not exclude the possibility that postnatal exposure is influential also.