Persistent Organic Pollutants and the Association with Maternal and Infant Thyroid Homeostasis: A Multipollutant Assessment

Abstract

Background:Disruption of thyroid homeostasis has been indicated in human studies targeting effects of persistent organic pollutants (POPs). Influence on the maternal thyroid system by POPs is of special interest during pregnancy because such effects could impair infant thyroid homeostasis.Objectives:We investigated the association between POPs and thyroid-stimulating hormone (TSH) and thyroid hormones (THs) in mother and child pairs from the Northern Norway Mother-and-Child Contaminant Cohort Study (MISA).Methods:Nineteen POPs and 10 thyroid parameters were analyzed in serum from 391 pregnant women in their second trimester. In addition, TSH concentrations in heel-prick samples from the infants were analyzed by the Norwegian Newborn Screening program. Association studies with a multipollutant approach were performed using multivariate analyses; partial least squares (PLS) regression, hierarchical clustering, and principal component analysis (PCA).Results:Several POPs were significantly associated with TSH and THs: a) PFOS was positively associated with TSH; b) PCBs, HCB, and nonachlors were inversely associated with T3, T4, and FT4; and, c) PFDA and PFUnDA were inversely associated with T3 and FT3. After mutual adjustments for the other contaminants, only PFDA and PFUnDA remained significantly associated with T3 and FT3, respectively. Infants born to mothers within the highest TSH quartile had 10% higher mean concentrations of TSH compared with children born to mothers in the lowest TSH quartile.Conclusion:The present results suggest that background exposures to POPs can alter maternal thyroid homeostasis. This research contributes to the understanding of multipollutant exposures using multivariate statistical approaches and highlights the complexity of investigating environmental concentrations and mixtures in regard to maternal and infant thyroid function.Citation:Berg V, Nøst TH, Pettersen RD, Hansen S, Veyhe AS, Jorde R, Odland JØ, Sandanger TM. 2017. Persistent organic pollutants and the association with maternal and infant thyroid homeostasis: a multipollutant assessment. Environ Health Perspect 125:127–133; http://dx.doi.org/10.1289/EHP152

Thyroid function disruptors: from nature to chemicals

“…In a study of prenatal HCB exposure, the effect of HCB depended on the genotype of the gene encoding the D1 (Dio1) enzyme, suggesting that D1s play a role in the disruption of THs following exposure to HBC (Llop et al 2017). Similar studies have shown that diminished T3 levels caused by HBC exposure during pregnancy can interfere with the TH levels in early newborns and affect neurodevelopment (Takser et al 2005, Maervoet et al 2007, Berg et al 2017.…”

Gestational diabetes and offspring birth size at elevated environmental pollutant exposures

“…Exposure to certain POPs, such as DDE, PFOS and PFOA, has been previously proposed to alter the secretion and function of human sex steroids and thyroid hormones (Berg et al 2016; Ferguson et al 2012), induce inflammation, mitochondrial dysfunction and oxidative stress (Kim and Lee 2014; Myre and Imbeault 2014), promote adipogenesis through activation of the peroxisome proliferator activated receptor gamma (PPARγ) (Janesick and Blumberg 2016), and alter lipid peroxidation and pancreatic beta cell function (Al-Eryani et al 2015). Findings from experimental studies also support an interference of mercury exposure to lipid peroxidation and pancreatic beta cell function (Chen et al 2006 and 2010; Moreira et al 2012), though data on metabolic effects of mercury are sparse (Heindel et al 2016).…”

Immunotoxic and hepatotoxic effects of perfluoro-n-decanoic acid (PFDA) on female Harlan Sprague–Dawley rats and B6C3F1/N mice when administered by oral gavage for 28 days

“…cell-mediated immunity (Nelson et al 1992), and thyroid hormone homeostasis (Harris et al 1989;Berg et al 2016). However, many of these effects were observed following IP exposure at levels that induced acute toxicity and morbidity.…”

“…Although evidence is limited, rodent studies indicate that PFDA may affect the immune system, as indicated by thymic atrophy, reversible bone marrow hypocellularity, and alterations in thyroid hormone levels (George and Anderson 1986;Kelling et al 1987;Harris et al 1989;Nelson et al 1992). Published reports have documented the occurrence of PFDA in human blood (Olsen et al 2011;Denys et al 2014) and breast milk (Fujii et al 2012;Motas Guzman et al 2016), and the correlation of PFDA levels with thyroid hormone homeostasis (Berg et al 2016;Kim et al 2016). The objective of this study was to evaluate potential adverse effects of PFDA to the immune system in female Harlan Sprague-Dawley rats and B 6 C 3 F 1 /N mice.…”