Exposure to Perflouroalkyl acids and foetal and maternal thyroid status: a review

Abstract

Background Exposure to perfluorinated-alkyl-acids (PFAAs) is ubiquitous. PFAAs are hormone-disrupting compounds that are strongly suspected to affect mother-child-health such as fetal growth. Thyroid disruption is a plausible mechanism of action. We aim to summarize the epidemiological evidence for the relation between prenatal and postnatal exposure to PFAAs and disruption of thyroid homeostasis in mothers and/or infants. Method Fifteen original publications on PFAAs concentrations and thyroid hormones (TH) in pregnant women and/or infants were found upon a literature search in the PubMed database. Information on exposure to seven PFAAs congeners [Perfluorooctane sulfonate (PFOS), Perfluorooctanoate (PFOA), Perfluorohexane sulfonate (PFHxS), Perfluorononanoic acid (PFNA), Perfluorodecanoic acid (PFDA), Perfluoroundecanoic acid (PFUnA), and Perfluorododecanoic acid (PFDoA)] and thyroid stimulating hormone (TSH), free and total thyroxine (FT4 and TT4), free and total triiodothyronine (FT3 and TT3), T3RU (Free triiodothyronine resin uptake) and FT4-index (FT4I) levels were recorded. We evaluated sampling of maternal TH by trimester, and infant TH by sex stratification. Reported associations between mother or infant PFAAs and TH were not uniformly assessed in the selected studies. Results Ten out of the fifteen studies examined maternal PFAAs concentration and TSH level. Seven studies showed significant associations between TSH and exposure to six PFAAs congeners, most of them were positive. Maternal T4 and T3 were investigated in nine studies and five studies found inverse associations between exposure to six PFAAs congeners and TH (TT3, TT4, FT3, FT4 and FT4I) levels. Eight of the fifteen studies investigated PFAAs concentrations and infant TSH. Infant TSH level was significantly affected in four studies, positively in three studies. Nine studies investigated infant T4 and T3 and seven studies found significant associations with PFAAs exposure. However, both inverse and positive significant associations with infant TH were found eliciting no clear direction. Conclusion Results indicate a mainly positive relationship between maternal PFAAs concentrations and TSH levels, and suggestion of an inverse association with T4 and/or T3 levels. Associations of infant TH with PFAAs concentration were less consistent.

Prenatal exposure to persistent organic pollutants and metals and problematic child behavior at 3–5 years of age: a Greenlandic cohort study

“…the estrogen and androgen receptors and thus modulating their signaling 2 , 3 . In addition, studies show that POPs can disrupt thyroid hormones in rodent’s such as mice and rats 1 , 4 – 6 as well as in human 7 , 8 . Heavy metals are considered systemic toxicants known to affect and damage multiple organ systems even at lower levels of exposure and some of them are classified as ‘known’ and ‘probable’ human carcinogens 9 .…”

Chronic exposure to perfluorohexane sulfonate leads to a reproduction deficit by suppressing hypothalamic kisspeptin expression in mice

“…To date, several epidemiological studies have identified associations between PFHxS and altered liver, thyroid, energy and lipid metabolism, protein biosynthesis, and immune function, which may be indirectly involved in the reproductive toxicity caused by PFHxS [55][56][57][58]. In addition, AVPV-and ARC-kisspeptin neurons express prolactin receptors, suggesting the possible participation of prolactin in the toxicity of PFHxS [59,60].…”

Chronic Exposure to Perfluorohexane Sulfonate Leads to a Reproduction Deficit by Suppressing Hypothalamic Kisspeptin Expression in Mice

“…To date, several epidemiological studies have identi ed associations between PFHxS and altered liver, thyroid, energy and lipid metabolism, protein biosynthesis, and immune function, which may be indirectly involved with the reproductive toxicity caused by PFHxS [46][47][48][49]. In addition, AVPV-and ARC-kisspeptin neurons express prolactin receptors, suggesting the possible participation of prolactin in the toxicity of PFHxS [50][51].…”