Prenatal and Postnatal Impact of Perfluorooctane Sulfonate (PFOS) on Rat Development: A Cross-Foster Study on Chemical Burden and Thyroid Hormone System

Abstract

Perfluorooctane sulfonate (PFOS), an environmentally persistent organic pollutant, has been reported to be transferred to the developing organisms via both placenta and breast milk. A cross-foster model was used to determine whether prenatal or postnatal exposure to PFOS alone can disturb the TH homeostasis in rat pups, and if so, which kind of exposure is a major cause of TH level alteration. Pregnant rats were fed standard laboratory rodent diet containing 0 (control) or 3.2 mg PFOS/kg throughout gestation and lactation period. On the day of birth, litters born to treated and control dams were cross-fostered, resulting in the following groups: unexposed control (CC), pups exposed only prenatally (TC), only postnatally (CT) or both prenatally and postnatally (TT). Serum and liver PFOS concentrations, serum total thyroxine (T4), total triiodothyronine (T3), reverse T3 (rT3) levels, and hepatic expression of genes involved in TH transport, metabolism, and receptors were evaluated in pups at the age of postnatal days (PNDs) 0, 7, 14, 21, or 35. PFOS body burden level in pups in group CT increased, while those in group TC dropped as they aged. Neither total T3 nor rT3 in pups was affected by PFOS exposure. Gestational exposure to PFOS alone (TC) significantly (p < 0.05) decreased T4 level in pups on PNDs 21 and 35, 20.3 and 19.4% lower than the control on the same PND, respectively. Postnatal exposure to PFOS alone (CT) also induced T4 depression on PNDs 21 and 35, 28.6 and 35.9% lower than controls, respectively. No significant difference in T4 level (p > 0.05) was observed between TC and CT on these two time points. None of the selected TH related transcripts was affected by PFOS in pups on PND 0. Only transcript level of transthyretin, TH binding protein, in group TT significantly increased to 150% of the control on PND 21. The results showed that prenatal PFOS exposure and postnatal PFOS exposure induced hypothyroxinemia in rat pups to a similar extent, which suggested that in utero PFOS exposure and postnatal PFOS accumulation, especially though maternal milk, are matters of great concern.

Perinatal Exposure to Perfluorooctane Sulfonate Affects Glucose Metabolism in Adult Offspring

“…It is known that PFOS can cross placenta and through lactation to impose developmental effects on fetus and neonates [25], [31], [36]–[40]. To investigate if the increase of liver weight might cause disturbance to liver functions as reported in the toxicological models in adult animals [22], [23], [26], [41], [42], the mRNA expression levels of hepatic genes targeting lipid metabolism were measured in the F 1 pups and were found to be modulated.…”

Concentration of perfluorinated compounds and cotinine in human foetal organs, placenta, and maternal plasma

“…In rodents, exposure to high doses of PFOS and PFOA during pregnancy reduced postnatal survival, birth weight, growth of the pups, and disturbed lactation (Lau et al, 2004;Olsen et al, 2009). Further, both pre-and postnatal PFAS exposure has been associated with hypothyroidism and significantly decreased T4 levels in pups (Yu et al, 2009). PFASs, particularly PFOA and PFNA, may induce synthesis of the oestrogen-responsive biomarker protein vitellogenin, leading to an oestrogen-like activity in rainbow trout (Benninghoff et al, 2011).…”

Thyroid disruption effects of environmental level perfluorooctane sulfonates (PFOS) in Xenopus laevis

“…Environmental levels of chemicals may adversely affect thyroid system and disturb thyroid function. There were reports that PFOS exposure induced THs deficiency (Yu et al 2009a(Yu et al , 2010 and THs alteration (Yu et al 2009b;Curran et al 2008) in rats, and alteration of thyroid homeostasis in mice (Fair et al 2011;Fuentes et al 2006). PFOS may exert its effects in the bumblebee partially through an endocrine disrupting action via the insect molting hormone or ecdysteroid receptor (Mommaerts et al 2011).…”