Information on placental transfer and adverse outcomes of short-chain per- and polyfluoroalkyl substance (PFASs) is limited, and factors responsible for PFAS placental transfer are still unclear. In the present study, concentrations of 21 PFASs were analyzed in 132 paired maternal and cord serum samples collected from residents in Beijing, China, and the placental transfer efficiency (PTE) of each PFAS was calculated. PTEs of short-chain perfluoroalkyl acids (PFAAs), including PFBA (146%), PFBS (97%), PFPeA (118%), and PFHxA (110%), were first reported, and a complete U-shaped trend of PTEs from C4 to C13 of perfluoroalkyl carboxylic acids (PFCAs) was obtained. Positive association between maternal weight and PTE of perfluorooctanesulfonate (PFOS) (p < 0.05) and negative association between maternal PFBA concentration and birth length (p < 0.01) were observed. Using in vitro experiments, we further determined equilibrium dissociation constants (K ds) of human serum albumin (HSA)–PFAS complexes (K d‑HP), serum proteins–PFAS complexes (K d‑SP), and liver-fatty acid binding protein (L-FABP)–PFAS complexes (K d‑LP) and found that they were all significantly correlated with PTEs of PFASs. The correlation coefficient was 0.92, 0.89, and 0.86, respectively (p < 0.01 in all three tests), suggesting that K ds of protein (serum)–PFAS complexes can play an important role in trans-placental transfer of PFASs in human and K d‑HP plays a pivotal role.

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Both iron deficiency and hyperglycemia are highly prevalent globally for pregnant women. Iron supplementation is recommended during pregnancy to control iron deficiency. The purposes of the review are to assess the oxidative effects of iron supplementation and the potential relationship between iron nutrition and gestational diabetes. High doses of iron (~relative to 60 mg or more daily for adult humans) can induce lipid peroxidation in vitro and in animal studies. Pharmaceutical doses of iron supplements (e.g., 10× RDA or more for oral supplements or direct iron supplementation via injection or addition to the cell culture medium) for a short or long duration will induce DNA damage. Higher heme-iron intake or iron status measured by various biomarkers, especially serum ferritin, might contribute to greater risk of gestational diabetes, which may be mediated by iron oxidative stress though lipid oxidation and/or DNA damage. However, information is lacking about the effect of low dose iron supplementation (≤60 mg daily) on lipid peroxidation, DNA damage and gestational diabetes. Randomized trials of low-dose iron supplementation (≤60 mg daily) for pregnant women are warranted to test the relationship between iron oxidative stress and insulin resistance/gestational diabetes, especially for iron-replete women.