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Background Previous research indicated that isomers and alternatives of per- and polyfluoroalkyl substances (PFAS) probably disturb glucose metabolism; however, current epidemiological evidence on the associations of PFAS with fasting blood glucose is inconsistent. Besides, studies on the joint association of multiple components of PFAS and fasting blood glucose as well as the key component are scarce. Objective To evaluate the associations of PFAS isomers and alternatives with fasting blood glucose and their joint effects, as well as identify the key component among population without glucose metabolism problems. Methods We selected 923 adults without glucose metabolism problems or missing data from the Isomers of C8 Health Project in China (2015—2016). Serum PFAS isomers and alternatives and fasting blood glucose were measured using ultra-performance liquid chromatography coupled with tandem mass spectrometry (UPLC-MS/MS) and automatic biochemical analyzer. We applied multiple linear regression to explore the associations of 16 pollutants which were detected among over 80% participants with fasting blood glucose. Meanwhile, we utilized qgcomp and Bayesian kernel machine regression (BKMR) models to explore the joint effects of PFAS isomers and alternatives mixture on target outcome indicators and identify the key component. Results The average age among the 923 participants in this study was (62.4±13.8) years old, including 472 men (51.1%) and 451 women (48.9%). Among selected PFAS isomers and alternatives, the highest serum concentration was ∑3+4+5m-PFOS (perfluoro-3/4/5-methylheptanesulfonate) with a median concentration of 10.20 ng·mL−1. The concentrations of linear perfluorooctane sulfonate (n-PFOS, 9.61 ng·mL−1), perfluorooctanoic acid (PFOA, 4.55 ng·mL−1), linear perfluorohexane sulfonic acid (n-PFHxS, 2.48 ng·mL−1), 6:2 chlorinated polyfluorinated ethersulfonic acid (6:2 Cl-PFESA, 1.90 ng·mL−1), perfluoro-6-methylheptanesulfonate (iso-PFOS, 1.85 ng·mL−1), perfluorobutanoic acid (PFBA, 1.81 ng·mL−1), perfluorinated n-nonanoic acid (PFNA, 1.39 ng·mL−1), and perfluoro-1-methylheptanesulfonate (1m-PFOS, 1.27 ng·mL−1) were higher than 1.00 ng·mL−1. After being adjusted for selected confounders, PFAS isomers and alternatives were positively associated with fasting blood glucose. With 1 ln unit concentration increment of 6:2 Cl-PFESA and PFNA, the estimated changes of fasting blood glucose were 0.18 (95%CI: 0.13, 0.23) mmol·L−1 and 0.24 (95%CI: 0.18, 0.30) mmol·L−1, respectively. The multi-pollutant models indicated a joint association of PFAS isomers and alternatives mixture with fasting blood glucose. The BKMR models reveals that as the quantiles of mixture elevated from the 50th to the 75th percentile, the values of fasting blood glucose increased 0.25 (95%CI: 0.21, 0.30) mmol·L−1, and the posterior inclusion probability of PFNA was 0.92, implying that PFNA was the key component. Conclusion PFAS isomers and alternatives are positively associated with fasting blood glucose. PFNA is the key component of the joint association.
RESUMO
Per- and polyfluoroalkyl substances (PFASs) are persistent organic pollutants (POPs). They are widely used in food packaging, tableware coating, stain resistant furniture, and other industrial production. Humans are exposed to PFASs on a daily basis through drinking water and intaking food, use of consumer products containing PFASs, and occupational exposure during the production of PFASs or related products. A growing body of toxicological studies has shown that PFASs exposure disrupts the thyroid hormone (TH) system and causes hypothyroidism, which is further supported by population epidemiological studies. PFASs can damage thyroid follicular cells and sodium/iodine transporters to impair iodine uptake by thyroid cells. They interfere with the synthesis of thyroglobulin, reduce the activity of thyroid peroxidase, and affect the synthesis and secretion of TH. They interfere with TH transportation and biological effects via TH competitive binding thyroid transporter or thyroid hormone receptor. They suppress TH signaling pathway and deiodinase activity, interfere negative feedback mechanism, and accelerate TH metabolism and excretion. The processes of TH synthesis, transport, degradation, and biological effects may all be affected by PFASs exposure. This paper described possible toxic mechanisms of PFASs on the thyroid from four aspects: TH biosynthesis, transport, action on target cells, and metabolic excretion stage, and summarized the thyroid toxicity associated with PFASs exposure.
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Per- and polyfluoroalkyl substances (PFASs) represent a group of organic chemicals with structures consisting of fluorinated carbon backbone in different lengths, and they are bioaccumulative and endocrine-disrupting. Humans can be exposed to PFASs through a variety of routes such as inhalation, ingestion, and dermal contact. Population studies have found that PFASs can be detected in urine, blood, and follicular fluid from females. Toxicological studies have demonstrated that PFASs can cause adverse reproductive health outcomes, including decreased fertilization and implantation rate, disturbance of reproductive hormone levels, abnormal egg cell development, and abnormal fetal absorption and fetal development. Limited epidemiological studies have also revealed that exposure to environmental levels of PFASs is related to female reproductive health, but the conclusions remain inconsistent. This study aimed to review the PFAS exposure levels and epidemiological research results from different biological samples in the female population, as well as the female reproductive toxicity and mechanisms of PFASs, and further elaborate the effects of environmental PFAS exposure on female reproduction health.