Chemosphere · 2022
Prenatal exposure to perfluorooctane sulfonate alternatives and associations with neonatal thyroid stimulating hormone concentration: A birth cohort study.
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Cao Zhongqiang, Li Junwei, Yang Meng, Gong Hongjian, Xiang Feiyan, Zheng Hao, Cai Xiaonan, Xu Shunqing, Zhou Aifen, Xiao Han
Аннотация
BACKGROUND: Chlorinated polyfluorinated ether sulfonic acids (Cl-PFESA) and perfluorobutane sulfonate (PFBS), used as perfluorooctanesulfonate (PFOS) alternatives, were indicated as thyroid hormone disruptive toxicants in experimental studies. However, it is unclear whether prenatal exposure to Cl-PFESA and PFBS affects neonatal thyroid stimulating hormone (TSH) in human.
OBJECTIVE: To disclose the relationships between prenatal Cl-PFESAs and PFBS exposure and neonatal thyroid-stimulating hormone (TSH) levels based on a perspective cohort study.
METHODS: A total of 1015 pairs of mother and newborn were included from an ongoing birth cohort study in Wuhan, China, between 2013 and 2014. Six PFASs in cord blood sera and TSH concentration in neonatal postpartum heel sticks blood were quantified. Mixed linear and weighted quantile sum (WQS) regression models were applied to assess the individual and combination effects of PFASs exposure on neonatal TSH levels with multiple covariates adjustments.
RESULTS: After adjusting for potential confounders and other five PFASs, for each 1-ng/mL increase of PFBS or 8:2 Cl-PFESA, was negatively associated with 25.90% (95%CI: 37.37%, -12.32%; P < 0.001) and 27.19% (95%CI: 46.15%, -1.55%; P = 0.033) change in TSH in male but not female infants, respectively. No significant association was found between other PFASs exposure and neonatal TSH. Higher PFAS mixture in cord blood was significantly associated with decrease TSH concentration in all newborns (β = -0.36; 95%CI: 0.58, -0.13; P = 0.001) identified by WQS regression model. PFBS, PFOS and 6:2 Cl-PFESA were the major contributors to the neonatal TSH decrement with the weights of 56.50%, 18.71%, 12.81% among PFAS mixture, respectively.
CONCLUSIONS: our prospective cohort study suggested a negative association of cord serum PFBS and 8:2 CI-PFESA with TSH concentration in newborns, especially for boys. Additional studies are required to elaborate on the underlying biological mechanisms, especially for PFBS.
OBJECTIVE: To disclose the relationships between prenatal Cl-PFESAs and PFBS exposure and neonatal thyroid-stimulating hormone (TSH) levels based on a perspective cohort study.
METHODS: A total of 1015 pairs of mother and newborn were included from an ongoing birth cohort study in Wuhan, China, between 2013 and 2014. Six PFASs in cord blood sera and TSH concentration in neonatal postpartum heel sticks blood were quantified. Mixed linear and weighted quantile sum (WQS) regression models were applied to assess the individual and combination effects of PFASs exposure on neonatal TSH levels with multiple covariates adjustments.
RESULTS: After adjusting for potential confounders and other five PFASs, for each 1-ng/mL increase of PFBS or 8:2 Cl-PFESA, was negatively associated with 25.90% (95%CI: 37.37%, -12.32%; P < 0.001) and 27.19% (95%CI: 46.15%, -1.55%; P = 0.033) change in TSH in male but not female infants, respectively. No significant association was found between other PFASs exposure and neonatal TSH. Higher PFAS mixture in cord blood was significantly associated with decrease TSH concentration in all newborns (β = -0.36; 95%CI: 0.58, -0.13; P = 0.001) identified by WQS regression model. PFBS, PFOS and 6:2 Cl-PFESA were the major contributors to the neonatal TSH decrement with the weights of 56.50%, 18.71%, 12.81% among PFAS mixture, respectively.
CONCLUSIONS: our prospective cohort study suggested a negative association of cord serum PFBS and 8:2 CI-PFESA with TSH concentration in newborns, especially for boys. Additional studies are required to elaborate on the underlying biological mechanisms, especially for PFBS.