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Pyrethroid insecticides have been extensively used in China and worldwide, while their effects on thyroid functions are rarely explored, especially in susceptible pregnant women. To assess the association between 3-phenoxybenzoic acid (3PBA), a major urinary metabolite of pyrethroids, and thyroid hormone levels in pregnant women in China. Three hundred and seventy-four pregnant women were recruited during the admission for delivery (third trimester of pregnancy) in a local hospital in Shandong, China during December 2011 to December 2013. Pyrethoids exposure was assessed by examining urinary metabolite of 3PBA levels. Thyroid hormones were detected by measuring serum concentrations of thyroid stimulating hormones (TSH), total triiodothyronine (TT3), free triiodothyronine (FT3), total thyroxine (TT4) and free thyroxine (FT4). Multiple linear regression models were used to investigate the associations between 3PBA concentrations and thyroid hormones levels. The detection frequency of 3PBA was 90.4%, with a median concentration of 1.14 μg/g creatinine. After adjusted for potential confounders, we found a significant negative relationship between 3PBA and serum FT3 (β = −0.06, 95% CI = −0.11 to −0.01) as well as an inverse dose dependent association (p for trend = 0.023). No significant association was found between 3PBA concentrations and other thyroid hormones. Our findings indicated that pyrethroid exposure was widespread and negatively associated with serum FT3 concentrations in pregnant women in northern China. Given to the widespread of pyrethroid exposure and critical role thyroid homeostasis plays during pregnancy, more studies are warranted to explore their relationships as well as underlying mechanisms. • Pyrethroid insecticides have been increasingly used in individual household and for agricultural purposes. • We assessed the pyrethroid exposure in pregnant women in northern China and explored their potential effects on thyroid functions. • The median concentration of pyrethroid urinary metabolite 3PBA was 1.14 μg/g creatinine (detection frequency as 90.4%. • A significant negative association between urinary 3PBA concentrations and serum FT3 levels was observed. [ABSTRACT FROM AUTHOR]

Human exposure to polybrominated diphenyl ethers (PBDEs) has been increasing over the last three decades in China and around the world. Animal studies suggest that PBDEs could reduce blood levels of thyroid hormones, but it is unclear whether PBDEs disrupt thyroid function in humans. We used data from a prospective birth cohort of 123 pregnant women who were enrolled between September 2010 and March 2011 in Shandong, China. We measured the concentrations of eight PBDE congeners (n = 106) and five thyroid hormones (n = 107) in cord serum samples. We examined the relationship between prenatal exposure to PBDEs and thyroid function (n = 90). Median concentrations of BDEs 47, 99, 100, and 153 (detection frequencies > 75%) were 3.96, 8.27, 3.31, and 1.89 ng/g lipid, respectively. A 10-fold increase in BDE-99 and Σ 4 PBDEs (the sum of BDEs 47, 99, 100, and 153) concentrations was associated with a 0.41 μg/dL (95% confidence interval [CI]: 0.10 to 0.72) and 0.37 μg/dL (95% CI: 0.06 to 0.68) increase in total thyroxine levels (TT 4 ), respectively. No associations were found between other individual congeners and any of the five thyroid hormones. Our study suggests that prenatal exposure to PBDEs may be associated with higher TT 4 in cord blood. Given the inconsistent findings across existing studies, our results need to be confirmed in additional studies. [ABSTRACT FROM AUTHOR]

Although animal studies suggested that prenatal cadmium exposure can cause neurodevelopmental deficits, little is explored in human populations, or its mechanism. We investigated the association between prenatal cadmium exposures and infants' developmental quotients (DQs) based on the Gesell Developmental Schedules (gross motor, fine motor, adaptive, language, and social domains) at 12 months of age and explored the role of brain-derived neurotrophic factor (BDNF) in prenatal cadmium-induced neurodevelopmental deficits in Shandong, China, by enrolling 300 mothers between September 2010 and December 2011. Maternal blood cadmium concentration (median, 1.24 μg/L) was negatively associated with social domain DQs and BDNF levels in cord serum. A 10-fold increase in maternal cadmium levels was associated with a 5.70-point decrease in social domain DQs, a 4.31-point decrease in BDNF levels. BDNF levels were positively associated with social domain DQs. These data suggest that prenatal low-level cadmium exposure has adverse effects on neurodevelopment. BDNF may play an important role in the decline of social domain DQs induced by prenatal low-level cadmium exposure. [ABSTRACT FROM AUTHOR]

Background Although studies in laboratory animals demonstrate neurodevelopmental deficits caused by prenatal or postnatal organophosphate pesticide (OP) exposure, there is limited evidence on effects induced by not only prenatal but also postnatal exposure of children to OPs. Methods We measured diethylphosphate (DE), dimethylphosphate (DM), and total dialkylphosphate (DAP) metabolites in maternal and child urine at 12 and 24 months of age and examined their relationship with developmental quotients (DQs) in 12-month-old infants and 24-month-old children in Shandong, China. Results The median concentrations of total DAP metabolites (DAPs) in child urine [371.97 nmol/g creatinine (12-month-old infants), 538.64 nmol/g creatinine (24-month-old children)] were higher than those in maternal urine (352.67 nmol/g creatinine). Prenatal OP exposure was negatively associated with 24-month-old children's DQs, especially among boys. A 10-fold increase in prenatal DEs and DAPs was associated with a 2.59- and 2.49-point decrease in social domain DQ scores in 24-month-old children ( n = 262), respectively. However, positive association of postnatal exposure to OPs and 24-month-old children's DQs was observed ( n = 237). Neither prenatal nor postnatal exposure to OPs was related to 12-month-old infants' DQs. Conclusions These data suggested that prenatal OP exposure could adversely affect children's neurodevelopment at 24 months of age, especially among boys. The prenatal period might be a critical window of OP exposure. In view of the positive association with postnatal OP exposure, it is necessary to interpret findings with caution. [ABSTRACT FROM AUTHOR]

Polybrominated diphenyl ethers (PBDEs) are widely used in commercial and household products. Few human studies have examined the effects of PBDE exposure on female reproductive function. We recruited 207 pregnant women when they were admitted for labor from September 2010 to February 2012 as part of a birth cohort study, the Laizhou Wan Birth Cohort study. Maternal sera were analyzed for eight PBDE congeners (BDE-28, -47, -85, -99, -100, -153, -154, and -183) and four sex hormones. BDE-153 exhibited the highest serum level (median 4.67 ng/g lipid), followed by BDE-99 (median 3.45 ng/g lipid) and BDE-28, -47, and -100 (medians near 2 ng/g lipid). BDE-28, -47, -99, -100, and -153 were the most frequently detected (> 90%) congeners. Follicle-stimulating hormone (FSH) levels were negatively associated with PBDE exposure. For each natural log unit increase in BDE-47, 100, and ∑ 5 PBDEs, FSH levels changed − 1.19 IU/L (95% confidence interval [CI]: − 1.32, − 1.02), − 1.17 IU/L (95%CI: − 1.36, − 1.01) and − 1.26 IU/L (95%CI: − 1.55, − 1.02) respectively. BDE-85, − 153, and − 183 were associated with adverse reproductive effects, including an increased risk of threatened abortion (odds ratio [OR] [95% CI]: 1.30 [1.03, 1.62], 1.04 [1.01, 1.08], and 1.03 [1.01, 1.06], respectively). BDE-153 was associated with an increased risk of premature birth (adjusted OR [95% CI]:1.05 [1.01, 1.09]), and BDE-28 was associated with longer time to pregnancy (adjusted OR [95% CI]: 1.34 [1.03, 1.76]). These findings suggest that maternal PBDE exposure may be inversely associated with female reproductive function. [ABSTRACT FROM AUTHOR]