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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 MeHg is a confirmed neurotoxin at sufficiently high dosages, the effect of prenatal low-level Hg exposure on infant neurodevelopment is still unknown. Four hundred ten mother-infant pairs were recruited in rural northern China from September 2010 to September 2012. We investigated maternal diet during pregnancy, collected maternal and umbilical blood samples, and tested infant neurodevelopment using Gesell developmental schedules (GDS) at the age of 1 year old. The geometric means (GM) of Hg exposure in maternal and umbilical blood were 0.72 and 1.2 μg/L, respectively. Positive associations between Hg levels and the frequency of total fish consumption were found (Spearman's correlation, r = 0.09 for maternal Hg, r = 0.14 for umbilical Hg, p < 0.01). After adjusting for confounding factors, we found a log-unit increase in umbilical blood Hg levels was associated with a 4.22-point (95 % confidence interval (95 %CI) 0.77 to 7.67) increase in the adaptive domain and a 4.06-point (95 %CI 0.51 to 7.62) increase in the social domain. No significant association has been found between other domains and Hg levels in our study. In further analysis, we noticed the positive correlation between the developmental quotient (DQ) scores of the adaptive domain and frequencies of total fish consumption ( p = 0.04). Our results failed to indicate the adverse effects between prenatal Hg exposure and infant neurodevelopment. However, given the low-level Hg exposure and its predominant source, the potential positive associations in our study may be attributed to the beneficial nutrients of fish consumption. [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]

Exposure to lead early in life may be a risk factor for fetal growth, but little is known about the effects of low-level prenatal lead exposure on birth outcomes. We measured maternal and cord blood lead levels and examined their associations with birth outcomes. Mother–infant pairs (n = 252) were recruited from a rural area located on the south coast of Laizhou Bay between 2010 and 2011. The median levels of maternal and cord blood lead were 3.20 and 2.52 μg/dL, respectively. Increasing maternal blood lead exposure was associated with decreasing birth weight (β = −148.99; 95% CI, −286.33 to −11.66), and a significant negative relationship was found between cord blood lead levels and birth length (β = −0.84; 95% CI, −1.52 to −0.16). Low-level prenatal lead exposure may adversely affect fetal growth. These results may be important for public health and have implications regarding the recommended blood lead levels. [Copyright &y& Elsevier]

Phenolic compounds are among the endocrine disruptors which are widely used in daily life products. Studies in laboratory animals showed reproductive and developmental effects. In spite of widespread exposure to phenols, only few studies examined their effects on human development. This study was designed to investigate the relationship between antenatal phenol exposure and birth outcomes in a Chinese obstetric population. Four hundred ninety-six mother-infant pairs recruited from the Laizhou Wan prospective birth cohort in northern China between 2010 and 2013 were included in the study. We measured two phenol metabolites in maternal urine at delivery and examined their associations with birth outcomes including birth weight, crown–heel length, head circumference, gestational age, and ponderal index. Median levels of bisphenol A (BPA) and triclosan (TCS) in urine were 1.07 and 0.50 μg/g creatinine, respectively. After adjusting for confounders, a 10-fold increase in BPA levels was associated with a 0.63 cm [95% confidence interval (CI): 0.25 to 1.01] increase in birth length among boys, but not among girls. No associations were found between TCS levels and any birth outcomes. The positive association of prenatal low-level BPA exposures with anthropometric measures observed among boys, suggests gender differences in the response to antenatal phenol exposure. Given the variability in urinary phenol levels reported during pregnancy, our findings based on levels of the target biomarkers in a single urine sample need to be confirmed in additional studies. [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]

The use of polybrominated diphenyl ethers (PBDEs) has been dramatically increasing over the last two decades in China. Animal studies suggest that prenatal exposure to PBDEs may result in neurodevelopmental deficits. Two hundred thirty-two participating mothers were recruited from a prospective birth cohort in rural northern China between September 2010 and February 2012. We analyzed 232 cord blood specimens for selected PBDE congeners and examined their association with children's developmental quotients (DQs) at 12 ( n =192) and 24 ( n =149) months of age based on the Gesell Developmental Schedules (motor, adaptive, language, and social domains). There were no substantial differences by demographic characteristics among the three time points: baseline, 12 and 24 months of age. Median cord blood levels of PBDE congeners 47, 99, 100, and 153 were 3.71, 6.70, 2.63, and 2.19 ng/g lipid, respectively. At 12 months of age, neither the individual nor total (the sum of BDEs 47, 99, 100, and 153) congener levels were associated with any of the four domain DQs. However, at 24 months of age, a 10-fold increase in BDE-99 levels was associated with a 2.16-point decrease [95% confidence interval (CI): −4.52, −0.20] in language domain DQs and a 10-fold increase in BDE-47 levels was associated with a 1.89-point decrease (95% CI: −3.75, −0.03) in social domain DQs. Prenatal exposure to PBDEs was associated with lower DQs in young children. The results contribute to the growing evidence that PBDEs could act as developmental neurotoxicants,and the findings have implications for children's environmental health in China. [ABSTRACT FROM AUTHOR]