Caifeng Wang

Reproductive endocrine-disrupting effects of triclosan: Population exposure, present evidence and potential mechanisms

Triclosan has been used as a broad-spectrum antibacterial agent for over 40 years worldwide. Increasing reports indicate frequent detection and broad exposure to triclosan in the natural environment and the human body. Current laboratory studies in various species provide strong evidence for its disrupting effects on the endocrine system, especially reproductive hormones. Multiple modes of action have been suggested, including disrupting hormone metabolism, displacing hormones from hormone receptors and disrupting steroidogenic enzyme activity. Although epidemiological studies on its effects in humans are mostly negative but conflicting, which is typical of much of the early evidence on the toxicity of EDCs, overall, the evidence suggests that triclosan is an EDC. This article reviews human exposure to triclosan, describes the current evidence regarding its reproductive endocrine-disrupting effects, and discusses potential mechanisms to provide insights for further study on its endocrine-disrupting effects in humans.

Association between prenatal exposure to polybrominated diphenyl ethers and young children's neurodevelopment in China.

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 childrens 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 childrens environmental health in China.

Prenatal low-level phenol exposures and birth outcomes in China

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 0.50μg/g creatinine, respectively. After adjusting for confounders, a 10-fold increase in BPA levels was associated with a 0.63cm [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.

Exposure to polybrominated diphenyl ethers and female reproductive function: A study in the production area of Shandong, China

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 4.67ng/g lipid), followed by BDE-99 (median 3.45ng/g lipid) and BDE-28, -47, and -100 (medians near 2ng/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 ∑5PBDEs, FSH levels changed -1.19IU/L (95% confidence interval [CI]: -1.32, -1.02), -1.17IU/L (95%CI: -1.36, -1.01) and -1.26IU/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.

Association Between Organophosphate Pesticide Exposure and Thyroid Hormones in Pregnant Women

Background: Use of organophosphate pesticides (OPs) is widespread in China. Although animal studies suggested that OP exposure could affect thyroid function, little is explored in human populations. Methods: We investigated levels of OP exposure in pregnant women and the relationship between OPs and thyroid hormones in Shandong, China. We enrolled 637 pregnant women from April 2011 to December 2013. OP exposure was assessed by a questionnaire administered to the pregnant women in the hospital and by analyses of urinary dialkylphosphate (DAP) metabolites of OPs in pregnant women (n = 413). We measured the concentration of five thyroid hormones in serum samples in pregnant women (n = 325) and analyzed the association between DAP metabolites of OPs and thyroid hormones (n = 325). Results: Median levels of DAP metabolites were 9.81 &mgr;g/L for dimethylphosphate (DMP), 0.79 &mgr;g/L for dimethylthiophosphate (DMTP), 5.00 &mgr;g/L for diethylphosphate (DEP), and 0.78 &mgr;g/L for diethylthiophosphate (DETP), which were higher than those reported in developed countries. We found that the total DAP concentration (the sum of DMP, DMTP, DEP, and DETP) in urine was positively associated with free T4 levels (&bgr; = 0.137; 95% confidence interval [CI] = 0.012, 0.263) and negatively associated with thyroid-stimulating hormone levels (&bgr; = −0.145; 95% CI = −0.242, −0.048). Conclusions: The findings suggest that OP exposure may be associated with changes in thyroid function in pregnant women. Given that urinary OP levels in pregnant women in Shandong were much higher than those reported in developed countries, further studies on the effects of OP exposure on thyroid function in pregnant women in China are warranted.

Impacts of prenatal triclosan exposure on fetal reproductive hormones and its potential mechanism

BACKGROUND Triclosan (TCS) has been widely detected in pregnant women. The reproductive endocrine-disrupting effects of TCS have been observed in humans and animals. Little is known about the potential impact of prenatal TCS exposure on fetal reproductive development as well as its potential mechanism. OBJECTIVES We investigated the potential effect of prenatal TCS exposure on fetal reproductive hormones in cord blood and its potential mechanism in relation to placental steroidogenic enzymes. METHODS Urinary TCS was detected among 537 healthy pregnant women from a prospective cohort in China. Four reproductive hormones in cord blood, namely E2 (n=430), T (n=424), LH (n=428) and FSH (n=373), and three steroidogenic enzymes in placenta, namely P450arom (n=233), 3β-HSD (n=227) and 17β-HSD (n=222), were measured. RESULTS Prenatal TCS exposure was associated with increased testosterone concentrations in cord blood in a dose-dependent manner. Infants with prenatal TCS levels >0.6μg/L had, on average, a 0.23ng/mL (95% CI: 0.05, 0.45, p=0.02) higher testosterone concentrations in cord blood compared to those with prenatal TCS levels <0.1μg/L. Of note, prenatal TCS exposure was associated with increased testosterone and decreased E2 concentrations in cord blood among male infants. Adverse associations were found between the prenatal TCS exposure and concentrations of three placental steroidogenic enzymes. 3β-HSD and P450arom demonstrated mediating effects in the association between prenatal TCS exposure and testosterone concentrations in cord blood. CONCLUSIONS Our findings suggested potential impacts of prenatal TCS exposure on reproductive hormones in cord blood mediated by steroidogenic enzymes, and male infants were more vulnerable.