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Environ Int. 2018 Feb;111:279-286. doi: 10.1016/j.envint.2017.11.007. Epub 2017 Nov 15.

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

Author information

1
Department of Environmental Health, School of Public Health, Shanghai Jiao Tong University School of Medicine, Shanghai, China; School of Nursing, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
2
Department of Environmental Health, School of Public Health, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
3
MOE and Shanghai Key Laboratory of Children's Environmental Health, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
4
Department of Environmental Health, School of Public Health, Shanghai Jiao Tong University School of Medicine, Shanghai, China; MOE and Shanghai Key Laboratory of Children's Environmental Health, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. Electronic address: tianmiejp@sjtu.edu.cn.

Abstract

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.

KEYWORDS:

Cord blood; Placenta; Prenatal exposure; Reproductive hormone; Steroidogenic enzymes; Triclosan

PMID:
29150338
DOI:
10.1016/j.envint.2017.11.007
[Indexed for MEDLINE]

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