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

Abstract

BackgroundTriclosan (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. ObjectivesWe 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. MethodsUrinary 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. ResultsPrenatal 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. ConclusionsOur findings suggested potential impacts of prenatal TCS exposure on reproductive hormones in cord blood mediated by steroidogenic enzymes, and male infants were more vulnerable.