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O30-1 Maternal exposure to endocrine disrupting chemicals (perfluoro-alkyls, phthalates and pcb/dioxins) and children’s reproductive hormone levels at birth; the hokkaido study on environment and children’s health
  1. Reiko Kishi,
  2. Atsuko Araki,
  3. Chihiro Miyashita,
  4. Sachiko Itoh,
  5. Houman Goudarzi
  1. Hokkaido University Centre for Environmental and Health Sciences, Sapporo, Japan

Abstract

Perinatal period is very important for the growth of fetuses. Disrupted endocrine environment during the perinatal period is considered to influence on the reproductive health in adulthood. The present study aimed to investigate the effects of prenatal exposure to perfluoro-alkyls, phthalates, and PCB/dioxins on fetal reproductive hormones. Among 514 participants of the Sapporo cohort in Hokkaido, JAPAN, 447 maternal blood samples were available for the PFOS/PFOA measurements. We also measured 493 samples for MEHP (the first metabolite of DEHP) and 426 samples for 17 PCDDs/PCDFs and 12 DL-PCB congeners. Two hundreds ninety-five infant cord samples were available for reproductive hormone measurements. We analysed cord blood levels of estradiol (E2), testosterone (T), progesterone (P4), cortisol, cortisone, DHEA, androstenedione, LH, FSH, SHBG, prolactin (PRL), inhibin B, and INSL3. The participants completed a self-administered questionnaire regarding information on maternal demographic characteristics. Medical records were obtained at delivery for information regarding maternal pregnancy complications, gestational ages, congenital anomalies, and infant gender and weight. In the fully adjusted linear regression analyses of the male infants, maternal PFOS levels were positively associated with E2 and reduced levels of T/E2, P4, and inhibin B. Among the female infants, there were significant inverse associations between PFOS levels and P4 and PRL levels. We also found a dose-response relationship of prenatal PFOS exposure with glucocorticoid and DHEA levels. Similarly, maternal MEHP levels were found to be associated with P4, inhibin B, and INSL3 for males only. Regarding dioxin-like compounds (DLCs), significant inverse associations were found between cord blood levels of PRL and Inhibin B, as well as DHEA among males. We found marginal correlations with DLCs and T/„E2 among females. As conclusions, these results suggest that fetal synthesis and secretion of reproductive hormones may be affected by in utero exposure to our background level of perfluoro-alkyls, phtalates and PCB/dioxins.

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