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The Association of Prenatal Exposure to Perfluorinated Chemicals with Glucocorticoid and Androgenic Hormones in Cord Blood Samples : The Hokkaido Study

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Title: The Association of Prenatal Exposure to Perfluorinated Chemicals with Glucocorticoid and Androgenic Hormones in Cord Blood Samples : The Hokkaido Study
Authors: Goudarzi, Houman Browse this author →KAKEN DB
Araki, Atsuko Browse this author →KAKEN DB
Itoh, Sachiko Browse this author →KAKEN DB
Sasaki, Seiko Browse this author →KAKEN DB
Miyashita, Chihiro Browse this author →KAKEN DB
Mitsui, Takahiko Browse this author →KAKEN DB
Nakazawa, Hiroyuki Browse this author →KAKEN DB
Nonomura, Katsuya Browse this author →KAKEN DB
Kishi, Reiko Browse this author →KAKEN DB
Issue Date: Jan-2017
Publisher: National Institute of Environmental Health Sciences, National Institutes of Health, U.S. Department of Health and Human Services
Journal Title: Environmental Health Perspectives
Volume: 125
Issue: 1
Start Page: 111
End Page: 118
Publisher DOI: 10.1289/EHP142
Abstract: Background: Perfluorinated chemicals (PFCs) disrupt cholesterol homeostasis. All steroid hormones are derived from cholesterol, and steroid hormones such as glucocorticoids and androgenic hormones mediate several vital physiologic functions. However, the in utero effects of PFCs exposure on the homeostasis of these steroid hormones are not well understood in humans. Objectives: We examined the relationship between prenatal exposure to perfluorooctane sulfonate (PFOS)/perfluorooctanoate (PFOA) and cord blood levels of glucocorticoid and androgenic hormones. Methods: We conducted a hospital-based birth cohort study between July 2002 and October 2005 in Sapporo, Japan (n = 514). In total, 185 mother-infant pairs were included in the present study. Prenatal PFOS and PFOA levels in maternal serum samples were measured using liquid chromatography-tandem mass spectrometry (LC-MS-MS). Cord blood levels of glucocorticoid (cortisol and cortisone) and androgenic hormones [dehydroepiandrosterone (DHEA) and androstenedione] were also measured in the same way. Results: We found a dose-response relationship of prenatal PFOS, but not PFOA, exposure with glucocorticoid levels after adjusting for potential confounders. Cortisol and cortisone concentrations were -23.98-ng/mL (95% CI: -0.47.12, -11.99; p for trend = 0.006) and -63.21-ng/mL (95% CI: -132.56, -26.72; p for trend < 0.001) lower, respectively, in infants with prenatal PFOS exposure in the fourth quartile compared with those in the first quartile. The highest quartile of prenatal PFOS exposure was positively associated with a 1.33-ng/mL higher DHEA level compared with the lowest quartile (95% CI: 0.17, 1.82; p for trend = 0.017), whereas PFOA showed a negative association with DHEA levels (quartile 4 vs. quartile 1: -1.23 ng/mL, 95% CI: -1.72, -0.25; p for trend = 0.004). We observed no significant association between PFCs and androstenedione levels. Conclusions: Our results indicate that prenatal exposure to PFCs is significantly associated with glucocorticoid and DHEA levels in cord blood.
Type: article
Appears in Collections:環境健康科学研究教育センター (Center for Environmental and Health Sciences) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: Houman Goudarzi

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