Sachiko Itoh1, Atsuko Araki1, Takahiko Mitsui2, Chihiro Miyashita1, Houman Goudarzi1, Seiko Sasaki3, Kazutoshi Cho4, Hiroyuki Nakazawa5, Yusuke Iwasaki5, Nobuo Shinohara6, Katsuya Nonomura7, Reiko Kishi8. 1. Center for Environmental Health and Sciences, Hokkaido University, Sapporo, Japan. 2. Department of Urology, Hokkaido University Hospital, Sapporo, Japan. 3. Department of Public Health, Hokkaido University Graduate School of Medicine, Sapporo, Japan. 4. Department of Obstetrics and Genecology, Hokkaido University Hospital, Sapporo, Japan. 5. Department of Analytical Chemistry, Faculty of Pharmaceutical Sciences, Hoshi University, Tokyo, Japan. 6. Department of Renal and Genitourinary Surgery, Hokkaido University Graduate School of Medicine, Sapporo, Japan. 7. Department of Renal and Genitourinary Surgery, Hokkaido University Graduate School of Medicine, Sapporo, Japan; Kushiro Rosai Hospital, Kushiro, Japan. 8. Center for Environmental Health and Sciences, Hokkaido University, Sapporo, Japan. Electronic address: rkishi@med.hokudai.ac.jp.
Abstract
BACKGROUND: Exposure to perfluoroalkyl substances (PFASs) may disrupt reproductive function in animals and humans. Although PFASs can cross the human placental barrier, few studies evaluated the effects of prenatal PFAS exposure on the fetus' reproductive hormones. OBJECTIVE: To explore the associations of prenatal exposure to perfluorooctane sulfonate (PFOS) and perfluorooctanoate (PFOA) with cord blood reproductive hormones. METHODS: In the prospective birth cohort (Sapporo cohort of the Hokkaido study), we included 189 mother-infant pairs recruited in 2002-2005 with both prenatal maternal and cord blood samples. PFOS and PFOA levels in maternal blood after the second trimester were measured via liquid chromatography-tandem mass spectrometry. We also measured cord blood levels of the fetuses' reproductive hormones, including estradiol (E2), total testosterone (T), progesterone (P4), inhibin B, insulin-like factor 3, steroid hormone binding globulin, follicle-stimulating hormone, and luteinizing hormone, and prolactin (PRL). RESULTS: The median PFOS and PFOA levels in maternal serum were 5.2ng/mL and 1.4ng/mL, respectively. In the fully adjusted linear regression analyses of the male infants, maternal PFOS levels were significantly associated with E2 and positively, and T/E2, P4, and inhibin B inversely; PFOA levels were positively associated with inhibin B levels. Among the female infants, there were significant inverse associations between PFOS levels and P4 and PRL levels, although there were no significant associations between PFOA levels and the female infants' reproductive hormone levels. CONCLUSIONS: These results suggest that the fetal synthesis and secretion of reproductive hormones may be affected by in utero exposure to measurable levels of PFOS and PFOA.
BACKGROUND: Exposure to perfluoroalkyl substances (PFASs) may disrupt reproductive function in animals and humans. Although PFASs can cross the human placental barrier, few studies evaluated the effects of prenatal PFAS exposure on the fetus' reproductive hormones. OBJECTIVE: To explore the associations of prenatal exposure to perfluorooctane sulfonate (PFOS) and perfluorooctanoate (PFOA) with cord blood reproductive hormones. METHODS: In the prospective birth cohort (Sapporo cohort of the Hokkaido study), we included 189 mother-infant pairs recruited in 2002-2005 with both prenatal maternal and cord blood samples. PFOS and PFOA levels in maternal blood after the second trimester were measured via liquid chromatography-tandem mass spectrometry. We also measured cord blood levels of the fetuses' reproductive hormones, including estradiol (E2), total testosterone (T), progesterone (P4), inhibin B, insulin-like factor 3, steroid hormone binding globulin, follicle-stimulating hormone, and luteinizing hormone, and prolactin (PRL). RESULTS: The median PFOS and PFOA levels in maternal serum were 5.2ng/mL and 1.4ng/mL, respectively. In the fully adjusted linear regression analyses of the male infants, maternal PFOS levels were significantly associated with E2 and positively, and T/E2, P4, and inhibin B inversely; PFOA levels were positively associated with inhibin B levels. Among the female infants, there were significant inverse associations between PFOS levels and P4 and PRL levels, although there were no significant associations between PFOA levels and the female infants' reproductive hormone levels. CONCLUSIONS: These results suggest that the fetal synthesis and secretion of reproductive hormones may be affected by in utero exposure to measurable levels of PFOS and PFOA.
Authors: Julia E Rager; Jacqueline Bangma; Celeste Carberry; Alex Chao; Jarod Grossman; Kun Lu; Tracy A Manuck; Jon R Sobus; John Szilagyi; Rebecca C Fry Journal: Reprod Toxicol Date: 2020-02-23 Impact factor: 3.143