Changes in steroid metabolism among girls with precocious puberty may not be associated with urinary levels of bisphenol A

Lee, Su Hyeon; Kang, Se Mi; Choi, Man Ho; Lee, Jeongae; Park, Mi Jung; Kim, Shin Hye; Lee, Won Yong; Ji, Hong; Chung, Bong Chul

doi:10.1016/j.reprotox.2013.03.008

Cited by 40 publications

(20 citation statements)

References 32 publications

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“…In humans, equivocal data have been obtained. BPA excretion was not associated with changes in pubertal timing in several studies (Ferguson et al, , b,c; Lee et al, , b).…”

Section: Bisphenol Amentioning

confidence: 86%

The effect of maternal exposure to endocrine disrupting chemicals on fetal and neonatal development: A review on the major concerns

Mallozzi¹,

Bordi²,

Garo³

et al. 2016

Birth Defects Research Pt C

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There is a widespread exposure of general population, including pregnant women and developing fetuses, to the endocrine disrupting chemicals (EDCs). These chemicals have been reported to be present in urine, blood serum, breast milk, and amniotic fluid. Endocrine disruptions induced by environmental toxicants have placed a heavy burden on society, since environmental exposures during critical periods of development can permanently reprogram normal physiological responses, thereby increasing susceptibility to disease later in life-a process known as developmental reprogramming. During development, organogenesis and tissue differentiation occur through a continuous series of tightly-regulated and precisely-timed molecular, biochemical, and cellular events. Humans may encounter EDCs daily and during all stages of life, from conception and fetal development through adulthood and senescence. Nevertheless, prenatal and early postnatal windows are the most critical for proper development, due to rapid changes in system growth. Although there are still gaps in our knowledge, currently available data support the urgent need for health and environmental policies aimed at protecting the public and, in particular, the developing fetus and women of reproductive age. Birth Defects Research (Part C) 108:224-242, 2016. © 2016 Wiley Periodicals, Inc.

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“…In humans, equivocal data have been obtained. BPA excretion was not associated with changes in pubertal timing in several studies (Ferguson et al, , b,c; Lee et al, , b).…”

Section: Bisphenol Amentioning

confidence: 86%

The effect of maternal exposure to endocrine disrupting chemicals on fetal and neonatal development: A review on the major concerns

Mallozzi¹,

Bordi²,

Garo³

et al. 2016

Birth Defects Research Pt C

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“…In these studies, one of 1,151 girls 6–8 years of age (Wolff et al 2010) and another of 192 girls 9 years of age (Wolff et al 2008a), BPA exposure was not associated with accelerated breast or pubic hair development. In a study of 82 patients with precocious puberty and 32 patients without precocious puberty, BPA exposure was not associated with precocious puberty (Lee SH et al 2014). However, in a study of 110 girls with precocious puberty and 100 girls without precocious puberty, BPA was associated with increased uterine and ovarian volume (Qiao et al 2010).…”

Section: Puberty and Sexual Receptivitymentioning

confidence: 95%

Bisphenol A and Reproductive Health: Update of Experimental and Human Evidence, 2007–2013

Peretz

Vrooman

Ricke

et al. 2014

Environ Health Perspect

475

301

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Background: In 2007, an expert panel reviewed associations between bisphenol A (BPA) exposure and reproductive health outcomes. Since then, new studies have been conducted on the impact of BPA on reproduction.Objective: In this review, we summarize data obtained since 2007, focusing on a) findings from human and animal studies, b) the effects of BPA on a variety of reproductive end points, and c) mechanisms of BPA action.Methods: We reviewed the literature published from 2007 to 2013 using a PubMed search based on keywords related to BPA and male and female reproduction.Discussion: Because BPA has been reported to affect the onset of meiosis in both animal and in vitro models, interfere with germ cell nest breakdown in animal models, accelerate follicle transition in several animal species, alter steroidogenesis in multiple animal models and women, and reduce oocyte quality in animal models and women undergoing in vitro fertilization (IVF), we consider it an ovarian toxicant. In addition, strong evidence suggests that BPA is a uterine toxicant because it impaired uterine endometrial proliferation, decreased uterine receptivity, and increased implantation failure in animal models. BPA exposure may be associated with adverse birth outcomes, hyperandrogenism, sexual dysfunction, and impaired implantation in humans, but additional studies are required to confirm these associations. Studies also suggest that BPA may be a testicular toxicant in animal models, but the data in humans are equivocal. Finally, insufficient evidence exists regarding effects of BPA on the oviduct, the placenta, and pubertal development.Conclusion: Based on reports that BPA impacts female reproduction and has the potential to affect male reproductive systems in humans and animals, we conclude that BPA is a reproductive toxicant.Citation: Peretz J, Vrooman L, Ricke WA, Hunt PA, Ehrlich S, Hauser R, Padmanabhan V, Taylor HS, Swan SH, VandeVoort CA, Flaws JA. 2014. Bisphenol A and reproductive health: update of experimental and human evidence, 2007–2013. Environ Health Perspect 122:775–786; http://dx.doi.org/10.1289/ehp.1307728

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“…In humans, equivocal data have been obtained. BPA excretion was not associated with changes in pubertal timing in several studies (11)(12)(13). Increased urinary BPA levels were observed either in precocious puberty (14) or in relation with late menarche (15).…”

mentioning

confidence: 88%

Delayed Neuroendocrine Sexual Maturation in Female Rats After a Very Low Dose of Bisphenol A Through Altered GABAergic Neurotransmission and Opposing Effects of a High Dose

et al. 2016

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Rat sexual maturation is preceded by a reduction of the interpulse interval (IPI) of GnRH neurosecretion. This work aims at studying disruption of that neuroendocrine event in females after early exposure to a very low dose of bisphenol A (BPA), a ubiquitous endocrine disrupting chemical. Female rats were exposed to vehicle or BPA 25 ng/kg·d, 25 μg/kg·d, or 5 mg/kg·d from postnatal day (PND)1 to PND5 or PND15. Exposure to 25 ng/kg·d of BPA for 5 or 15 days was followed by a delay in developmental reduction of GnRH IPI studied ex vivo on PND20. After 15 days of exposure to that low dose of BPA, vaginal opening tended to be delayed. In contrast, exposure to BPA 5 mg/kg·d for 15 days resulted in a premature reduction in GnRH IPI and a trend toward early vaginal opening. RNA sequencing analysis on PND20 indicated that exposure to BPA resulted in opposing dose effects on the mRNA expression of hypothalamic genes involved in gamma aminobutyric acid A (GABAA) neurotransmission. The study of GnRH secretion in vitro in the presence of GABAA receptor agonist/antagonist confirmed an increased or a reduced GABAergic tone after in vivo exposure to the very low or the high dose of BPA, respectively. Overall, we show for the first time that neonatal exposure to BPA leads to opposing dose-dependent effects on the neuroendocrine control of puberty in the female rat. A very low and environmentally relevant dose of BPA delays neuroendocrine maturation related to puberty through increased inhibitory GABAergic neurotransmission.

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Changes in steroid metabolism among girls with precocious puberty may not be associated with urinary levels of bisphenol A

Cited by 40 publications

References 32 publications

The effect of maternal exposure to endocrine disrupting chemicals on fetal and neonatal development: A review on the major concerns

The effect of maternal exposure to endocrine disrupting chemicals on fetal and neonatal development: A review on the major concerns

Bisphenol A and Reproductive Health: Update of Experimental and Human Evidence, 2007–2013

Delayed Neuroendocrine Sexual Maturation in Female Rats After a Very Low Dose of Bisphenol A Through Altered GABAergic Neurotransmission and Opposing Effects of a High Dose

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