Endocrine-Disrupting Chemicals: Prepubertal Exposures and Effects on Sexual Maturation and Thyroid Activity in the Female Rat. A Focus on the EDSTAC Recommendations

Goldman, Jerome M.; Laws, Susan C.; Balchak, Sharon K.; Cooper, Ralph L.; Kavlock, Robert J.

doi:10.1080/10408440091159185

Cited by 145 publications

(61 citation statements)

References 289 publications

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“…The Endocrine Disruptor Screening and Testing Advisory Committee (EDSTAC) to the EPA developed a tiered screening and testing strategy. Tier 1 includes a specific pubertal female assay in rats [117][118][119][120] (Fig 2), and a pubertal male rat assay has been proposed as 1 of the alternative assays. In the pubertal female assay, weanling rats are dosed daily by gavage with the test agent for ϳ20 days.…”

Section: Assessment Of Puberty In Toxicologic Studiesmentioning

confidence: 99%

Public Health Implications of Altered Puberty Timing

et al. 2008

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Changes in puberty timing have implications for the treatment of individual children, for the risk of later adult disease, and for chemical testing and risk assessment for the population. Children with early puberty are at a risk for accelerated skeletal maturation and short adult height, early sexual debut, potential sexual abuse, and psychosocial difficulties. Altered puberty timing is also of concern for the development of reproductive tract cancers later in life. For example, an early age of menarche is a risk factor for breast cancer. A low age at male puberty is associated with an increased risk for testicular cancer according to several, but not all, epidemiologic studies. Girls and, possibly, boys who exhibit premature adrenarche are at a higher risk for developing features of metabolic syndrome, including obesity, type 2 diabetes, and cardiovascular disease later in adulthood. Altered timing of puberty also has implications for behavioral disorders. For example, an early maturation is associated with a greater incidence of conduct and behavior disorders during adolescence. Finally, altered puberty timing is considered an adverse effect in reproductive toxicity risk assessment for chemicals. Recent US legislation has mandated improved chemical testing approaches for protecting children's health and screening for endocrinedisrupting agents, which has led to changes in the US Environmental Protection Agency's risk assessment and toxicity testing guidelines to include puberty-related assessments and to the validation of pubertal male and female rat assays for endocrine screening.

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Section: Assessment Of Puberty In Toxicologic Studiesmentioning

confidence: 99%

Public Health Implications of Altered Puberty Timing

et al. 2008

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“…The individual variation in the changes of estrous cyclicity, persistent estrus or diestrus, was considered to be due to the difference of the sensitivity to the effect of EGME in each animal. Regarding the delay of puberty onset at 100 mg/kg, GnRH agonists or antagonists, dopamine receptor agonists, or estrogen antagonists are known to induce the delay of VO (Goldman et al, 2000). Considering this report, EGME possibly disrupts the HPG axis during the juvenile to peripubertal periods such as increases in gonadotropin or decreases in gonadotropin, PRL, or E 2 , which results in the delay of VO.…”

Section: Discussionmentioning

confidence: 89%

“…The experimental design including dosing period was modified according to the Endocrine Distruptor Screening and Testing Advisory Committee (EDSTAC) Tier I Female Pubertal Screening Protocol (Goldman et al, 2000). EGME was orally administered to juvenile female rats (9 animals/group) for 21 days, at a dose level of 50, 100, or 300 mg/kg from PND 21 to 41.…”

Section: Experimental Designmentioning

confidence: 99%

The effects of ethylene glycol monomethyl ether on female reproductive system in juvenile rats

et al. 2017

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-Ethylene glycol monomethyl ether (EGME), which is widely used in various industrial products, is known for adverse effects on the reproductive system in adult rats. However, the effects of EGME on reproductive development in juvenile rats have not been demonstrated. In order to investigate the effects of EGME on the female reproductive system and pubertal development in juvenile rats, EGME was administered to female Sprague Dawley rats from postnatal day 21 to 41 at a dose level of 0, 50, 100, or 300 mg/kg. The animals were examined for general condition, body weight, vaginal opening (VO), estrous cyclicity, and histopathology of reproductive organs. EGME treatment resulted in a prolonged estrous cycle interval characterized by persistent diestrus at 50 mg/kg without effects on body weight, timing of VO, or histology of the reproductive organs. EGME at 100 mg/kg induced decreases in body weight gain, a delay of VO, and irregular estrous cycle with absence of corpora lutea and hypertrophy of uterine epithelium indicating disturbance of the ovulatory process associated with hormonal effect. At 300 mg/kg, there was significant delay of puberty due to severe growth retardation. The present results revealed that irregular estrous cycle is a first indicator of the effects of EGME on the female reproductive system in juvenile rats, with delayed pubertal onset and ovulatory process disturbance at a higher dose.

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“…This resulted in a congressional mandate under the Food Quality Protection Act and Safe Drinking Water Amendments (26,27) for the U.S. EPA to develop screening programs for compounds with estrogenic and other endocrine activities. These assays were developed by the Endocrine Disruptor Screening and Testing Advisory Committee (EDSTAC) and include a series of both in vitro and in vivo bioassays that can detect endocrine-active chemicals (28,29). Figure 1 illustrates some industrial compounds that exhibit estrogenic activity.…”

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confidence: 99%

“…Human exposure to these estrogenic compounds in the diet is relatively low and is accompanied by significantly higher levels of phytoestrogens such as flavonoids, other hydroxylated aromatics present in vegetables, fruits, nuts, and other products (22). The EDSTAC has outlined several in vitro and in vivo bioassays for estrogenic compounds (28,29), and these assays can provide data on relative estrogenic potencies for individual compounds or estrogen equivalents (EQs) for mixtures (30,31). For example, we have used multiple bioassays to show that the EQs in 200 mL of red wine (30) were at least 1,000 times higher than EQs for the average daily intake of known estrogenic pesticides in the diet.…”

mentioning

confidence: 99%