In utero effects of chemicals on reproductive tissues in females

Miller, Kimberly P.; Borgeest, Christina; Greenfeld, Chuck; Tomic, Dragana; Flaws, Jodi A.

doi:10.1016/j.taap.2003.07.016

Cited by 94 publications

(50 citation statements)

References 151 publications

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“…During early pregnancy, when organs are developing, the fetus is especially vulnerable. Maternal chemical exposures can, therefore, significantly affect fetal development by compromising placental development and exchange, as well as hormonal signaling needed for in utero fetal growth (Miller et al 2004). PAHs can affect in utero fetal development by binding to the aryl hydrocarbon receptor (AhR) causing anti-estrogenic activity, through increased metabolism and depletion of endogenous estrogens, (Carpenter et al 2002) thus disrupting the endocrine system by altering steroid function.…”

Section: Discussionmentioning

confidence: 99%

Biomarkers of exposure to combustion by-products in a human population in Shanxi, China

Naufal

Zhu

et al. 2009

J Expo Sci Environ Epidemiol

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Emissions of complex mixtures of polycyclic aromatic hydrocarbons (PAHs) and other compounds into the environment represent a potential threat to the health of humans. Information regarding the dose and duration of exposure is essential to determine the degree of risk and to identify sensitive receptors within a population. Although measurements of chemical concentrations in air may be used to estimate exposures, internal biomarkers provide more accurate information regarding the dose of exposure and retention of toxic chemicals. This study was conducted in a population in rural China exposed to PAHs from a variety of sources. The study population was located in an area known to have an elevated incidence of birth defects. Parents of children born with a neural tube defect (NTD) were recruited as case participants and parents of children born with no visible birth defect were recruited as controls. The study was designed to test the hypothesis that parents of children born with a NTD would exhibit a biomarker of exposure at higher levels than the parents of a child with no visible birth defect. A total of 35 mothers and 32 fathers were recruited as case participants, and 18 mothers and 19 fathers were recruited as control participants. Venous blood was collected from the study participants by hospital staff as soon as possible following the birth of the child. PAHs were isolated from the whole blood by solvent extraction and DNA was isolated from a separate aliquot of blood for 32 Ppostlabeling to measure bulky adducts. Single Nucleotide Polymorphisms (SNPs) in phase II enzymes were also monitored in an attempt to identify sensitive receptors. Both total and carcinogenic PAH (cPAH) concentrations were elevated in the parents of case children. Both values were elevated significantly in mothers, whereas only cPAH concentrations were elevated significantly in fathers. Levels of DNA adducts were highly variable and displayed a reverse pattern to that of PAH levels in blood. None of the polymorphisms evaluated were correlated with PAH levels or DNA adducts. For mothers, whose total PAH concentration was above the median concentration, the age-adjusted odds ratio (OR) for having a child with a NTD was 8.7. Although this suggests that PAHs may be a contributing factor to the risk of NTDs, the lack of a correlation with DNA adducts would suggest a possible non-genotoxic mechanism. Alternatively, the PAHs may be a surrogate for a different exposure that is more directly related to the birth defects. The results have shown that blood levels of PAHs may be used to identify populations exposed to elevated concentrations of combustion by-products.

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Section: Discussionmentioning

confidence: 99%

Biomarkers of exposure to combustion by-products in a human population in Shanxi, China

Naufal

Zhu

et al. 2009

J Expo Sci Environ Epidemiol

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“…DMBA and BAP) that indirectly may alter levels of hormones by depleting follicles before they reach the steroid-producing antral stage. The topic of PAHinduced depletion of preantral follicles has been briefly reviewed elsewhere (Miller et al 2004). One study using isolated preantral follicles from rats showed that treatment with BAP (R1.5 ng/ml) inhibited follicular growth, and decreased E 2 and anti-Mü llerian hormone output (Neal et al 2010).…”

Section: Polycyclic Aromatic Hydrocarbonsmentioning

confidence: 99%

Endocrine-disrupting chemicals in ovarian function: effects on steroidogenesis, metabolism and nuclear receptor signaling

Craig¹,

Wang²,

Flaws³

2011

Reproduction

Self Cite

225

123

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Endocrine-disrupting chemicals (EDCs) are exogenous agents with the ability to interfere with processes regulated by endogenous hormones. One such process is female reproductive function. The major reproductive organ in the female is the ovary. Disruptions in ovarian processes by EDCs can lead to adverse outcomes such as anovulation, infertility, estrogen deficiency, and premature ovarian failure among others. This review summarizes the effects of EDCs on ovarian function by describing how they interfere with hormone signaling via two mechanisms: altering the availability of ovarian hormones, and altering binding and activity of the hormone at the receptor level. Among the chemicals covered are pesticides (e.g. dichlorodiphenyltrichloroethane and methoxychlor), plasticizers (e.g. bisphenol A and phthalates), dioxins, polychlorinated biphenyls, and polycyclic aromatic hydrocarbons (e.g. benzo[a]pyrene).

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“…When prescribed to pregnant mothers, DES adversely affected When considering the female reproductive system of DES-exposed individuals, abnormalities were primarily manifested within the reproductive tract (vagina, cervix, uterus, and oviduct). To a limited extent these abnormalities present in the form of malignant tumors, whereas, to larger extent reproductive tract malformations, reproductive dysfunction, and poor pregnancy outcomes have been documented (reviewed in [121,122]). …”

Section: -Effects Of Estrogenic and Anti-androgenic Endocrine Disrupmentioning

confidence: 99%

“…To a limited extent these abnormalities present in the form of malignant tumors, whereas, to larger extent reproductive tract malformations, reproductive dysfunction, and poor pregnancy outcomes have been documented (reviewed in [121,122]). …”

Section: A-estrogenic Endocrine Disruptorsmentioning

confidence: 99%

Developmental exposure to environmental endocrine disruptors: Consequences within the ovary and on female reproductive function☆

Uzumcu

Zachow

2007

Reproductive Toxicology

114

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Female reproductive function depends upon the exquisite control of ovarian steroidogenesis that enables folliculogenesis, ovulation, and pregnancy. These mechanisms are set during fetal and/or neonatal development and undergo phases of differentiation throughout pre-and post-pubescent life. Ovarian development and function are collectively regulated by a host of endogenous growth factors, cytokines, gonadotropins, and steroid hormones as well as exogenous factors such as nutrients and environmental agents. Endocrine disruptors represent one class of environmental agent that can impact female fertility by altering ovarian development and function, purportedly through estrogenic, anti-estrogenic, and/or anti-androgenic effects. This review discusses ovarian development and function and how these processes are affected by some of the known estrogenic and anti-androgenic endocrine disruptors. Recent information suggests not only that exposure to endocrine disruptors during the developmental period causes reproductive abnormalities in adult life but also that these abnormalities are transgenerational. This latter finding adds another level of importance for identifying and understanding the mechanisms of action of these agents. 1-IntroductionThe primary function of an adult ovary is to produce the steroid and protein hormones needed to support (1) the development and maturation of ovarian follicles (i.e., folliculogenesis) including oocytes, (2) ovulation, and (3) the initiation and maintenance of pregnancy in mammals. In order for this to collectively occur, the secretion of ovarian hormones is tightly regulated by the neuroendocrine system and is locally controlled by many intraovarian feedback mechanisms (reviewed in [1]).Two major developmental events within the ovary are follicular assembly (i.e., the formation of primordial follicles) and the primordial-to-primary follicle transition (the "initial" recruitment) [1]. The initial phase of folliculogenesis is regulated by paracrine growth factors Correspondence: Dr. Mehmet Uzumcu, Department of Animal Sciences, School of Environmental and Biological Sciences, Rutgers, The State University of New Jersey, 84 Lipman Drive, New Brunswick, NJ Supported by NIH grant R21 ES013854-01A1 (MU) and funds from Robert Wood Johnson Medical School-UMDNJ (RZ).Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author ManuscriptReprod Toxicol. Author manuscript; available in PMC 2007 August 21. Published in final edited form as:Reprod Toxicol. 2007 ; 23(3): 337-352. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-...

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In utero effects of chemicals on reproductive tissues in females

Cited by 94 publications

References 151 publications

Biomarkers of exposure to combustion by-products in a human population in Shanxi, China

Biomarkers of exposure to combustion by-products in a human population in Shanxi, China

Endocrine-disrupting chemicals in ovarian function: effects on steroidogenesis, metabolism and nuclear receptor signaling

Developmental exposure to environmental endocrine disruptors: Consequences within the ovary and on female reproductive function☆

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