Grantee Research Project Results
2017 Progress Report: Novel Methods to Assess the Effects of Chemicals on Child Development
EPA Grant Number: R835434Center: Water Innovation Network for Sustainable Small Systems
Center Director: Reckhow, David A.
Title: Novel Methods to Assess the Effects of Chemicals on Child Development
Investigators: Schantz, Susan L.
Institution: University of Illinois Urbana-Champaign
EPA Project Officer: Hahn, Intaek
Project Period: June 1, 2013 through May 31, 2018 (Extended to May 31, 2019)
Project Period Covered by this Report: June 1, 2017 through May 31,2018
Project Amount: $3,962,727
RFA: Children's Environmental Health and Disease Prevention Research Centers (with NIEHS) (2012) RFA Text | Recipients Lists
Research Category: Children's Health , Human Health
Objective:
Project 1: Joint Effects of Endocrine Disruptors, Diet and BMI on Child Development
The major goals of this project are: 1) to assess sources of exposure to phthalates, bisphenol A (BPA) and other endocrine disrupting chemicals (EDCs) during the prenatal and adolescent periods; 2) to examine the association of prenatal or adolescent exposure to phthalates, BPA and other EDCs (and interactions among these exposures) with physical, behavioral and cognitive development in infants and adolescents; 3) to assess the potential for a high fat diet (HFD)/obesity during two critical periods -- prenatal or adolescent -- to interact with chemical exposure to influence physical, behavioral and cognitive development; and 4) to investigate the association of prenatal exposure to phthalates, BPA and other EDCs with markers of oxidative stress or inflammation in maternal and cord blood. In addition, we hypothesize that associations of exposure with these outcomes will vary by child sex.
Project 2: Endocrine Disrupting Chemicals, Diet, and Gonadal Toxicity
The proposed studies were designed to test the hypothesis that bisphenol A (BPA), phthalate, and high fat diet exposure interact to increase oxidative stress in developing and adolescent gonads, leading to infertility, early reproductive senescence, and transgenerational effects on fertility in the offspring. To test this hypothesis, the following specific aims will be completed: 1) determine if high fat diet and BPA/phthalate/phthalate mixture exposure increase oxidative stress in the gonads of female and male mice, 2) determine if high fat diet and BPA/phthalate/phthalate mixture exposure destroy germ cells and cause epigenetic changes known to reduce germ cell quality in the gonads of female and male mice, and 3) determine if high fat diet and BPA/phthalate/phthalate mixture exposure cause infertility and early reproductive senescence in the F-1F3 generations in mice.
Project 3: Endocrine Disruptors and Diet: Effects on the Developing Cortex
To examine exposure to BPA or an environmentally relevant phthalate mixture crossed with a high fat diet on offspring during the perinatal or adolescent period. The end points are cognitive and emotional behaviors, neuroanatomical changes in the medial prefrontal cortex, genetic expression changes as well as levels of inflammatory cytokines.
Community Outreach and Translation Core
Aim 1. To develop a strong Community Outreach and Translation Core (COTC) that is informed by the Community Advisory Board (CAB) and Dr. Susan Korrick, the Center’s Pediatric Health Specialist, and that works bi-directionally with the PI’s of the Center. The CAB and PI’s will work together in an iterative manner using feedback from stakeholders in developing dissemination materials.
Aim 2. Through stakeholder partnerships formed in the CAB, disseminate emerging knowledge about the effects of chemical exposure and high fat diets during the prenatal period, on the developing young child, and during adolescence.
Progress Summary:
Project 1: Joint Effects of Endocrine Disruptors, Diet and BMI on Child Development
For the prospective birth cohort component of this project, the fifth reporting period has been devoted to five things: (1) continued recruitment of pregnant women into the study, (2) data collection from enrolled women throughout their pregnancies and at birth, (3) cognitive and physical assessments of offspring born to study participants, (4) preparation of the dataset collected during the earlier P20 Formative Center stage of our research for statistical analysis and publication, and (5) presentations of our work at national scientific conferences. As of August, 2018 563 pregnant women have been enrolled in the study and a total of 462 of study participants had given birth. Earlier we developed and implemented new state-of-the-art procedures for assessing cognition of infants during the first year of life. We are currently assessing cognitive functions including recognition memory, attention and information processing speed at 1-5 weeks of age, 4-5 months of age and 7-8 months of age in infants born to women in this study, and following up with mothers to assess behavior and language development in toddlers at 27-29 and 36-38 months of age. In addition, we recently started detailed assessments of physical, behavioral, cognitive and language development in the children at 46-48 months of age. All of the infant assessments are computer automated and the 4-5 and 7-8 month assessments make use of infrared eye tracking technology to track the infant’s looking behavior.
For the adolescent component of this project, our research to date has been devoted to completion of data collection. We have leveraged data from an ongoing prospective birth cohort, the New Bedford Cohort (NBC), in combination with work performed as part of our previous Children's Center. The current project, a key component of this leveraged work, was collection of urine samples (for EDC exposure measurements) on 200 NBC adolescents. We successfully completed adolescent urine sample collection and analysis. Eighty one % of adolescents examined during the data collection provided at least one urine sample and 144 (70%) of these provided 2 urines, collected approximately one week apart. As part of the parent study assessments, we have completed prospectively collected neurobehavioral assessments, home assessments, height, weight, diet, medical, demographic, lifestyle and exposure information on these 205 children all of which are key data for this project's analyses. We now have results for urine samples analyzed for ECDs at the CDC where levels of 11 common phthalate metabolites and 8 phenols (BPA, triclosan, butyl paraben, methyl paraben, propyl paraben, benzophenone-3, 2,4-dichlorophenol and 2,5-dichlorophenol) were measured as well as recent phthalate (e.g., DINCH metabolites) and BPA chemical substitutes (e.g., bisphenol S and F). We have begun finalizing the epidemiologic analyses of the association of EDC exposures with adverse neurobehavior in adolescents and recently submitted our first paper based on these finding for publication.
Project 2: Endocrine Disrupting Chemicals, Diet, and Gonadal Toxicity
First, we tested the hypothesis that prenatal exposure to DEHP disrupts ovarian functions in the F1, F2, and F3 generations of female mice. Our data indicate that in the F1 generation, prenatal exposure to DEHP disrupted body and organ weights, decreased folliculogenesis, and increased serum 17β-estradiol levels. In the F2 generation, exposure to DEHP decreased body and organ weights, dysregulated folliculogenesis, and disrupted serum progesterone levels. In the F3 generation, DEHP exposure accelerated folliculogenesis. These data suggest that prenatal exposure to DEHP leads to adverse multigenerational and transgenerational effects on ovarian function.
Second, we tested the hypothesis that prenatal exposure to DEHP accelerates the onset of puberty, disrupts birth outcomes, and reduces fertility-related indices in the F1, F2, and F3 generations of female mice. Our data indicate that in the F1 generation, prenatal DEHP exposure accelerated the onset of puberty and disrupted fertility-related indices. In the F2 generation, DEHP exposure accelerated the onset of puberty, increased the female to male sex ratio, and disrupted fertility-related indices. In the F3 generation, DEHP exposure accelerated the onset of puberty, increased the female to male sex ratio, decreased female pup anogenital index, and reduced fertility-related indices. Collectively, the data show that prenatal DEHP exposure at environmentally relevant doses accelerates the onset of puberty, disrupts birth outcomes, and disrupts fertility-related indices; thus, suggesting that DEHP causes female reproductive problems in a multigenerational and transgenerational manner.
Third, we tested the hypothesis that prenatal DEHP exposure affects follicle numbers, estrous cyclicity, and hormone levels in multiple generations of 1-year-old mice. Prenatal DEHP exposure altered estrous cyclicity (750 mg/kg/day), increased the presence of ovarian cysts (750 mg/kg/day), and decreased total follicle numbers (750 mg/kg/day) in the F1 generation. It also decreased anogenital distance (200 µg/kg/day) and altered follicle numbers (200 µg/kg/day and 500 mg/kg/day) in the F2 generation, and it altered estrous cyclicity (20 and 200 µg/kg/day, 500 and 750 mg/kg/day) and decreased folliculogenesis (200 µg/kg/day and 500 mg/kg/day) in the F3 generation. Further, prenatal DEHP increased estradiol levels (F1 and F3), decreased testosterone levels (F1, F2, and F3), decreased progesterone levels (F2), altered gonadotropin hormone levels (F1 and F3), and decreased inhibin B levels (F1 and F3). Collectively, these data show that prenatal exposure to DEHP has multi- and transgenerational effects on female reproduction, and it may accelerate reproductive aging.
Fourth, we investigated the changes in gene expression in the ovary from female mice prenatally and ancestrally exposed to DEHP in the F1, F2, and F3 generations. This led us to identify 104 genes that are upregulated and 73 genes that are downregulated by ancestral exposure to DEHP. Pathway analysis showed that the PI3K-AKT, cyclins and cell cycle regulation, and extra-cellular matrix receptor interaction pathways are altered in the F3 ovaries. Functional annotation gene clustering analysis suggested that ancestral exposure to DEHP also causes differential expression of genes important for positive regulation of cell proliferation (21 genes), negative regulation of apoptotic processes and cell death (24 genes), cellular response to hormone stimulus (14 genes), and organ morphogenesis (17 genes). Collectively, these data indicate that ancestral DEHP exposure causes transgenerational changes in the expression of genes and pathways in the ovary that are important for ovarian functions and fertility.
Fifth, we tested the hypothesis that prenatal exposure to a phthalate mixture alters sex steroid hormones in a multi- and transgenerational manner in female mice. At PND 21, prenatal phthalate mixture exposure decreased estradiol and testosterone levels, but did not affect progesterone levels in the F1 generation. At PND 60, phthalate mixture decreased estradiol, progesterone, and testosterone levels in the F1 generation. Further, ancestral phthalate mixture exposure increased estradiol levels at PND 60 in the F2 generation. Lastly, ancestral phthalate mixture exposure did not affect hormone levels at PND 21, but it increased estradiol levels and decreased progesterone and testosterone levels at PND 60 in the F3 generation. Overall, these data suggest that prenatal exposure to an environmentally relevant phthalate mixture induces some multi- and transgenerational effects on sex steroid hormone levels in female mice.
Sixth, we tested the hypothesis that maternal exposure to DEHP impairs neurobehavior and recognition memory in her male offspring via oxidative damage in the hippocampus. Our data indicate that prenatal exposure to DEHP causes elevated anxiety-like behavior and impaired recognition memory. These behavioral changes may originate from neurodegeneration caused by oxidative damage and inflammation in the hippocampus. Decreased circulating testosterone level and expression of androgen receptor in the brain may be factors contributing to the impaired neurobehavior in the DEHP mice.
Finally, we collaborated with experts on the pituitary, brain, and immune system to determine whether BPA exposure affects the pituitary, brain, and immune system. We found that BPA exposure: 1) has unique sex specific effects on gene expression and Pomc repression in males and female pituitaries that may occur through different mechanisms, 2) leads to transgenerational changes in the expression of the imprinted gene, Meg3, in the brain, and 3) modulates peritoneal macrophage function in female mice involving SYMD2-H3K36 dimethylation. Collectively, these data indicate the BPA exposure may affect reproduction through multiple pathways in the gonads, pituitary, brain, and immune system.
Project 3: Endocrine Disruptors and Diet: Effects on the Developing Cortex
Perinatal BPA
Genetic analysis: BPA increased Erα expression perinatally and this increased continued into adulthood but only in females. Epigenetic markers were not changed. MicroRNAs associated with this receptor were also not significantly affected.
Neuroanatomy: Although in the expected direction, the increase in the number of neurons and glia in the medial prefrontal cortex in BPA exposed males did not reach significance. The number of synapses is also being quantified and is nearly finished.
Perinatal Phthalate mixture
Neuroanatomy: Long term effects in neuroanatomy were found in adults following perinatal phthalate exposure: The number of neurons and synapses were decreased in both sexes in the medial prefrontal cortex. This was concordant with deficits in behavior (cognitive flexibility reported last year) that relies on the prefrontal cortex.
Perinatal high fat diet
Neuroanatomy: The number of neurons and glia were quantified in the prefrontal cortex in the animals that received a zero dose of phthalates. There was no effect detected in adults.
Overall Summary
Perinatal exposure to relatively low doses of environmentally relevant mixture of phthalates results in deficits in cognitive behavior that are aligned with a decrease both the number of neurons and the number of synapse in the medial prefrontal cortex. The effects of perinatal BPA are, in comparison, more subtle. The phthalates affect both sexes while BPA mainly affects males. There were few interactions between perinatal exposure a high fat diet and either BPA or an environmentally relevant mixture of phthalates on previous reported behavioral measures. Thus the neuroanatomical quantification concentrated on the phthalate groups.
Community Outreach and Translation Core
Expansion of the Community Advisory Board. In response to the retirement of some board members and following discussions with the remaining board members, we have expanded the board to include representation from Early Childhood. New organizations represented include: Ever Thrive Illinois: Champions for Healthy Communities (Chicago, IL); School of Healthy Studies, Northern Illinois University (DeKalb, IL)
Follow up on Child Care Provider Environmental Health Knowledge. We have continued to follow up on the interest generated from a state-wide conference that addressed environmental health in child care and a state-wide survey of child care providers, both with indicated that base knowledge about environmental influences on children’s health was very low and that there was great interest in learning more. We have conducted 40 in-depth semi-structured interviews with child care providers across the state to assess their baseline knowledge of environmental influences on children’s health. We are also working with a state-wide advocacy group with educational materials in response to a new State of Illinois rule, currently under public comment, that mandates that all child care providers receiving child care subsidies conduct annual water testing for lead.
Social Media Outreach We have an active presence on Facebook, Twitter, podcasts, and websites that is aimed at child care providers and parents.
University-Based Child and Family Policy Consortium/Society for Research in Child Behavior Webinar. Barbara Fiese, Brenda Koester, and Susan Buchanan were invited to present a webinar “Environmental Influences on Children’s Health and Development” that reached close to 150 participants. http://www.familyresiliency.illinois.edu/environmental-influences-childrens-health-and-development-webinar-available; https://www.youtube.com/watch?v=rwcXOYkw0Z8
Co-Lead PEHSU/Children’s Centers COTC “Social Media Workgroup” efforts. The goal of this group is to increase the capacity of the CEHC/PEHSU network for utilizing social media platforms for community education & outreach.
Continue Participation in Pharmaceuticals and Personal Care Products in Environment Consortium at Illinois. This consortium gathers scientists, outreach and translation professionals, and interested community members on a monthly basis for webinars and speakers that are made available to the general public.
Future Activities:
Project 1: Joint Effects of Endocrine Disruptors, Diet and BMI on Child Development
Over the coming year, we will continue to recruit pregnant women into the pregnancy and birth cohort, and will assess infants and children as they reach our designated follow up ages. We will continue to analyze data collected during the Formative P20 phase and submit additional papers for publication, and will continue to submit abstracts for presentation at national and international conferences. EDC data are now available on the adolescent cohort, thus, the focus in the coming year will be on data analyses to address study aims, as well as preparation of abstracts for presentation at scholarly meetings and manuscripts for publication.
Project 2: Endocrine Disrupting Chemicals, Diet, and Gonadal Toxicity
During the no cost extension period, we plan to finalize our work the transgenerational effects of DEHP and the phthalate mixture on female and male reproduction. Specifically, we plan to finish detailed histological evaluations of reproductive tissues collected from the F1, F2, and F3 generations. We also plan to finish measurements of sex steroid hormone levels as well as gonadotropin levels in the females and males from the F1, F2, and F3 generations. Further, we plan to investigate potential change(s) in epigenome of the affected females and males using tissues collected from the F1-F3 generations. Finally, we plan to publish the results as abstracts and manuscripts.
Project 3: Endocrine Disruptors and Diet: Effects on the Developing Cortex
A. Adolescent Phthalates. We have started the behavioral and neuroanatomical project of exposure to the phthalate mixture during adolescence. Quantifying both the behavioral and neuroanatomical effects of this exposure will take the remainder of the extension year.
B. Mechanisms for perinatal effects on neuron number. We are examining the mechanism for the lower number of neurons following perinatal exposure to the phthalate mixture. We are quantifying the number of neurons that divided at the peak of cortical neurogenesis through the BrdU marker. We also are quantifying the number of naturally dying cells (apoptosis) during the developmental pruning period. The study should be completed in the next 4 months.
C. Papers to be published. In addition to A. and B. above: 1. two papers on perinatal BPA effects, one of which is under re-review; 2. a paper on behavioral effects of the perinatal exposure to the phthalate mixture and high fat diet; 3. the paper comparing the neuroanatomical effects of perinatal high fat diet exposure.
Community Outreach and Translation Core
a) continued CAB meetings. Share with the CAB our survey and interview findings to develop new messaging and dissemination materials for child care providers. Work with CAB to develop agenda and theme for 2018 conference; b) complete research necessary to guide development of messaging to child care providers; c) develop short videos/public service announcements and accompanying educational materials, including social media messaging, targeted to child care providers and families; d) hold, in Spring 2019, a statewide conference for child care providers, advocates, and administrators, focused on environmental influences on children’s health in collaboration with state-wide partners; e) continue to co-lead Social Media Workgroup which will be developing social media message library, toolkit, and trainings throughout the year for the CEHC/PEHSU network; f) continue to Collaborate with Pharmaceuticals & Personal Care Products in the Environment Consortium at Illinois – We will continue to explore ways to work together with the group and will continue to participate in their annual Conference and monthly webinars.
References:
Journal Articles: 31 Displayed | Download in RIS Format
Other center views: | All 68 publications | 31 publications in selected types | All 31 journal articles |
---|
Type | Citation | ||
---|---|---|---|
|
Barakat R, Lin P-CP, Rattan S, Brehm ES, Canisso IF, Abosalum ME, Flaws JA, Hess R, Ko C. Prenatal exposure to DEHP induces premature reproductive senescence in male mice. Toxicological Sciences 2017;156(1):96-108. |
R835434 (2016) R835434 (2017) |
Exit Exit Exit |
|
Berger A, Ziv-Gal A, Cudiamat J, Wang W, Zhou C, Flaws JA. The effects of in utero bisphenol A exposure on the ovaries in multiple generations of mice. Reproductive Toxicology 2016;60:39-52. |
R835434 (2015) |
Exit Exit Exit |
|
Brehm E, Rattan S, Gao L, Flaws JA. Prenatal exposure to di(2-ethylhexyl) phthalate causes long-term transgenerational effects on female reproduction in mice. Endocrinology 2018;159(2):795-809. |
R835434 (2017) |
Exit Exit |
|
Drobna Z, Henriksen AD, Wolstenholme JT, Montiel C, Lambeth PS, Shang S, Harris EP, Zhou C, Flaws JA, Adli M, Rissman EF. Transgenerational effects of bisphenol A on gene expression and DNA methylation of imprinted genes in brain. Endocrinology 2018;159(1):132-144. |
R835434 (2017) |
Exit Exit |
|
Eckstrum KS, Edwards W, Banerjee A, Wang W, Flaws JA, Katzenellenbogen JA, Kim SH, Raetzman LT. Effects of exposure to the endocrine-disrupting chemical bisphenol A during critical windows of murine pituitary development. Endocrinology 2018;159(1):119-131. |
R835434 (2017) |
Exit Exit |
|
Gal A, Lin P-C, Barger AM, MacNeill AL, Ko C. Vaginal fold histology reduces the variability introduced by vaginal exfoliative cytology in the classification of mouse estrous cycle stages. Toxicologic Pathology 2014;42(8):1212-1220. |
R835434 (2013) |
Exit Exit |
|
Kiester B, Sloane S, Fujimoto E, Fiese B, Su L. What Do Childcare Providers Know about Environmental Influences on Children's Health? Implications for Environmental Health Literacy Efforts. INTERNATIONAL JOURNAL OF ENVIRONMENTAL RESEARCH AND PUBLIC HEALTH 2021;18(10):5489. |
R835434 (Final) |
Exit Exit |
|
Kougias DG, Cortes LR, Moody L, Rhoads S, Pan Y-X, Juraska JM. Effects of perinatal exposure to phthalates and a high-fat diet on maternal behavior and pup development and social play. Endocrinology 2018;159(2):1088-1105. |
R835434 (2017) |
Exit Exit |
|
Kougias DG, Sellinger EP, Willing J, Juraska JM. Perinatal exposure to an environmentally relevant mixture of phthalates results in a lower number of neurons and synapses in the medial prefrontal cortex and decreased cognitive flexibility in adult male and female rats. Journal of Neuroscience 2018;38(31):6864-6872. |
R835434 (2017) |
Exit Exit |
|
Li Q, Davila J, Kannan A, Flaws JA, Bagchi MK, Bagchi IC. Chronic exposure to bisphenol A affects uterine function during early pregnancy in mice. Endocrinology 2016;157(5):1764-1774. |
R835434 (2016) |
Exit Exit |
|
Li Q, Lawrence CR, Nowak RA, Flaws JA, Bagchi MK, Bagchi IC. Bisphenol A and phthalates modulate peritoneal macrophage function in female mice involving SYMD2-H3K36 dimethylation. Endocrinology 2018;159(5):2216-2228. |
R835434 (2017) |
Exit Exit |
|
Niermann S, Rattan S, Brehm E, Flaws JA. Prenatal exposure to di-(2-ethylhexyl) phthalate (DEHP) affects reproductive outcomes in female mice. Reproductive Toxicology 2015;53:23-32. |
R835434 (2014) R835434 (2015) |
Exit Exit Exit |
|
Oakley OR, Kim KJ, Lin PC, Barakat R, Cacioppo JA, Li Z, Whitaker A, Chung KC, Mei W, Ko C. Estradiol synthesis in gut-associated lymphoid tissue: leukocyte regulation by a sexually monomorphic system. Endocrinology 2016;157(12):4579-4587. |
R835434 (2016) |
Exit Exit |
|
Peretz J, Vrooman L, Ricke WA, Hunt PA, Ehrlich S, Hauser R, Padmanabhan V, Taylor HS, Swan SH, VandeVoort CA, Flaws JA. Bisphenol A and reproductive health: update of experimental and human evidence, 2007-2013. Environmental Health Perspectives 2014;122(8):775-786. |
R835434 (2013) R835434 (2014) R834593C001 (Final) R835436 (2014) R835436 (2015) R835436 (2017) |
|
|
Rattan S, Zhou C, Chiang C, Mahalingam S, Brehm E, Flaws JA. Exposure to endocrine disrupting chemicals during adulthood: consequences for female fertility. Journal of Endocrinology 2017;233(3):R109-R129. |
R835434 (2017) |
Exit Exit Exit |
|
Rattan S, Brehm E, Gao L, Niermann S, Flaws JA. Prenatal exposure to di(2-ethylhexyl) phthalate disrupts ovarian function in a transgenerational manner in female mice. Biology of Reproduction 2018;98(1):130-145. |
R835434 (2017) |
Exit Exit |
|
Rattan S, Brehm E, Gao L, Flaws JA. Di(2-ethylhexyl) phthalate exposure during prenatal development causes adverse transgenerational effects on female fertility in mice. Toxicological Sciences 2018;163(2):420-429. |
R835434 (2017) |
Exit Exit |
|
Richardson KA, Hannon PR, Johnson-Walker YJ, Myint MS, Flaws JA, Nowak RA. Di(2-ethylhexyl) phthalate (DEHP) alters proliferation and uterine gland numbers in the uteri of adult exposed mice. Reproductive Toxicology 2018;77:70-79. |
R835434 (2017) |
Exit Exit Exit |
|
Sellinger E, Kougias D, Drzewiecki C, Juraska J. Behavioral effects in adult rats exposed to low doses of a phthalate mixture during the perinatal or adolescent period. NEUROTOXICOLOGY AND TERATOLOGY 2020;79(106886). |
R835434 (Final) |
Exit Exit |
|
Wang W, Hafner KS, Flaws JA. In utero bisphenol A exposure disrupts germ cell nest breakdown and reduces fertility with age in the mouse. Toxicology and Applied Pharmacology 2014;276(2):157-164. |
R835434 (2013) R835434 (2014) |
Exit Exit Exit |
|
Wise LM, Sadowski RN, Kim T, Willing J, Juraska JM. Long-term effects of adolescent exposure to Bisphenol A on neuron and glia number in the rat prefrontal cortex: differences between the sexes and cell type. Neurotoxicology 2016;53:186-192. |
R835434 (2014) R835434 (2015) |
Exit Exit Exit |
|
Wise LM, Hernández-Saavedra D, Boas SM, Pan YX, Juraska JM. Perinatal high-fat diet and bisphenol A:effects on behavior and gene expression in the medial prefrontal cortex. Developmental Neuroscience 2018;21:1-16. |
R835434 (Final) |
Exit Exit |
|
Yazdy MM, Coull BA, Gardiner JC, Aguiar A, Calafat AM, Ye X, Schantz SL, Korrick SA. A possible approach to improving the reproducibility of urinary concentrations of phthalate metabolites and phenols during pregnancy. Journal of Exposure Science & Environmental Epidemiology 2018;28(5):448-460. |
R835434 (2017) R835434 (Final) |
Exit Exit |
|
Zhou C, Wang W, Peretz J, Flaws JA. Bisphenol A exposure inhibits germ cell nest breakdown by reducing apoptosis in cultured neonatal mouse ovaries. Reproductive Toxicology 2015;57:87-99. |
R835434 (2014) R835434 (2015) |
Exit Exit Exit |
|
Zhou C, Gao L, Flaws JA. Exposure to an environmentally relevant phthalate mixture causes transgenerational effects on female reproduction in mice. Endocrinology 2017;158(6):1739-1754. |
R835434 (2016) |
Exit Exit |
|
Zhou C, Flaws JA. Effects of an environmentally relevant phthalate mixture on cultured mouse antral follicles. Toxicological Sciences 2017;156(1):217-229. |
R835434 (2016) |
Exit Exit |
|
Zhou C, Gao L, Flaws JA. Prenatal exposure to an environmentally relevant phthalate mixture disrupts reproduction in the F1 female mice. Toxicology and Applied Pharmacology 2017;318:49-57. |
R835434 (2016) |
Exit Exit Exit |
|
Ziv-Gal A, Wang W, Zhou C, Flaws JA. The effects of in utero bisphenol A exposure on reproductive capacity in several generations of mice. Toxicology and Applied Pharmacology 2015;284(3):354-362. |
R835434 (2014) R835434 (2015) |
Exit Exit Exit |
|
Ziv-Gal A, Flaws JA. Evidence for bisphenol A-induced female infertility: a review (2007-2016). Fertility and Sterility 2016;106(4):827-856. |
R835434 (2016) |
Exit Exit Exit |
|
Strakovsky RS, Schantz SL. Impacts of bisphenol A (BPA) and phthalate exposures on epigenetic outcomes in the human placenta. Environmental Epigenetics 2018;4(3):dvy022 (18 pp.). |
R835434 (2017) |
Exit Exit Exit |
|
Strakovsky RS, Schantz SL. Using experimental models to assess effects of bisphenol A (BPA) and phthalates on the placenta:challenges and perspectives. Toxicological Sciences 2018 |
R835434 (2017) |
Exit |
Supplemental Keywords:
Adolescent health, bisphenol A, BPA, children's health, cognition, endocrine disruptors, epidemiology, growth, neurobehavior, phenols, phthalates, prenatal exposure, ovary, testis, gonads, oxidative stress, diet, indoor air, food, beverages, plastics, cleaning products, personal care products, manufactured fragrances and scents, packaging, exposure, health effects, human health, metabolism, vulnerability, sensitive populations, infants, children, age, diet, sex, susceptibility, cumulative effects, chemicals, toxics, EDCs, endocrine-disrupting chemicals, public policy, survey, preferences, administrative policies and procedures, social science, epidemiology, public health, early care and education, child development, communication, interviews, observation, science translation, Great Lakes, Midwest, Illinois, EPA Region 5, Mississippi River watershed, child care, plastics manufacturing, food processing, pediatricsRelevant Websites:
http://ikids.beckman.illinois.edu Exit
http://familyresiliency.illinois.edu/research/COTC Exit Exit
Progress and Final Reports:
Original AbstractThe perspectives, information and conclusions conveyed in research project abstracts, progress reports, final reports, journal abstracts and journal publications convey the viewpoints of the principal investigator and may not represent the views and policies of ORD and EPA. Conclusions drawn by the principal investigators have not been reviewed by the Agency.
Project Research Results
- Final Report
- 2016 Progress Report
- 2015 Progress Report
- 2014 Progress Report
- 2013 Progress Report
- Original Abstract
31 journal articles for this center