Grantee Research Project Results
2013 Progress Report: The UCSF Pregnancy Exposures to Environmental Chemicals (PEEC) Children's Center
EPA Grant Number: R835433Center: Center for Integrative Research on Childhood Leukemia and the Environment - 2015
Center Director: Metayer, Catherine
Title: The UCSF Pregnancy Exposures to Environmental Chemicals (PEEC) Children's Center
Investigators: Woodruff, Tracey J. , Gould, Robert , Fisher, Susan J. , Zlatnik, Marya , McMaster, Michael , Stotland, Naomi , Sutton, Patrice , Morello-Frosch, Rachel , Gerona, Roy , Sen, Saunak
Current Investigators: Woodruff, Tracey J.
Institution: University of California - San Francisco
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, 2013 through May 31,2014
Project Amount: $3,312,848
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:
R835433C001: Modeling the Effects of EDCs on Early Stages of Human Placental Development
The hypothesis of our PEEC Children’s Center is that environmental chemical exposures have harmful effects on human in utero development and on children’s health. Project 1 brings together a team of basic scientists who are investigating the impact of polybrominated diphenyl ether‐47 (PBDE‐47), a flame retardant, and perfluorooctanoic acid (PFOA), a repellent, on formation of the human placenta. The goal of the project is to map, at high resolution, the effects of these chemicals on the transcriptome (Aim 1), the epigenome (Aim 2) and the functional consequences of the alterations we observe (Aim 3). In Aim 1, we will use our in vitro model of human placentation and an unbiased approach, RNA‐seq, to understand the pathways in which PBDE‐47 and/or PFOA are working in terms of effects on trophoblast function. Aim 2 uses the same experimental design to carry out a comprehensive analysis of the effects of these chemicals on histone modifications and DNA methylation. Finally, in Aim 3, we will study the functions of molecules that are targets of the environmental chemicals of interest and which we suspect play important roles in human placental development. These experiments will employ functional and molecular analyses that will allow us to phenotype human trophoblast cells and their defining properties in relation to environmental chemical exposures.
R835433C002: Mid‐Gestational Exposure to EDCs and Effects on Placental Development
Our project tests the hypotheses that (1) polybrominated diphenyl ethers (PBDEs), perfluorinated chemicals (PFCs) and select environmental organic acids (EOAs) accumulate differently in human fetuses than in pregnant women during the second trimester of pregnancy; and (2) these chemical exposures negatively impact placental development and function, an important outcome that can adversely affect in utero growth, prenatal development, birth weight, and thus, childhood and adult health. Compelling scientific data show that human in utero development is highly susceptible to disruption by exposure to chemicals, in particular endocrine disrupting agents, but a major impediment to understanding these risks is the lack of human data on fetal exposures and on the mechanisms by which chemicals can adversely impact in utero development. Through our work as a Formative Center, we provided some of the first human data characterizing mid‐gestation chemical exposures and mechanisms of adverse effects.
Specifically, we detected PBDEs, PFCs and EOAs such as bisphenol‐A (BPA) in 99–100% of the pregnant women and 95–100% of fetuses (liver and umbilical cord blood) in our study population. In addition, in vitro experiments that employed our novel human trophoblast progenitor cell (TBPC) model of placental development demonstrated that environmentally relevant doses of PBDE‐47 (a PBDE congener) compromised TBPC self‐renewal in an undifferentiated state while promoting differentiation (see Project 1, Aim 1). Both effects are hallmarks of poor placental development and have been shown to be risk factors for reduced fetal growth, preterm delivery and preeclampsia. Our project will significantly advance this promising line of research to include a larger sample size, a more diverse set of biological specimens and a wider range of measured chemicals. We will also test the impact of these chemicals on in utero development by assessing the relationship between direct measures of chemical exposure and morphological and molecular markers that enable an assessment of placentation. Accordingly, our specific aims are to:
- Compare maternal serum, placenta and fetal liver levels of a broad range of chemicals through traditional and novel biomonitoring approaches. We will collect matched biological specimens from 130 pregnant women obtaining elective second trimester pregnancy terminations (excluding cases in which pregnancies are complicated by fetal anomalies or maternal smoking). We will analyze the samples for 17 PBDEs and 12 PFCs. We will also use a novel biomonitoring approach based on Time‐of‐Flight Liquid Chromatography‐Mass Spectrometry (LC‐QTOF/MS) combined with traditional analytic methods to identify and quantify exposure to the five most frequently detected EOAs in our study population. We will compare measurements of these 34 chemicals in maternal serum to those in the placenta and fetal liver. Thus, at the conclusion of these experiments, we will have a much broader understanding of the most significant environmental chemical exposures during pregnancy and the relationships between levels detected in the maternal blood, placenta and fetus.
- Evaluate the relationship between placental disruption and exposure to PBDEs, PFCs and select EOAs. We will measure known morphological and molecular markers of placental development in the second trimester placentas that are collected in Aim 1. Then we will evaluate the relationship of these markers to individual and cumulative metrics of PBDE, PFC and EOA exposure measured in the same placental samples. Additionally, the goal of Project 1 is to identify novel PBDE and PFC placental targets (specifically, PBDE‐47 and PFOA, respectively). In Aim 3 of that Project, we will also evaluate the relationship between these endpoints, which will be analyzed in the same placental samples, and individual and cumulative metrics of PBDE, PFC and EOA exposure. Thus, at the conclusion of these experiments, we will have important new information about the placental effects of endocrine disrupting chemicals.
Working with our Community Outreach and Translation Core, we will translate our findings to the clinical and policy communities, thus providing key inputs for improving public policy approaches to identifying, assessing and preventing human risks from these endocrine disrupting chemicals.
R835433C003: Effects of EDCs and Chronic Psychosocial Stress on Fetal Growth
This project will examine the hypothesis that prenatal exposures to endocrine disrupting chemicals (EDCs) affect fetal growth outcomes such as birth weight and small for gestational age (SGA), and whether these adverse effects are magnified by chronic psychosocial stress. We will conduct a prospective study in an economically and ethnically diverse group of pregnant women in order to evaluate two important types of environmental exposures: (1) EDCs—polybrominated diphenyl ethers (PBDEs) and perfluorinated chemicals (PFCs); and (2) chronic psychosocial stress, using objective and subjective measures of participants’ perceived stress, social standing, physical and social environments, and biomarkers of chronic stress response. We hypothesize that exposure to both EDCs and stress may have synergistic effects on fetal growth. Accordingly, this project has three specific aims:
- Evaluate the relationship between prenatal PBDE and PFC exposures and birth weight. Hypothesis: Higher levels of PBDEs and PFCs in maternal serum are independently associated with lower birth weight and SGA, and concurrent exposures to these two classes of compounds have cumulative effects on birth weight. We will measure PBDEs and PFCs in serum from pregnant women (N = 450) during their second trimester and collect demographic, pregnancy history and birth outcome data at delivery to analyze the following outcomes: (1) birth weight, (2) low birth weight (less than 2500 grams), and (3) SGA (birth weight less than the 10th percentile for the infant’s gestational age based on growth curves accounting for race/ethnicity and sex).
- Evaluate the relationship between measures of chronic psychosocial stress in the maternal‐fetal unit and birth weight outcomes. Hypothesis: Exposures to chronic stress is associated with lower birth weight and SGA. We will collect three types of chronic stress measurements: 1) metrics based on participants’ perceptions of their social standing and their chronic stress exposures in household, neighborhood and work environments; 2) geocoded metrics of neighborhood socioeconomic status and civic engagement capacity; and 3) biological markers of chronic stress response in the maternal‐fetal unit, including telomere length in umbilical cord leukocytes and corticotropin releasing hormone (CRH) levels in maternal plasma. We will examine whether fetal and maternal biomarkers of stress response mediate the relationship between perceptual and geocoded measures of chronic stress exposure and adverse birth weight effects.
- Assess whether exposure to chronic psychosocial stress in the maternal‐fetal unit modifies the relationship between PBDE and PFC exposures and birth weight outcomes. Hypothesis: The effects of prenatal PBDE and PFC exposures on birth weight are modified by exposure to chronic stress in the maternal‐fetal unit. We will evaluate potential interactions between the chemical exposures and chronic stress exposure on birth weight. Our approach to modeling chemical and chronic stress exposures will be informed by our analytical results from Aims 1 and 2.
The ethnic and economic diversity of our study population will provide a unique advantage for enhancing scientific understanding about the range of prenatal exposures to persistent and ubiquitous EDCs and their effects on fetal growth.
Core A: Community Outreach and Translation Core (COTC)
Aim 1: Communicate the science broadly;
Aim 2: Harness the evolving science to health care;
Aim 3: Advance prevention‐based public policy
Core B: Administrative Core
Aim 1: Provide the administrative support for the Center.
Aim 2: Facilitate the communication and interactions within and outside of the Center.
Aim 3: Facilitate the career development and mentoring of the Faculty Development Investigator (FDI) and junior researchers.
Aim 4: Monitor the progress toward achieving the Center’s goals.
Progress Summary:
R835433C001: Modeling the Effects of EDCs on Early Stages of Human Placental Development
During the first project year, we made significant progress on Aims 1 and 2. With regard to Aim 1, we performed experiments designed to establish (1) the relevant timing of in vitro exposure, (2) dosing regimens, and (3) exposure durations for PBDE‐47 and PFOA that will be used for future RNA‐seq experiments. We are conducting these experiments in primary cultures of human cytotrophoblast (CTB) cells, a model system that we have used for more than 20 years to study placentation in normal pregnancy and in pregnancy complications. We are using this model in place of the trophoblast progenitor cell (TBPC) lines that we have established from human chorionic membranes. We chose the primary culture model to leverage transcriptomic and epigenomic data generated by our participation in the NIH‐funded Roadmap Epigenome Mapping Center and in microarray‐based gene expression profiling studies we have recently published (Zhou, et al., J Clin. Invest., 2013). From these experiments, we gained significant practical knowledge that will be applied to this project in using next‐generation sequencing to study DNA methylation, histone modifications and RNA expression.
To apply our CTB culture system to toxicological investigations, we characterized the dynamic morphological and molecular changes that occur over time in unexposed CTBs to determine relevant in vitro exposure windows. Using a combination of analyses, including time‐lapse imaging of cell movement/behavior, immunolocalization and/or RT‐PCR of molecules involved in CTB identity/function (e.g., integrins, cytokeratins, proteinases), and time‐course microarray data, we have identified a time point in culture (15 h post‐initial plating) to initiate chemical exposures. This initial exposure period will coordinate with significant CTB movement/aggregation on a morphological level, and, in parallel, dynamic changes in biological pathways regulating CTB function (e.g., cell migration/motility, cell communication, tissue remodeling) on a molecular level. These characteristics are essential components of trophoblast invasion of the endometrium during the establishment of the maternal/fetal interface.
We have also completed initial PBDE‐47 and PFOA toxicity studies in CTBs to determine relevant concentration ranges and exposure durations. We measured cell viability and lactate dehydrogenase activity―a marker of relative cell death―in order to determine relevant doses for future experiments. We included concentrations which are physiologically relevant for pregnant women and occupational exposures and toxicologically effective in vitro. Both PBDE‐47 and PFOA impact these two endpoints in a dose‐dependent manner, with significant effects observed at the highest concentrations tested (n ≥ 5 independent experiments). With PBDE‐47, we conducted these assessments in eight separate experiments and did not observe any significant effect of gestational age on sensitivity. With these established concentration ranges of PBDE‐47 and/or PFOA, we are currently characterizing potential upstream effects of cytotoxicity, monitoring caspase 3 activity (apoptosis) and oxidative stress to determine time‐dependent responses associated with chemical exposure. Additionally, in a dose‐ and time‐dependent manner, we are investigating the effects of PBDE‐47 and/or PFOA on key molecules related to CTB function using RT‐PCR. Once complete, this data will help us finalize the concentrations and time point(s) to be used for analysis of transcriptomic and epigenomic changes.
Additionally, we now have data from the Roadmap Epigenome Mapping Center, which was completed with support from this grant and which provides a wealth of information we can use to understand the effects of exposing CTBs to PBDEs and PFOA. In these experiments, we analyzed the transcriptome and epigenome of purified CTBs, chorionic villi, chorionic membranes and basal plate. The analysis includes gene expression levels measured by RNA‐seq, DNA methylation, Chip‐seq targeting specific histone modifications and mIR expression. PCA analysis of the global methylation pattern showed that these extraembryonic cells/tissues form a distinct cluster as compared to human embryonic stem cells (hESCs), fetal brain and all other samples that Roadmap has analyzed. Analysis of the DNA methylation and histone modification patterns of CTBs revealed that these extraembryonic cells are globally hypomethylated in comparison to hESCs and other fetal and adult tissues analyzed. Differentially methylated regions (DMEs) included key gene regulatory regions and transposable elements that are typically highly methylated in other cell types. This is particularly relevant since expression of retrotransposons and endogenous retroviruses is prevalent in the placenta, likely due to their hypomethylated state. Hypomethylated regulatory regions for genes that are important for extraembryonic/trophoblast development included hypoxia‐inducible factor (HIF) 1‐alpha, HIF 1‐beta, TEAD4 (required for trophectoderm specification in mouse blastocysts), and E‐box consensus sequences that bind basic helix‐loop‐helix transcription factors. Pathway analysis of the RNA‐seq data revealed inflammatory response, chemokine activity and leukocyte migration to be among the major gene groups upregulated in extraembryonic tissues.
Identification of the epigenetic landscape of CTBs and other extraembryonic tissues gives us important baseline information for understanding, in detail, the effects of exposing these cells to PBDEs and PFOA. It allows us to conduct targeted analyses in addition to our global exploration of the epigenetic changes induced by exposures. Aim 3 experiments are designed to analyze the functions of molecules that are targets of the environmental chemicals of interest and which we suspect play important roles in human placental development. The deep understanding of the normal transcriptomic and epigenomic landscape of CTBs that we are now developing will help put the data we generate in the exposure experiments in the proper context and inform these targeted analyses.
This project is providing significant professional development opportunities for a postdoctoral fellow in the laboratory, Dr. Joshua Robinson. He has been working on this project with T32 support from a training grant administered by the UCSF Center for Reproductive Sciences. He was recently awarded a K99, Pathways to Independence Grant entitled, “Polybrominated Diphenyl Ether Effects on Human Neuronal Development.” His growing expertise in using in vitro model systems for studying the developmental effects (in humans) of gestational exposures to environmental chemicals is the direct result of participation in this project.
R835433C002: Mid‐Gestational Exposure to EDCs and Effects on Placental Development
Although we are still in the very early stages of this project, we have already produced a number of accomplishments and developed infrastructure for the project as we prepare to begin recruitment and sample collection. We hired and trained one research assistant and developed study databases, data entry forms, and data quality assurance and control plans. With collaborative efforts of the San Francisco General Hospital (SFGH) Women’s Option Center (WOC), we developed a joint consent form and IRB for several of our ongoing research projects at the WOC, including the current project. We also developed the study protocol, study instructions and exposure assessment questionnaire, and translated study material to Spanish. All study personnel have undergone required trainings for Human Subjects Research, Biosafety and Blood‐borne Pathogens trainings. We obtained institutional approvals for our project, including IRB/Human Subjects Approval, Biological Use Authorization and SFGH research approvals. We have purchased lab supplies and biospecimen collection material necessary for carrying out study activities. All biospecimen collection materials have been sent to our collaborators to test for possible contamination of chemicals of interest (PBDEs and PFCs). Methods for PBDE analysis in serum and liver have already been developed by our collaborators at California Department of Toxic Substances (DTSC), Drs. Myrto Patreas and June‐ Soo Park. Methods development for PBDE analysis in placenta is in its final stage, and method development results will presented during the upcoming EPA site visit. Methods for PFCs analysis in serum, liver and placenta are currently under development by our collaborator, Dr. Roy Gerona at the UCSF Department of Clinical Toxicology. Dr. Roy Gerona has already completed methods for nontargeted analysis of EOAs in serum using LC‐QTOF/MS and is preparing a manuscript for publication. In collaboration with Drs. Michael McMaster and Susan Fisher, we have tested and completed a protocol for placenta collection and placental marker analyses (morphological and molecular markers of placental development).
R835433C003: Effects of EDCs and Chronic Psychosocial Stress on Fetal Growth
The first half of Fund Year 1 (FY) was spent developing the infrastructure for the project. We hired and trained two research assistants and developed study databases, data entry forms, and data quality assurance and control plans. We also developed the study protocol, stress assessment and chemical exposure questionnaire, and translated all study material to Spanish. All study personnel have undergone required trainings for Human Subjects Research, APeX, Biosafety and Blood‐borne Pathogens. We obtained institutional approvals for our project, including IRB/Human Subjects Approval, Biological Use Authorization, San Francisco General Hospital (SFGH) and Moffitt‐Long Hospital (MLH) research approvals. We have purchased lab supplies and biospecimen collection material necessary for carrying out study activities. All biospecimen collection materials have been sent to our collaborators to test for possible contamination by chemicals of interest (PBDEs and PFCs). We initiated participant recruitment efforts at SFGH in April 2014 and at MLH in May 2014. The first few months of recruitment were slow due to some staff turnover, training of new staff and adjusting recruitment activities to clinic flow. Thus far, we have recruited 35 participants (16 from SFGH and 19 from MLH), and 1 participant has delivered. A summary of the demographics demonstrating ethnic and socioeconomic diversity of our study population can be found in Table 1. Methods for PBDE analysis in serum have already been developed by our collaborators at California Department of Toxic Substances, Drs. Myrto Patreas and June‐Soo Park. Methods for PFCs analysis in serum are currently under development by our collaborator, Dr. Roy Gerona at the UCSF Department of Clinical Toxicology.
Table 1: Project III Patient Recruitment | ||
|
SFGH |
MLH |
Age (range, mean) |
18‐41, 30 |
26-38, 33 |
Race/Ethnicity |
8 |
1 |
Hispanic |
||
African American/Black |
3 |
5 |
White |
1 |
9 |
Asian |
1 |
2 |
Other |
3 |
2 |
Combined Household Income |
|
|
< 20K |
7 |
1 |
20 – 49K |
4 |
3 |
50 – 99K |
2 |
5 |
100 – 149K |
1 |
4 |
150 – 199K |
0 |
2 |
≥200K |
0 |
4 |
Don’t Know/Missing |
2 |
0 |
Education Attainment |
|
|
High school/GED or below |
10 |
0 |
Some college or AA degree |
3 |
2 |
Bachelor’s degree |
2 |
6 |
Master’s degree |
1 |
6 |
Ph.D./M.D./DDS |
0 |
5 |
Core A: Community Outreach and Translation Core (COTC)
Aim 1: Communicate the Science Broadly: Distributed 2,284 electronic and 5,458 hard copies of our All That Matters series of patient‐centered brochures; were quoted in 116 print or online media outlets; had 9,935 unique visitors to the website; made a total of 25 presentations to clinical and policy audiences and to the public on reproductive environmental health science (N = 16) and on our Navigation Guide systematic review methodology (N = 9); used Facebook and Twitter to communicate the science four times per week.
Aim 2: Harness the Evolving Science to Health Care: A critical outcome of our efforts was publication of the American Congress of Obstetricians and Gynecologists (ACOG) and the American Society for Reproductive Medicine (ASRM) Committee Opinion, “Exposure to Toxic Environmental Agents,” and a companion white paper in September 2013. The Opinion recognizes that “patient exposure to toxic environmental chemicals and other stressors is ubiquitous, and preconception and prenatal exposure to toxic environmental agents can have a profound and lasting effect on reproductive health across the life course.” The ACOG/ASRM Opinion, which legitimates efforts by health professionals to take action to prevent exposure to toxic chemicals, is a major milestone in our efforts to institutionalize environmental health among health professionals. June 2013—Held the Visionary Leadership Awards Reception at The Endocrine Society (TES) Meeting. The meeting included stirring addresses on the relevance of environmental exposures to patient health and the need for improved policy by Teresa Woodruff, President‐elect of The Endocrine Society (TES); Linda Giudice, President of the ASRM; and Jeanne Conry, President of ACOG. October 2013—The H. John Heinz III Center for Science, Economics & Environment held the Presidents for Prevention event, an information session focused on environmental risk factors contributing to the development of women’s cancers. PRHE was a co‐sponsor of the event and deeply involved in its planning. Approximately 100 distinguished policy makers and leaders of governmental and nongovernmental scientific and environmental health advocacy organizations were in attendance. At the event, the presidents of three of the nation’s leading professional medical and scientific societies, ACOG, ASRM and TES, delivered the scientific consensus that exposure to environmental chemicals impacts health outcomes within both contemporary lifetimes and the lifetimes of future generations. The full briefing can be viewed here: http://www.youtube.com/watch?v=5WCEWiaclec. Exit Collaborated with the UCSF Pediatric Environmental Health Specialty Unity (PEHSU) on creating educational opportunities for OB/GYN residents in reproductive environmental health. See: http://prhe.ucsf.edu/prhe/pdfs/PEEC_OBGYNEd_poster.pdf. Exit Our PEEC Center’s Dr. Marya Zlatnik and Dr. Mark Miller of the UCSF PEHSU are spearheading this collaboration. An outcome of their efforts is that Dr. Betsy O’Donnell, a first year UCSF MFM fellow, is currently doing a reproductive and environmental health elective under their direction; our COTC’s Director of Health Professional Outreach Education, Dr. Robert Gould, served as an active member of the California Preconception Care Council, the UCSF Sustainability Committee and as a collaborator in the followup to the USEPA/ATSDR 2012 Strategic Planning for Reproductive Environmental Health meeting, which for the first time brought together leaders from federal agencies, professional medical and nursing organizations, pediatricians, obstetricians, occupational medicine physicians, policy makers, and academics to explore issues related to health outcomes and prenatal environmental exposures to toxic chemicals.
Aim 3: Advance Prevention‐Based Public Policy: As an outcome of the ACOG/ASRM Opinion, leaders of the ACOG, ASRM, the American Academy of Pediatrics and the March of Dimes held a briefing on April 7, 2014 in Washington, D.C., titled, “What the Elk River Chemical Spill Exposed: The Links Between the Environment and the Health of Our Most Vulnerable (A Panel Discussion With the Nation’s Leading Physicians Dedicated to the Health of Pregnant Women, Infants, Children and Families).” The briefing was sponsored by the Senate Committee on Health Education, Labor, and Pensions (HELP). Dr. Gould was a featured speaker at a California Legislative Informational Briefing on Pesticides, presenting the findings of our Pesticides Matters white paper for reproductive health professionals. We submitted two sets of written comments and attended a public hearing on the Cal‐OSHA Standards Board’s actions regarding the California Hazard Communication Standard (HCS). We advanced uptake of the Navigation Guide systematic review methods through nine meetings and briefings with decision makers in key federal and state agencies, including with key governmental and clinical organizational leaders (i.e., USEPA, Institute of Medicine, World Health Organization and the National Academy of Sciences), as well as scientists and advocates. Held three Navigation Guide Work Group Webinars. Submitted written comments to National Toxicology Program on its draft OHAT approach for systematic review and evidence integration for literature‐based health assessments. Submitted written recommendations to Cal‐EPA for summarizing data from epidemiological and toxicological studies, specifically commenting on the example tables that were presented to the Developmental and Reproductive Toxicant Identification (DART) Committee.
Core B: Administrative Core
PEEC principal investigators and staff met monthly, with the exception of February and July 2014, to discuss progress on each project. We rotated through projects, designating one project or the COTC to give a 25-minute presentation on their progress, followed by a Q&A session. The Administrative Core addressed program-related topics such as Quality Assurance, professional meetings, External Advisory Committee selection and other Center information. In early 2014, we began rotating between an in‐person meeting, a Web‐based meeting, and a 2‐hour quarterly meeting.
We began the project with a 2‐hour kick‐off meeting on September 11, 2013, facilitated by Annemarie Charlesworth. At this meeting, each project and core presented on the work that they would be doing. We also completed a work plan exercise wherein project/core principal investigators met with their staff to discuss the aims and goals of their project and to generate a timeline to guide and measure progress. The kick‐off meeting concluded with discussions on fund spending, data quality management, and reporting.
In January 2014, the Center began using Basecamp as a centralized online hub for organizing the Administrative Core and storing Center‐related, nonsensitive files (logos, templates, etc.).
Children’s Environmental Health Center (CEHC) Calls and Annual Meeting
Principal investigators and staff from the Center attended 10 CEHC teleconferences. Six principal investigators, including the Center principal investigator, attended the EPA and NIEHS Children’s Centers Grantee Meeting on October 28, 2013. The PEEC Center principal investigator, Tracey Woodruff, served on the planning committee for the meeting.
External Committee and EAC Meeting
The External Advisory Committee (EAC) was selected between the months of November 2013 and February 2014. We had some difficulty in finding a community‐based advocate, but in the end, we selected two members to fill the role. Our EAC is composed of six individuals. They are:
- Jeanne Conry, M.D., Ph.D., The Permanente Medical Group, Roseville, CA
- Russ Hauser, M.D., M.P.H., Sc.D., Harvard School of Public Health, Boston, MA
- Lauren Zeise, Ph.D., CalEPA Office of Environmental Health Hazard Assessment (OEHHA), Oakland, CA
- Gilbert C. Gee, Ph.D., Kaiser Permanente, Los Angeles, CA
- Yoel Sadovsky, M.D., Magee‐Women’s Research Institute & Foundation, Pittsburgh, PA
- Xochitl Castañeda, Ph.D., University of California, Berkeley, Berkeley, CA
We are trying to schedule our first meeting with the EAC but we have run into several scheduling issues. We are currently looking at dates in December and January. Our committee is made up of individuals with complex schedules, so finding a meeting date that works for everyone has proven challenging. Once we have a date, the meeting will be held in San Francisco at a location to be determined.
Quality Assurance
A Quality Management Plan was created and signed by EPA QA Manager Lisa Doucet in November 2013.
Standard Operating Procedures (SOPs) and Quality Assurance Project Plans (QAPPs) are in place in each location where samples are being collected and stored. A Quality Assurance audit will take place on September 29 and 30, 2014, during which time the CQAM will review SOPs, QAPPs and lab compliance. Recommendations will be made, if necessary, and an audit report will be sent to EPA staff.
Virtual Home and Patient Information Distribution
The Administrative Core has created a section of the PRHE website to showcase the PEEC Children’s Center (http://prhe.ucsf.edu/prhe/PEEC_childrens_center.html). However, UCSF’s Department of Ob/GYN and RS is switching to a Drupal‐based platform in Q2 of 2014. At this point, the PEEC Center will have its own dedicated site.
Contact and Communication with NIEHS and EPA
The Center has maintained continuous communication with EPA and NIEHS in addition to participating in the monthly Children’s Center calls and attending the annual Children’s Centers Grantee Meeting. Dr. Woodruff has communicated with NIEHS and EPA program officers during in‐person meetings, email exchanges and telephone calls during the course of this project period.
Junior Faculty and Postdoctoral Fellow Mentoring
Dr. Woodruff has met regularly with postdoctoral fellows associated with the center. Further, she helped facilitate Dr. Ami Zota’s transition to a junior faculty member at George Washington University School of Public Health. She has regularly met with Dr. Gerona, the proposed Faculty Development Investigator (FDI) who will replace Dr. Zota, and has written him into several grant applications. Further, they have co-authored two publications and are planning on at least four more.
Future Activities:
R835433C001: Modeling the Effects of EDCs on Early Stages of Human Placental Development
At the beginning of the Year 2, we will complete the experiments designed to establish the dosing regimens of PBDEs ± PFOA with regard to their effects on CTB morphology, differentiation and toxicity. We will then proceed to the RNA‐seq experiments and validating the expression patterns of the transcripts that are differentially expressed after exposure to the chemicals of interest. During this time, we will also complete our analyses of the data that we have obtained so far on the transcriptome and epigenome of purified CTBs and tissues of the extraembryonic compartment. Also during year 2, we may begin the analyses of PBDE‐47 ± PFOA effects on the epigenome. We will begin with the methylation analyses. We will coalesce these datasets with the RNA‐seq results to choose the targets on which the functional analyses will concentrate.
R835433C002: Mid‐Gestational Exposure to EDCs and Effects on Placental Development
In the next reporting period, we will begin patient recruitment and collection of biospecimens at SFGH. Target enrollment is 185 women in their second trimester, and we anticipate recruiting approximately two‐thirds of the study participants in the next reporting period. During that time, we will also begin to measure PBDE and PFC levels in matched samples of maternal serum, fetal liver and placenta, conduct nontargeted analysis of EOA’s in matched samples, and begin morphological and molecular assessment of placenta samples.
R835433C003: Effects of EDCs and Chronic Psychosocial Stress on Fetal Growth
With study infrastructure in place, we expect to enroll 2–4 participants each week from each study site (SFGH and MLH) and finish enrollment by the end of Year 3. We will complete method development for PFCs before the end of Year 2, and start chemical analysis for both PBDEs and PFCs at the beginning of Year 3. We will also begin stress biomarker analysis at the beginning of Year 3.
Core A: Community Outreach and Translation Core (COTC)
Continued advancement of our aims.
Core B: Administrative Core
We will continue holding monthly meetings and retreats in the next project period.
Members of the PEEC Children’s Center will attend the 2014 Children’s Centers Grantee Meeting and, given the opportunity, will present the progress of the Center to attendees of the meeting. Several members will stay for PPTOX following the Children’s Center meeting.
We plan to hold a meeting with the PEEC EAC in December 2014 or January 2015. Administrative Core staff will invite NIEHS and EPA program officers to attend the meeting and will communicate the results of the meeting after the meeting has concluded.
The Administrative Core will submit audit information to EPA staff and program officers to keep them in the loop on the Quality Assurance efforts of the Center. The CQAM will continue to monitor changes in QAPPs and SOPs, if any, and report those changes to the EPA Quality Assurance Manager.
The Center will continue to engage program officers and send them any manuscripts that are produced within the upcoming project period.
Center principal investigators will continue to engage trainees and provide them with career development opportunities.
Journal Articles: 48 Displayed | Download in RIS Format
Other center views: | All 77 publications | 54 publications in selected types | All 48 journal articles |
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Type | Citation | ||
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Abrahamsson D, Park J, Singh R, Sirota M, Woodruff T. Applications of Machine Learning to In Silico Quantification o Chemicals without Analytical Standards. Journal of Chemical Information and Modeling 2020;60(6):2718-2727. |
R835433 (Final) R835643 (Final) |
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Abrahamsson D, Siddharth A, Young T, Sirota M, Park J, Martin J, Woodruff T. In Silico Structure Predictions for Non-targeted Analysis: From Physicochemical Properties to Molecular Structures. JOURNAL OF THE AMERICAN SOCIETY FOR MASS SPECTROMOTY 2022;33(7):1134-1147 |
R835433 (Final) |
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Abrahamsson D, Brueck C, Prasse C, Lambropoulou D, Koronaiou L, Wang M, Park J, Woodruff T. Extracting Structural Information from Physicochemical Property Measurements Using Machine Learning-A New Approach for Structure Elucidation in Non-targeted Analysis. ENVIRONMENTAL SCIENCE & TECHNOLOGY 2023;27(40):14827-14838 |
R835433 (Final) R835643 (Final) |
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Bland G, Abrahamsson D, Wang M, Zlatnik M, Morello-Frosch R, Park J, Sirota M, Woodruff T. Exploring applications of non-targeted analysis in the characterization of the prenatal exposome. SCIENCE OF THE TOTAL ENVRIONMENT 2023;912(169458) |
R835433 (Final) |
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Casey JA, Karasek D, Ogburn, EL, Goin DE, Dang K, Braveman PA, Morello-Frosch R. Coal and oil power plant retirements in California:association with reduced preterm birth among populations nearby. American Journal of Epidemiology 2018;187(8):1586-1594. |
R835433 (2017) R835433 (Final) |
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Casey JA, Gemmill A, Karasek D, Ogburn, EL, Goin DE, Morello-Frosch R. Increase in fertility following coal and oil power plant retirements in California. Environmental Health 2018;17(1):44 (10 pp.). |
R835433 (2017) R835433 (Final) |
Exit Exit |
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Di Renzo GC, Conry JA, Blake J, DeFrancesco MS, DeNicola N, Martin Jr. JN, McCue KA, Richmond D, Shah A, Sutton P, Woodruff TJ, van der Poel SZ, Giudice LC. International Federation of Gynecology and Obstetrics opinion on reproductive health impacts of exposure to toxic environmental chemicals. International Journal of Gynaecology and Obstetrics 2015;131(3):219-225. |
R835433 (2015) R835433 (Final) |
Exit Exit Exit |
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Gerona RR, Pan J, Zota AR, Schwartz JM, Friesen M, Taylor JA, Hunt PA, Woodruff TJ. Direct measurement of bisphenol A (BPA), BPA glucuronide and BPA sulfate in a diverse and low-income population of pregnant women reveals high exposure, with potential implications for previous exposure estimates: a cross-sectional study. Environmental Health 2016;15:50 (14 pp.). |
R835433 (2015) R835433 (2017) R835433 (Final) |
Exit Exit |
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Gerona RR, Schwartz JM, Pan J, Friesen MM, Lin T, Woodruff TJ. Suspect screening of maternal serum to identify new environmental chemical biomonitoring targets using liquid chromatography-quadrupole time-of-flight mass spectrometry. Journal of Exposure Science & Environmental Epidemiology 2018;28(2):101-108. |
R835433 (2017) R835433 (Final) R835643 (2017) |
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Goin D, Abrahamsson D, Wang M, Jiang T, Park J, Sirota M, Morello-Frosch R, DeMicco E, Zlatnik M, Woodruff T. Disparities in chemical exposures among pregnant women and neonates by socioeconomic and demographic characteristics:A nontargeted approach. ENVIRONMENTAL RESEARCH 2022;215(1):114158. |
R835433 (Final) |
Exit Exit |
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Goin D, Abrhamsson D, Wang M, Park J, Sirota M, Morello-Frosch R, DeMicco E, Trowbridge J, Augt L, O'Connell S, Ladella S, Zlatnik M, Woodruff T. Investigating geographic differences in environmental chemical exposures in maternal and cord sera using non-targeted screening and silicone wristbands in California. JOURNAL OF EXPOSURE SCIENCE AND ENVIRONMENTAL EPIDEMIOLOGY 2022;. |
R835433 (Final) |
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Huang H, Wang A, Morello-Frosch R, Lam J, Sirota M, Padula A, Woodruff TJ. Cumulative risk and impact modeling on environmental chemical and social stressors. Current Environmental Health Reports 2018;5(1):88-99. |
R835433 (2017) R835433 (Final) |
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Johnson PI, Sutton P, Atchley DS, Koustas E, Lam J, Sen S, Robinson KA, Axelrad DA, Woodruff TJ. The Navigation Guide—evidence-based medicine meets environmental health: systematic review of human evidence for PFOA effects on fetal growth. Environmental Health Perspectives 2014;122(10):1028-1039. |
R835433 (2014) R835433 (Final) |
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Johnson PI, Koustas E, Vesterinen HM, Sutton P, Atchley DS, Kim AN, Campbell M, Donald JM, Sen S, Bero L, Zeise L, Woodruff TJ. Application of the Navigation Guide systematic review methodology to the evidence for developmental and reproductive toxicity of triclosan. Environment International 2016;92-93:716-728. |
R835433 (2015) R835433 (2016) R835433 (Final) |
Exit Exit Exit |
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Koustas E, Lam J, Sutton P, Johnson PI, Atchley DS, Sen S, Robinson KA, Axelrad DA, Woodruff TJ. The Navigation Guide—evidence-based medicine meets environmental health:systematic review of nonhuman evidence for PFOA effects on fetal growth. Environmental Health Perspectives 2014;122(10):1015-1027. |
R835433 (2014) R835433 (Final) |
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Lam J, Koustas E, Sutton P, Johnson PI, Atchley DS, Sen S, Robinson KA, Axelrad DA, Woodruff TJ. The Navigation Guide—evidence-based medicine meets environmental health:integration of animal and human evidence for PFOA effects on fetal growth. Environmental Health Perspectives 2014;122(10):1040-1051. |
R835433 (2014) R835433 (Final) |
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Lam J, Lanphear BP, Bellinger D, Axelrad DA, McPartland J, Sutton P, Davidson L, Daniels N, Sen S, Woodruff TJ. Developmental PBDE exposure and IQ/ADHD in childhood: a systematic review and meta-analysis. Environmental Health Perspectives 2017;125(8):086001 (20 pp.). |
R835433 (2016) R835433 (2017) R835433 (Final) |
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Lam J, Kotas E, Sutton P, Padula A, Cabana M, Vesterinen H, Griffiths C, Dickie M, Daniels N, Whitaker E, Woodruff T. Exposure to formaldehyde and asthma outcomes:A systematic review, meta-analysis, and economic assessment. PLOS ONE 2021;16(3):e0248258. |
R835433 (Final) |
Exit |
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Lam J, Sutton P, Kalkbrenner A, Windham G, Halladay A, Koustas E, Lawler C, Davidson L, Daniels N, Newschaffer C, Woodruff T. A Systematic Review and Meta-Analysis of Multiple Airborne Pollutants and Autism Spectrum Disorder. PLoS One. 2016 Sep 21;11(9):e0161851. doi:10.1371/journal.pone.0161851. PubMed PMID:27653281; PubMed Central PMCID:PMC5031428. |
R835433 (2016) R835433 (Final) |
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McHale CM, Osborne G, Morello-Frosch R, Salmon AG, Sandy MS, Solomon G, Zhang L, Smith MT, Zeise L. Assessing health risks from multiple environmental stressors: moving from G×E to I×E. Mutation Research 2018;775:11-20. |
R835433 (2017) R835433 (Final) |
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Morello-Frosch R, Cushing LJ, Jesdale BM, Schwartz JM, Guo W, Guo T, Wang M, Harwani S, Petropoulou SE, Duong W, Park J-S, Petreas M, Gajek R, Alvaran J, She J, Dobraca D, Das R, Woodruff TJ. Environmental chemicals in an urban population of pregnant women and their newborns from San Francisco. Environmental Science & Technology 2016;50(22):12464-12472. |
R835433 (2015) R835433 (2017) R835433 (Final) |
Exit Exit Exit |
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Morgan RL, Thayer KA, Bero L, Bruce N, Falck-Ytter Y, Ghersi D, Guyatt G, Hooijmans C, Langendam M, Mandrioli D, Mustafa RA, Rehfuess EA, Rooney AA, Shea B, Silbergeld EK, Sutton P, Wolfe MS, Woodruff TJ, Verbeek JH, Holloway AC, Santesso N, Schunemann HJ. GRADE: assessing the quality of evidence in environmental and occupational health. Environment International 2016;92-93:611-616. |
R835433 (2015) R835433 (2016) R835433 (Final) |
Exit Exit Exit |
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Parry E, Zota AR, Park J-S, Woodruff TJ. Polybrominated diphenyl ethers (PBDEs) and hydroxylated PBDE metabolites (OH-PBDEs): a six-year temporal trend in Northern California pregnant women. Chemosphere 2018;195-777-783. |
R835433 (2017) R835433 (Final) |
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Pelch K, Reade A, Kwiatkowski C, Merced-Nieves F, Cavalier H, Schultz K, Wolffe T, Varshavsky J. The PFAS-Tox Database:A systematic evidence map of health studies on 29 per-and polyfluoroalkyl substances. ENVIRONMENTAL INTERNATIONAL 2022;167(107408). |
R835433 (Final) |
Exit Exit |
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Roadmap Epigenomics Consortium, Kundaje A, Meuleman W, Ernst J, Bilenky M, Yen A, Heravi-Moussavi A, Kheradpour P, Zhang Z, Wang J, Ziller MJ, Amin V, Whitaker JW, Schultz MD, Ward LD, Sarkar A, Quon G, Sandstrom RS, Eaton ML, Wu YC, Pfenning AR, Wang X, Claussnitzer M, Liu Y, Coarfa C, Harris RA, Shoresh N, Epstein CB, Gjoneska E, Leung D, Xie W, Hawkins RD, Lister R, Hong C, Gascard P, Mungall AJ, Moore R, Chuah E, Tam A, Canfield TK, Hansen RS, Kaul R, Sabo PJ, Bansal MS, Carles A, Dixon JR, Farh KH, Feizi X, Karlic R, Kim AR, Kulkarni A, Li D, Lowdon R, Elliott G, Mercer TR, Naph SJ, Onuchic V, Polak P, Rajagopal N, Ray P, Sallari RC, Siebenthall KT, Sinnott-Armstrong NA, Stevens M, Thurman RE, Wu J, Zhang B, Zhou X, Beaudet AE, Boyer LA, De Jager PL, Farnham PJ, Fisher SJ, Haussler D, Jones SJ, Li W, Marra MA, McManus MT, Sunyaev S, Thomson JA, Tlsty TD, Tsai LH, Wang W, Waterland RA, Zhang MQ, Chadwick LH, Bernstein BE, Costello JF, Ecker JR, Hirst M, Meissner A, Milosavljevic A, Ren B, Stamatoyannopoulos JA, Wang T, Kellis M. Integrative analysis of 111 reference human epigenomes. Nature 2015;518(7539):317-330. |
R835433 (2014) R835433 (Final) |
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Robinson JF, Kapidzic M, Gormley M, Ona K, Dent T, Seifikar H, Hamilton EG, Fisher SJ. Transcriptional dynamics of cultured human villous cytotrophoblasts. Endocrinology 2017;158(6):1581-1594. |
R835433 (2016) R835433 (2017) R835433 (Final) |
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Robinson J, Hamilton E, Lam J, Chen H, Woodruff T. Differences in cytochrome p450 enzyme expression and activity in fetal and adult tissues. PLACENTA 2020;100:35-44. |
R835433 (Final) R834678 (Final) |
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Solomon GM, Morello-Frosch R, Zeise L, Faust JB. Cumulative environmental impacts: science and policy to protect communities. Annual Review of Public Health 2016;37:83-96. |
R835433 (2015) R835433 (2017) R835433 (Final) |
Exit Exit |
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Stotland NE, Sutton P, Trowbridge J, Atchley DS, Conry J, Trasande L, Gerbert B, Charlesworth A, Woodruff TJ. Counseling patients on preventing prenatal environmental exposures--a mixed-methods study of obstetricians. PLoS ONE 2014;9(6):e98771 (7 pp.). |
R835433 (2014) R835433 (Final) |
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Sutton PM, Giudice LC, Woodruff TJ. Moving from awareness to action on preventing patient exposure to toxic environmental chemicals. American Journal of Obstetrics and Gynecology 2016;214(5):555-558. |
R835433 (2015) R835433 (Final) |
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Sutton, P, Woodruff, TJ, Conry, J, Giudice, LC. Exposure to toxic chemicals:reproductive health professionals speak about the first 1,000 days. San Francisco Medicine 2014;87(9):12-13. |
R835433 (2014) R835433 (Final) |
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Uyghurturk D, Goin D, Martinez-MierEA, Woodruff T, DenBesten P. Maternal and fetal exposures to fluoride during mid-gestation among pregnant women in northern California. ENVIRONMENTAL HEALTH 2020;19(1):38. |
R835433 (Final) |
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Vandenberg LN, Ågerstrand M, Beronius A, Beausoleil C, Bergman A, Bero LA, Bornehag CG, Boyer CS, Cooper GS, Cotgreave I, Gee D, Grandjean P, Guyton KZ, Hass U, Heindel JJ, Jobling S, Kidd KA, Kortenkamp A, Macleod MR, Martin OV, Norinder U, Scheringer M, Thayer KA, Toppari J, Whaley P, Woodruff TJ, Ruden C. A proposed framework for the systematic review and integrated assessment (SYRINA) of endocrine disrupting chemicals. Environmental Health 2016;15(1):74. |
R835433 (2015) R835433 (Final) |
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Vandenberg LN, Gerona RR, Kannan K, Taylor JA, van Breemen RB, Dickenson CA, Liao C, Yuan Y, Newbold RR, Padmanabhan V, Vom Saal FS, Woodruff TJ. Erratum to: A round robin approach to the analysis of bisphenol A (BPA) in human blood samples. Environmental Health 2016;15:43. |
R835433 (2017) R835433 (Final) |
Exit Exit |
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Varshavsky J, Zota A, Woodruff T. A Novel Method for Calculating Potency-Weighted Cumulative Phthalates Exposure with Implications for Identifying Racial/Ethnic Disparities among Reproductive-Aged Women in NHANES 2001-2012. ENVIRONMENTAL SCIENCE & TECHNOLOGY 2016;5(19):10616-10624. |
R835433 (Final) |
Exit Exit |
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Varshavsky J, Morello-Frosch R, Woodruff T, Zota A. Dietary sources of cumulative phthalates exposure among the general population in NHANES 2005-2014. ENVIRONMENT INTERNATIONAL 2018;115:417-429. |
R835433 (Final) |
Exit Exit |
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Varshavsky J, Morello-Frosch R, Harwani S, Snider M, Petropoulou S, Park J, Petras M, Reynolda P, Nguyen T, Quach T. A Pilot Biomonitoring Study of Cumulative Phthalates Exposure among Vietnamese American Nail Salon Workers. INTERNATIONAL JOURNAL OF ENVIRONMENTAL RESEARCH AND PUBLIC HEALTH 2020;17(1). |
R835433 (Final) |
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Varshavsky J, Smith A, Wang A, Hom E, Izano M, Huang H, Padula A, Woodruff T. Heightened susceptibility:A review of how pregnancy and chemical exposures influence maternal health. Reproductive Toxicology 2020;92(SI):14-56. |
R835433 (Final) R835643 (Final) |
Exit Exit |
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Vesterinen HM, Johnson PI, Koustas E, Lam J, Sutton P, Woodruff TJ. In support of EHP's proposal to adopt the ARRIVE guidelines. Environmental Health Perspectives 2013;121(11‐12):A325. |
R835433 (2013) R835433 (2014) R835433 (Final) |
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Vesterinen HM, Morello-Frosch R, Sen S, Zeise L, Woodruff TJ. Cumulative effects of prenatal-exposure to exogenous chemicals and psychosocial stress on fetal growth: systematic-review of the human and animal evidence. PLoS One 2017;12(7):e0176331 (29 pp.). |
R835433 (2017) R835433 (Final) |
Exit Exit |
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Wang A, Padula A, Sirota M, Woodruff TJ. Environmental influences on reproductive health: the importance of chemical exposures. Fertility and Sterility 2016;106(4):905-929. |
R835433 (2016) R835433 (2017) R835433 (Final) R835643 (2016) R835643 (2017) |
Exit Exit |
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Wang A, Gerona RR, Schwartz JM, Lin T, Sirota M, Morello-Frosch R, Woodruff TJ. A suspect screening method for characterizing multiple chemical exposures among a demographically diverse population of pregnant women in San Francisco. Environmental Health Perspectives 2018;126(7):077009 (13 pp.). |
R835433 (2017) R835433 (Final) |
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Woodruff TJ, Sutton P. The Navigation Guide systematic review methodology: a rigorous and transparent method for translating environmental health science into better health outcomes. Environmental Health Perspectives 2014;122(10):1007-1014. |
R835433 (2014) R835433 (Final) |
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Zota AR, Linderholm L, Park JS, Petreas M, Guo T, Privalsky ML, Zoeller RT, Woodruff TJ. Temporal comparison of PBDEs, OH-PBDEs, PCBs, and OH-PCBs in the serum of second trimester pregnant women recruited from San Francisco General Hospital, California. Environmental Science & Technology 2013;47(20):11776-11784. |
R835433 (2017) R835433 (Final) |
Exit Exit Exit |
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Zota AR, Mitro SD, Robinson JF, Hamilton EG, Park JS, Parry E, Zoeller RT, Woodruff TJ. Polybrominated diphenyl ether (PBDEs) and hydroxylated PBDE metabolites (OH-PBDEs) in maternal and fetal tissues, and associations with fetal cytochrome P450 gene expression. Environment International 2018;112:269-278. |
R835433 (2017) R835433 (Final) |
Exit Exit Exit |
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Zota A, Mitro S, Robinson J, Hamilton E, Park J, Parry E, Zoeller R, Woodruff J. Polybrominated diphenyl ethers PBDEs and hydroxylated PBDE metabolites OH-PBDEs in maternal and fetal tissues, and associations with fetal cytochrome P450 gene expression. ENVIRONMENT INTERNATIONAL 2018;112:269-278. |
R835433 (Final) |
Exit Exit |
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Morello-Frosch R, Cushing LJ, Jesdale BM, Schwartz JM, Guo W, Guo T, Wang M, Harwani S, Syrago-Petropoulou SSE, Duong W, Park J-S, Petreas M, Gajek R, Alvaran J, She J, Dobraca D, Das R, Woodruff TJ (2016) Environmental Chemicals in an Urban Population of Pregnant Women and their Newborns from San Francisco. Environ Sci and Technol DOI:10.1021/acs.est.6b03492. |
R835433 (2016) |
Exit Exit Exit |
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Johnson PI, Sutton P, Koustas E, Vesterinen HM, Woodruff TJ. Response to correspondence by Heather Lynch, Julie Goodman and Nancy Beck Re:"Application of the Navigation Guide systematic review methodology to the evidence for developmental and reproductive toxicity of triclosan". Environ Int. 2017 Feb 21. pii:S0160-4120(17)30231-3. doi:10.1016/j.envint.2017.02.007. [Epub ahead of print] PubMed PMID:28236502. |
R835433 (2016) R835433 (Final) |
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Supplemental Keywords:
Endocrine disrupting chemicals, EDCs, environmental chemical exposure, human placental development, perfluorooctanoic acid, PFOAs, polybrominated diphenyl ether, PBDEs, perfluorinated chemicals, PFCs, trophoblast progenitor cell, TBPCs, psychosocial stress, cytotrophoblast cell, CTBs;Relevant Websites:
YouTube: Prevention of Women's Cancers Exit
Reproductive Environmental Health Education for OB/GYN Specialists (PDF) (PDF, 1pp, 174kb) Exit
UCSF: Pregnancy Exposures to Environmental Chemicals (PEEC) Children's Center 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
- 2017 Progress Report
- 2016 Progress Report
- 2015 Progress Report
- 2014 Progress Report
- Original Abstract
48 journal articles for this center