Author Archives: Sarah Phillips

Fall 2019 Seminar Series

Category : Symposium

Duke University Program in Environmental Health & Toxicology

Fall 2019 Seminar Series (Pharm 847-S/ENV 847-S)

Fridays 11:45 a.m. – 1:00 p.m.

Field Auditorium, Grainger Hall unless otherwise noted


Sept 6    Phillip West, Texas A&M University College of Medicine, Mitochondrial Control of Innate Immunity in Health and Disease

Sept 13  Rashmi Joglekar, PhD Candidate, Nicotine and Sexualization of the Brain

Sept 20  Alison Harrill, NIEHS, Assessing chemical risks unique to genetically sensitive subpopulations using Diversity Outbred mice

Sept 27  Sven-Eric Jordt, Duke University School of Medicine, The role of TRPA1 receptor in toxicology

Oct 4      Dan Richter, Duke University Nicholas School of the Environment, and Emmanuel Obeng-Gyasi, North Carolina A&T, Urban Lead Legacy: A Soil Scientist’s Perspective

Oct 11    Symposium: Bridging Across Levels of Analysis to Advance Neurotoxic Risk Determination: Toxicology for the Second Fifth of the 21st Century, 8:30 am – 3:00 pm, Symposium Chair: Dr. Edward D. Levin

Oct 18    Michael Falvo, US Dept. Veterans Affairs, Airborne Hazards in the Deployment Environment: Implications for US Military Veterans

Oct 25    Scott Kennedy, University of Washington, The Rise of Somatic Mutations During Aging and the Tools to Study Them

Nov 1     Michelle Block, Indiana University School of Medicine, Microglia and the Lung Brain Axis:  Implications for CNS Disease?

Nov 8     James Crall, Harvard University, Pesticides and pollinators: Identifying the behavioral impacts of chronic neonicotinoid exposure in bumblebees

Nov 15   Michael Slimak, US EPA, EPA’s Sustainable and Healthy Communities (SHC) Research Program

Nov 22   Christine Payne, Duke University Dept. of Mechanical Engineering & Materials Science, Nanoparticle-cell interactions: Importance for human health

Nov 29   Thanksgiving Break

Dec 6     Rafael Trevisan, Duke University post-doctoral researcher, Using zebrafish as a model to investigate the potential threat of nanoplastics to aquatic species

Dec 13   Justin Conley, US EPA, Fetal and neonatal effects of in utero exposure to perfluoroalkyl ether acids

Summer 2019 Internships!

Category : News

Summer 2019 Research Internship

Application deadline is 5:00 pm EST, Friday, February 1, 2019.

The World Health Organization defines environmental health as “encompassing the assessment and control of those environmental factors that can potentially affect health. It is targeted towards preventing disease and creating health-supportive environments.” The field of environmental health is multi-disciplinary and requires scientific contributions from many fields to elucidate threats to human health. 

The Superfund Research Program (SRP) is a network of university grants funded by the National Institute of Environmental Health Sciences (NIEHS) designed to seek solutions to the complex health and environmental issues associated with toxic chemicals found at the nation’s hazardous waste sites. The Duke University NIEHS-funded Superfund Research Center (SRC) focuses on early, low-dose exposures to toxins and their developmental impacts that are usually only evident during later life stages. Full-time summer research internship opportunities are now open for both undergraduate and Master’s students (can be studying Biology, Psychology, Neuroscience, Engineering, Environmental Sciences, Science Communication, etc.) in the SRC projects and cores below:

Project 1: Cholinergic and Monoaminergic Mechanisms of Persistent Neurobehavioral Toxicity. The focus of this project is to better understand what happens in the brain when someone who is already being exposed to one chemical (nicotine from cigarette smoke or dexamethasone from preterm labor therapy) is exposed to chemicals such as organophosphate pesticides, PAHs, and/or polybrominated diphenyl ethers (PBDEs).

Project 3: Persistent Mitochondrial and Epigenetic Effects of Early Life Toxicant Exposure. Growing evidence suggests that chemicals of interest to Superfund stakeholders can have persistent, toxic effects on the mitochondria, and that some individuals may be more sensitive to the effects due to genetic differences. This project aims to test which important Superfund chemicals and chemicals of emerging concern are mitochondrial toxicants; whether effects from exposure are persistent throughout life and into subsequent generations; and whether the effects are stronger for individuals from some genetic backgrounds.

Project 4: Mechanisms and Consequences of Evolved Adaptation to Environmental Pollution. This project continues the Duke Superfund Research Center’s (SRC’s) long-standing research in the Elizabeth River in Virginia. For years, polycyclic aromatic hydrocarbons (PAHs) were discharged into the river from several wood treatment facilities that employed creosote. Researchers from the Duke SRC have spent years studying a fish species native to the area, the killifish (Fundulus heteroclitus) and its response to living in contaminated environments. Their research has found that killifish at contaminated sites exhibit pollution-driven adaptation to high levels of PAHs at these sites. Current research is examining fitness costs associated with this evolved resistance, and with the killifish and zebrafish models, mechanisms of PAH developmental toxicity and later life consequences of embryonic exposures to low levels of PAHs.

Neurobehavioral Toxicity Core. This core supports the Center’s projects by providing information concerning neurobehavioral consequences of exposure to toxicants, including pesticides, flame retardants, and polycyclic aromatic hydrocarbons. Neurotoxicant impacts are evaluated using in vivo models with rats, zebrafish and killifish. Neurobehavioral functions investigated include sensorimotor function, learning, memory, attention, and emotional response. This core connects the findings of mechanistic studies to functional consequences in living organisms.

 Research Translation Core. The Research Translation Core (RTC) uses science communication (also called research translation) techniques to share the Center’s research results with critical members of the scientific, governmental, and lay community. The RTC works closely with the Community Engagement Core (CEC – see below for more information on this core) to support their mission of engaging communities around environmental health. Students affiliated with this core will support research translation projects and activities to effectively communicate research findings of the Center to scientists, policy-makers, and interested/affected community stakeholders. Summer interns with the RTC work on a variety of projects, but typically focus on one project that is central to their time at Duke. In the past, these projects have included work on the effectiveness of fish consumption advisories and communicating information about soil contamination to community gardeners.

Community Engagement Core. This core works with communities across North Carolina affected by environmental contaminants. Communities can contact us with short-term requests for information related to environmental contamination or with proposals for longer term engagement through participatory research projects and/or education and outreach activities. By “community engagement,” we mean working in an ongoing way with a community, listening closely to their needs and learning from their experiences.

Analytical Chemistry Core. This core fosters the evaluation of contaminant exposure to humans and wildlife and the determination of contaminant distribution in the environment. The core provides routine quantitative and qualitative analysis of organic and metal contaminants on a routine basis to investigators in support of Duke SRC research projects. The ACC also develops novel methods for emerging contaminants of concern in environmental and biological samples on an as-needed basis. Finally, the ACC serves as a consulting and training resource for cutting-edge analytical chemistry needs within the Duke SRC.

Positions are open to students currently enrolled in a four-year postsecondary institution (either as an undergraduate or as a master’s student). Candidate must be legally authorized to work in the USA. Visa sponsorship is not available. All summer trainees will be paid a $12/hour and are expected to work full-time for 10 weeks for a maximum of 35 hours per week (start and end dates are flexible between mid-May through mid-August). Students will visit other Superfund Center labs located on Duke’s campus, participate in weekly research discussions, lab meetings, seminars, and workshops.

Applicants should email a (1) cover letter explaining their educational background and interest in research + specifying ONE or TWO projects/cores or PIs of interest, and (2) resume/CV addressed to: 

Dr. Joel Meyer, Director of Training Core AND Ms. Sarah Phillips, Administrator

The deadline for application submission is Friday, February 1, 2019.

 Questions regarding project descriptions, summer expectations or benefits should contact Sarah Phillips by email. Please do not directly contact individual PIs.

Toxicology Seminar Series: Dr. Lisa Satterwhite, Thursday, February 1st.

Category : toxseminar


Our Toxicology Seminar Series, is taking place this Thursday, February 1, from 11:45 am – 1:00 pm in Field Auditorium, Environment Hall, on Duke’s West Campus. During Thursday’s seminar, Dr. Lisa Satterwhite will be speaking about her research with the Latino farmworker communities of eastern NC. Her talk is entitled “Pesticide Exposure and Predictive Genomics: Finding Early Stage Asymptomatic Disease.”

Dr. Satterwhite initiated an ongoing field study in 2010 after learning of severe birth defects among Latina farmworkers. She will share information about the first genomic signature for pesticide exposure that is highly similar to Parkinson’s disease and early results of neurodevelopmental deficits in children and youth who do farmwork. She will end with predictive risk models based on the electronic medical record that can be applied to any diagnosis related to an environmental exposure.

Dr. Satterwhite earned her PhD in molecular cell biology at Johns Hopkins University School of Medicine where she identified mechanisms that cells use to delay cytokinesis until after chromosome segregation has begun. She studied classical yeast genetics and chromosome segregation in the Department of Molecular Biology at Princeton University as a Damon Runyon Walter Winchell Fellow. Satterwhite joined Duke Biomedical Engineering to study health inequity in Latino migrant farmworkers and agricultural communities of eastern NC, to collaborate with Duke Photonics to create diagnostic optical signatures for sickle cell anemia and cancer, and to teach a class where students do original research towards an early stage pancreatic cancer diagnostic. She and her lab also partner with the NICHES, a children’s environmental health and prevention research center at Duke.



Seminar: Nov. 10, Jessica Brandt

Category : Uncategorized

Our seminar speaker on Friday, November 10, from 12:00 – 1:20pm in Field Auditorium, Environment Hall, will be our own Jessica Brandt, a 5th year UPEH/ITEHP PhD candidate in Dr. Rich Di Giulio and Dr. Emily Bernhardt’s labs. She will be speaking about “Tracing coal ash through aquatic food webs: enrichment, bioaccumulation, and toxicity.”


Please find the abstract of her talk below:

Coal-fired power plants are the largest point source of environmental pollution in the US and release an estimated 1 million metric tons of pollutants (i.e., coal combustion residuals or CCRs) to aquatic ecosystems each year. In the past, research on the ecotoxicological consequences of this waste stream have focused on selenium and the US EPA has recently revised their selenium criteria for the improved protection of aquatic life. In this talk, I will describe the current selenium burden in CCR-receiving systems as it relates to these revised criteria for surface waters and fish tissues, and discuss how sub-teratogenic levels of selenium exposure can compromise the ecological fitness of freshwater fishes. Finally, I will present the CCR waste stream as a multivariate mix of toxicologically-relevant stressors and consider how ecosystem-specific features influence the magnitude and duration of CCR impacts in lakes with decades-long histories of inputs from adjacent power plants.

Seminar: Nov. 3, Dr. Andrew Whitehead, UC Davis

Category : Uncategorized

Our speaker this Friday, November 3, is Dr. Andrew Whitehead from UC Davis. We be in Field Auditorium, Environment Hall, on Duke’s West Campus, for his talk from 12:00 pm – 1:20 pm. Please join us!

Dr.  Whitehead will be speaking about “The Solution to Pollution is … Evolution? The Genomic Basis of Rapid Adaptation in Killfish.” The abstract for his talk is below:

A hallmark of biological systems is their ability to evolve and adapt to changing environmental conditions. In particular, species have been successfully evolving adaptations to chemical poisons for billions of years. They key challenge in the anthropocene is the severity and pace of change of the chemical environment. What are the attributes of species that contribute to their adaptive potential in the face of such environmental change, and what kinds of genetic changes are necessary to rescue species from extinction? Killifish are abundant in estuaries along the Atlantic coast of North America, including in sites polluted with common and persistent organic pollutants. Rapid adaptive evolution has increased the frequency of genetic variants that contribute to heritable chemical tolerance in polluted sites. We present an analysis of 400 whole genome sequences and transcriptomics to reveal the genes and pathways that affect chemical sensitivity in these populations. Importantly, this evolutionary process, coupled with our analysis, has revealed the types of sensitivity-affecting mutations that remain fit in nature. We also present some preliminary QTL mapping that links sensitivity to particular classes of chemicals to particular genes. We propose a comparative QTL mapping program to link sensitivity to specific chemicals (dioxins, PCBs, PAHs) and resistance to particular developmental phenotypes (cardiovascular system and craniofacial developmental abnormalities) in multiple genetic backgrounds. This program should reveal the types of mutations, and the genes and pathways in which they may occur, that affect sensitivity to multiple developmental syndromes upon exposure to environmental pollution while maintaining animal fitness in the real world

Reminder – if you are coming from off-campus, we can help you with parking. Please email Sarah Phillips for more info.

HELP US BEING GREEN – bring your personal drinkware and/or plates!

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Seminar: October 27, Laura Maurer, PhD, MPH, ExxonMobil Biomedical Sciences, Inc.

Category : Uncategorized

A friendly reminder about the upcoming Friday, October 27, UPEH/ITEHP Seminar from 12:00 pm – 1:20 pm in Love Auditorium, LSRC B101, on Duke’s West Campus. Laura Maurer, PhD, MPH, will be speaking about “Applying toxicological data to regulatory decision making.”

Dr. Maurer was postdoc in the Nicholas School from 2014-2016 in Joel Meyer’s lab. Prior to her time in Durham, she did her thesis work in toxicology at the University of Michigan. Following her time at Duke, Laura took a position in industry as a toxicologist with ExxonMobil Biomedical Sciences, Inc. which involves multiple toxicology-related roles and a few non-toxicology-related ones.

Reminder: if you are coming from off-campus, we can help you with parking. Please contact Sarah Phillips at for more information.

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Seminar: Oct. 20, Robert Tighe, MD, Duke University Medical Center

Category : Uncategorized

Please join us on Friday, October 20, at 12:00 pm in Field Auditorium, Environment Hall, to hear Dr. Robert Tighe speak about “Links between pulmonary macrophage function and environmental exposures.”

Dr. Tighe is an Assistant Professor of Medicine at the Duke University School of Medicine within the Pulmonary, Allergy and Critical Care unit.

See abstract below for specific information regarding his talk on Friday.

The research focus of our laboratory is to identify susceptibility factors and candidate pathways, relevant to host biological responses to environmental pollutants. By carefully dissecting these links, his lab is gaining insight into how environmental pollutants acutely induce respiratory symptoms and exacerbate chronic lung diseases. This can lead to targeted therapeutics and/or identify susceptible populations. We focus on macrophages as central mediators of pulmonary responses to environmental pollutants. To do this, we have developed advanced techniques using flow cytometry to define macrophages and immune cells in the lung of rodents and humans. In the present talk, I will discuss the use of flow cytometry techniques to define immune populations in the lung and also discuss ways that air pollution modifies macrophage functions.

Seminar: Oct. 13, Dr. Christopher Kassotis, PhD

Category : Uncategorized

Please join us on Friday, October 13, at 12:00 pm in Field Auditorium, Environment Hall, to hear Dr. Chris Kassotis speak about “Mechanisms of adipogenic activity of environmental contaminants and mixture.” Dr. Kassotis is currently an NRSA postdoctoral research fellow in the Nicholas School of the Environment. He works in Dr. Heather Stapleton’s lab and is researching the ability of and mechanisms through which various indoor contaminants and house dust may promote adipogenesis (lipid accumulation in fat cells and/or fat cell proliferation) and contribute to potential adverse metabolic health in children.

See abstract below for specific information regarding his talk on Friday. 

Obesity and metabolic disorders are a large societal concern and generate significant human health care costs. Recently, attention has focused on the potential for environmental contaminants to act as metabolic disruptors through disruption of nuclear hormone receptors. Our work has sought to evaluate the potential for diverse environmental contaminants to promote fat cell development, using an in vitro model of adipogenesis. These mouse pre-adipocytes, when exposed to “active” chemicals, differentiate into adipocytes, undergo morphological changes, accumulate triglycerides, and eventually come to resemble a mature human white fat cell. Our recent work has found that numerous indoor semivolatile organic contaminants can promote fat cell differentiation, and that mixtures of these chemicals present in house dust are also sufficient to drive differentiation at low, environmentally relevant levels. Our next steps are digging deeper into mechanisms, causative chemicals, and potential health impacts from exposure.

Seminar: October 6, Dr. Rebecca Fry, UNC

Category : Uncategorized

On Friday, October 6, at 12:00 pm in Environment Hall’s Field Auditorium, Dr. Rebecca Fry will present a talk entitled “The Placental Epigenome as a Driver of the Developmental Origins of Health and Disease.

Dr. Fry serves as the Director of the UNC Superfund Research Program and is a professor with the Department of Environmental Sciences and Engineering. The abstract for her talk is below:

The placenta serves as a transient organ that is responsible for the regulation of the prenatal environment and is critical for optimal fetal development. It acts as a nutrient transporter and produces critical hormones to maintain pregnancy and support the fetus. In contrast to these essential functions, the placenta may also serve as a source of exposure for toxic substances, dysregulated hormone signaling and immune-related proteins. Such exposures including maternal stress, excess hormones, cytokines or environmental toxicants impact fetal health and influence later-life health outcomes. An increasing body of literature supports sex-specific birth and later-life outcomes in relation to adverse in utero environments. For example, sex-specific perinatal and later life outcomes have been linked to toxic substance exposure, maternal stress and maternal immune status. It is likely that sexdependent health outcomes in infants may be associated with sexual dimorphism of the placenta. In support of this, physiologic differences between placentas obtained from male or female pregnancies have been observed. While key physiological differences have been observed in male and female placentas, the underlying mechanisms are not well established. Epigenetic regulation may underlie not only the physiologic differences observed between male and female placentas but later life health outcomes. For instance, key differences in chromatin structure have been observed between male and female placentas, suggesting that there is a role for epigenetic regulation in placental sexual dimorphism. Understanding epigenetic regulation in the placenta is important given the modifiability of its epigenome in response to prenatal stressors, and its role as a mediator of the developmental origins of health and disease. Additionally, because certain epigenomic marks are stable over time, it is possible that changes to the fetal placenta methylome explain the sex-based differences in later-life disease risks. These data provide key insights into sexual dimorphism of the placental methylome as a driver of differential susceptibility to adverse prenatal environmental conditions and later life health.

Seminar: Friday, Sept. 29, Andrea Baccarelli, MD, PhD

Category : Uncategorized

On Friday, September 29, at 12:00 pm in Environment Hall’s Field Auditorium, Dr. Andrea Baccarelli will present a talk entitled “Mitochondriomics and Epigenetics in Human Air Pollution Studies – New Findings and Methodological Challenges.” Dr. Baccarelli serves as the Environmental Health Sciences Department Chair and the Director of the Laboratory of Precision Environmental Biosciences at Columbia University. His research explores epigenetic and molecular mechanisms as potential functional pathways linking exposures to environmental pollutants to human disease.

Please see the abstract for his talk below:

The amount of scientific research linking environmental exposures and human health outcomes continues to grow; yet few studies have teased out the mechanisms involved in environmentally-induced diseases. Cells can respond to environmental stressors in many ways: inducing oxidative stress/inflammation, changes in energy production and epigenetic alterations. Mitochondria, tiny organelles that each retains their own DNA, are exquisitely sensitive to environmental insults and are thought to be central players in these pathways. While it is intuitive that mitochondria play an important role in disease processes, given that every cell of our body is dependent on energy metabolism, it is less clear how environmental exposures impact mitochondrial mechanisms that may lead to enhanced risk of disease. My presentation will highlight (i) the importance of exploring environmental mitochondriomics in environmental health sciences, (ii) why environmental mitochondriomics is well suited to biomarker development in this context, and (iii) how molecular and epigenetic changes in mitochondria and mitochondrial DNA (mtDNA) may reflect exposures linked to human health outcomes.

April 2020