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.
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
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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 email@example.com for more information.
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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.”
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.
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.
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.
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.
Join us on Friday, September 22! A Superfund-themed symposium will be held in Environment Hall on Duke University’s West Campus from 9:00 am – 5:00 pm.
Bill Suk, PhD, Director of the Superfund Research Program at NIEHS, will give a keynote lecture to start the day. Investigators from each of the Duke Superfund Center’s research projects and support cores will provide an overview of their work, and trainees will present research highlights during the afternoon session.
Please RSVP here. Please park in the Bryan Center – parking passes will be given during the symposium.
Kickoff: Duke University Superfund Research Center (SRC)
Fall 2017 Symposium: hosted by the Duke University Program in Environmental Health
Field Auditorium, Environment Hall, Duke University West Campus
8:30 – 9:00 am Registration and Continental Breakfast
9:00 – 9:15 am Welcome and Introductions, Dr. Heather Stapleton, Deputy Director, Duke University SRC
9:15 – 10:00 am Keynote: History of the Superfund Program, Dr. Bill Suk, Director, NIEHS Superfund Research Program
10:00 – 10:20 am History and Highlights of the Duke University SRC, Dr. Rich Di Giulio, Director, Duke University SRC
10:20 – 10:35 am Coffee Break
10:35 am – 12:30 pm Overview of Center: PI speed talks (7 minutes + 3 for questions)
12:30 – 1:45 pm Lunch (provided)
1:45 – 3:45 pm Trainee Speed Talks – Topically Organized (17 minutes + 3 for questions)
3:45 – 4:30 pm Discussion: Promoting Collaborations
What opportunities are we missing? What help/resources (other projects, cores, etc.) would we each like to advance our research?