• Friday, March 4, 2022

    10:00 AM -12:00 PM
    Location: zoom (email shawn.tucker @ oregonstate.edu for full info)

    2022 PNWC-TEHR Pilot Project Ignite Talks


    Applications for the Strategic Initiative Awards:

    1. Dr. Diana Rohlman (OSU) “Wildfire Smoke and Infant Health”
    2. Dr. Sarah Rothenberg (OSU) “Reducing Methylmercury Exposure through Fish Consumption in Lane County, Oregon”
    3. Dr. Manuel Garcia-Jaramillo (OSU) “Identification and Evaluation of Toxic Contaminant Mixtures in Surface Water from the Portland Harbor Superfund Site Using Effect-Directed Analysis Coupled to Non-target High-Resolution Mass Spectrometry”


    Applications for the Vanguard Awards:

    1. Dr. Veronica Irvin (OSU) “Development of a treatment decision aid for home environmental contaminants using a mobile approach”
    2. Dr. Siva Kolluri (OSU) “p27/Kip1 cell cycle inhibitor as an unexpected regulator of PAH toxicity”
    3. Dr. Lew Semprini (OSU) “Cometabolic Treatment of 1,2,3-Trichloropropane in Hydrogel Beads and the Evaluation of Toxicity Reduction Using Embryonic Zebrafish Assays”
    4. Dr. Karen Guillemin (UO) “Modulation of tissue iron by microbiota, inflammation, and environmental exposures”
    5. Dr. Susan Tilton (OSU) “Development of a 3D respiratory co-culture model for assessing toxicity to chemicals from wildfire smoke”
  • Friday, February 4, 2022

    11:00-12:00 PM
    Location: Email [email protected] for zoom invite

    Rebalancing Agrochemical Cycles: From The Molecular To Systems Level

    Leanne Gilbertson, PhD
    Associate Professor of Environmental Engineering Fulton C. Noss Faculty Fellow
    University of Pittsburgh

    Immense agrochemical inputs, including pesticides and nutrients, are required for crop production and their use is incredibly inefficient. When considered at the global scale, these inefficiencies have tremendous economic and environmental consequences caused by emissions to the atmosphere (e.g., greenhouse gases) and surrounding water bodies (e.g., eutrophication). There are also massive losses of embodied resources and emissions when agrochemicals do not reach their target. As such, there is an opportunity for innovative solutions to have a big impact on an industry that is critical to the wellbeing of the global population. Yet, choices we make about the raw materials we use and how we design new technologies to increase performance have upstream (e.g., embodied resources) and downstream (e.g., emissions) implications. A combined approach that involves design decisions at the molecular level with systems-level analyses is necessary to preclude shifting burdens to other life cycle stages and to uncover high impact contributors across the life cycle. In this talk, I will discuss research from my group that aims at defining and addressing agrochemical use inefficiencies in crop production, including (i) evaluating tradeoffs of proposed nanotechnology solutions, (ii) sustainably designing carriers for delivering agrochemicals more efficiently to roots, and (iii) modeling nitrate transport and uptake in soil.   

  • Friday, January 7, 2022

    11:00am - 12:00pm (PST)
    Location: zoom (email shawn.tucker @ oregonstate.edu for full info)

    Exosomes and extracellular vesicles in environmental toxicology – new approaches to assess the impact of environmental exposures on human health

    Andrea Baccarelli, MD PhD
    Chair and Professor of Environmental Health Sciences, Director, Precision Environmental Health Laboratory
    Director, P30 Center for Environmental Health in Northern Manhattan Columbia University Mailman School of Public Health, New York, NY

    My lab studies a cell-to-cell communication system that the body uses to maintain homeostasis. When environmental exposures disrupt homeostatic communication patterns, we seek to detect those shifts by “listening in” to the communications mediated by circulating extracellular vesicles (EVs). EVs are tiny (<1 µm) membrane-bound vesicles, which encompass exosomes, microvesicles, microparticles and other types of vesicles, released into the bloodstream by human cells and can be easily studied in blood samples. EVs contain cargo, such as non-coding RNAs, that can act on the recipient cell to modify it. My lab found overall patterns, based on the concentrations of EVs and their cargo, before disease develops. We also determined that EV-based communication is highly sensitive to environmental exposures. However, human data on EVs as a potential mediator of environmental toxicity are limited. I will present evidence from human environmental studies indicating that EV encapsulated miRNAs may mediate effects caused by toxic exposures. In these investigations, we have shown that exposures, including air pollution, BPA and other chemicals, strongly modify the EV-miRNA profiles. I will present data demonstrating that altered EV-miRNA profiles are associated with disease. Based on current evidence, I will propose possible models for the interplay between toxicants and EVs in human health and disease.

  • Friday, December 3, 2021

    Location: Zoom

    Environmental Chemical Impact on the Host-Microbiome Interaction

    Andrew D. Patterson, PhD
    Pennsylvania State University

    The field of toxicology has long suggested that host microbiota could influence the disposition and toxicity of environmental chemicals. Early correlative studies of heavy metal exposure identified the microbiota as contributing to host toxicity. However, technological limitations necessary for cataloging the microbiota community structure and for characterizing their metabolic capabilities have hitherto hindered progress in this area. Technological advances including sequence-based identification and functional characterization via mass spectrometry-based metabolite profiling have begun to shed light on how microbes influence and/or impact toxicity outcomes. Data will be presented to highlight key aspects of gut microbiota-host interaction and how environmental chemicals (dioxins, furans, polychlorinated biphenyls) can impact this important connection.

  • Friday, November 5, 2021

    1:00-2:00 PM
    Location: Zoom

    The Silent Spring of Obesogens: Translational Mechanisms of Obesity Caused by DDT Exposure Across Lifetimes

    Michele A. La Merrill, PhD MPH
    Associate Professor of Department of Environmental Toxicology
    UC Davis

    Adult and prenatal exposures to the pesticide DDT and its metabolite DDE have been associated with risk of obesity in subsequent generations of people, mice and rats in numerous studies.  Our research indicates that these obesogenic effects are caused by impaired metabolism. We have observed that prenatal exposure to DDT or DDE impairs body heat production in mice from their first week of life to 9 months of age. Indeed, metabolic reductions in thermogenesis, the production of body heat, are associated not just with DDT and DDE exposures, but also with numerous pharmaceuticals and genes that are known to cause obesity. Epigenome studies in both mice and humans with DDT and DDE exposures have revealed extensive changes in DNA methylation enriching the thermogenesis pathway, including changes in DNA methylation of upstream signaling and substrate regulation pathways. Defects in the thermogenic function but not the structure of mouse brown adipose tissue and cultured brown adipocytes have observed. Additionally, prenatal DDT reduces the innervation of mouse brown adipose tissue, and the upstream synaptic connectivity is reduced by either DDT or DDE exposure prenatally. This body of research evidence indicates that both DDT and DDE act as obesogens by targeting both brown adipose and the sympathetic nervous system to impair thermogenesis. 

  • Friday, October 1, 2021

    3:00-4:00 PM
    Location: Contact us for Zoom info


    Shohreh F. Farzan, PhD
    Asst Professor of Environmental Health, Dept of Population and Public Health Sciences
    Keck School of Medicine, University of Southern California

    A growing body of evidence supports a role for environmental contaminants, such as air pollutants and toxic metals, in the development and progression of cardiometabolic disease in adults. However, relatively little is known about the influence of these exposures on cardiovascular and metabolic disease risk during vulnerable lifestages, such as childhood, adolescence and pregnancy. For example, pregnancy may act as a window of susceptibility to environmental exposures, but relatively few studies have explored the effects of environmental contaminants on maternal prenatal and postpartum health. Among children, in utero and early life exposures may impact subclinical markers of cardiovascular dysfunction, with potential implications for cardiovascular health trajectories. As such, these lifestages may represent critical periods for intervention, as exposures during these times may exacerbate the risk of long-term cardiometabolic health effects. In this seminar, Dr. Farzan will discuss emerging research in this area, with examples from her work investigating the role of prenatal environmental exposures and psychosocial stressors on maternal perinatal cardiometabolic health, as well as the role of metals and air pollutants on subclinical indicators of cardiovascular disease risk from childhood to young adulthood. 

  • Friday, August 6, 2021

    1:00-2:00 PM
    Location: LINC 128 and online, for those interested, contact us for the zoom link

    Environmental Epitranscriptomics: Dynamic Rna Modifications And Environmental Health Sciences

    Fred Tyson, PhD
    Program Director in the Genes, Environment and Health Branch of the Division of Extramural Research and Training(DERT)

    Fred Tyson is a Program Director in the Genes, Environment and Health Branch of the Division of Extramural Research and Training (DERT) at the National Institute of Environmental Sciences. He received his PhD in cell biology and developmental genetics from Rutgers University.   Postdoctoral training in molecular genetics was obtained at Sloan-Kettering followed by additional training in molecular oncology at Duke.  Tyson served as a Senior Staff Fellow at NIEHS in the Laboratory of Molecular Toxicology and as a Senior Scientist at the Saccamanno Cancer Research Institute in Grand Junction, CO. As an NIEHS program officer, Tyson has developed a research portfolio that employs multi-disciplinary approaches to address environmental health science issues.  He has supported diverse research programs in environmental justice, health disparities, genomics, epigenomics, epitranscriptomics and marine toxicology. His current portfolio responsibilities include oversight of grants and programs addressing lung cancer, electronic nicotine delivery systems, oceans and human health as well as programs that address how environmental exposures may perturb epigenomic and epitranscriptomic processes. He has worked with trans-NIH programs as well as leading components of Common Fund supported initiatives as well as working across agencies such as the NSF, FDA, CDC and NOAA to advance environmental health science research priorities.  

  • Friday, July 9, 2021

    1:00-2:00 PM
    Location: For those interested, contact us for the zoom link

    Application Of Single Cell Transcriptomics To Mechanistic Toxicology

    Peer Karmaus, Phd
    Staff Scientist
    National Institute of Environmental Health Sciences

    Toxicology testing has traditionally relied on rudimentary single endpoint outcomes. With the advent of single cell technologies, the biological unit of the cell can be interrogated at the mechanistic level. With recent advances in single cell transcriptomics, an unprecedented level of detail is now revealed on a per cell basis. These technologies now allow the assessment of population heterogeneity and the effect of chemical perturbation on cellular heterogeneity. Here Dr. Karmaus will discuss an example of applying single cell transcriptomics for evaluating the attenuation of T cell activation by atrazine. 

    Peer Karmaus is a Staff Scientist at the National Institute for Environmental Health Sciences and an Adjunct Assistant Professor at Michigan State University. His research focuses on how metabolism in innate and adaptive immune cells dictate cell fate and function.  

  • Thursday, July 8, 2021

    1:00-2:00 PM
    Location: LINC 128 and online (click link below for recording)

    Identification Of Sars-cov-2 Host Factors Using Genome Wide Crispr Screens

    Chris Vulpe MD, PhD
    Professor, Center for Environmental and Human Toxicology
    University of Florida

    The COVID-19 pandemic has resulted in 153 million infections and 3.2 million deaths as of May 2021. While effective vaccines are being administered globally, there is still a great need for antiviral therapies as potentially antigenically distinct SARS-CoV-2 variants continue to emerge across the globe. Viruses require host factors at every step in their life cycle, representing a rich pool of candidate targets for antiviral drug design. To identify host factors that promote SARS-CoV-2 infection with potential for broad-spectrum activity across the coronavirus family, we carried out a collaborative effort with Dr. Michel Norris and Dr. Stephanie Karst to perform genome-scale CRISPR knockout screens in two cell lines (Vero E6 and HEK293T ectopically expressing ACE2) with SARS-CoV-2 and the common cold-causing human coronavirus OC43. We identified multiple genes and functional pathways that have been previously reported to promote human coronavirus replication as well as novel genes and pathways. Of note, host factors involved in cell cycle regulation were enriched in our screens as were several key components of the programmed mRNA decay pathway. We identified novel candidate antiviral compounds targeting a number of factors revealed by our screens. Our studies substantiate and expand the growing body of literature focused on understanding key human coronavirus-host cell interactions and exploit that knowledge for rational antiviral drug development. 

  • Sunday, July 4, 2021

    1:00-2:00 PM

    Interrogating Microglia As A Critical Mediator Of Pfos-induced Neurotoxicity

    Jessica Plavicki
    Manning Assistant Professor of Pathology and Laboratory Medicine
    Brown University

    Per- and Polyfluoroalkyl Substances (PFAS) are a class of global toxicants that are resistant to environmental degradation. Exposure to perfluorooctane sulfonate (PFOS), a prevalent PFAS congener, dampens adaptive immune responses in children. However, it is not known whether PFOS exposure affects the development and function of microglia, the resident innate immune cells in the brain. Using a single cell image analysis pipeline, we found that PFOS exposure produced a rounded, activated microglia morphology in developing zebrafish. PFOS-exposed embryos exhibited a heightened microglial response to brain injury. The exacerbated responses were not due to changes in inflammatory cytokine signaling or an increase in cell death; therefore, we examined other factors in the microenvironment that may modulate microglial development and behavior. Using the photoconvertible calcium indicator CaMPARI, we observed increased neural activity following PFOS exposure. The observed increase may reflect aberrant connectivity associated with the failure of microglia to refine neural networks. Alternatively, the increase in neuronal firing may drive the observed activated microglial phenotypes and alter microglial response to injury. Using optogenetics, we were able to induce a ramified, less activated state in microglia and rescue the exacerbated microglial response to brain injury. We are currently conducting experiments to determine if neural silencing is sufficient to rescue the altered microglial morphology in PFOS-exposed embryos and the microglial response to brain injury.