Annual Meeting Home | SOT Home | | Contact Us | Join | Site Map | Help


Share this page.

Continuing Medical Education (CME) Courses

The Clinician-Scientist Engagement (CSE) Task Force of the Society of Toxicology identified five CME sessions that offer educational opportunities that support physicians and other healthcare providers’ improvement in their competence in patient care, medical knowledge, practice-based learning and improvement, interpersonal and communication skills, professionalism, and systems-based practice.

SOT is pleased to offer the following CME workshop, symposium, and regional interest sessions during the SOT Annual Meeting on Monday, March 14, through Thursday, March 17, in the New Orleans Ernest N. Morial Convention Center.

Schedule:

Workshop Session: Transient Receptor Potential A1 (TRPA1) Cation Channels: Fluttering Hearts, Headaches and Hot Flashes—Can One “Environmental Sensor” Be the Cause of All the Pain?

Monday, March 14, 2016, 9:30 AM–12:15 PM
Room 208

Theme: Advances in Neurotoxicology

Accreditation Statement: This activity has been planned and implemented in accordance with the accreditation requirements and policies of the Accreditation Council for Medical Education (ACCME) through the joint providership of The University of Arkansas for Medical Sciences (UAMS) College of Medicine and the Society of Toxicology (SOT).  The UAMS College of Medicine is accredited by the ACCME to provide continuing medical education for physicians.

Designation Statement:  The UAMS College of Medicine designates this live activity for a maximum of 2.75 AMA PRA Category 1 Credit(s)™.  Physicians should claim only the credit commensurate with the extent of their participation in the activity.

Target Audience: Physicians and other health care providers

Learning Objectives: After the activity, the participant will be able to:
(1) Identify environmental irritants that activate TRPA1 and their most common sources ; (2) Describe the interaction between volatile toxics such as acrolein and the TRPA1 channel and its role in the health effects of inhaled toxicants; (3) Explain the various different health effects of TRPA1 agonists to patients or individuals who are at higher risk of adverse responses (i.e. elderly); (4) Associate exposure to irritants in tobacco smoke with cardiopulmonary toxicity and appraise the effects of several e-cigarette flavorants; (5) Describe the integrated and protective role of TRPA1 receptors against inhaled toxics; (6) Describe the role of TRPA1 and environmental irritants in triggering the trigeminovascular reflex and migraine; (7) Identify how lifestyle and environmental exposures can alter individual epigenetics; (8) Associate lifestyle and environmental factors with changes in pain threshold and heat sensitivity.

Chairperson(s): Mehdi Hazari, US EPA, Research Triangle Park, NC, and Daniel J. Conklin, University of Louisville, Louisville, KY.

The following Specialty Sections recommend this sessions as being of special interest to its members:

    • Cardiovascular Toxicology Specialty Section
    • Inhalation and Respiratory Specialty Section
    • Neurotoxicology Specialty Section

The role of transient receptor potential (TRP) cation channels, particularly TRPA1, in numerous toxicological pathways has garnered great interest over the last decade. These investigations have focused on the ability of TRPA1 to act as an “environmental sensor” for chemical irritants such as acrolein, formaldehyde and chloramines, which are found in disinfectants, but also as a mediator of pain, inflammation and acute physiological changes given it is a target of reactive oxygen species such as hydrogen peroxide, and even endogenous agonists such as 4-hydroxy-nonenol. These features as well as its presence on sensory neurons throughout the body make TRPA1 an important component in the mode of toxicity of not only gaseous irritants, but also chemicals transmitted in water or by direct contact with the skin. Although it has become clear that TRPA1 contributes to the acute adverse health effects of exposure, new studies have now revealed that it is also involved in the development and progression of chronic diseases. This latter phenomenon is likely related to variations in the TRPA1 gene which manifest at a young age but also due to a lifetime of accrued epigenetic changes that essentially alter the responsiveness of an individual to a given exposure. Therefore, this session will highlight the newly understood multifaceted roles of TRPA1 in environmental sensing. The presentations will focus on a broad array of topics including how TRPA1 mediates acute cardiovascular effects after inhalation of air pollutants.  Findings will show that inhalation of not only typical TRPA1-activating gaseous irritants, but also particulate matter, causes cardiac arrhythmogenesis as well as vascular responses through TRPA1 mediated mechanisms.  Attendees will also hear about the role of TRPA1 in the “masking” effects of flavorants such as menthol and cinnamon in e-cigarettes, which has important implications in both studying the health effects of these alternative tobacco products and their potential regulation. In addition, chemical sensitivity to environmental irritants will also be explored in relation to TRPA1 and trigeminal-vascular mechanisms, which are nasal sensory pathways that alter blood flow to the brain and are linked to episodic headaches. Finally, the broader implications of TRPA1 variability, lifestyle and environment will be addressed from an epigenetic perspective in a study of identical twins to demonstrate links to susceptibility and chronic pain.

9:30 AM–9:35 AM

Introduction
Mehdi Hazari, US EPA, Research Triangle Park, NC.

9:35 AM–10:05 AM

TRP Ion Channels as Key Targets of Tobacco and Electronic Cigarette Irritants and Flavor Additives
Sven E. Jordt, Duke University, Durham, NC.

10:05 AM–10:35 AM

Examining the Role of TRPA1 in Air Pollution-induced Cardiac Arrhythmias and Autonomic Imbalance
Mehdi Hazari, US EPA, Research Triangle Park, NC.

10:35 AM–11:05 AM

From Tobacco Smoke to Gas Attacks: How TRPA1 Modulates Cardiopulmonary Toxicity of Acrolein
Daniel J. Conklin, University of Louisville, Louisville, KY.

11:05 AM–11:35 AM

TRPA1 and Meningeal Vasodilatation Due to Environmental
Irritants—Mechanisms of Migraine

Joyce Hurley, Indiana University, Indianapolis, IN.

11:35 AM–12:05 PM

Epigenetic Changes in the TRPA1 Promoter Show Pain Sensitivity is Affected by Lifestyle and Environment
Stephen McMahon, King’s College-London, London, UK.

12:05 PM–12:15 PM

Panel Discussion/Q&A

Regional Interest Session: The Toxicological Implications of the Gulf Oil Spill: Research Accomplishments and Research Needs

Monday, March 14, 2016, 9:30 AM–12:15 PM
Room R08

Theme:  Health and Environmental Impacts of Man-Made and Naturally Released Toxicants

Accreditation Statement: This activity has been planned and implemented in accordance with the accreditation requirements and policies of the Accreditation Council for Medical Education (ACCME) through the joint providership of The University of Arkansas for Medical Sciences (UAMS) College of Medicine and the Society of Toxicology (SOT). The UAMS College of Medicine is accredited by the ACCME to provide continuing medical education for physicians.

Designation Statement: The UAMS College of Medicine designates this live activity for a maximum of 2.75 AMA PRA Category 1 Credit(s)™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

Target Audience: Physicians and other health care providers

Learning Objectives: After the activity, the participant will be able to:
(1) Examine the role of toxicological science in addressing human exposure to environmental contaminants associated with technological disasters; (2) Describe transdisciplinary environmental epidemiological study designs tailored to addressing complex population-based environmental health threats; (3) Apply the findings associated with the impact of interactions between chemical and non-chemical stressors on human health in clinical- and other health care delivery settings.

Chairperson(s): Bernard Goldstein, University of Pittsburgh, Pittsburgh, PA, and Maureen Lichtveld, Tulane University, New Orleans, LA.

The following Specialty Section recommends this session as being of special interest to its members:

    • Risk Assessment Specialty Section

This session will focus on existing toxicological research concerning the impact of Gulf oil spill on human health, discuss the many remaining uncertainties requiring toxicological research, and review the availability to toxicological scientists of the more than $1 billion that has or will be spent in different programs on research related to preventing and to understanding the potential impact of future oil spills affecting American coastal waters and communities. More than five years ago the Deepwater Horizon explosion released millions of barrels of oil into the Gulf of Mexico over a five month period. The chemical and physical characteristics of this crude oil changed over time due to its interaction with sea and shore and sun. Much of it was burned at sea, releasing combustion products. An unprecedented amount of a chemical dispersant sprayed on the oil spill added to the potential toxicological implications. The potential impact on seafood safety also has been a significant issue with concern both about health effects to those ingesting seafood as well as the economic and social implications to Gulf communities dependent on gathering seafood.  After the spill, a Society of Toxicology Working Group developed a two page description of the toxicological implications aimed broadly at the public and at decision makers. www.toxicology.org/pm/Deepwater_oil_spill.pdf.  This serves as a baseline for the proposed seminar which will be co-chaired by Dr. Maureen Lichtveld, the chair of the Department of Global Environmental Health Sciences at Tulane University School of Public Health and Tropical Medicine who has been actively involved in the oil spill response, and Dr Bernard Goldstein of the University of Pittsburgh who has reviewed the subject with Dr. Lichtveld  (New Engl J Med 364:1334–48, 2011)  and has  been significantly involved in three of the programs funding oil spill activities.  Dr. Goldstein was also involved n the SOT Communications Strategy that led to the SOT Working Group document.  The opening presentation will be by Dr. Linda Birnbaum, Director of the NIEHS, who will provide an overview of the NIEHS response which has led to funding of the large majority of oil spill toxicological research, and of future research needs. This will be followed by scientists directly involved in research related to the oil spill. Dr. Cornelius Elferink of the University of Texas Medical Branch will present studies related to petrogenic PAH contamination in Gulf seafood and its implications to local seafood consumers, including use of a PAH assay dependent on Aryl Hydrocarbon Receptor responsiveness. Dr. Jeffrey Wickliffe will present information from the NIEHS Consortia (Tulane, Texas Medical Branch, University of Florida and Louisiana State University) relevant to assessing the risks of seafood contamination. Dr. Maureen Lichtveld will discuss the utilization of toxicological research in epidemiological studies evaluating the impact of the oil spill and of other Gulf area stressors on the health of vulnerable populations. Lastly, Dr. Goldstein will build upon the previous presentations, discuss the extent to which toxicological research has provided answers to the questions about potential human health impacts raised by the SOT Working Group, and  describe the many active research initiatives providing funding for oil spill research and critique the extent to which toxicological research has been included.

9:30 AM–9:40 AM Introduction

9:40 AM–10:15 AM

Gulf Oil Spill Response: Health Research, Community-Academic Partnerships, Lessons Learned, and Future Preparedness
Linda S. Birnbaum, National Institute of Environmental Health Sciences, Research Triangle Park, NC.

10:15 AM–10:40 AM

A Toxicological Assessment of Petrogenic PAH Contamination in Gulf Seafood Following the Deepwater Horizon Oil Disaster
Cornelis J. Elferink, University of Texas Medical Branch, Galveston, TX.

10:40 AM–11:05 AM

Human Health Risk Assessments Regarding Consumption of Fish and Shellfish from the Northern Gulf of Mexico Following the Deepwater Horizon Accident: Results Across Three Academic Research Consortia
Jeffrey Wickliffe, Tulane University, New Orleans, LA

11:05 AM–11:30 AM

Linking Bench to Trench: Embedding Toxicological Science in Environmental Epidemiologic Studies to Unravel Complex Health Threats in Gulf Coast Reproductive Age Women and Infants
Maureen Lichtveld, Tulane University, New Orleans, LA.

11:30 AM–11:55 AM

Opportunities and Needs for Toxicological Research Related to the Gulf Oil Spill
Bernard Goldstein, University of Pittsburgh, Pittsburgh, PA.

11:55 AM–12:15 PM

Panel Discussion/Q&A

Symposium Session: Sulfur Mustard Poisoning: Mechanisms of Dermal and Pulmonary Toxicity and New Treatment Approaches

Wednesday, March 16, 2016, 9:30 AM–12:15 PM
Room R02

Theme: Health and Environmental Impacts of Man-Made and Naturally Released Toxicants

Accreditation Statement: This activity has been planned and implemented in accordance with the accreditation requirements and policies of the Accreditation Council for Medical Education (ACCME) through the joint providership of The University of Arkansas for Medical Sciences (UAMS) College of Medicine and the Society of Toxicology (SOT). The UAMS College of Medicine is accredited by the ACCME to provide continuing medical education for physicians.

Designation Statement: The UAMS College of Medicine designates this live activity for a maximum of 2.75 AMA PRA Category 1 Credit(s)™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

Target Audience: Physicians and other health care providers

Learning Objectives: After the activity, the participant will be able to:
(1) Describe the toxicological concerns regarding sulfur mustard and specifically the incapacitating eye, skin, and respiratory tract damage produced by this chemical; (2) Discuss the mechanisms of toxicity of sulfur mustard on the skin, lungs, eyes  and bone marrow and why it is a carcinogen; (3) Describe the current treatment for sulfur mustard-induced blisters, including mechanical dermabrasion, surgery and laser debridement (“lasablation”), in addition to symptomatic and supportive treatment; (4) Describe current treatment approaches for sulfur mustard-induced lung damage using anti-inflammatory agents (e.g., steroids), antioxidants (e.g., tocopherols, melatonin, acetylcysteine, nitric oxide synthase inhibitors), and protease inhibitors (e.g., doxycycline, aprotinin, ilomastat); (5) Describe new therapeutic strategies for sulfur mustard-induced tissue damage (e.g. stem cells, antioxidants) and pitfalls in therapy (e.g. PARP-inhibitors); (6) Discuss the principles of a rapid test using an antibody for the reliable detection of pure sulfur mustard on the skin.

Chairperson(s): Allister Vale, University of Birmingham, Birmingham, United Kingdom, and Horst Thiermann, Bundeswehr Institute of Pharmacology and Toxicology, Munich, Germany.

The following Specialty Section recommends this session as being of special interest to its members:

    • Clinical and Translational Toxicology Specialty Section

Sulfur mustard (Bis(2-chloroethyl) sulphide; SM), a chemical sometimes referred to as mustard gas, is a liquid which boils at 217°C and freezes at 13°C to 15°C, which explains its persistence in the environment. Droplets of SM released in an explosion can pose a risk to health from inhalation, ingestion of contaminated food and water, as well as contact with the skin and eyes. SM was first used as a chemical warfare agent almost 100 years ago (12 July 1917) in Belgium in WWI. Since then it has been deployed in Ethiopia, in China, in the Yemen and in Iran with several hundred thousand casualties resulting. The potential further use of SM in military conflicts and by terrorists remains a threat that if realised would result in a large number of casualties with severely incapacitating eye, skin, respiratory tract, and possibly systemic, damage. SM produces acute damage to the skin (blisters, skin necrosis), to the eyes (corneal damage with temporary blindness) and to the respiratory tract (nose bleeds, tracheobronchitis and acute respiratory distress syndrome), and it can be lethal at high concentrations. SM depresses bone marrow function which may lead to secondary infection. Long-term disability due to respiratory complications is common. SM is also a recognized human carcinogen. Following SM inhalation, DNA damage, apoptosis, and autophagy  are observed in the lung, along with increased expression of activated caspases and DNA repair enzymes, biochemical markers of these activities. This is associated with inflammatory cell accumulation in the respiratory tract and increased expression of tumor necrosis factor-a and other pro-inflammatory cytokines, as well as reactive oxygen and nitrogen species. Matrix metalloproteinases are also upregulated in the lung and skin after SM exposure, which are thought to contribute to the detachment of epithelial cells from basement  membranes and disruption of the pulmonary epithelial barrier. Findings that production of inflammatory mediators correlates directly with altered lung function suggests that they play a key role in toxicity. Following skin contact with SM, keratinocytes of the stratum basale in the skin appear to be the most sensitive to its cytotoxic actions, and blistering involves the detachment of these cells from the supporting basal lamina of the basement membrane of the epidermal-derma junction. Studies on SM and its analogs in animals suggest that individual or combination therapies using anti-inflammatory agents (e.g., steroids), antioxidants (e.g., tocopherols, melatonin, acetylcysteine, nitric oxide synthase inhibitors), and protease inhibitors (e.g., doxycycline, aprotinin, ilomastat), may be effective in ameliorating the toxicity of SM-induced lung damage in humans. Experimentally, single and multiple infusions of mesenchymal stem cells have reduced SM-induced edema, necrosis, inflammation, and death at 5 weeks post-exposure.  In addition to symptomatic and supportive treatment for SM-induced blisters, mechanical dermabrasion and laser debridement (“lasablation”) have both produced an increased rate of wound healing in animal models and may be of benefit in a clinical context. A rapid test using an antibody for the reliable detection of pure SM on the skin, which gives a result within 10 minutes, has been developed.

9:30 AM–10:00 AM

Sulfur Mustard: History of Use and Features of  Exposure
Allister Vale, University of Birmingham, Birmingham, United Kingdom.

10:00 AM–10:30 AM

Pathophysiology of Sulfur Mustard-induced Skin Lesions and Current Therapeutic Options
Paul Rice, Dstl Porton Down, Salisbury, United Kingdom.

10:30 AM–11:00 AM

Sulfur Mustard-induced Toxic Lung Injury: Mechanisms of Toxicity
Alfred Sciuto, US Army Medical Research Institute of Chemical Defense, Aberdeen, MD.

11:00 AM–11:30 AM

Sulfur Mustard-induced Pulmonary Injury: Current Therapeutic Approaches to Mitigating Toxicity
Debra Laskin, Rutgers University, Piscataway, NJ.

11:30 AM–12:00 Noon

Novel Developments and Advanced Molecular Targets for Diagnosis and Treatment of Sulfur Mustard-induced Cell Damage
Horst Thiermann, Bundeswehr Institute of Pharmacology and Toxicology, Munich, Germany.

12:00 Noon–12:15 PM

Panel Discussion/Q&A

Workshop Session: “Breaking Bad”—Cardiovascular Autophagy Gone Rogue: A Putative Mechanism of Toxicity and a Drug Target in Disease

Wednesday, March 16, 2016, 2:00 PM–4:45 PM
Room 217

Accreditation Statement: This activity has been planned and implemented in accordance with the accreditation requirements and policies of the Accreditation Council for Medical Education (ACCME) through the joint providership of The University of Arkansas for Medical Sciences (UAMS) College of Medicine and the Society of Toxicology (SOT). The UAMS College of Medicine is accredited by the ACCME to provide continuing medical education for physicians.

Designation Statement: The UAMS College of Medicine designates this live activity for a maximum of 2.75 AMA PRA Category 1 Credit(s)™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

Target Audience: Physicians and other health care providers

Learning Objectives:After the activity, the participant will be able to:
(1) Describe cellular autophagy: (2) Discuss cardiovascular autophagy as an emerging therapeutic and toxicological endpoint; (3) Explain how drugs/toxicants promote cardiovascular pathology via autophagic imbalance; (4) Identify drugs that can target cardiovascular autophagy in a way that attenuates cardiovascular pathology.

Chairperson(s): Leslie C. Thompson, US EPA, Research Triangle Park, and Tammy R. Dugas, Louisiana State University, Baton Rouge, LA.

The following Specialty Sections recommend this session as being of special interest to its members:

    • Cardiovascular Toxicology Specialty Section
    • Mechanisms Specialty Section
    • Regulatory and Safety Evaluation Specialty Section

Christian de Duve coined the word “autophagy” in 1963 during his studies of the lysosome. In the 1970s autophagy was identified as a toxicological mechanism in acute liver damage caused by dimethylnitrosamine and in 1983 rubomycin injection was used to generate a model of myocardial insufficiency in rats by impairing autophagic function in the heart. Autophagy is a tightly regulated process within cells that includes 1) molecular marking of damaged or dysfunctional cellular constituents; and 2) degrading/recycling those marked cellular constituents. Essentially autophagy is a waste management system for cells. By cleaning up worn, aged, and damaged cellular constituents, autophagy helps maintain overall cellular health, function and efficiency. Disruption of autophagy can have adverse effects on cardiovascular function and impaired autophagy has been implicated in cardiovascular pathologies and toxicity responses to various pharmaceuticals and environmental toxicants. Abnormal autophagic processes have been well documented in cardiovascular disease and are increasingly being targeted for therapeutic approaches. Thus, autophagy in the cardiovascular system is emerging as an important toxicological and therapeutic endpoint. This session will highlight the clinical consequences of impaired autophagy on normal cardiovascular function, discuss emerging evidence linking alterations in autophagy to cardiotoxicity responses to antineoplastic agents, and examine autophagic consequences in vascular endothelial cells following treatment with drugs used to treat HIV. Finally, this session will highlight evidence that propose targeting autophagy as a therapeutic strategy in different vascular diseases. Namely, evidence will be presented describing targeted increase in autophagy to improve endothelial cell-mediated diabetic vasculopathy and decrease smooth muscle proliferation in conditions of atherosclerosis and restenosis.

2:00 PM–2:05 PM

Overview
Leslie C. Thompson, US EPA, Research Triangle Park, NC.

2:05 PM–2:37 PM

Clinical Perspective on Cardiovascular Autophagy
Monte S. Willis, University of North Carolina Chapel Hill, Chapel Hill, NC.

2:37 PM–3:09 PM

Contributions of Mitophagy in Cumulative Doxorubicin-induced Cardiomyopathy
Kendall B. Wallace, University of Minnesota, Duluth, MN.

3:09 PM–3:41 PM

Cycles of Injury and Repair via Mitophagy Associated with Chronic Exposures and Premature Senescence
Tammy R. Dugas, Louisiana State University, Baton Rouge, LA.

3:41 PM–4:13 PM

Autophagy as a Drug Target in Diabetic Vascular Disease
Jessica L. Fetterman, Boston University, Boston, MA.

4:13 PM–4:45 PM

Verapamil, Autophagy and Vascular Smooth Muscle Antiproliferation
Daniel J. Conklin, University of Louisville, Louisville, KY.

Workshop Session: Potential Health and Environmental Effects of Unconventional Hydraulic Fracturing

Thursday, March 17, 2016, 9:30 AM–12:15 PM
Room R04

Theme: Health and Environmental Impacts of Man-Made and Naturally Released Toxicants

Accreditation Statement: This activity has been planned and implemented in accordance with the accreditation requirements and policies of the Accreditation Council for Medical Education (ACCME) through the joint providership of The University of Arkansas for Medical Sciences (UAMS) College of Medicine and the Society of Toxicology (SOT). The UAMS College of Medicine is accredited by the ACCME to provide continuing medical education for physicians.

Designation Statement:  The UAMS College of Medicine designates this live activity for a maximum of 2.75 AMA PRA Category 1 Credit(s)™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

Target Audience: Physicians and other health care providers

Learning Objectives: After the activity, the participant will be able to:
(1) Explain the process of unconventional gas well drilling; (2) Predict potential areas of exposure risk to both workers and the populace; (3) Classify potentially harmful chemical exposures that may require acute clinical care; (4) Describe the regulatory protections that prevent untoward ecological and human health exposures; (5) Formulate air and water exposure risks based on proximity to well development; (6) Differentiate the potential acute toxicity associated with drilling activities with the potential chronic toxicities associated with on-going regional gas well development; (7) Identify critical environmental behaviors and exposure pathways of toxic substances that may be released during the hydraulic fracturing process; (8) Predict possible immune effects in humans following exposure to produced water based on animal immunotoxicological data.

Chairperson(s): Travis L. Knuckles, West Virginia University, Morgantown, WV, and Judith Zelikoff, New York University Medical Center, Tuxedo, NY.

The following Specialty Sections recommend this sessions as being of special interest to its members:

    • Ethical, Legal and Social Issues Specialty Section
    • Mixtures Specialty Section
    • Occupational and Public Health Specialty Section

Unconventional gas well development in the Marcellus Shale geological formation has reached an all-time high in recent years.  As such, many rural communities and regions are experiencing increased industrial activities and possibly air pollutant exposures from shale gas extraction activities. The burgeoning development of unconventional gas well sites has the potential to contribute to poor outdoor and indoor air and water quality. In particular, concentrations of particulate matter (PM) in the fine (<2.5 um, PM2.5) and ultrafine (<0.1 um, PM0.1) size ranges and volatile organic compounds (VOCs) may be increased in areas surrounding drilling operations. Furthermore, water quality issues have been reported in areas of hydraulic fracturing activity. However, potential exposures to complex mixtures of toxicants and the health effects on workers and on nearby residents are poorly understood. This multi-faceted symposium will begin with a discussion on the basics of hydraulic fracturing and the potential occupational exposures. Next, a presentation on the regulatory policies and proposals that are currently in place at the state and federal levels. The third presentation will explore the potential mechanisms of exposure to the surrounding communities. A talk on air and water chemistry and the exposome will follow, and the workshop will conclude with relevant findings in animal models on the toxicological impacts of air and water samples collected on/nearby a drilling site. This cutting-edge presentation will provide the audience with a chance to better understand unconventional gas and oil drilling and reach their own conclusions on this passionate topic. Prompted by the passion underscoring this topic, a 15 minute Question & Answer Panel discussion will follow the presentations.

9:30 AM–10:04 AM

Overview of Unconventional Oil and Gas Exploration and Production and Possible Occupational Exposures
John Snawder, National Institute for Occupational Safety and Health, Cincinnati, OH.

10:04 AM–10:33 AM

Current State and Federal Regulatory Policies and Proposals Regarding Unconventional Natural Gas Drilling, and the Environmental Impacts of Drill Cuttings
Terry Polen, West Virginia Department of Environmental Protection, Charleston, WV.

10:33 AM–11:02 AM

An Approach to Studying Potential Acute and Chronic Disease Associated with Unconventional Natural Gas Development Operations
Michael McCawley, West Virginia University, Morgantown, WV.

11:02 AM–11:31 AM

Hydraulic Fracturing, Chemical Constituents and the Exposome
Beizhan Yan, Columbia University, Palisades, NY.

11:31 AM–12:00 Noon

Wide-ranging Toxicological Effects of Produced Water from Hydraulic Fracturing in a Mouse Model
Judy Zelikoff, New York University Medical Center, Tuxedo, NY.

12:00 Noon–12:15 PM

Panel Discussion/Q&A

Jointly Provided by: UAMS College of Medicine and SOT


CSE Task Force

Richard Y. Wang, DO (Chair)
William D. Atchison, PhD
John G. Benitez, MD, MPH
Jeffrey Brent, MD, PhD
Robert Hoffman, MD
Michael Kosnett, MD
Melissa McDiarmid, MD, MPH
Kenneth McMartin, PhD
Kenneth S. Ramos, MD, PhD
Tao Wang, MD, PhD
John A. Wisler, PhD, DABT