Superfund Research Program
The NIEHS Superfund Research Program (SRP) hosted a seminar series to examine the interactions between environmental exposures and infectious agents in the development of disease. The series highlighted researchers from around the country who are exploring this relationship between environmental exposures, infectious agents, and immune response.
Session I - Introduction to Infectious Agents and Their Interactions with Environmental Exposures
October 17, 2016 • 2:00 – 4:00 p.m. EDT
An archive of this webinar is available on EPA's CLU-IN Training & Events Webpage.
The first session of this series introduced the topic and provided examples illustrating the interplay between environmental exposures and infectious agents.
Presenters:
- Karl Western, M.D., National Institute of Allergy and Infectious Diseases
- Rita Loch-Caruso, Ph.D., University of Michigan, Northeastern University SRP Center
- José Cordero, M.D., University of Georgia, Northeastern University SRP Center
- Thomas Kensler, Ph.D., University of Pittsburgh
Moderator:
- William Suk, Ph.D., Director, NIEHS Superfund Research Program
Karl Western, M.D., from the National Institute of Allergy and Infectious Diseases (NIAID), set the stage by providing an introduction from the perspective of his institute. The establishment of the EPA in 1970 resulted in NIAID losing much of its mission in infection and the environment. NIAID is increasingly engaged in an effort to predict the next epidemic disease and to deal with it before it impacts heavily on human populations. In order to be successful in this effort, NIAID needs to strengthen or establish working relationships with veterinary, agricultural, and environmental research partners.
Rita Loch-Caruso, Ph.D., a professor at the University of Michigan and project leader for the Northeastern University SRP Center, discussed her work related to toxicant-microbial interactions in infection of human extraplacental membranes. Her study evaluated the potential for S-(1,2-dichlorovinyl)-l-cysteine (DCVC), a carcinogenic metabolite of trichloroethylene (TCE), to modify host defense responses of gestational tissues to Group B Streptococcus, a leading cause of adverse pregnancy outcomes. Her research team found that DCVC decreased pathogen-stimulated release of mediators important for host defense against infectious microorganisms in extraplacental membranes.
José Cordero, M.D., who is also a part of the Northeastern SRP Center, introduced their ongoing work on the Zika virus in Puerto Rico, including research on whether exposures to environmental chemicals can have the unintentional effect of amplifying risks of Zika during pregnancy.
Thomas Kensler, Ph.D., a professor at the University of Pittsburgh, discussed his research on the relationship between aflatoxins and hepatitis B in the development of hepatocellular carcinoma (HCC). HCC, the most common form of liver cancer, is among the leading causes of cancer death in most parts of the developing world. He discussed studies that have examined the interaction of hepatitis B virus (HBV) and aflatoxin as independent and interactive risk factors for liver cancer and discussed his work to understand better the underlying mechanisms driving this multiplicative interaction.
Session II - Environmental Chemicals and Immune Response
October 31, 2016 • 1:00 - 3:00 p.m. EDT
An archive of this webinar is available on EPA's CLU-IN Training & Events Webpage.
In the second session of this series, speakers presented innovative research on how environmental chemicals alter immune response.
Presenters:
- Philippe Grandjean, M.D., D.M.Sc., University of Southern Denmark, Harvard School of Public Health
- Bruce Stanton, Ph.D., Dartmouth College
- Syed Hashsham, Ph.D., Michigan State University
Moderator:
- Demia Wright, Public Health Educator, NIEHS Worker Training Program
Philippe Grandjean, M.D., D.M.Sc., a professor at the Harvard School of Public Health, described his research linking elevated exposure to perfluorinated compounds with reduced immune response to vaccinations.
Bruce Stanton, Ph.D., a professor at Dartmouth College and Director of the Dartmouth SRP Center, discussed his research on the effects of arsenic on Pseudomonas aeruginosa infections in the lung by adversely affecting the innate immune response. Inorganic and organic forms of arsenic, at levels relevant to exposures in the U.S., have adverse effects on cytokine secretion by human bronchial epithelial cells and macrophages, thereby disrupting the ability of the lungs to clear bacterial infections.
Syed Hashsham, Ph.D., a professor at Michigan State University (MSU) and MSU SRP Center project leader, talked about his ongoing research related to the role of keystone bacteria in modulating the immune system and their interaction with the host in response to dioxin exposure. Concepts related to microbial community modeling and tracking also were presented.
Session III - Co-Exposures in the Lung
November 7, 2016 • 1:00 - 3:00 pm EST
An archive of this webinar is available on EPA's CLU-IN Training & Events Webpage.
The third session of this series focused on interactions between environmental exposures and infectious agents in the lung.
Presenters:
- Steven Kleeberger, Ph.D., National Institute of Environmental Health Sciences
- Fenna Sillé, Ph.D., Johns Hopkins University, former University of California, Berkeley SRP trainee
- Stephania Cormier, Ph.D., University of Tennessee Health Science Center, Louisiana State University SRP Center
Moderator:
- Michael Humble, Ph.D., National Institute of Environmental Health Sciences
Steven Kleeberger, Ph.D., a principal investigator in the NIEHS Intramural Research Program, described his work to understand the mechanisms of Respiratory Syncytial Virus (RSV) infection and disease severity and how that relates to exposure to environmental insults. His findings may help identify individuals at risk for severe RSV infection.
Fenna Sillé, Ph.D., an assistant professor at Johns Hopkins University and former University of California, Berkeley SRP postdoctoral researcher, discussed how early-life exposure to arsenic permanently changes the immune system and increases infectious disease risk later in life, using Mycobacterium tuberculosis in the lung as the model. Their observations in Chile suggest that arsenic impacts critical processes that occur in early life, such as the developing immune system, thereby contributing to increased mortality risk from cancer, bronchiectasis and tuberculosis (TB) later in life. As part of their studies, they observed metabolic and immunogenic alterations in arsenic exposed macrophages and mice as well as effects on TB pathogenicity in vivo. Together, their data elucidates how arsenic influences infectious disease risk in exposed populations.
Stephania Cormier, Ph.D., a professor at the University of Tennessee Health Science Center and Center Director of the Louisiana State University SRP Center, discussed the relationship between environmentally-persistent free radicals (EPFRs) and severity of respiratory viral infections. Exposure to elevated levels of particulate matter containing EPFRs is associated with increased risk of morbidity and mortality from respiratory tract viral infections in children. She also discussed how early-life exposure to EPFRs elicits active immunosuppressive and demonstrate the role of Tregs and IL10 in enhanced influenza severity. Finally, she demonstrated that blocking such immune responses can protect against severe disease.
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