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February 11, 2019 | 11:00 a.m. - 12:00 p.m.
Category: Seminar
Location: Integrative Biosciences Center Conference Room 1D | Map
6135 Woodward Ave.
Detroit , MI 48202
Cost: Free
Audience: Academic Staff, Alumni, Community, Current Graduate Students, Current Undergraduate Students, Faculty, Staff

Presentation hosted by

Department of Pharmacology,

Institute of Environmental Health Sciences,

and the Center for Urban Responses to Environmental Stressors

Monday, February 11, 2019

11:00 a.m. to 12:00 noon

6135 Woodward Ave., Detroit, MI  48202

Michael Petriello, Ph.D.

University of Kentucky, Cardiovascular Research Center

"Impacts of halogenated persistent organics on cardiometabolic disease biomarkers and atherosclerotic risk"

 

Dr. Petriello earned his B.S. in biology/environmental sciences from Muhlenberg College and his Ph.D. in toxicology from the University of Kentucky.

Abstract:

Cardiovascular and related metabolic disorders are largely caused by genetic (heritable) and environmental factors. Understanding how these factors intersect to determine individual disease risk is a critical challenge in developing personalized approaches to the diagnosis and treatment of the disease.  Well-studied “lifestyle-dependent” determinants of increased cardiometabolic disease risk include smoking, physical inactivity, and poor nutrition, but emerging data now implicate exposures to persistent environmental pollutants as an important contributor to inter-individual variability in cardiovascular disease (CVD) risk. Interestingly, emerging diet-derived biomarkers such as trimethylamine N-oxide (TMAO) have strong positive relationships with heart disease risk, and Dr. Petriello's research has recently shown that a class of persistent organic pollutants known as dioxins can increase TMAO formation in preclinical models and are positively associated with circulating TMAO in residents of Anniston, Alabama. Interestingly, these associations were evident only in women and diminish as BMI increases. To study mechanisms related to this unexpected observation, Dr. Petriello and the research team he works with has characterized a mouse model of pollutant exposure that develops atherosclerosis but not adipose tissue expansion. They examined the effects of a dioxin-like pollutant, PCB 126, on markers of systemic inflammation, hepatic steatosis, modulation of gut microbiota, and atherosclerotic lesion size. Mice exposed to PCB 126 exhibited significantly increased plasma inflammatory cytokine levels, increased accumulation of hepatic fatty acids, reduced cecum bacteria alpha diversity, significantly increased Firmicutes to Bacteroidetes ratio, and accelerated atherosclerotic lesion formation in the aortic root. As environmental exposures to PCBs and other dioxins have decreased in recent decades, they have begun to investigate a paradigm of nutrient/toxicant interactions in emerging classes of halogenated pollutants including per- and polyfluoroalkyl substances (PFAS) which have been shown previously to positively associate with other clinically relevant biomarkers of CVD including total and/or low density lipoprotein (LDL) cholesterol in cross-sectional epidemiological studies. Most recently, they developed an LC-MS-based method to quantiate multiple PFAS in serum/plasma and have begun to investigate associations between cholesterol levels and pollutant exposure in rural individuals living in Eastern Kentucky (Appalachia) who are undergoing a diet and lifestyle-based intervention to reduce cardiometabolic disease risk. Preliminarly results show significant positive associations between multiple PFAS and cholesterol levels, but these associations are dependent on efficacy of the intervention.

For more information about this event, please contact Julie O'Connor at 313-577-8845 or julie.oconnor@wayne.edu.