The Science of DioxinJuly 20, 2016 | |
Kentucky Researchers Say They Have Identified Potential Link Between Pollutants and Human Disease Risk
Michael Petriello, a postdoctoral fellow working with researchers at the University of Kentucky Superfund Research Center (the “U.K. S.R.C.”), is reporting that he discovered a mechanism that may link exposure to environmental pollutants to increased human disease risk.
Michael Petriello, who is working with Bernhard Hennig, director of the U.K. SRC, and Andrew Morris, of the university’s Healthcare Division of Cardiovascular Medicine who has a joint appointment at the Lexington Veterans Affairs Medical Center in Lexington, Kentucky, said that, “A goal of our work is to identify human populations that are highly sensitive to pollutant-induced disease.”
In laboratory experiments, Petriello said that he found that exposure to a class of pollutants called polychlorinated biphenyls (“PCBs”) can increase levels of an enzyme in the liver that generates a metabolite in the blood called tri methylamine N-oxide (“TMAO”). The university said in a statement that these observations “may be relevant to other widespread classes of environmental pollutants termed dioxins and dioxin-like chemicals because these pollutants could also increase levels of a liver enzyme critical for TMAO production in lab models.”
“Dr. Petriello’s research clearly shows that exposure to PCBs increases the circulating levels of TMAO, a biomarker of increased risks for cardiovascular disease,” Hennig said.
The U.K. SRC group now is working with researchers at the Centers for Disease Control and Prevention (“CDC”) to see if the relationship between exposure to environmental pollutants and circulating TMAO levels observed in the lab also happens in people.
“Once we identify interactions between diet and toxicology, such as this observed link between TMAO and PCBs, we may be better equipped to educate and engage the public on ways to minimize risk,” Petriello said.
Hennig added, “What makes Dr. Petriello’s discoveries significant is the fact that we can now use biomarkers like TMAO to estimate the cardiovascular risk of PCB exposure in humans.”
The university observed that the findings in the research, “Dioxin-like pollutants increase hepatic flavin containing monooxygenase (FMO3) expression to promote synthesis of the pro-atherogenic nutrient biomarker trimethylamine N-oxide from dietary precursors,” that TMAO was formed by metabolism of dietary lipids that were particularly rich in meat and dairy products, suggested that diets that reduced consumption of these lipids to decrease TMAO levels “might be particularly beneficial for people who are exposed to these kinds of pollutants.”