Studies have shown that perinatal exposure of rats and mice to common flame retardants found in household items permanently reprograms liver metabolism, often leading later in life to insulin resistance and non-alcoholic fatty liver disease.
Now, research led by University of Massachusetts Amherst School of Public Health and Health Sciences associate professor of environmental health sciences, Dr. Alexander Suvorov, with co-authors in Moscow, Russia, has identified the likely mechanism responsible for the pollutant’s effect: an altered liver epigenome.
“Changes in the liver epigenome can explain those functional changes in the liver,” Dr. Suvorov explains. “We looked at two different epigenetic mechanisms and there were changes in both.”
Published in Epigenomics, the study showed that environmentally relevant exposure to polybrominated diphenyl ether (PBDE) through the umbilical cord and breast milk permanently changed liver metabolism in rats. The mother rats were fed enough PBDEs to cause concentrations in their fat similar to those found in humans living in big cities in the U.S.
“The pups never got exposed directly, yet it altered the way their liver works forever,” says Dr. Suvorov. “Normally when you remove the stressor, the organ will recover. But in this case, it’s not recovering. Epigenetic changes can persist in a row of cellular divisions and can even propagate through generations.”
In the U.S., concentrations of PBDEs in human tissues is still increasing, even though the industry stopped using the flame retardants in 2013. “These chemicals are extremely stable, and they bioaccumulate and bioconcentrate,” Dr. Suvorov says. “Likely we will be exposed for another 50 years or so. Even more important, we have never deeply analyzed the long-term effects of exposure.”Tags: Friday Letter Submission, Publish on December 20