How dust bunnies might make kids gain weight

Chemicals in house dust may trigger a receptor linked to obesity—and children ingest about 50 milligrams of it a day, says Heather Stapleton. "We are continuing to build on this research to determine what type of health effects may be caused by this level of activation in children." (Credit: iStockphoto)

Some chemicals commonly found in house dust may trigger a key receptor linked to human obesity, preliminary research suggests.

The study adds to a growing body of evidence that a wide range of chemical mixtures used as flame retardants and added to lubricants, hydraulic fluids, and plastics can bind to the PPARgamma receptor and, under the right conditions, activate it.

This activation during early development “may be a key factor in obesity,” says Heather Stapleton, associate professor of environmental ethics and sustainable environmental management at Duke University’s School of Environment.

PPARgamma—short for peroxisome proliferator-activated nuclear receptor gamma—regulates fat metabolism, cell proliferation, and cell death.

50 mg of dust a day

Previous studies have shown that many chemicals, including the widely used organophosphates and polybrominated diphenyl ether (PDBE) metabolites, can bind to PPARgamma. But the studies also showed that binding to the receptor did not always activate it.

To better understand whether environmental exposures can trigger the receptor’s “on switch,” researchers conducted their new study using a reporter gene assay to monitor PPARgamma activation in house dust samples.

They chose to study chemicals in dust samples because indoor dust is an important pathway through which humans—especially infants and young children—become exposed to environmental contaminants. Young children ingest about 50 milligrams of house dust a day, according to US EPA estimates.

Mix of chemicals

Published in Environmental Science & Technology, the analysis shows that 28 of 30 semivolatile compounds commonly found in indoor dust were “weak or moderate” PPARgamma agonists—meaning they could bind to and activate the receptor.

“But what was very interesting,” Stapleton says, “was the level of activation observed following exposure to an environmentally relevant mixture of these contaminants in house dust samples.”

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The researchers found signs of significant PPARgamma activation in more than half of the 25 dust samples collected from homes, offices, and gyms, at a level of exposure that would be similar to a child’s daily dose.

Further research is now under way to test the laboratory findings in conditions that simulate the type of chronic, low-level exposure to these chemicals that occurs in the real world.

“We are continuing to build on this research to determine what type of health effects may be caused by this level of activation in children,” Stapleton says.

Mingliang Fang, a PhD student working with Stapleton, and Thomas F. Webster, professor of environmental health at the Boston University School of Public Health are coauthors of the study.

The National Institute of Environmental Health Sciences and Boston University School of Public Health funded the research.

Source: Duke University