Study finds no evidence that phthalates are responsible for increased childhood obesity

April 6, 2016

Dr. Jessie Buckley

Dr. Jessie Buckley

Jessie Buckley, PhD, a postdoctoral research associate in the UNC Gillings School of Global Public Health’s Department of Epidemiology, was featured in the “Science Selection” section of Environmental Health Perspectives for her recent research on phthalates and obesity in children.

The research findings show no evidence of a connection between phthalates – chemicals commonly found in consumer products, which some scientists claim alter metabolism – and the increasing prevalence of childhood obesity.

Buckley was lead author of the paper, titled “Prenatal Phthalate Exposures and Childhood Fat Mass in a New York City Cohort,” published online April 1 by Environmental Health Perspectives. Other co-authors from the Gillings School include Stephanie Engel, PhD, David Richardson, PhD, and Julie Daniels, PhD, all associate professors in the Department of Epidemiology, as well as Michelle Mendez, PhD, assistant professor in the Department of Nutrition, and Amy Herring, PhD, professor and associate chair in the Department of Biostatistics.

While a small number of studies have suggested that prenatal exposure to certain environmental chemicals may be partially responsible for upward-trending levels of childhood obesity, Buckley’s research found no association between prenatal phthalate exposure and increased body fat.

In fact, the research showed that high rates of exposure to di(2-ethylhexyl) phthalate (DEHP), a chemical commonly used in consumer products like toys, cosmetics and food packaging, was actually associated with lower body fat in children.

In the course of the study, the co-authors measured phthalate exposure levels in pregnant women in the third trimester, then followed up to measure fat mass in the women’s children. Children were measured between one and three times, with the final visit occurring between seven and nine years of age.

The findings about the effects of DEHP exposure contradict the hypothesis that phthalates are environmental ‘obesogens,’ or chemicals that can slow metabolism. This finding was already supported, to a degree, by previous studies in animals that linked postnatal DEHP exposure to lower body fat, but Buckley’s study is the first to examine prenatal exposure in humans.

“Most human studies of phthalates and adiposity have assessed postnatal exposures,” Buckley explains, “but we focused on prenatal exposures because susceptibility to obesity is thought to be ‘programmed’ during fetal development. This makes the fetus particularly sensitive to environmental exposures that affect fat development and accumulation.”

Study limitations include the reliance on a single urine sample taken during the third trimester of pregnancy, which is important to note because phthalates have very short half-lives. Also, the statistically significant association for DEHP and lower body fat was seen only in the group of children with the highest exposure level.

Buckley warns against reading too much into the results. “In this small collection of literature,” she says, “there is still no agreement on what, if any, associations to expect in relation to prenatal phthalate exposure and child growth.”


Gillings School of Global Public Health contact: David Pesci, director of communications, (919) 962-2600 or


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