High Phthalate Levels Linked to Obesity in Children

Nancy A. Melville

June 25, 2012

June 25, 2012 (Houston, Texas) — Children who are obese show significantly higher levels of serum di-ethylhexyl phthalate (DEHP) compared with nonobese children, and the concentrations of DEHP appear to increase the risk for obesity in a dose-dependent manner, according to a study presented here at ENDO 2012: The Endocrine Society 94th Annual Meeting.

Phthalates, synthetic chemicals found in consumer packaging and a variety of products ranging from medical devices to toys and cosmetics, have been linked in some studies to obesity in adults; however, there is limited research on the exposure of children to these chemicals.

A research team led by Mi Jung Park, MD, PhD, from Sanggye Paik Hospital and Inje University College of Medicine in Seoul, Korea, evaluated the serum levels of DEHP in 204 Korean children, aged 6 to 13 years, including 15 children who were obese and 99 nonobese control patients.

Measurements of serum DEHP levels, analyzed by gas chromatography/mass spectrometry, showed geometric mean serum DEHP levels to be higher in the obese children compared with in the control children (53.8 ± 191.5 ng/mL vs 107.0 ± 341.5 ng/mL; P < .0001).

Significant correlations were further seen with DEHP levels and covariates including body mass index (r, 0.194; P = .015), serum alanine aminotransferase (r, 0.159; P = .047), uric acid (r, 0.166; P = .038), and body fat mass (r, 0.170; P = .029).

Each elevated quartile of serum DEHP correlated with an increased risk for obesity in a dose-dependent manner. For quartile 2, there was an odds ratio [OR] of 1.25 (95% confidence interval [CI], 0.51 - 3.01); for quartile 3, the OR was 3.63 (95% CI, 1.48 - 8.91); and for quartile 4, the OR was 5.04 (95% CI, 2.00 - 12.71).

The correlation remained even after adjusting for age, sex, physical activity, household income, and daily calorie intake.

There were no significant correlations between serum DEHP and high-density lipoprotein cholesterol, triglyceride, fasting blood sugar, and fasting insulin.

Dr. Park noted that the obesity correlation was expected because of previous findings in adults. However, the dose-dependent relationship between levels of DEHP and obesity were not expected.

"I was very surprised to see the dose-dependent correlation between DEHP levels and obesity risk," Dr. Park told Medscape Medical News.

"Phthalates in human studies are very limited. Only few studies based on the [National Health and Nutrition Examination Survey] data in US showed significant association between phthalate and waist circumference or body mass index in adults," Dr. Park said.

"We proved a significant association between phthalate and fat mass in children," he asserted.

He speculated that the mechanism driving phthalate-related weight gain has to do with peroxisome proliferator-activated receptor γ (PPARγ) activation, as well as antithyroid and antiandrogenic effects.

"PPARγ is master regulator of adipogenesis, lipid metabolism, and phthalate potentiate adipogenesis," Dr. Park explained.

"Thyroid disruption is known to involve the programming of future body weight gain. In addition, phthalates are suspected as having an antiandrogen effect, which may potentiate obesity, since androgen lowers [body mass index]."

The authors called for prospective studies to better examine potential causal links between DEHP exposure and childhood obesity.

"Phthalates are ubiquitous in our lives, and these results alert the public to recognize the possible harm and make efforts to reduce this exposure," Dr. Park said.

Dr. Park has disclosed no relevant financial relationships.

ENDO 2012: The Endocrine Society 94th Annual Meeting: Abstract SAT-574. Presented June 23, 2012.

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