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Published on: June 2, 2023
Early-Life Phthalate Exposure and Adiposity at 8 Years of Age
Jessica Shoaff1, George D Papandonatos1, Antonia M Calafat2
1Department of Epidemiology, Brown University School of Public Health , Providence, Rhode Island, USA.
Insights
Early phthalate exposure did not increase child adiposity. Postnatal exposure to di(2-ethylhexyl) phthalate (∑DEHP) and monoethyl phthalate (MEP) showed timing-dependent associations with child body fat.
Area of Science:
- Environmental Health Sciences
- Pediatric Endocrinology
- Toxicology
Background:
- Early-life exposure to phthalates is suspected to influence child adiposity.
- Prior research has not identified specific windows of vulnerability to phthalate exposure during development.
Purpose of the Study:
- To investigate the relationship between child adiposity at age 8 and repeated urinary phthalate metabolite levels from gestation through childhood.
- To identify critical periods of vulnerability to phthalate exposure concerning child adiposity.
Main Methods:
- Quantified nine urinary phthalate metabolites in 219 mother-child pairs up to two times prenatally and six times from ages 1-8.
- Measured child body mass index (BMI), waist circumference, and percent body fat at age 8.
- Employed statistical methods to assess phthalate-adiposity associations at each exposure window and model exposure trajectories.
Main Results:
- Prenatal phthalate concentrations were not associated with increased child adiposity.
- Monobenzyl phthalate (MBzP) showed inverse associations with adiposity throughout pregnancy and childhood.
- Associations for di(2-ethylhexyl) phthalate (∑DEHP) and monoethyl phthalate (MEP) metabolites with adiposity varied by exposure timing; for example, higher ∑DEHP at 1 and 5 years were linked to decreased and increased body fat, respectively. MEP at 5 and 8 years was associated with higher adiposity.
Conclusions:
- No evidence of an obesogenic effect from prenatal phthalate exposure was found in this cohort.
- Postnatal exposure to MEP and ∑DEHP exhibited timing-dependent associations with child adiposity.
- Specific postnatal windows, particularly later in childhood for MEP and ∑DEHP, may be more critical for phthalate-related adiposity effects.
Background:
Early-life phthalate exposure may influence child adiposity, but prior studies have not determined if there are periods of enhanced vulnerability to phthalates.
Objective:
To examine the relationship between child adiposity at 8 y of age and repeated urinary biomarkers of phthalate exposure from gestation through childhood to determine if there are distinct periods of vulnerability.
Methods:
In 219 mother-child pairs from Cincinnati, Ohio, we quantified nine urinary phthalate metabolites up to two times prenatally and six times from 1-8 y of age. We measured child body mass index (BMI), waist circumference, and percent body fat at 8 y of age. To identify periods of vulnerability, we used two statistical methods to estimate phthalate-adiposity associations at each visit, test differences in phthalate-adiposity associations across visits, and model trajectories of phthalate concentrations for children at different levels of adiposity.
Results:
Prenatal phthalate concentrations were not associated with excess child adiposity. Monobenzyl phthalate (MBzP) concentrations during pregnancy and childhood were inversely associated with adiposity. The associations of di(2-ethylhexyl) phthalate (∑DEHP) metabolites and monoethyl phthalate (MEP) with child adiposity depended on the timing of exposure. A 10-fold increase in ∑DEHP at 1 and 5 y was associated with a 2.7% decrease [95% confidence interval (CI): -4.8, -0.5] and 2.9% increase (95% CI: 0.3, 5.5) in body fat, respectively. MEP concentrations at 5 and 8 y of age were associated with higher child adiposity, but earlier childhood concentrations were not.
Conclusion:
In this cohort, we did not find evidence of an obesogenic effect of prenatal phthalate exposure. Positive associations between postnatal MEP and ∑DEHP concentrations depended on the timing of exposure. https://doi.org/10.1289/EHP1022.
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