Early-Life Phthalate Exposure and Adiposity at 8 Years of Age

Jessica Shoaff, George D Papandonatos, Antonia M Calafat, Xiaoyun Ye, Aimin Chen, Bruce P Lanphear, Kimberly Yolton, Joseph M Braun, Jessica Shoaff, George D Papandonatos, Antonia M Calafat, Xiaoyun Ye, Aimin Chen, Bruce P Lanphear, Kimberly Yolton, Joseph M Braun

Abstract

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.

Figures

Figure 1.
Figure 1.
Adjusted difference in child body fat percentage at 8 y of age per 10-fold increase in urinary phthalate metabolite concentrations during pregnancy and at 1, 2, 3, 4, 5, and 8 y of age in the Health Outcomes and Measures of the Environment (HOME) Study. Adjusted for maternal age at delivery, race, marital status, insurance, income, education, parity, cotinine, depressive symptoms, midpregnancy body mass index (BMI), food security, prenatal fruit/vegetable and fish consumption, prenatal vitamin use, child sex, and child age at the 8-y visit. Monoethyl phthalate (MEP), mono-n-butyl phthalate (MnBP), mono-isobutyl phthalate (MiBP), mono(3-carboxypropyl) phthalate (MCPP), monobenzyl phthalate (MBzP). Di(2-ethylhexyl) phthalate (∑DEHP) metabolites is the sum of mono(2-ethyl-5-hydroxyhexyl) phthalate (MEHHP), mono(2-ethyl-5-oxohexyl) phthalate (MEOHP), and mono(2-ethyl-5-carboxypentyl) phthalate (MECPP). We did not quantify urine concentrations of MnBP and MiBP at 1–3 years of age because we detected the parent compounds of these metabolites in the diaper inserts. Interaction p-value indicating whether the timing of exposure modifies the association between phthalate concentrations and body fat was MnBP (p=0.78), MiBP (p=0.77), MEP (p=0.07), MBzP (p=0.83), MCPP (p=0.19), and ∑DEHP (p=0.09). Results for BMI z-score and waist circumference were similar, as the outcomes were highly correlated with each other (Pearson r≥0.8).
Figure 2.
Figure 2.
Adjusted trajectories of urinary MBzP concentrations in Health Outcomes and Measures of the Environment (HOME) Study children at the 25th, 50th, and 90th percentiles of body fat percent at 8 y of age. Adjusted for maternal age at delivery, race, marital status, insurance, income, education, parity, cotinine, depressive symptoms, midpregnancy body mass index (BMI), food security, prenatal fruit/vegetable and fish consumption, prenatal vitamin use, child sex, and child age at the 8-y visit.
Figure 3.
Figure 3.
Adjusted trajectories of urinary MEP concentrations in Health Outcomes and Measures of the Environment (HOME) Study children at the 25th, 50th, and 90th percentiles of body fat percent at 8 y of age. Adjusted for maternal age at delivery, race, marital status, insurance, income, education, parity, cotinine, depressive symptoms, midpregnancy body mass index (BMI), food security, prenatal fruit/vegetable and fish consumption, prenatal vitamin use, child sex, and child age at the 8-y visit.
Figure 4.
Figure 4.
Adjusted trajectories of urinary ∑DEHP concentrations in Health Outcomes and Measures of the Environment (HOME) Study children at the 25th, 50th, and 90th percentiles of body fat percent at 8 y of age. Adjusted for maternal age at delivery, race, marital status, insurance, income, education, parity, cotinine, depressive symptoms, midpregnancy body mass index (BMI), food security, prenatal fruit/vegetable and fish consumption, prenatal vitamin use, child sex, and child age at the 8-y visit. Di(2-ethylhexyl) phthalate (∑DEHP) metabolites is the sum of mono(2-ethyl-5-hydroxyhexyl) phthalate (MEHHP), mono(2-ethyl-5-oxohexyl) phthalate (MEOHP), and mono(2-ethyl-5-carboxypentyl) phthalate (MECPP).

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