Phthalates are hypothesized to cause obesity, but few studies have assessed whether prenatal phthalate exposures are related to childhood body mass index (BMI).
We included 707 children from three prospective cohort studies enrolled in the US between 1998 and 2006 who had maternal urinary phthalate metabolite concentrations measured during pregnancy, and measures of weight and height at ages 4 to 7 years. We calculated age- and sex-standardized BMI z scores and classified children with BMI percentiles ≥85 as overweight/obese. We used mixed effects regression models to estimate associations between a 1 standard deviation increase in natural log phthalate metabolite concentrations and BMI z scores and overweight/obesity. We estimated associations in multiple metabolite models adjusted for confounders, and evaluated heterogeneity of associations by child’s sex, race/ethnicity, and cohort.
Mono-3-carboxypropyl phthalate concentrations were positively associated with overweight/obese status in children (odds ratio [95% credible interval] = 2.1 [1.2, 4.0]) but not with BMI z scores (β = −0.02 [−0.15, 0.11]). We did not observe evidence of obesogenic effects for other metabolites. However, monoethyl phthalate and summed di-(2-ethylhexyl) phthalate metabolites (∑DEHP) concentrations were inversely associated with BMI z scores among girls (monoethyl phthalate beta = −0.14 [−0.28, 0.00]; ∑DEHP beta = −0.12 [−0.27, 0.02]).
Maternal urinary mono-3-carboxypropyl phthalate, a nonspecific metabolite of several phthalates, was positively associated with childhood overweight/obesity. Metabolites of diethyl phthalate and DEHP were associated with lower BMI in girls but not in boys, suggesting that prenatal exposures may have sexually dimorphic effects on physical development.
From the aDepartment of Epidemiology, Gillings School of Global Public Health, University of North Carolina, Chapel Hill, NC; bDepartment of Epidemiology, Brown University School of Public Health, Brown University, Providence, RI; cDepartment of Environmental Health Sciences, Columbia Center for Children’s Environmental Health, Mailman School of Public Health, Columbia University, New York, NY; dDepartment of Nutrition, Gillings School of Global Public Health, University of North Carolina, Chapel Hill, NC; eDivision of General and Community Pediatrics, Department of Pediatrics, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH; fDivision of Laboratory Sciences, National Center for Environmental Health, Centers for Disease Control and Prevention, Atlanta, GA; gDepartment of Community and Preventative Medicine, Mount Sinai School of Medicine, New York, NY; hChild and Family Research Institute, BC Children’s and Women’s Hospital, Vancouver, Canada; iFaculty of Health Sciences, Simon Fraser University, Burnaby, Canada; jDepartment of Biostatistics, Gillings School of Global Public Health, and Carolina Population Center, University of North Carolina, Chapel Hill, NC; and kDepartment of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY.
Submitted 24 April 2015; accepted 5 January 2016.
Supported by the National Institute of Environmental Health Sciences (NIEHS) of the National Institutes of Health (NIH) under Award Number R21ES021700. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH. JPB was supported by training grants from NIEHS (T32 ES007018) and the Eunice Kennedy Shriver National Institute of Child Health and Human Development (T32-HD052468-05). AHH was supported by a grant from NIEHS (ES020619). The Mount Sinai Children’s Environmental Health Study was supported by grants from NIEHS (ES009584), US EPA (R827039 and RD831711), ATSDR, and The New York Community Trust. The Columbia Children’s Environmental Health Center was supported by grants from NIEHS (P50 ES09600, RO1 ES013543, RO1 ES08977, RO1 ES11158), US EPA (R827027, R82860901), Irving General Clinical Research Center (Grant RR00645), Bauman Family Foundation, Gladys and Roland Harriman Foundation, Hansen Foundation, W. Alton Jones Foundation, New York Community Trust, Educational Foundation of America, New York Times Company Foundation, Rockefeller Financial Services, Horace W. Smith Foundation, Beldon Fund, John Merck Fund, New York Community Trust, and V. Kann Rasmussen Foundation. The Cincinnati HOME Study was supported by NIEHS (P30ES10126) and NIEHS/EPA (PO1 ES11261).
The authors report no conflicts of interest.
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Correspondence: Jessie P. Buckley, Department of Epidemiology, University of North Carolina at Chapel Hill, CB #7435, Chapel Hill, NC 27599. E-mail: firstname.lastname@example.org.