Background: Prenatal exposure to endocrine-disrupting chemicals such as persistent organic pollutants (POPs) may increase risk of obesity later in life.

Objective: We examined the relation of in utero POPs exposure to offspring obesity and cardiometabolic risk factors at 4 years of age in the Rhea mother–child cohort in Crete, Greece ( n = 689).

Methods: We determined concentrations of polychlorinated biphenyls (PCBs), dichlorodiphenyldichloroethylene (DDE), and hexachlorobenzene (HCB) in first-trimester maternal serum. We measured child weight, height, waist circumference, skinfold thicknesses, blood pressure (BP), blood levels of lipids, C-reactive protein, and adipokines at 4 years of age. Childhood obesity was defined using age- and sex-specific cut points for body mass index (BMI) as recommended by the International Obesity Task Force.

Results: On multivariable regression analyses, a 10-fold increase in HCB was associated with a higher BMI z -score (adjusted β = 0.49; 95% CI: 0.12, 0.86), obesity [relative risk (RR) = 8.14; 95% CI: 1.85, 35.81], abdominal obesity (RR = 3.49; 95% CI: 1.08, 11.28), greater sum of skinfold thickness (β = 7.71 mm; 95% CI: 2.04, 13.39), and higher systolic BP (β = 4.34 mmHg; 95% CI: 0.63, 8.05) at 4 years of age. Prenatal DDE exposure was associated with higher BMI z -score (β = 0.27; 95% CI: 0.04, 0.5), abdominal obesity (RR = 3.76; 95% CI: 1.70, 8.30), and higher diastolic BP (β = 1.79 mmHg; 95% CI: 0.13, 3.46). PCBs were not significantly associated with offspring obesity or cardiometabolic risk factors.

Conclusions: Prenatal exposure to DDE and HCB was associated with excess adiposity and higher blood pressure levels in early childhood.

Citation: Vafeiadi M, Georgiou V, Chalkiadaki G, Rantakokko P, Kiviranta H, Karachaliou M, Fthenou E, Venihaki M, Sarri K, Vassilaki M, Kyrtopoulos SA, Oken E, Kogevinas M, Chatzi L. 2015. Association of prenatal exposure to persistent organic pollutants with obesity and cardiometabolic traits in early childhood: the Rhea mother–child cohort (Crete, Greece). Environ Health Perspect 123:1015–1021;  http://dx.doi.org/10.1289/ehp.1409062

Address correspondence to M. Vafeiadi, Department of Social Medicine, Faculty of Medicine, University of Crete, P.O. Box 2208, Heraklion 71003, Crete, Greece. E-mail: [email protected]

We thank all the cohort participants for their generous collaboration.

The Rhea project was financially supported by European Union (EU) grants for specific projects (EU FP6-2003-Food-3-NewGeneris; EU FP6. STREP HiWATE; EU FP7 ENV.2007.1.2.2.2. Project no. 211250 ESCAPE; EU FP7-2008-ENV-1.2.1.4 Envirogenomarkers; EU FP7-HEALTH-2009-single stage CHICOS; EU FP7 ENV.2008.1.2.1.6. Proposal no. 226285 ENRIECO; EU-FP7-HEALTH-2012 Proposal no. 308333 HELIX), MeDALL (FP7 European Union project, no. 264357), and the Greek Ministry of Health (Program of Prevention of obesity and neurodevelopmental disorders in preschool children, in Heraklion district, Crete, Greece: 2011–2014; “Rhea Plus”: Primary Prevention Program of Environmental Risk Factors for Reproductive Health, and Child Health: 2012–15). E.O. was supported by the U.S. National Institutes of Health (K24 HD069408).

The authors declare they have no actual or potential competing financial interests.

Received: 11 August 2014 Accepted: 21 April 2015 Advance Publication: 24 April 2015 Final Publication: 1 October 2015

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