Abstract

Introduction: Prenatal exposure to persistent organic pollutants (POPs) has been linked to elevated body mass index (BMI) in recent birth cohort studies, but whether the current background exposure levels relate to other cardiometabolic (CM) risk components is underexplored. In the Spanish INMA Birth Cohort Study we have shown that prenatal POP exposures are associated with rapid growth and overweight risk in the first year of life.1 Building upon prior evidence, we have now evaluated the associations of POP exposures with CM risk at age 4 years. Methods: We analysed 1180 mother-child pairs from three Spanish regions followed from pregnancy (2003/8) to childhood, with POP concentrations measured in 1st trimester pregnancy serum (ng/g lipid, log2). Overweight was defined as an age- and sex-specific BMI z-score≥ 85th WHO percentile. Total cholesterol, triglycerides, high- and low-density lipoprotein cholesterol were measured in child non-fasting blood collected at 4 years (n=664). Hierarchical cluster analysis defined groups of lower or higher CM risk based on BMI and metabolic biomarkers. Linear regression and generalized linear models assessed the associations adjusting for confounders selected using directed acyclic graphs. Results: Prenatal DDE exposure was associated with increased risk of overweight (RR per exposure doubling [95% CI]=1.09 [1.01, 1.18]) overall, and increased CM risk in boys (RR [95% CI]= 1.11 [1.00, 1.23]) (girls: RR~1, p-sex int.=0.10). Prenatal HCB exposure was associated with a slight mean increase in BMI z-scores (β [95% CI]= 0.05 [0.01, 0.10]; p-sex int.=0.35) and non-significantly related to overweight and CM risks. Prenatal PCB exposure was associated with increased risk of overweight in girls (RR [95% CI] = 1.26 [1.01, 1.58]) (boys: RR~1, p-sex int.=0.04) and unrelated to CM risk. Conclusion: Associations between prenatal POP exposures and infant growth persist and lead to increased overweight and CM risks in childhood. 1Valvi, Obesity 2014

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