Abstract
Few studies have investigated longitudinal associations between early life phthalate exposure and subsequent obesity and cardiovascular risks in children with inconsistent results. We aimed to evaluate the associations between phthalate exposure during gestation and childhood with offspring obesity and cardiometabolic risk factors in 500 mother-child pairs from the Rhea pregnancy cohort in Crete, Greece. Seven phthalate metabolites [monoethyl phthalate (MEP), mono-n-butyl phthalate (MnBP), mono-isobutyl phthalate (MiBP), monobenzyl phthalate (MBzP), mono(2-ethylhexyl) phthalate (MEHP), mono(2-ethyl-5-hydroxyhexyl) phthalate (MEHHP), and mono(2-ethyl-5-oxohexyl) phthalate (MEOHP)] were quantified in spot urine samples collected from mothers (1st trimester) and their children at 4 years of age. We calculated the molar sum of DEHP metabolites (MEHP, MEHHP, MEOHP). We measured child weight, height, waist circumference, skinfold thicknesses, blood pressure (BP), and lipids at 4 and 6 years and leptin, adiponectin, and C-reactive protein at 4 years. We used generalized estimating equations to examine associations at each age and tested for interaction by sex. Child exposure to phthalate metabolites was associated with lower BMI z-scores in boys and higher BMI z-scores in girls. Each 10-fold increase in ΣDEHP was associated with a change in waist circumference of −2.6 cm (95% CI: −4.72, −0.48) in boys vs. 2.14 cm (95% CI: −0.14, 4.43) in girls (p-sex interaction = 0.003) and a change in waist-to-height ratio of −0.01 (95% CI: −0.03, 0.01) in boys vs. 0.02 (95% CI: 0.01, 0.04) in girls (p-sex interaction = 0.006). Phthalate metabolite concentrations at age 4 were negatively associated with systolic and diastolic blood pressure. MEP was associated with lower systolic BP z-scores (adj. β = −0.22; 95% CI: −0.36, −0.08) at 4 years. MnBP and MBzP were associated with lower diastolic BP z-scores (adj. β = −0.13; 95%CI: −0.23, −0.04, and adj. β = −0.11; 95% CI: −0.21, −0.01, respectively). A 10-fold increase in MiBP was associated with 4.4% higher total cholesterol levels (95% CI: 0.2, 8.7). Prenatal phthalate exposure was not consistently associated with child adiposity and cardiometabolic measures. Our findings suggest that early life phthalate exposure may affect child growth and adiposity in a sex-specific manner and depends on the timing of exposure.
Highlights
Childhood obesity is a risk factor for obesity-related health outcomes such as cardiovascular and other chronic diseases later in life and one of the most common public health problems and challenges globally
To control for confounding, we considered maternal and child covariates that were of a priori interest as independent predictors of child adiposity and growth or that may be related to phthalate levels: maternal pre-pregnancy BMI, maternal age at birth, parity, maternal educational level [low level: ≤9 years of mandatory schooling, medium level: >9 years of schooling up to attending post-secondary school education and high level: attending university or having a university/technical college degree], smoking during pregnancy, gestational weight gain [GWG], ethnic origin (Greek, non-Greek), residence, delivery type
Fifty-six percent of the children included in the analysis were boys, their mean (±standard deviation (SD)) birth weight was 3,203 (± 462.8) g and the average (±SD) gestation was 38.2 (± 1.5) weeks
Summary
Childhood obesity is a risk factor for obesity-related health outcomes such as cardiovascular and other chronic diseases later in life and one of the most common public health problems and challenges globally. The global prevalence of childhood overweight and obesity has increased over the last three decades to 124 million in 2016 [1] and if current trends continue, the World Health Organization (WHO) predicts that 70 million young children will be overweight or obese by 2025 [2]. Obesity and associated risk factors, such as high blood pressure and dyslipidemia, in childhood can induce changes in metabolism and contribute to the development of atherosclerosis in adulthood [4]. Obesogens-chemicals that inappropriately regulate and promote lipid accumulation and adipogenesis-may contribute to obesity development, especially when exposure occurs during pregnancy and early life [7,8,9]
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