Prenatal exposure to phthalates and phenols and preclinical vascular health during early adolescence

Abstract

Background and aim: Exposure to endocrine-disrupting chemicals may increase cardiovascular risk from early life, but studies in children have shown inconsistent results, most focused on analysis of single chemicals, and none included measures of micro-vascularization as early preclinical markers. This study aimed to evaluate the association between prenatal exposure to phthalates and phenols and macro- and microvascular health during early adolescence. Methods: Using data from a Spanish birth cohort (n = 416), prenatal exposure to eight phthalate metabolites and seven phenols (bisphenol A, four parabens, benzophenone-3, triclosan) were assessed using first and/or third trimester spot-urine concentrations. Macrovascular health (systolic and diastolic blood pressure (SBP and DBP, mmHg), pulse wave velocity (PWV, m/s)) and microvascular health (central retinal artery/vein equivalent (CRAE/CRVE, mu m)), were measured at 11 years old. Linear regression models assessed associations for individual chemicals and Bayesian weighted quantile sum regression (BWQS) evaluated the overall association of the phthalate and phenol mixture with cardiovascular health. Results: In single exposure models, bisphenol-A was associated with decreased PWV (beta per doubling of exposure = -0.06; 95% CI: -0.10, -0.01). Mono-iso-butyl phthalate was associated with an increase in CRAE (beta = -1.89; 95% CI: 0.34, 3.44). Methyl- and butyl-parabens were associated with a decrease in CRVE (beta = 0-.71; 95% CI: -1.41, -0.01) and (beta = -0.96; 95% CI: -1.57, -0.35), respectively. No statistically significant associations were observed between any of the exposures and SBP or DBP. BWQS models showed no evidence of associations between the phthalate and phenol mixture and any of the outcomes. Conclusions: Our results provide little evidence to suggest that prenatal exposure to phthalates and phenols is associated with macro- or microvascular health during early adolescence, except a few associations with certain compounds. Errors in exposure measurement and reduced variability in cardiovascular measures at this early age limit our ability to draw strong conclusions.