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Phthalate-associated hypertension in premature infants: a prospective mechanistic cohort study

Randall Jenkins1, Shane Tackitt2, Ladawna Gievers3

  • 1Department of Pediatrics, Oregon Health & Science University, 707 SW Gaines Road, Mail Code CDRC-P, Portland, OR, 97239, USA. jenkinra@ohsu.edu.

Pediatric Nephrology (Berlin, Germany)
|April 28, 2019
PubMed

Insights

Postnatal exposure to di-(2-ethylhexyl) phthalate (DEHP) in premature infants is linked to increased blood pressure. This exposure may activate the mineralocorticoid receptor (MR) pathway, contributing to hypertension in this vulnerable population.

Area of Science:

  • Neonatal Medicine
  • Pediatric Endocrinology
  • Environmental Health Science

Background:

  • Phthalates, including di-(2-ethylhexyl) phthalate (DEHP), are environmental contaminants with known associations to adverse health outcomes.
  • Elevated exposure to DEHP in premature infants has raised concerns regarding potential impacts on cardiovascular health.
  • Previous studies suggest a correlation between phthalate exposure and increased blood pressure in pediatric populations.

Purpose of the Study:

  • To investigate the relationship between DEHP exposure and systolic blood pressure (SBP) in premature infants.
  • To determine if DEHP exposure is associated with the activation of the mineralocorticoid receptor (MR) pathway.
  • To explore the mediating role of 11β-HSD2 activity and sodium transporter expression in DEHP-induced SBP changes.

Main Methods:

  • A prospective observational cohort study design was employed, monitoring premature infants for 8 months post-birth.
  • Infants were assessed for DEHP metabolite presence in urine, correlating with intravenous (IV) and respiratory tubing exposures.
  • Linear regression and urinary exosome analysis were used to evaluate DEHP's impact on SBP index and potential mechanistic pathways involving MR and 11β-HSD2.

Main Results:

  • Nine out of eighteen infants developed transient idiopathic hypertension.
  • DEHP metabolites were detected in urine, with higher IV and respiratory DEHP exposures observed in hypertensive infants.
  • DEHP exposure from IV fluids significantly correlated with SBP index, and urinary cortisol/cortisone ratio indicated 11β-HSD2 inhibition, suggesting MR activation.

Conclusions:

  • Postnatal DEHP exposure is significantly associated with increased blood pressure and hypertension in premature infants.
  • The mechanism involves the activation of the mineralocorticoid receptor (MR) pathway, likely through the inhibition of the enzyme 11β-HSD2.
  • These findings highlight the potential cardiovascular risks of DEHP exposure in neonates and underscore the need for monitoring and mitigation strategies.
Abstract

Keywords:
Blood pressureHypertensionNeonatalPhthalates

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