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Can oxybenzone cause Hirschsprung's disease?

Joseph C DiNardo1, Craig A Downs2

  • 1Vesuvius, VA, 24483, USA.

Reproductive Toxicology (Elmsford, N.Y.)
|March 5, 2019
PubMed
Summary

Oxybenzone, an endocrine disruptor in sunscreens, crosses the placenta. High maternal levels are linked to Hirschsprung

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Area of Science:

  • Environmental Health
  • Developmental Toxicology
  • Endocrinology

Background:

  • Oxybenzone is a common UV filter in sunscreens.
  • It is an endocrine disrupting chemical (EDC) that can penetrate skin and placental barriers.
  • Studies detect oxybenzone in maternal and fetal blood samples.

Purpose of the Study:

  • To investigate the association between maternal oxybenzone exposure and Hirschsprung's Disease (HSCR).
  • To examine oxybenzone's effect on neural crest cell migration in vitro.
  • To assess fetal exposure levels from typical sunscreen use.

Main Methods:

  • Analysis of oxybenzone levels in pregnant women's urine.
  • In vitro testing using human cell lines to assess cell migration and function.
  • Modeling of fetal exposure based on maternal blood levels.

Main Results:

  • Maternal urinary oxybenzone levels correlated with neonatal HSCR.
  • Low oxybenzone concentrations disrupted human cell migration and function, mimicking HSCR.
  • Sufficient oxybenzone transfers to the fetus to inhibit neural crest cell migration.

Conclusions:

  • Maternal exposure to oxybenzone from sunscreen may increase the risk of HSCR in neonates.
  • Oxybenzone's interference with neural crest cell development is a potential mechanism for HSCR.
  • Further research is needed to understand the full impact of sunscreen chemicals on fetal development.
Keywords:
EmbryogenesisHirschsprung’s diseaseInhibition of neural crest cell migrationOxybenzone

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