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