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Published on: March 6, 2018
Environmental phenols and pubertal development in girls
Mary S Wolff1, Susan L Teitelbaum1, Kathleen McGovern1
1Department of Preventive Medicine, Icahn School of Medicine at Mount Sinai, 1 Gustave L. Levy Place Box 1057, New York, NY 10029, USA.
Environmental phenols impact child puberty. Some phenols delayed breast development, while others, like triclosan, accelerated it. Further research is needed on these widespread exposures.
Area of Science:
- Environmental health
- Endocrinology
- Pediatric development
Background:
- Widespread environmental exposure to phenols is documented globally, with potentially high levels in children.
- Phenols possess diverse hormonal activities, yet their impact on child reproductive development remains understudied, primarily based on limited cross-sectional data.
Purpose of the Study:
- To prospectively investigate the association between urinary phenol concentrations and pubertal development timing in girls.
- To identify specific phenols that may influence the onset of breast and pubic hair development.
Main Methods:
- A prospective cohort study involving 1239 U.S. girls aged 6-8 years, followed annually for 7 years.
- Measurement of ten urinary phenols (e.g., benzophenone-3, enterolactone, bisphenol A, parabens, triclosan) at enrollment.
- Utilized Cox proportional hazards ratios and Kaplan-Meier analyses to assess risks of earlier or later puberty onset.
Main Results:
- Enterolactone and benzophenone-3 were associated with a 5-6 month delay in breast development.
- Triclosan and 2,5-dichlorophenol were linked to earlier breast development (4-9 months sooner).
- Body size mediated the association between enterolactone and breast development, suggesting potential antiadipogenic or thyroid-agonist roles for these phenols.
Conclusions:
- Certain ubiquitous environmental phenols show significant associations with altered pubertal timing in girls.
- Findings suggest potential antiadipogenic (benzophenone-3, enterolactone) and thyroid-agonist (triclosan, 2,5-dichlorophenol) mechanisms.
- Further investigation is warranted to confirm these results and identify critical windows of susceptibility for phenol exposure during development.
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