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site on endocrine disruption
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Fact SheetsPrecocious Puberty
Issue: Premature sexual development is linked to exposure to estrogenic contaminants.
Background: Precocious puberty has been reported in children exposed to environmental contaminants. Premature breast bud development was reported in young girls in Puerto Rico with exposure to phthalate esters. In Michigan premature puberty was recently reported in young girls with exposure to brominated diphenyl ethers.
Trends: The age of puberty onset has been suggested to be decreasing over at least two decades. However, the extent and persistence of the decline remains controversial. Moreover, there is no data available for regional differences in the sexual development.
Consistency of the data: Too few studies have been conducted to permit an evaluation of the consistency of the data in this area.
Experimental evidence: Animal studies have shown that exposure to environmental contaminants with estrogenic activity (chemicals that mimic some or all of the actions of estrogens) can accelerate the onset of puberty onset.
Biological plausibility: The biological trigger for the onset of puberty remains unknown. However, it is clear that estrogens accelerate the onset of sexual development. Hence, it is plausible that environmental estrogens can accelerate sexual development if present at sufficient concentration. It can be argued that if estrogenic contaminants can induce this effect then we should also be concerned about exposure to dietary phytoestrogens that are plant estrogens that although they have much shorter half life than man-made chemicals are much more potent.
Conclusion: Overall the literature does not support the contention that environmental chemicals or dietary factors are having widespread effects on human sexual development. Nevertheless, accelerated sexual development is plausible in individuals exposed to high concentrations of estrogenic substances.
Key Papers on this issue:
