A landmark study suggesting that American girls are reaching puberty at an earlier age has stimulated a wide ranging debate about whether sexual development is taking place more rapidly, if so, what is causing it, and what should be done about it.

There are no clear answers. The issue is very difficult to study in people, especially as the historical data on timing of puberty are very limited.

[an overview of factors proposed to influence the rate of sexual development]
[More on the landmark study and the debate it has stimulated]
[Additional findings on timing of sexual developments in people]

While the science on people is uncertain, experiments with animals demonstrate conclusively that the pace and pattern of sexual development is vulnerable to chemical contamination in utero or shortly after birth. Two clear patterns emerge: that exposure to estrogen mimics reduces the age of puberty in females, while exposure to compounds that interfere with androgens (like testosterone) delays puberty in males. This is readily evident in a compilation of known effects.

Below follow brief descriptions of several recent important studies carried out in the laboratory:

Howdeshell et al. found that when female mice are exposed in the womb by delivering low doses of bisphenol A through food to the mother that the female mice pass a milestone in sexual development significantly earlier than do unexposed mice.

They also show that position in the womb interacts with contamination: those females positioned between female litter mates were most affected by bisphenol a, while those between males were least affected. More...

Monosson, E, WR Kelce, C Lambright, J Ostby and LE Gray. 1999. Peripubertal exposure to the antiandrogenic fungicide, vinclozolin, delays puberty, inhibits the development of androgen-dependent tissues, and alters androgen receptor function in the male rat. Toxicology and Industrial Health 15:65-79.

Vinclozolin is a well-studied fungicide that interferes at low levels of exposure with the interaction of androgens with their receptor. Exposure to anti-androgenic compounds like vinclozolin alters reproductive development of male mammals, including inducing female-like characteristics. In this paper Gray et al. document that vinclozolin delays pubertal development in males. This is because a series of events leading to and during puberty are dependent upon androgenic hormone signalling. Puberty delays can also be induced with other antiandrogenic substances like p,p'-DDE, methoxychlor, linuron and dibutyl phthalate.

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