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
are no clear answers. The issue is very difficult to study in people,
especially as the historical data on timing of puberty are very
overview of factors proposed to influence the rate of sexual development]
on the landmark study and the debate it has stimulated]
findings on timing of sexual developments in people]
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.
follow brief descriptions of several recent important studies carried
out in the laboratory:
K, AK Hotchkiss, KA Thayer, JG Vandenbergh and FS vom Saal. 1999.
Plastic bisphenol A speeds growth and puberty. Nature 401:
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.
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.
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
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.