on bisphenol A
O and S Oishi. 2000. Disposition of Orally Administered 2,2-Bis(4-hydroxyphenyl)
propane (Bisphenol A) in Pregnant Rats and the Placental Transfer
to Fetuses. Environmental
Health Perspectives 108:931-935.
this laboratory experiments with rats, Takahashi and Oishi confirm
and extend an earlier paper by Miyakoda
showing that orally-ingested bispenol A rapidly enters the maternal
bloodstream and then quickly appears in fetal blood, reaching higher
peak concentrations in the fetus than in the mother. "The results
suggest that the absorption and distribution of BPA in maternal
organs and in fetuses are extremely rapid and that BPA can easily
pass through the placenta. The placenta is not a barrier to BPA."
is important because of the ubiquity of exposure
to bisphenol A through a wide diversity of modern products and
the extreme potency of bisphenol A in disrupting fetal development.
Low levels of fetal bisphenol A, for example, alter prostrate
size and hormonal sensitivity in adult mice and also advance
the age of puberty
in mice. These laboratory experiments produce results that are consistent
with certain human epidemiological trends but to date lack scientific
certainty linking the observed effects in animals to observed trends
did they do?
Takahashi and Oishi exposed pregnant female rats to high doses of
bisphenol A and then at varying times after exposure examined the
concentration of BPA in the blood and tissue of the mother and its
fetal offspring. They used high doses to make detection reliable,
and argue that the dose that they used is not outside of the range
that will allow their results to be extrapolated to BPA kinetics
at low doses.
did they find?
They found that within 10 minutes of ingesting BPA, the compound
could be measured within the maternal and fetal blood. Maximum blood
concentrations were reached 20 minutes after exposure, and levels
declined thereafter. In maternal blood the decline after the peak
was approximately 100-fold over 10 hours, whereas in the fetus the
decline after the peak was somewhat slower. Fetal concentrations
became higher than maternal concentrations, following a kinetic
pattern also observed in diethylstilbestrol:
manner in which fetal BPA levels become higher than maternal
plasma levels after the maximum maternal plasma level occurs
may resemble that of DES, one of the most potent nonsteroidal
synthetic estrogens. BPA, 2,2-bis(4-hydroxyphenyl)propane, is
somewhat structurally related to DES, 3,4-bis(4-hydroxyphenyl)-3-hexene.
DES is rapidly absorbed and distributed and cleared in maternal
organs, and its major site of accumulation is the liver. Maternally
administered DES is also rapidly distributed to fetuses in rats,
mice, hamsters, and monkeys ; the fetal level is 2-3 times that
in the maternal blood. DES deposits in fetal genital organs,
which may be responsible for the transplacental reproductive
toxicity. From our results, we determined that BPA is also rapidly
absorbed, distributed, and cleared, and the major organ of accumulation
is also the liver. After 40 min the fetal BPA concentration
is higher than in maternal blood."
does it mean?
importantly, this confirms earlier results that bisphenol A ingestion
by a female rodent quickly leads to exposure of the fetus. The digestive
and blood factors that buffer the developing fetus from natural
estrogen and from phytoestrogens do not eliminate exposure to bisphenol
A. Transfer to the fetus is very rapid, within minutes.
rapidity and efficiency of transfer has significant implications
for epidemiological studies of bisphenol A's impact in humans. It
implies that single exposures, for example via high rates of leaching
from a food container marketed as usable in microwave ovens, could
quickly but ephemerally pass into the mother, into the fetus, and
after lingering for several hours disappear. If the passage took
place during a critical, vulnerable window of development and provoked
an effect, the impact would be virtually impossible to link statistically
to the exposure via current epidemiological practices. This ephemerality
of the contaminant coupled with its high potency during passing
windows of development are important reasons why human epidemiology
is strongly biased toward false negatives (concluding a product
is safe when in fact it causes harm) in the study of endocrine disruption.