Our Stolen Futurea book by Theo Colborn, Dianne Dumanoski, and John Peterson Myers
 
 

 

 

background on bisphenol A

Takahashi, 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.


In this laboratory experiments with rats, Takahashi and Oishi confirm and extend an earlier paper by Miyakoda et al., 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."

This 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 in humans.

What 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.

What 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:

  "The 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."  

What does it mean?
Most 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.

The 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.

 

 
     

 

 

 

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