Schönfelder, G, W Wittfoht, H Hopp, CE Talsness, M Paul and I Chahoud. 2002. Parent Bisphenol A Accumulation in the Human Maternal-Fetal-Placental Unit. Environmental Health Perspectives 110:A703-A707.

background on BPA
Virtually all Americans exposed to BPA

One of the arguments offered against concerns about potential human effects of bisphenol A is that, at least in rats and mice, much of the "parent BPA" (the chemical form in which it is ingested) is quickly converted to another variant of BPA, BPA-monoglucoronide, which is biologically inactive. Further, most of the BPA is quickly excreted. Hence, the argument goes, little can be reaching the fetus to affect development.

That argument was already weakened by the observation that ingestion of very low levels of BPA by pregnant mice causes adverse effects in the offspring... even with the metabolic conversion to BPA-monoglucoronide and quick excretion.

Now in this article Schönfelder et al. empirically refute another part of the argument: their studies of pregnant women and their fetuses reveal biologically significant levels of "parent BPA" in the samples measured.

Thus bisphenol A reaches the human fetus in the womb at levels that are well within the ranges shown experimentally to alter development, and in its most powerful chemical form. This result increases the urgency of measures to reduce exposures to bisphenol A until questions about its safety can be resolved.

What did they do? Schönfelder et al. developed some new methods in analytical chemistry allowing them to measure bisphenol A reliably at extremely low levels within human tissue and serum. They then applied those methods to samples of blood and tissue taken during pregnancy and immediately birth, obtained from 37 mothers living in urban areas of Germany.

What did they find? They found bisphenol A in all human samples examined: placental tissue, mothers' blood plasma obtained during weeks 32-41 of pregnancy and placental tissue and umbilical cord blood plasma at birth.

Average BPA levels in maternal and fetal samples. The lower limit of detection for their technique was 0.01 ng/mL

Two details in their results are particularly intriguing.

• First, while average levels in fetal plasma were lower than maternal plasma (see figure above), in fact in 14 of the 37 mother-fetal comparisons, fetal concentrations were higher than the mother's. All but two of those involved male fetuses. The authors conclude that this fetal accumulation of BPA is likely to be a result of the absence of enzymes in the fetus capable of metabolizing BPA to its biologically-inert form. The full range of these detoxification enzymes is not developed until after an infant reaches the age of 3 months.
• Second, male fetal concentrations were higher than female, even after correcting for a positive correlation between body weight and BPA fetal concentration. The authors suggest that this may be due to sexual differences in metabolism, or maternal differences in exposure to BPA in consumer products, somehow linked to the sex of the fetus.

What does it mean? It is no longer possible to claim that the human fetus is somehow protected from biologically-active form of bisphenol A, or that levels that reach the fetus are so low as to be irrelevant. Seen against the backdrop of mounting experimental studies with animals showing adverse effects on fetal development, within the range of exposures reported by Schönfelder et al., this new work reinforces the need for taking immediate steps to reduce human exposures to BPA until safety issues can be resolved.

The authors cautiously observe:

They leave unaddressed the broader policy question:

Given three types of observations:

• animal experiments demonstrating low level adverse effects of bisphenol A
• epidemiological trends in people consistent with predictions based on animal and in vitro experiments, and
• Schönfelder et al.'s demonstration of fetal exposure to BPA at levels comparable to those capable of causing developmental effects in animals

should regulators wait until epidemiological proof of human harm, or act now to reduce exposures?

Sufficient evidence is now available on bisphenol A to make highly plausible a series of human effects. The burden of proof should be reversed. Rather than waiting for scientific certainty of harm, steps to reduce human exposures should begin now, only to be curtailed if further research shows definitively that the mounting evidence has exaggerated bisphenol A's potential effects.