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.
argument was already weakened by the observation that ingestion
low levels of BPA by pregnant mice causes adverse effects in
the offspring... even with the metabolic conversion to BPA-monoglucoronide
and quick excretion.
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.
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.
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.
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.
BPA levels in maternal and fetal samples. The lower limit
of detection for their technique was 0.01 ng/mL
details in their results are particularly intriguing.
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.
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.
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
authors cautiously observe:
etiology of many adverse reproductive outcomes among humans
is poorly understood. A growing body of scientific evidence
indicates that a number of chemicals to which humans are in
contact—including natural and synthetic hormones, organometals,
pesticides, persistent environmental pollutants, monomers,
and additives used in the plastic industry—may interfere
with the endocrine system, potentially causing adverse effects
to both wildlife and humans.
for concern include evidence for a number of trends: There
are indications for an increase in the incidence of some hormonally
sensitive carcinomas, decrease in sperm count and quality,
and increased obesity and earlier puberty occurring in girls,
as well as altered physical and mental development in children.
date, there is no evidence that ingestion of BPA at levels
estimated to occur by typical environmental exposure has adverse
effects in humans; a causal relationship of the observed effects
with BPA has not yet been adequately established. Long-term
follow-up studies are needed to assess the adverse effects
of BPA exposure in early life. Further studies on human exposure
to BPA are needed to address the question whether maternal
exposure to BPA can lead to adverse health effects in offspring."
leave unaddressed the broader policy question:
three types of observations:
experiments demonstrating low level adverse effects of bisphenol
trends in people consistent with predictions based on animal and
in vitro experiments, and
et al.'s demonstration of fetal exposure to BPA at levels
comparable to those capable of causing developmental effects in
regulators wait until epidemiological proof of human harm, or act
now to reduce exposures?
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.