Concerns over the chemical, which is used as a sealant in the linings of food and beverage containers and in the making of hard plastics, have focused largely on fetuses and newborns who, it has been suggested, may be more vulnerable to BPA because they have not developed the ability to deactivate it.
But a team of researchers from the U.S. Food and Drug Administration and the National Toxicology Program studying the pharmacokinetics of BPA, or the way the chemical is processed in the body, are finding that BPA is effectively metabolized by the mother, the placenta and even the fetus itself.
The study, which began in 2010, first looked at BPA as it was metabolized in pregnant mice and rats. After finding that the rodents and fetuses were able to deactivate the chemical, the researchers began studying BPA in monkeys, a species more closely related to humans.
BPA was administered to the monkeys via injection into the bloodstream, meaning that the chemical bypassed the digestive tract, where the researchers have found that a significant amount of BPA metabolization takes place. The results of this most recent trial showed that the fetus was exposed to less than half of the amount of active BPA administered to the mother.
And that level is much higher than the level a human would naturally be exposed to, explained Daniel Doerge, a chemist with FDA’s National Center for Toxicological Research and the study’s lead researcher in an email to Food Safety News.
“We need to keep in mind that this dose is more than 1000-fold above realistic human daily aggregate exposure to women of child-bearing age, which would certainly produce levels in the fetus far below the levels detectable by current analytical methodology,” said Doerge.
When BPA is ingested – the most common route of exposure to the chemical – it is reduced to undetectable levels in the fetus, the study showed.
“The net result is that more than 99% of dietary BPA is detoxified by conversion to BPA-G before it enters the bloodstream for delivery into the tissues where even more metabolism can occur,” explained Doerge.
The study also revealed that BPA was deactivated in monkeys at a much higher rate than it was in the rodents.
“The result is that newborn monkeys have about ten-fold lower internal exposures to BPA than newborn rodents,” said Doerge.
It is important to note that pharmacokinetics studies do not look at the effects of BPA on pregnant mothers or on fetuses but rather the way the body changes and removes the chemical before it reaches the tissues of the fetus.
At harmful levels, BPA is thought to be an endocrine disruptor, which mimics the effects of hormones in the body and can lead to developmental and behavioral problems in fetuses and infants. The 10 pharmacokinetics studies that have been conducted since 2010 show not that BPA is not harmful, but that harmful BPA is metabolized and deactivated by the body.
The team’s research has also addressed the theory that BPA that does reach the fetus might collect there, and potentially become active again.
“Our work also tested a hypothesis that BPA-G could be ‘reactivated’ to BPA and ‘accumulated’ in the fetus. Our results showed that this does not occur and, in addition, the fetus gradually acquires its own metabolic capacity to detoxify BPA throughout gestation.
Doerge says the next step in his team’s research is to study BPA pharmacokinetics in humans.
“We are currently investigating BPA pharmacokinetics in human volunteers in conjunction with the National Toxicology Program of the National Institute of Environmental Health Science,” he said. “These studies will serve as a bridge between earlier human studies and our current studies in animal models.”
A 2011 study on dietary BPA exposure showed that after 20 test subjects consumed high levels of BPA, no active BPA was detected in samples of the participants’ urine taken hourly for 24 hours after ingestion. High levels of detoxified BPA were detected.
The FDA, which is in charge of regulating BPA, says that while “BPA is safe at the very low levels that occur in some foods,” and assessment that is “based on review by FDA scientists of hundreds of studies including the latest findings from new studies initiated by the agency,” it is also taking steps to reduce the amount of BPA while it continues to study the risk of BPA exposure.
The agency banned the use of BPA in baby bottles and sippy cups in July of 2012, but said the ban was because theses products aren’t made with the chemical anymore, and regulating this use has been rendered obsolete.
Bisphenol A is currently banned in some types of containers in 11 U.S. states, including California, Connecticut, Delaware, Maine, Maryland, Massachusetts, Minnesota, New York, Vermont, Washington and Wisconsin. Laws in Canada, the European Union, China, Malaysia, South Africa and Argentina also prohibit BPA in products intended for small children. Australia and Japan have initiated voluntary bans.
France has proposed a ban on the chemical in the European Union, but it has been blocked by six other countries.
The European Food Safety Authority issued an opinion on fetus exposure to BPA in 2008:
“Taking account of data in human neonates on compounds structurally related to BPA which undergo glucuronidation/sulphation, the Panel considers that there is sufficient capacity in the neonate to conjugate BPA at doses below 1 mg/kg bw (the Panel noted that exposures at the TDI of 0.05 mg/kg bw are 20 fold lower than this).”© Food Safety News