The analysis of 150 BPA exposure studies was presented at the American Association for the Advancement of Science's annual meeting by toxicologist Justin Teeguarden of the Department of Energy's Pacific Northwest National Laboratory, Washington.
Teeguarden also evaluated 130 toxicity studies that referred to exposure as low dose and looked at the chemical’s toxicity in animals and cells in the lab, in the work supported by the US Environmental Protection Agency (EPA).
Low dose confusion
According to his analysis the "low doses" span a range of concentrations and only 0.8% to 7% of the exposures in the studies are in the range of human contact.
He found the range of concentrations spans from 10 grams per kilogram of weight per day down to 100 picograms per kilogram of weight per day (a picogram is one millionth of a gram).
Teeguarden questioned the relevance of studies citing low-dose as automatically relevant to human exposure.
“The term low-dose cannot be understood to mean either relevant to human exposures or in the range of human exposures. However, this is in fact what it has come to mean to the public, as well as many in the media.”
He said the low dose moniker had been used to promote selected toxicity studies, possibly in arguments to ban BPA.
"For BPA and all chemicals, we need more accurate language to present these findings so the public and scientists in other disciplines can understand how human exposures compare to exposures in laboratory studies reporting toxicity."
In the 150 exposure studies, Teeguarden looked to see if BPA concentrations were high enough to be a significant source of estrogen-like activity in the blood.
BPA binds to the same proteins that estrogen does, called estrogen receptors, however it does so more weakly than estrogen, so to trigger biological effects through receptors, concentrations have to be high enough in the blood.
Human blood levels of BPA were expected to be below levels required for significant binding to four of the five key estrogen receptors to cause biological effects.
Richard Sharpe, from the University of Edinburgh, Scotland also presented at the annual meeting and said most human exposure to BPA occurs via diet and the gut where most BPA is inactivated with further inactivation in the liver.
“…if BPA causes the human disorders with which it has been associated, it would mean that BPA was an extremely potent toxic chemical; so potent, that if it was injected into experimental animals…at human exposure levels it would be expected to cause major disorders in the animals, and yet many such studies show no effects or only mild effects.”