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Bisphenol A Health Effects

BPA was first recognized to have estrogenic activity as a synthetic drug in 1936 long before it was used to form polycarbonate plastic and resins in the early 1950s. Interest and concern about the health effects of BPA have been growing, following reports that the health effects seen in exposed animals are also on the rise in humans. These include breast and prostate cancer, regional decline in sperm counts, abnormal penile/urethra development in males, early sexual maturation in females, increasing neurobehavioral problems, increasing prevalence of obesity and type 2 diabetes, and immune system effects.

Low-Dose Effects

Most BPA health effect studies prior to 1997 were conducted on laboratory animals at doses close to or higher than the level EPA set as a “reference dose” (RfD), a benchmark of maximum acceptable daily exposure. EPA chose the lowest dose tested (50 mg/kg/day) as a Lowest Observed Adverse Effect Level (LOAEL). In 1988 the Agency then divided this dose by a 1,000-fold safety factor to calculate the maximum concentration it believed would be health-protective (50 μg/kg/day), even if experienced daily over a lifetime. This choice was based upon “high dose experiments” conducted by the U.S. National Toxicology Program in 1982. A 1,000-fold safety factor would normally provide an ample margin of protection against adverse health effects, if the experiments had thoroughly explored whether effects occur at lower doses. They did not.

Since 1997, more than 100 additional peer-reviewed studies have reported health effects in animals from BPA doses beneath the EPA Reference Dose (RfD), which has remained unchanged since 1988. For the purposes of this report, “low-dose” is defined as exposures beneath the EPA RfD. Many scientists have reported diverse abnormal endocrine effects in both terrestrial and aquatic animals at doses far lower than the LOAEL used to set the EPA RfD. And BPA has been detected circulating in human blood in parts per billion (ppb) concentrations that would not be explained if exposures were occurring at the EPA RfD.

Scientists now believe that there are at least two mechanisms by which BPA disrupts normal endocrine function. BPA can act as a weak estrogen, binding to the estrogen receptor. Alternatively, BPA can block the effect of stronger natural estrogens, inhibiting estrogen function. They are commonly assumed to act through the estrogen receptors in the cell nucleus that regulate gene expression. Several other mechanisms of BPA action are thought to be relevant to its biological effect. BPA may bind to the recently discovered membrane estrogen receptor. Activation of these receptors regulates cell signaling and influences gene expression. In addition, BPA produces changes in DNA structure by adding methyl groups to DNA, silencing their expression. These later two mechanisms do not respond in the same way to BPA as the classic receptors, and may have very different response to low doses of BPA. These latter effects have been reported at exceptionally low part per trillion doses, nearly 1,000 times lower than the effect level used to establish the current EPA RfD.

 

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