been found to leach from plastic products, more so in high temperatures and basic or acidic conditions, such as during autoclaving.2 This becomes more alarming with the pressing problem of global warming.3 Food is also considered the most significant source of BPA exposure worldwide. In fact, BPA has already been detected in almost all of urine samples collected from USA.4
When BPA is imbibed, it is metabolized by the liver into BPA glucuronide, which is excreted through the urine.5 BPA is an estrogenic monomer that binds weakly to nuclear estrogen receptors. In fact, its binding to estrogen receptors is 1000 – 10, 000-fold lower than the natural hormone E2.6 Currently, it is now polymerized to make polycarbonate plastic, which is now extensively used in the manufacture of food and beverage cans and dental materials.
The potency of BPA partly results from the low dose needed to produce a physiologic response. This is because the activation of the effector is longer than the actual hormone-receptor binding, or the number of receptors is greater than the number of molecules. Thus, despite the low affinity of BPA to the receptor, low concentrations still initiate a response. In fact, the linear concentration between receptor occupancy and hormone concentration is preserved only up to 10% receptor occupancy. Above this, saturation of response occurs first, and saturation of receptor follows.7
BPA mimics the activity of 17β-estradiol, posing a strong estrogenic activity. With just 10 – 20 nM, it was seen to competitively bind to estrogen receptors, proliferation of MCF-7 breast cancer cells, induction of progesterone receptors, and reversal estrogen action by tamoxifen. It induces proliferative and stimulatory changes in estrogen targets.8
There is a major concern to public health due to its high potential for human exposure and to its demonstrated toxicity (endocrine disruptor effect). A growing number of health experts and consumers are becoming concerned

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