Research: Bisphenol A (BPA) Causes 100x More Harm Than Previously ImaginedSayer Ji An alarming new study establishes that the commonly used chemical bisphenol Aused in tens of thousands of consumer products, and its lesser known but increasingly prevalent analogs, bisphenol S and F, are several orders of magnitude more disruptive to the endocrine systems of the developing male human fetus than previous toxicological risk assessments were capable of determining. The new study was published in the journal Fertility and Sterility and titled, A new chapter in the bisphenol A story: bisphenol S and bisphenol F are not safe alternatives to this compound. As we have documented extensively in the past, the authors of the new study raise concerns that as awareness of bisphenol As clearly demonstrated toxicity grows and it loses favor within the marketplace, manufacturers are increasingly substituting it with chemically similar bisphenol compounds whose toxicities are less well characterized. As a result, consumers who conscientiously buy ostensibly BPA-free products are being mislead into thinking they are bisphenol free and therefore safe. The new study employed an innovative organotypic culture system that took tissue samples from mouse, rat and human fetal testis, in order to create an experimental model that would accurately reproduce some of the dynamics observable within in vivo (living organism-based) systems that are not ascertainable within conventional in vitro (cell-based) models. They termed this experimental environment the fetal testis assay (FeTA) system. Disturbingly, they found: With the use of a culture system that we developed (fetal testis assay [FeTA]), we previously showed that 10nmol/L BPA reduces basal testosterone secretion of human fetal testis explants and that the susceptibility to BPA is at least 100-fold lower in rat and mouse fetal testes. [emphasis added] In other word, the endocrine-disruptive effect of bisphenol A particularly its ability to suppress the testosterone-mediated mascularization process during embryogenesis may be at least 100 times more toxic than previously believed. How so? Conventional toxicological risk assessments of novel new chemicals like bisphenol A are invariably performed on rodents, with effects (lethal dose 50%/LD50) extrapolated to humans based merely on body weight differences. What these do not account for is the contrasting ontological differences between cells of different species. Nor do these acute lethal response studies (LD50) account for the non-linear response between dose and effect (i.e. monotonicity). An accumulating body of scientific evidence has forced an acknowledgment today that the low-dose effects of chemicals on hormonal systems include the following counterintuitive response: a lower dose may have more profoundly disruptive effects on our hormonal system than higher doses. This concept may be so counterintuitive, that it begs for deeper explanation. For instance, if chemical compound X at 1 milligram induces programmed cell death within an exposed cell, and .01 milligram of compound X induces a phenotypal change in the cell consistent with cancer, it will be the latter effect (the lower dose) that may be more detrimental in the long term, as cell death follows with stem-cell mediated replacement of the damaged differentiated cell; whereas chemically-induced carcinogenesis may result in the death of the entire organism). Case in point: Using the FeTA system, we previously reported that basal testosterone secretion by human testes was not affected by 10,000 nmol/L DES, but it was reduced by concentrations as low as 10 nmol/L of BPA. Conversely, 10 nmol/L and 100 nmol/L BPA did not affect testosterone secretion by both mouse and rat testes, and 10,000 nmol/L BPA was needed to observe a significant reduction (58). The researchers also noted that during the development of the nascent male human in embryogenesis exposure to bisphenols in the 6.5th and 14th gestational weeks the window known to be critical for what is known as the masculinization programming window these chemicals are likely contributing to the alarming worldwide increase in male reproductive disorders, such as such as hypospadias [abnormally placed urinary hole], cryptorchidism [the absence of one or both of the testicles], incomplete development or agenesis of prostate and seminal vesicles, and reduction of the anogenital distance (AGD) [the distance from the anus to the genitalia] and penis length. Clearly, conventional toxicology, where the assumption is that a higher concentration of a toxic substance is linearly connected to a higher quantifiable adverse response, is no longer realistic. Living systems are highly dynamic and complex and one can never predict how a xenobiotic chemical will affect it. Any biologically incompatible chemical, introduced at a critically important developmental window, could result in untold adverse effects. The point is to eliminate unnecessary exposures, instead of abiding by what regulators consider an acceptable level of harm. Clearly, the time is now to call for a ban of bisphenol containing products. While 3.4 millions tons are produced annually, with 20% of this being used as epoxy resin to coat food and beverage metallic cans, we can no longer pretend, given the latest research, that this chemical is not causing massive damage to exposed populations. The researchers comment: Bisphenol A (BPA) is a widely studied typical endocrine-disrupting chemical, and one of the major new issues is the safe replacement of this commonly used compound. Bisphenol S (BPS) and bisphenol F (BPF) are already or are planned to be used as BPA alternatives. With the use of a culture system that we developed (fetal testis assay [FeTA]), we previously showed that 10nmol/L BPA reduces basal testosterone secretion of human fetal testis explants and that the susceptibility to BPA is at least 100-fold lower in rat and mouse fetal testes. Here, we show that addition of LH in the FeTA system considerably enhances BPA minimum effective concentration in mouse and human but not in rat fetal testes. Then, using the FeTA system without LH (the experimental conditions in which mouse and human fetal testes are most sensitive to BPA), we found that, as for BPA, 10nmol/L BPS or BPF is sufficient to decrease basal testosterone secretion by human fetal testes with often nonmonotonic dose-response curves. In fetal mouse testes, the dose-response curves were mostly monotonic and the minimum effective concentrations were 1,000nmol/L for BPA and BPF and 100nmol/L for BPS. Finally, 10,000nmol/L BPA, BPS, or BPF reducedInsl3expression in cultured mouse fetal testes. This is the first report describing BPS and BPF adverse effects on a physiologic function in humans and rodents. On a Brighter Note While chemicals like BPA represent a source of great harm, there is plenty of research revealing that we can mitigate and/or undo some of the damage associated with its ubiquitous exposure, when eliminating it all together is not an option. In line with our mission: Education Equal Empowerment, we have gathered up abstracts from the National Library of Medicine indicating the in-built resilience of biological systems to attenuate the adverse effects of these chemicals, such as: Clearly, the best case scenario is avoiding exposure to bisphenols whenever possible. However, simply accepting a thermal receipt at a purchase, or consuming a meal whose ingredients derive from canned foods, makes avoidance a very difficult proposition. We hope that this research will foment a movement to pressure manufacturers and regulators to clamp down on the use ofbisphenols. This article first appeared at GreenMedInfo. Please visit to access their vast database of articles and the latest information in natural health. The population reduction scheme in the uS is in overdrive. Protect yourself. Most all soy is GMO! Watch the documentary The Disappearing Male 