Currently, no federal agency tests the toxicity of new materials before they are allowed on the market… ! ? ! ?
Common BPA substitute, BPS, disrupts heart rhythms in females
Abstract:
” … In the current study, the investigators perfused, or flowed, BPS through the arteries of each animal’s pumping heart, after stimulating the heart with the hormone catecholamine to mimic stress. For a control group, 30 rat hearts received only catecholamine and no BPS.
Exposure to BPS rapidly increased the heart rate of female rats and under the stress condition led to arrhythmias—heart rhythm abnormalities—far greater than in the control rats that did not receive BPS, Wang reported. Electocardiograms demonstrated that BPS caused extra heartbeats and a racing heartbeat, also known as ventricular tachycardia. In male rats, BPS reportedly did not have this rapid impact on the heart… ”
Exposure to BPA Substitute Causes Hyperactivity and Brain Changes in Fish
Abstract:
” …At the peak time of neuronal birth, the number of neurons in BPA-exposed fish rose 170 percent compared with unexposed fish, Kurrasch stated. In similar experiments using BPS, the number of neurons in exposed fish increased 240 percent. These results, she explained, suggest that BPA and BPS could lead to altered brain connections and might explain the hyperactivity they observed in another experiment. Specifically, the research team used movement tracking software to evaluate behavioral changes in young fish and found that fish exposed during brain development to either BPA or BPS were hyperactive, but unexposed fish were not… ”
Bisphenol S Disrupts Estradiol-Induced Nongenomic Signaling in a Rat Pituitary Cell Line: Effects on Cell Functions
Abstract:
Background:
Bisphenol-A (BPA) is a well-known endocrine disruptor that imperfectly mimics the effects of physiologic estrogens via membrane-bound estrogen receptors (mERα, mERβ, and GPER/GPR30), thereby initiating nongenomic signaling. Bisphenol S (BPS) is an alternative to BPA in plastic consumer products and thermal paper.
Objective:
To characterize the nongenomic activities of BPS, we examined signaling pathways it evoked in GH3/B6/F10 rat pituitary cells alone and together with the physiologic estrogen estradiol (E2). Extracellular signal-regulated kinase (ERK)– and c-Jun-N-terminal kinase (JNK)–specific phosphorylations were examined for their correlation to three functional responses: proliferation, caspase activation, and prolactin (PRL) release.
Methods:
We detected ERK and JNK phosphorylations by fixed-cell immunoassays, identified the predominant mER initiating the signaling with selective inhibitors, estimated cell numbers by crystal violet assays, measured caspase activity by cleavage of fluorescent caspase substrates, and measured PRL release by radioimmunoassay.
Results:
BPS phosphoactivated ERK within 2.5 min in a nonmonotonic dose-dependent manner (10–15 to 10–7 M). When combined with 10–9 M E2, the physiologic estrogen’s ERK response was attenuated. BPS could not activate JNK, but it greatly enhanced E2-induced JNK activity. BPS induced cell proliferation at low concentrations (femtomolar to nanomolar), similar to E2. Combinations of both estrogens reduced cell numbers below those of the vehicle control and also activated caspases. Earlier activation of caspase 8 versus caspase 9 demonstrated that BPS initiates apoptosis via the extrinsic pathway, consistent with activation via a membrane receptor. BPS also inhibited rapid (≤ 1 min) E2-induced PRL release.
Conclusion:
BPS, once considered a safe substitute for BPA, disrupts membrane-initiated E2-induced cell signaling, leading to altered cell proliferation, cell death, and PRL release.
Most Plastic Products Release Estrogenic Chemicals: A Potential Health Problem That Can Be Solved
Abstract
Background:
Chemicals having estrogenic activity (EA) reportedly cause many adverse health effects, especially at low (picomolar to nanomolar) doses in fetal and juvenile mammals.
Objectives:
We sought to determine whether commercially available plastic resins and products, including baby bottles and other products advertised as bisphenol A (BPA) free, release chemicals having EA.
Methods:
We used a roboticized MCF-7 cell proliferation assay, which is very sensitive, accurate, and repeatable, to quantify the EA of chemicals leached into saline or ethanol extracts of many types of commercially available plastic materials, some exposed to common-use stresses (microwaving, ultraviolet radiation, and/or autoclaving).
Results:
Almost all commercially available plastic products we sampled—independent of the type of resin, product, or retail source—leached chemicals having reliably detectable EA, including those advertised as BPA free. In some cases, BPA-free products released chemicals having more EA than did BPA-containing products.
Conclusions:
Many plastic products are mischaracterized as being EA free if extracted with only one solvent and not exposed to common-use stresses. However, we can identify existing compounds, or have developed, monomers, additives, or processing agents that have no detectable EA and have similar costs. Hence, our data suggest that EA-free plastic products exposed to common-use stresses and extracted by saline and ethanol solvents could be cost-effectively made on a commercial scale and thereby eliminate a potential health risk posed by most currently available plastic products that leach chemicals having EA into food products.
Sources and More Information:
- Common BPA substitute, BPS, disrupts heart rhythms in females, Endocrine Society, Newsroom, 23-Jun-2014.
- Exposure to BPA Substitute Causes Hyperactivity and Brain Changes in Fish, Endocrine Society, Newsroom, 23-Jun-2014.
- Bisphenol S Disrupts Estradiol-Induced Nongenomic Signaling in a Rat Pituitary Cell Line: Effects on Cell Functions, Environ Health Perspect., DOI:10.1289/ehp.1205826, March 2013.
- Most Plastic Products Release Estrogenic Chemicals: A Potential Health Problem That Can Be Solved, Environ Health Perspect., PMC3222987, Jul 1, 2011.