New Mechanism of Toxic Plastics: Evidence That BPA and BPS Impact Heart Rate via GPER

Overview

Bisphenol A (BPA) and Bisphenol S (BPS) are chemicals used in hard plastics for food containers and are xenoestrogens, chemicals that mimic the hormone estrogen. BPA and BPS are thought to act through estrogen receptors α and β (ERα/β); however, typical BPA exposure levels are much lower than levels needed to bind ERα/β. Building off of my data from last year, which surprisingly found that BPA and BPS increase heart rate in Daphnia magna, this study aims to test my central hypothesis that BPA and BPS increase heart rate by binding a different receptor: G protein-coupled estrogen receptor (GPER). To test this hypothesis, I utilized a specific antagonist of GPER, the chemical G-15. Because GPER regulates calcium flow and therefore heart rate, I predicted that G-15 would suppress the effects of BPA or BPS on D. magna heart rate. I exposed D. magna to BPA or BPS in the absence or presence of G-15, as well as G-15 alone. After six days, I measured their heart rate. Similarly to what I observed last year, BPA and BPS increased D. magna heart rate, suggesting BPS is just as harmful as BPA. Additionally, the heart rate of D. magna exhibited a hyperbolic relationship with BPA and BPS concentration, suggesting that BPA and BPS saturate a receptor. More importantly, G-15 suppressed the effect of BPA and BPS on heart rate, suggesting that GPER is the receptor that mediates the effect of BPA and BPS on heart rate. Overall, my study suggests that at low concentrations BPA and BPS affect heart rate through GPER, which is in contrast to prior assumptions that BPA and BPS affect heart rate through ERα/β. My study has many implications for limiting the continued use of harmful plastics by screening for chemicals that bind GPER.

Competition history

• AJAS 2026 Category not listed

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