Assessing the Safety of a Replacement Chemical: Nongenomic Activity of Bisphenol S

Suspected links between bisphenol A (BPA) and adverse human health effects have spurred a search for replacement chemicals for use in common applications such as polycarbonate plastics, food can linings, and thermal papers.Bisphenol S (BPS) has been adopted for some uses.A new study now shows that low doses of BPS can disrupt nongenomic signaling pathways in cultured pituitary cells [EHP 121(3):352-358; Viñas and Watson].Nearly 93% of U.S. residents over age 6 carry measurable amounts of BPA in their bodies.The compound is suspected to contribute to the development of diseases such as diabetes, asthma, and cancer, and animal studies have shown it adversely affects reproduction.In contrast to genomic regulation, which involves receptors in the cell nucleus, nongenomic regulation involves receptors in the cell membrane.Since BPA can interact with cell-membrane estrogen receptors, researchers explored whether structurally similar BPS might likewise inf luence non genomic pathways.Treatments included various low doses of BPS alone and paired with estradiol, an endogenous estrogen.Measured responses included activation of ERK and JNK, mitogen-activated protein kinases involved in cell growth, proliferation, and apoptosis (programmed cell death); activation of caspases 8 and 9, enzymes that also are involved in apoptosis; and release of prolactin, a hormone that helps regulate hundreds of biological functions, including metabolism, reproduction, and lactation.