Several years ago, manufacturers of water bottles, food containers and baby products began facing increased governmental and public pressure to remove bisphenol A (BPA) – a key ingredient in the plastics they used – from their products. BPA has been linked by scientists to diabetes, asthma and cancer, as well as altered prostate and neurological development.

The industry responded by creating “BPA-free” products, which were made from plastic containing a compound called bisphenol S. In addition to having similar names, it turns out BPA and BPS share a similar structure and versatility. BPS is now known to be used in everything from currency to thermal receipt paper, and widespread human exposure to BPS was confirmed in a 2012 analysis of urine samples taken in the U.S., Japan, China and five other Asian countries.

And according to a new study by University of Texas Medical Branch at Galveston researchers, BPS also resembles BPA in a more problematic way. Like BPA, the study found that BPS disrupts cellular responses to the hormone estrogen, changing patterns of cell growth and death, as well as hormone release. Also like BPA, it does so at extremely low levels of exposure.

“Our studies show that BPS is active at femtomolar to picomolar concentrations just like endogenous hormones —that’s in the range of parts per trillion to quadrillion,” said UTMB professor Cheryl Watson, senior author of a paper on the study being published in Environmental Health Perspectives. “Those are levels likely to be produced by BPS leaching from containers into their contents.”

Watson and graduate student René Viñas conducted cell-culture experiments to examine the effects of BPS on a form of signaling that involves estrogen receptors — the “receivers” of a biochemical message — acting in the cell’s outer membrane instead of the cell nucleus. Where nuclear signaling involves interaction with DNA to produce proteins and requires hours to days, membrane signaling (also called “non-genomic” signaling) acts through much quicker mechanisms, generating a response in seconds or minutes.

Watson and Viñas focused on key biochemical pathways that are normally stimulated when estrogen activates membrane receptors. One, involving a protein known as ERK, is linked to cell growth; another, referred to as JNK, is tied to cell death. In addition, they examined the ability of BPS to activate proteins called caspases (also linked to cell death) and promote the release of prolactin, a hormone that stimulates lactation and influences many other functions.

“These pathways form a complicated web of signals, and we’re going to need to study them more closely to fully understand how they work,” Watson said. “On its own, though, this study shows us that very low levels of BPS can disrupt natural estrogen hormone actions in ways similar to what we see with BPA. That’s a real cause for concern.”

The study was supported by the Passport Foundation and the U.S. National Institutes of Health.