Assessing the safety of bpa and bps



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Assessing the safety of BPA and BPS

Bisphenol A is a synthetic compound used by companies for a variety of applications. The initial discovery of this compound was during pharmaceutical exploration intending to manufacture a synthetic estrogen in the early 1900s (Dodds, 1936). It was during this time publications regarding BPA’s estrogenic tendencies were released. Years later, BPA was reintroduced by chemists as a commercial product in epoxy resins and polycarbonate plastics. By the 1970s these products were utilized by nearly all US industries either directly or indirectly (Vogel, 2009).

BPA and BPS are ubiquitous across manufactured products. It is almost inevitable that an individual will come in contact with a product containing BPA every day. The diversity in applications this molecule provides makes it extremely useful in a variety of scenarios. Unfortunately it comes at a cost to public health. BPA and BPS have been identified to act as endocrine disrupting chemicals (EDCs) (Robertson, 2015). EDCs are exogenous agents that can interfere with species’ homeostasis through a variety of mechanisms. BPA and BPS are a subclass of EDCs referred to as “hormone mimics” and interrupt regular binding actions of the hormone, estrogen. Due to structural similarities, BPA and BPS have the potential to alter estrogenic activity and alter reproductive success (Rodchester, 2015).

From an industrial perspective, BPA is one of the most useful compounds in manufacturing. It can be found in a variety of products such as water bottles, packaging, receipts, helmets, medical supplies, and polycarbonates. Polycarbonates have been used for decades in a range of applications due to its lightweight, shatter-resistant nature.

The controversy regarding BPA regulation has become a heated topic among the scientific community and government agencies (Hentges, 2014). Claims scrutinizing the use of BPA in commercial products resulted in manufacturers marketing “BPA Free” alternatives in attempts to assuage environmental groups and public health advocates which lead to the introduction of BPA’s estrogenic cousin, BPS. In compliance with public demands, companies have turned to BPS as an alternative analogue. The introduction of BPS allowed for companies to eliminate use of BPA despite BPS having demonstrated comparable mechanisms of interference as BPA (Rodchester, 2015).

Over the past decade, studies evaluating the estrogenic effects of these compounds have provided strong evidence of adverse physiological impacts. Widespread exposure is one of the biggest concerns when considering BPA/BPS in the realm of public health. In 2008, the National Toxicology Program (NTP) expressed some concern for effects of BPA on the brain, behavior, and prostate gland in infants and children at current human exposures (Shelby, 2008). The release of this study and others expressing apprehension towards the safety of BPA increased the need for further investigation. During this time, regulation of BPA was repeatedly unsuccessful, never making it past federal government legislation. The Food and Drug Administration has banned the use of BPA in baby bottles due to age- dependent differences in metabolic capabilities, but has otherwise established the chemical to be “safe” at current human exposures (Hentges, 2014). Despite the EPA’s toxicity assessments and uncertainties of the NTP, BPA and BPS are not regulated under the Toxic Substance Control Act (Barraza, 2013).

Failure to regulate BPA and BPS production makes it hard to determine the level of toxicity. Further exploration of BPA has linked exposures to a number of negative health impacts (Robertson, 2015). Fetal exposures to estrogenic compounds can induce developmental abnormalities, predisposing individuals to a number of health concerns such as various cancers, decreased fertility, heart disease, and weakened immune systems (Robertson, 2015). Animal studies have been the primary source of data when assessing BPA. Neurotoxicity has been explored in mice and resulted in alternations to learning ability. Damage to DNA indicated that BPA exposure significantly altered spatial memory (Zhou, 2017). Similarly, BPA exposures in rats during development were later shown to heighten prostate cancer susceptibility due to early- life exposures (Prins, 2017). It is the alterations to development influenced by an increase in estrogenic chemicals that could give rise to precancerous characteristics or behavioral changes. These studies investigating low, chronic exposures serve as models that should be applied to public health. These findings are important because they were found under conditions consistent to what the public is exposed to.

These studies are just a sampling of examples that suggest negative effects due to BPA exposure. The assessments of chemical exposure to BPA or BPS however, are complicated and include extensive variables to consider. Understanding how BPA is processed in the body is important to understand the mechanisms of disruption and if the compound actually poses a potential risk. BPA is metabolized into two major products, Bisphenol A-sulfate and Bisphenol A-glucuronide, which are not biologically active in the same way as free BPA in the body (Shelby, 2008). In addition, BPA has a much lower binding affinity to the body’s estrogen receptors than estradiol (E2), the body’s most active form of estrogen (Acconcia, 2015). Findings linking homeostatic disruption with exposure to BPA or BPS have been interpreted widely in laboratory animals, but less tracked in humans; although the possibility that human development can be altered should also be considered (Shelby, 2008). In addition, BPS has been identified to act more efficiently than BPA and the body’s natural estrogenic hormones at binding the estrogen receptors (Rochester, 2015).

Due to variations in results, many studies have been questioned or disregarded as irrelevant. Dissonance among the scientific community has created a very confusing and incomplete understanding of BPA and BPS influence. Inconsistent results make it hard to label the products as toxic, which is why it is critical to continue the investigation.

Increasing demand of products containing BPA and BPS continues to influence the global consumption rate of these compounds. Automotive, construction, and electrical applications promote the use of BPA to maintain economic benefits (HIS MarkIt, 2016). Until a suitable alternative is introduced, companies will continue to utilize these compounds. Corporations argue that the release of BPA into the environment at current levels does not pose a threat because the biodegradation rate of BPA is rapid and as a result cannot persist within the environment (Hentges, 2014). Environmental occurrences however, must be considered because production rates continue to grow. Early life exposures to developing individuals of specialist species are especially sensitive to environmental changes making them more vulnerable to sub- lethal exposures (Prins, 2017). In addition, it is important to recognize that BPA and BPS are not the only chemicals in aquatic environments. The potential for co-exposures of chemicals in conjunction with other environmental stressors is severely understudied when assessing toxicity in aquatic environments.

In 2016, the Toxic Substance Control Act updated its regulatory procedures by implementing the Frank R. Lautenberg Chemical Safety for the 21st Century Act stating the following improvements; EPA reevaluation of existing chemicals, new risk- based safety standards, and increased public transparency of toxic chemicals (EPA, 2017). The new testing requirements will result in additional research of BPA and BPS. Unfortunately the guidelines contain unrealistic expectations for EPA regulation of hazardous chemicals. Insufficient timing and funding restricts the EPA from acting effectively to prevent toxic chemicals from becoming available for production. New studies will hopefully expand on the knowledge of BPA/ BPS safety and regulation.

As someone who studies EDC toxicity, it is frustrating to realize what drives regulations of hazardous chemicals. Economic growth seems to be prioritized over environmental and public health. Since my introduction to the world of environmental toxicology, I have become very aware of chemical exposures and the narrowing dichotomy between environmental and human health. As new chemicals continue to be introduced, it is inevitable that we will see adverse health effects with increased exposures. Even if levels of BPA are considered to be safe for humans at this time, we still do not fully understand the implications, especially when it comes to aquatic ecosystems and vulnerable species. This uncertainty should encourage limitations and regulations of BPA and BPS production to ensure the safety of consumers.

References:

Acconcia, F., Pallottini, V., Marino, M., 2015. Molecular mechanisms of action of BPA. National Institute of Health- Dose Response. 10.1177/1559325815610582

Barraza, L. (2013). A new approach for regulating bisphenol A for the protection of the public's health. Journal Of Law, Medicine & Ethics419-12. doi:10.1111/jlme.12030



Dodds EC, Lawson W. Synthetic oestrogenic agents without the phenanthrene nucleusNature. 1936;137(3476):996

Environmental Protection Agency. 2017. The Frank R. lautenberg chemical safety for the 21st century act: assessing and managing chemicals under TSCA. https://www.epa.gov/assessing-and-managing-chemicals-under-tsca/frank-r-lautenberg-chemical-safety-21st-century-act

Hentges, S. 2014. American Chemistry Council Facts About BPA. Underwriters Laboratory

IHS MarkIt. 2016. Chemical economics handbook- bisphenol A. https://www.ihs.com/products/bisphenol-chemical-economics-handbook.html

Prins, G. S., Shu-Hua, Y., Birch, L., Xiang, Z., Ana, C., Han, L., & ... van Breemen, R. B. (2017). Prostate cancer risk and DNA methylation signatures in aging rats following developmental BPA exposure: A dose-response analysis. Environmental Health Perspectives1251-12. doi:10.1289/EHP1050

Robertson, T., & Farrelly, T. (2015). Bisphenol A (BPA) exposure in New Zealand: a basis for discussion. Journal Of The Royal Society Of New Zealand45(4), 184-196. doi:10.1080/03036758.2015.1071271

Rochester, J., Bolden, A. 2015. Bisphenol S and F: A systematic review and comparison of the hormonal activity of bisphenol A substitutes. Environmental Health Perspectives, DOI:10.1289/ehp.1408989

Shelby, M. D. 2008. NTP-CERHR monograph on the potential human reproductive and developmental effects of bisphenol A. National Toxicology Program- Center of Risks to Human Reproduction, (22), NIH 08–5994

Vogel, S. 2009. The Politics of Plastics: The Making and Unmaking of Bisphenol A “Safety”. American Journal of Public Health. 10.2105/AJPH.2008.159228



Zhou, Y., Wang, Z., Xia, M., Zhuang, S., Gong, X., Pan, J., & ... Lu, S. (2017). Neurotoxicity of low bisphenol A (BPA) exposure for young male mice: Implications for children exposed to environmental levels of BPA. Environmental Pollution22940-48. doi:10.1016/j.envpol.2017.05.043


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