BPA Ban in California Passes, Despite Industry Spin

Sen. Dianne Feinstein has introduced legislation in the Senate that would ban BPA in infant food packaging, in addition to other food and beverage containers. You can bet that the industry spin is going to continue.
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On July 1, the California Assembly passed a bill that will ban the use of BPA in products for children less than 3 years of age - including baby bottles, sippy cups, infant formula and baby food. The bill, sponsored by Senator Fran Paveley, passed out of the Senate nearly a year ago but passage in the Assembly was largely delayed because of an aggressive distortion and misinformation campaign by the chemical industry.

I've blogged before about the spin tactics the chemical industry has schemed up - including "fear tactics" with claims that all canned food would disappear from store shelves if BPA bans were passed and "manipulating the legislative process" in state campaigns, like California's. In fact, an unprecedented $5 million was reportedly spent by the chemical industry to defeat this California bill. In addition, industry trade groups, such as the American Chemistry Council and the Grocery Manufacturer's Association have attempted to convince legislators and the public that the science on BPA's toxicity is far from clear and in fact that there are no credible studies that show BPA is harmful. Of course, this is not true but this strategy remains a big part of their distortion and disinformation campaign.

California is the eighth state to ban BPA in children's products, after Minnesota, Maryland, Wisconsin, Connecticut, Washington, Vermont, and New York. Other states and municipalities have BPA bans pending and Sen. Dianne Feinstein, D-Calif., has introduced legislation in the Senate that would ban BPA in infant food packaging, in addition to other food and beverage containers. You can bet that the industry spin is going to continue and there will be a lot of pressure to convince the Governor of California to veto this newly passed legislation. If you live in California, let him know your views and encourage him to sign SB 797: E-mail him at governor@governor.ca.gov.

Now I'd like to spend some time dispelling some of the myths propagated by the chemical industry, which are certainly going to resurface.

The industry arguments on BPA's safety often focus on three main points:

1) They suggest that academic studies should be disregarded because they do not use "Good Laboratory Practices", which are held up as the "gold standard" for a weight of evidence approach;

(2) They assert that existing rodent studies should be discarded because rats and mice metabolize BPA differently than humans such that BPA is more toxic in rodents;

(3) They contend that low-dose studies are not useful because only one researcher did them and used "unorthodox, unrealistic, and non-repeatable methods".

This reasoning is flawed in several important ways described below. Existing research on BPA is compelling and convincing for a wide variety of harmful health effects at low doses and has been replicated by many independent laboratories. While the additional research being conducted by federal agencies will provide insights into many issues involving BPA’s impacts on humans, current science supports taking action now to protect children from BPA. There is no valid scientific rationale for waiting for further study since the science is sufficiently clear today to support action.

"Good Laboratory Practices" is a standard for animal care and data collection required for industry laboratories in response to fraudulent practices documented in the 1970s. Industry-funded studies are required by EPA and FDA to follow so-called Good Laboratory Practices (GLP) standards, which include specified approaches to recordkeeping to facilitate audits and reduce fraud.(54 Fed. Reg. 34034 (August 17, 1989). GLP requirements are not associated with higher quality research, proper study design or correct statistical analysis.(i) In most cases, GLP studies have not even undergone scientific peer-review. GLP studies don’t necessarily use modern methods for evaluating chemicals and aren’t designed to grapple with the problems of low-dose exposures. The four GLP studies that FDA has relied upon for not acting on BPA have been harshly criticized in the peer-reviewed literature and the NTP rejected three of those studies in its review of BPA.(i)

In contrast, academic research which has found BPA to be harmful has been published in respected scientific journals and relies on the peer-review process to uphold scientific quality. NIH-funded research is subject to morestringent review then industry GLP-compliant studies. Peer-reviewed, non-GLP studies are routinely used in regulatory standard-setting by federal agencies, in particular by U.S. EPA.

Metabolic Pathways in animals and humans are important when considering BPA toxicity. However, the chemical industry often ignores scientific evidence indicating that fetuses and neonates are routinely exposed to the more active and toxic form of BPA. Infants and children do not metabolize chemicals such as BPA as effectively as adults.(ii) The liver is not the only organ capable of metabolizing BPA and some organs, such as the testes, are able to convert inactive forms of BPA into the more toxic active form.(iii iv v vi) In addition, recent scientific studies clearly indicate that BPA – in both its active and inactive form – can cross the placenta where the inactive form of BPA is converted to the active form.

Biomonitoring studies clearly show BPA is present in the human body at levels that are concerning for health impacts. (vii viii) Therefore, the fetus is being exposed to a toxic form of BPA during extremely vulnerable periods of development. (ix) While these levels are below current outdated regulatory standards, those standards are not based on the abundance of current scientific evidence demonstrating harmful health effects at low doses.

Low dose studies have been conducted by multiple scientists in multiple labs. Low levels of BPA, similar to those found in humans, have been demonstrated in dozens of well-conducted studies published in the peer-reviewed literature by many different independent, academic laboratories to cause adverse effects on the development of an animals’ reproductive system, brain and behavior, and potentially the metabolic system. Prenatal exposure has also been shown to increase susceptibility to prostate and mammary (breast) cancer later in life. Moreover, low doses of BPA, within the range of common human exposure, have been shown to interfere with prostate cancer treatment in human/animal models used to develop drugs for prostate treatment (x), and to interfere with the action of drugs used to treat breast cancer, in human breast cancer cells (xi).

It is simply wrong to suggest, as the chemical industry has, that only one researcher has found a problem, or that this research has not been repeated. Based on a literature review of reproductive and developmental effects in 2008, the National Toxicology Program (NTP) identified twelve low-dose studies as adequate for inclusion in their analysis. (xii) Many other studies have been published since then and in all over 200 studies have been published demonstrating evidence of harm after BPA exposure. As identified in the NTP report, BPA causes harmful effects at doses at or above 10 micrograms per kilogram of bodyweight per day. Exposures in formula-fed infants are estimated to be similar at 1 to 11 micrograms per kilogram of bodyweight per day.

Weight of Evidence is not determined by the outcome of one study. A weight of evidence approach is an evaluation of multiple studies using a variety of methods and approaches, done by different investigators. An evaluation of each individual study independent of others is not a realistic approach for determining whether or not a chemical is toxic, as every study has flaws. Based on multiple scientific studies, there is strong evidence that low doses of BPA exposure are harmful to health.

For example, in the case of neurodevelopment, there is: (1) in vitro evidence that BPA damages neuronal cells (xiii); (2) rodent data that BPA causes neurobehavioral abnormalities (xiv); (3) non-human primate data demonstrating neurobehavioral changes (xv); and (4) data demonstrating behavioral changes in human toddlers (xvi). When taken together, these studies make a compelling case that BPA causes neurodevelopmental effects. Similar lines of evidence can be drawn for effects of BPA in the prostate and mammary glands.

Based on the widespread exposure, especially in vulnerable populations, and the existing scientific data, current levels of exposure to BPA should not be considered safe and BPA should not be allowed for use in food packaging.


[i] Myers, J. P., F. S. vom Saal, et al. (2009). "Why public health agencies cannot depend on good laboratory practices as a criterion for selecting data: the case of bisphenol A." Environ Health Perspect 117 (3): 309-15.

[ii] Mykkanen, H., J. Tikka, et al. (1997). "Fecal Bacterial Enzyme Activities in Infants Increase with Age and Adoption of Adult-Type Diet." Journal of Pediatric Gastroenterology and Nutrition 25(3): 312-316.

[iii] Zalko, D., A. M. Soto, et al. (2003). "Biotransformations of bisphenol A in a mammalian model: answers and new questions raised by low-dose metabolic fate studies in pregnant CD1 mice." Environ Health Perspect 111(3): 309-19

[iv] Sakamoto, H., H. Yokota, et al. (2002). "Excretion of bisphenol A-glucuronide into the small intestine and deconjugation in the cecum of the rat." Biochim Biophys Acta 1573(2): 171-6.

[v] Stowell, C. L., K. K. Barvian, et al. (2006). "A Role for Sulfation-Desulfation in the Uptake of Bisphenol A into Breast Tumor Cells." 13(8): 891-897.

[vi] Miyakoda H, Tabata M, Onodera S, Takeda K 2000 Comparison of conjugative activity, conversion of bisphenol A to bisphenol A glucuronide, in fetal and mature male rat. J Health Sci 46:269-274

[vii] Nishikawa, M., H. Iwano, et al. (2010). "Placental Transfer of Conjugated Bisphenol A and Subsequent Reactivation in the Rat Fetus." Environ Health Perspect. 2010 Apr [Epub ahead of print]

[viii] Balakrishnan, B., K. Henare, et al. (2010). "Transfer of bisphenol A across the human placenta." American Journal of Obstetrics and Gynecology 202(4): 393.

[ix] Vandenberg, L. N., I. Chauhoud, et al. (2010). "Urinary, Circulating and Tissue Biomonitoring Studies Indicate Widespread Exposure to Bisphenol A." Environ Health Perspect. 2010 Mar 23. [Epub ahead of print]

[x] Wetherill, Y.B., J.K. Hess-Wilson, C.E.S. Comstock, S.A. Shah et al. (2006) Bisphenol A facilitates bypass of androgen ablation therapy in prostate cancer. Mol Cancer Ther 5(12) 3181-3190.

[xi] LaPensee, E.W, T.R. Tuttle, S.R. Fox and N Ben-Jonathon.(2009). "Bisphenol A at low nanomolar doses confers chemosresistance in estrogen receptor-α-positive and –negative breast cancer cells. Environ Health Perspect 117:175-180.

[xii] Chapin, R. E., J. Adams, et al. (2008). "NTP-CERHR expert panel report on the reproductive and developmental toxicity of bisphenol A." Birth Defects Res B Dev Reprod Toxicol 83(3): 157-395.

[xiii] Zhou, R., Z. Zhang, et al. (2009). "Deficits in development of synaptic plasticity in rat dorsal striatum following prenatal and neonatal exposure to low-dose bisphenol A." Neuroscience 159 (1): 161-71.


Miyagawa, K., M. Narita, et al. (2007). "Changes in central dopaminergic systems with the expression of Shh or GDNF in mice perinatally exposed to bisphenol-A." Nihon Shinkei Seishin Yakurigaku Zasshi

Summarized in Chapin, R. E., J. Adams, et al. (2008). "NTP-CERHR expert panel report on the reproductive and developmental toxicity of bisphenol A." Birth Defects Res B Dev Reprod Toxicol 83(3): 157-395. 159(1): 161-71. 27(2): 69-75.

[xiv] Summarized in Chapin, R. E., J. Adams, et al. (2008). "NTP-CERHR expert panel report on the reproductive and developmental toxicity of bisphenol A." Birth Defects Res B Dev Reprod Toxicol 83(3): 157-395.

[xv] Nakagami, A., T. Negishi, et al. (2009). "Alterations in male infant behaviors towards its mother by prenatal exposure to bisphenol A in cynomolgus monkeys (Macaca fascicularis) during early suckling period." Psychoneuroendocrinology

Leranth, C., T. Hajszan, et al. (2008). "Bisphenol A prevents the synaptogenic response to estradiol in hippocampus and prefrontal cortex of ovariectomized nonhuman primates." Proceedings of the National Academy of Sciences 105(37): 14187-14191. 34(8): 1189-97.

[xvi] Braun, J. M., K. Yolton, et al. (2009). "Prenatal bisphenol A exposure and early childhood behavior." Environ Health Perspect 117(12): 1945-52

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