Sign up to receive email updates, action alerts, health tips, promotions to support our work and more from EWG. You can opt-out at any time. [Privacy]


California Urged To Add Bisphenol-A (BPA) To Prop 65 Toxics List

California Urged To Add Bisphenol-A (BPA) To Prop 65 Toxics List

Friday, July 17, 2009

Oral testimony of Bill Allayaud,
Director of Government Affairs, California Office
Environmental Working Group

Meeting of California Office of Environmental Health and Hazard Assessment’s (OEHHA’s)
Developmental and Reproductive Toxicity Identification Committee

Oakland, California
July 15, 2009

Hello, my name is Bill Allayaud. I am the Director of Government Affairs for Environmental Working Group’s California office. I give these comments on behalf of Environmental Working Group, particularly our California Office Director Renee Sharp, who was unable to attend today’s meeting.

The Environmental Working Group (EWG) strongly urges the DART Committee to list bisphenol A (BPA) as a reproductive and developmental toxicant. We believe that the draft report prepared by OEHHA and the overall weight of evidence from laboratory studies clearly support this listing. OEHHA’s draft summary of the evidence details dozens of studies showing permanent effects to the male reproductive system, impacts to brain and behavior, and a variety of other low-dose effects, including early puberty and impairment of female reproductive development, including fertility.

I would like to make 3 main points to support the case for Prop 65 listing of BPA.

Point 1. Industry misrepresents findings of the NTP and FDA

Industries that produce or use BPA frequently misrepresent the state of the scientific evidence and regulatory decisions. In particular, the American Chemistry Council (ACC) and Grocery Manufacturers Association (GMA), in their written comments to the Committee, mischaracterize the findings on BPA toxicity of both the National Toxicology Program and the federal Food and Drug Administration.

In September 2008, the NTP published its final monograph on BPA, finding “clear evidence of adverse effects” for developmental toxicity at high doses. This alone would be a sufficient basis for adding BPA to the Reproductive and Developmental toxicants list.

The NTP went on to assess “the possible effects of current exposures to bisphenol A on human development and reproduction,” framing its conclusions in terms of a 5-level scale: negligible concern, minimal concern, some concern, concern, and serious concern.

The NTP expressed “some concern for the effects of BPA on brain, behavior, and prostate gland in fetuses, infants, and children at current human expo­sures to bisphenol A.” The NTP explains on its website, at, that the term-of-art “some concern” is the “midpoint” on its 5-level scale. It assigns the “some concern” ranking a deep yellow color, lighter than the alarm-red of “serious concern” but a sharp contrast to the green color of “negligible concern.”

NTP did assume minimal or negligible concern for some endpoints. But, when the Grocery Manufacturers Association asserts that the NTP “expressed only minimal or negligible concern regarding most alleged health effects,” it selectively ignores the most troubling NTP findings about BPA’s possible effects on the developing fetus and young child. This blatant attempt to mislead the panel, and the public, should not be allowed to stand.

Nor should the panel accept the claim by GMA and the American Chemistry Council that the NTP did not “formally” or “definitively” identify BPA as causing developmental or reproductive toxicity (ACC 2009, GMA 2009).

These verbal sleights-of-hand ignore the gravity of the NTP’s conclusions about BPA’s effects on the developing fetus and young child. The NTP did not, as the ACC and GMA imply, give BPA a green light – a green ranking. Instead, its monograph asserted that there were “critical data needs” for assessing the dangers of BPA at current human exposures, and it detailed nine types of research that should be pursued to fill crucial data gaps.

We would like to note that it is relatively unusual for the NTP to express such concerns about contaminant exposures for the general population, in this case all American pregnancies, infants and children. In the past, few chemical exposures have achieved the designation “some concern.” It is generally applied to very specific sub-populations. For example “some concern” describes the NTP’s assessment of the risks of fetal amphetamine exposure (NTP 2005).

Given that BPA exposure in early life is unnecessary and largely avoidable, the designation of “some concern” for the fetus, infant and young child is clearly a matter that should be seriously considered by regulatory bodies, despite industry’s assurances to the contrary.

ACC also misrepresents the status of the federal Food and Drug Administration’s safety review for BPA in food packaging. When the ACC claims that FDA has found that “an adequate margin of safety exists for BPA at current levels of exposure from food contact use,” it neglects to mention that last November, the agency’s Science Board firmly rejected the agency’s conclusion that present-day BPA exposures are safe. The Science Board found that the weight of evidence pointed to toxic effects at levels at least one order of magnitude lower than those considered by FDA (FDA 2008b). In fact, FDA’s draft assessment actually led the Science Board to conclude the present day exposures are unsafe: Science Board reviewers observed that FDA’s assessment “provide[s] sufficient scientific basis to conclude that Margins of Safety defined by FDA as ‘adequate’ are, in fact, inadequate.” (FDA 2008b)

Point 2. Scientific reviews by OEHHA, NTP and FDA advisors support listing BPA

Thorough reviews by OEHHA and the NTP, and the concerns raised by the FDA’s Science Board point to a consistent and credible association between low dose exposure to BPA during pregnancy and effects to the brain and reproductive system.

The NTP monograph finds compelling evidence of low dose toxicity, specifically citing 12 high-quality studies showing reproductive and developmental effects. Notably, 8 of the 12 studies use oral dosing directly relevant to a pregnant woman or newborn, and several employ concentrations as low as 10 micrograms per kilogram body weight (NTP 2008).

There is ample evidence of BPA’s toxicity to the male reproductive system, particularly the prostate. Many studies have found that developmental exposure to BPA causes a variety of functional changes, including abnormal differentiation of cytokeratin 10 cells, altered proliferation and differentiation of stromal cells, and epigenetic changes that predispose rats to later life prostate cancer (OEHHA 2009). These sensitive indicators of prostate impacts were simply not studied by industry-funded guideline studies, which often use more crude measures of toxicity.

BPA has been shown to provoke a variety of changes to brain development and behavior. The Canadian government used this body of research as the basis for listing BPA as “toxic.” It took immediate action to reduce infant exposures (Canada 2008). In the United States, both OEHHA and the NTP highlight studies showing loss of sexually dimorphic behavior as the strongest and most consistent findings of developmental toxicity. NTP highlights 7 high quality oral studies (Palanza 2002, Laviola 2005, Gioisa 2007, Ceccarelli 2007, Ryan 2006, Della Seta 2006, Negishi 2004). OEHHA adds that the effects noted in sex-differentiated behavioral studies are particularly well designed and performed, consistent with known impacts of estrogenic chemicals, and correctly focused on gestational exposures (OEHHA 2009).

We concur with OEHHA’s assessment and would like to call the Committee’s attention to 2 recently published studies confirming similar effects in non-human primates. These studies, which Dr. Sarah Janssen of NRDC described in written comments to OEHHA, extend the findings of loss of sexually dimorphic behavior in rodents to more closely related species (Adewal 2009, Nakagami 2009).

Point 3. Human exposure to BPA is widespread, and exposures are perilously close to toxic levels in low-dose studies

BPA is widely detected in Americans, including more than 92% of urine samples analyzed in CDC’s NHANES study (Calafat 2008). Despite industry assurances that the chemical is quickly metabolized and excreted, the “free” or unmetabolized form is commonly measured in human tissues. Most worrisome is the detection of free BPA in maternal serum, ovarian follicular fluid, umbilical cord blood and amniotic fluid (Ikezuki 2002), premature infant’s urine (Calafat 2009), and the placenta (Schonfelder 2002).

The widespread detection of a chemical with a rapid half-life suggests Americans have daily contact with BPA from common sources. Food and food packaging are thought to predominate. The Environmental Working Group tested 97 canned food and formula samples for BPA, a component of nearly all linings of metal food cans. We found detectable residues in more than half of the samples. Concentrations ranged from 1 to 385 parts per billion, with the highest concentrations noted in canned pasta, soup, tuna and vegetables (EWG 2007).

We calculated that a pregnant woman of average weight could consume from 0.5 to 1 ug BPA per kilogram of body weight by ingesting a single serving of a highly contaminated food. Because formula can make up 100% of their daily diet, infants fed liquid formula from metal cans had even higher daily exposure values. It is important to note that these intense exposures for bottle-fed infants likely persist over the duration of formula feeding. In 2008, the Canadian government confirmed EWG’s findings with tests of 56 liquid samples, many of which were produced in the United States (Cao 2008).

A recent Harvard University study found that polycarbonate drink bottles are another significant source of BPA for adults. College students’ BPA levels increased by nearly 70% over baseline when they began drinking all cold beverages from polycarbonate bottles. The researchers themselves cautioned that infants would be at increased risk because their bodies have not matured to the point that they can metabolize and excrete the chemical. We caution that drinking heated liquids from polycarbonate bottles would result in even more BPA leaching. Bottle-fed babies could receive all of their daily nutrition from these containers.

This research suggests that high-end adult exposures can routinely exceed 1 microgram per kilogram of body weight, and infant exposures can be even higher. As previously mentioned, the 12 studies NTP cites as the strongest evidence of low-dose toxicity use doses perilously close to the daily intake estimates for pregnant women, infants and children. Eight of the 12 studies administer BPA orally, making intake levels easily comparable to normal consumption by infants and children. The remaining 4 studies use subcutaneous dosing, which NTP has determined to be relevant for exposures to the developing fetus and neonate who have with impaired metabolic capacity (NTP 2008).

The lowest dose studies shown to affect brain and behavior and male reproductive development employ doses of just 10 micrograms BPA per kilogram of body weight, which is by any measure an unacceptably low margin of safety for effects as serious and permanent as those caused by BPA.

In closing, we urge the Committee to consider carefully today’s decision. BPA clearly meets the Committee’s 1993 criteria for listing as a reproductive and developmental toxicant on the basis of “sufficient evidence in experimental animals, such that extrapolation to humans is appropriate” (DART-IC 1993). This includes careful experimental design, relevant routes of exposure and dosing levels well below those that result in maternal or systemic toxicity. As the NTP and the FDA Science Board have determined, the weight of evidence supports concern for present-day BPA exposures. EWG urges the Committee to join these authoritative bodies and list BPA according to authority granted under California Proposition 65.

Thank you for this opportunity to comment.


ACC. 2009. American Chemistry Council comments to California’s DART-IC committee, June 30, 2009.

Adewale HB, Jefferson WN, et al. 2009. Neonatal Bisphenol-A Exposure Alters Rat Reproductive Development and Ovarian Morphology Without Impairing Activation of Gonadotropin Releasing Hormone Neurons. Biol Reprod: biolreprod.109.078261.

Calafat AM, Ye, X., Wong, L.Y., Reidy, J.A., Needham, L.L. 2008. Exposure of the U.S. Population to Bisphenol A and 4-tertiary-Octylphenol: 2003-2004 Environ Health Perspect 116(1): 39-44.

Calafat AM, Weuve J, Ye X, Jia LT, Hu H, Ringer S, et al. 2009. Exposure to bisphenol A and other phenols in neonatal intensive care unit premature infants. Environ Health Perspect 117(4): 639-644.

Canada. 2008. Proposed Risk Management Approach for Phenol, 4,4’-(1-methylethylidene) bis (Bisphenol A). Environment Canada-Health Canada. October, 2008. Available at:

Cao XL, Dufresne G, Belisle S, Clement G, Falicki M, Beraldin F, et al. 2008. Levels of bisphenol A in canned liquid infant formula products in Canada and dietary intake estimates. J Agric Food Chem 56(17): 7919-7924.

Carwile JL, Luu HT, Bassett LS, Driscoll DA, Yuan C, Chang JY, Ye X, Calafat AM, Michels KB. 2009. Use of Polycarbonate bottles and urinary bisphenol A concentrations. Environmental Health Perspectives, epub May 12th, 2009.
Ceccarelli I, Della Seta D, Fiorenzani P, Farabollini F, Aloisi AM. 2007. Estrogenic chemicals at puberty change ERalpha in the hypothalamus of male and female rats.Neurotoxicol Teratol. 29(1): 108-115.

DART-IC. 1993. Criteria for recommending chemicals for listing as known to the State to cause reproductive toxicity. Developmental and Reproductive Toxicity Identification Committee. November 1993.

Della Seta D, Minder I, Belloni V, Aloisi AM, Dessi-Fulgheri F, Farabollini F. 2006. Pubertal exposure to estrogenic chemicals affects behavior in juvenile and adult male rats. Horm Behav. 50(2): 301-307.

EWG. 2007. Bisphenol A: Toxic plastics chemical in canned food. Environmental Working Group.

Food and Drug Administration. 2008a. Draft assessment of bisphenol A for use in food contact applications. Available online at:

Food and Drug Administration. 2008b. Scientific peer-review of the draft assessment of bisphenol A for use in food contact applications. FDA Science Board Subcommittee on Bisphenol A. October 31, 2008. Available online at:

GMA. 2009. Grocery Manufacturers Association comments to California’s DART-IC committee, June 30, 2009.

Gioiosa L, Fissore E, Ghirardelli G, Parmigiani S, Palanza P (2007) Developmental exposure to low-dose estrogenic endocrine disruptors alters sex

Ikezuki Y, Tsutsumi, O., Takai, Y., Kamei, Y., Taketani, Y. 2002. Determination of bisphenol A concentrations in human biological fluids reveals significant early prenatal exposure. Hum Reprod 17(11): 2839-2841.

Laviola G, Gioiosa L, Adriani W, Palanza P. 2005. D-amphetamine-related reinforcing effects are reduced in mice exposed prenatally to estrogenic endocrine disruptors. Brain Res Bull. 65(3): 235-240.

Negishi T, Kawasaki K, Suzaki S, Maeda H, Ishii Y, Kyuwa S, Kuroda Y, Yoshikawa Y. 2004. Behavioral alterations in response to fear-provoking stimuli and tranylcypromine induced by perinatal exposure to bisphenol A and nonylphenol in male rats. Environ Health Perspect.112(11): 1159-1164.

NTP. 2005. NTP-CERHR Monograph on the Potential Human Reproductive and Developmental Effects of Amphetamines. National Toxicology Program. NIH Publication No. 05-4474.

NTP. 2008. NTP-CERHR Monograph on the Potential Human Reproductive and Developmental Effects of Bisphenol A. National Toxicology Program. NIH Publication No. 08-5994.

Nakagami A, Negishi T, 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. In press, epublished 2009 Apr 2.

OEHHA. 2009. Evidence on the Developmental and Reproductive Toxicity of Bisphenol A. Draft Report, May 2009. Reproductive and Cancer Hazard Assessment Branch,
Office of Environmental Health Hazard Assessment, California Environmental Protection Agency.

Palanza PL, Howdeshell KL, Parmigiani S, vom Saal FS. 2002. Exposure to a low dose of bisphenol A during fetal life or in adulthood alters maternal behavior in mice. Environ Health Perspect. 110(Suppl 3): 415-422.

Ryan BC, Vandenbergh JG. 2006. Developmental exposure to environmental estrogens alters anxiety and spatial memory in female mice. Horm Behav. 50(1): 85-93.

Schonfelder G, Wittfoht, W., Hopp, H., Talsness, C. E., Paul, M., Chahoud, I. 2002. Parent bisphenol A accumulation in the human maternal-fetal-placental unit. Environ Health Perspect 110(11): A703-707.