A Survey of Bisphenol A in U.S. Canned Foods
EWG's tests found:
Of all foods tested, chicken soup, infant formula, and ravioli had BPA levels of highest concern. Just one to three servings of foods with these concentrations could expose a woman or child to BPA at levels that caused serious adverse effects in animal tests.
For 1 in 10 cans of all food tested, and 1 in 3 cans of infant formula, a single serving contained enough BPA to expose a woman or infant to BPA levels more than 200 times the government's traditional safe level of exposure for industrial chemicals. The government typically mandates a 1,000- to 3,000-fold margin of safety between human exposures and levels found to harm lab animals, but these servings contained levels of BPA less than 5 times lower than doses that harmed lab animals.
BPA testing in canned food. We contracted with a national analytical laboratory to test 97 cans of food we purchased in March 2006 in three major, chain supermarkets in Atlanta, Georgia; Oakland, California; and Clinton, Connecticut. The lab tested 30 brands of food altogether, 27 national brands and 3 store brands. Among the foods we tested are 20 of the 40 canned foods most commonly consumed by women of childbearing age (CDC 2002), including soda, canned tuna, peaches, pineapples, green beans, corn, and tomato and chicken noodle soups. We also tested canned infant formula. The lab detected BPA in fifty-seven percent of all cans.
BPA is a heavily produced industrial compound that has been detected in more than 2,000 people worldwide, including more than 95 percent of 400 people in the United States. More than 100 peer-reviewed studies have found BPA to be toxic at low doses, some similar to those found in people, yet not a single regulatory agency has updated safety standards to reflect this low-dose toxicity. FDA estimates that 17% of the U.S. diet comprises canned food; they last examined BPA exposures from food in 1996 but failed to set a safety standard.
Recommendations
BPA is associated with a number of health problems and diseases that are on the rise in the U.S. population, including breast and prostate cancer and infertility. Given widespread human exposure to BPA and hundreds of studies showing its adverse effects, the FDA and EPA must act quickly to revise safe levels for BPA exposure based on the latest science on the low-dose toxicity of the chemical.
BPA is at unsafe levels in one of every 10 servings of canned foods (11%) and one of every 3 cans of infant formula (33%)
Source: Chemical analyses of 97 canned foods by Southern Testing and Research Division of Microbac Laboratories, Inc., North Carolina.
EWG calculated people's BPA exposures from canned food using the following assumptions: Calculations reflect a single adult serving, using label serving size and body weight of 60 kg (132 lbs); exposures for concentrated infant formula is calculated for exclusively formula-fed infant using average 3-month-old body weight (6 kg/13 lbs) and average daily formula ingestion (840 g/30 oz); formula is assumed diluted with water free of BPA. Estimated single-serving exposures are compared against BPA dose of 2 ug/kg/d linked in lab studies to permanent damage of reproductive system from in utero exposures and referenced as "toxic dose" in figure above (see Section 3 of this report).
Summary of findings
Widespread exposures, no safety standards. In studies conducted over the past 20 years, scientists have detected BPA in breast milk, serum, saliva, urine, amniotic fluid, and cord blood from at least 2,200 people in Europe, North America, and Asia (CERHR 2006). Researchers at the Centers for Disease Control and Prevention recently detected BPA in 95% of nearly 400 U.S. adults (Calafat et al. 2005). EWG-led biomonitoring studies have detected BPA in people from four states and the District of Columbia (EWG 2007). BPA ranks in the top two percent of high production volume chemicals in the U.S., with annual production exceeding a billion pounds (EPA 2006), and is so common in products and industrial waste that it pollutes not only people but also rivers, estuaries, sediment, house dust, and even air nearly everywhere it is tested.
Yet despite its ubiquity and toxicity, BPA remains entirely without safety standards. It is allowed in unlimited amounts in consumer products, drinking water, and food, the top exposure source for most people. The lack of enforceable limits has resulted in widespread contamination of canned foods at levels that pose potential risks. For instance, analysis of our tests reveals that for one of every five cans tested, and for one-third of all vegetables and pastas (ravioli and noodles with tomato sauce), a single serving would expose a pregnant woman to BPA at levels that fall within a factor of 5 of doses linked to birth defects — permanent damage of developing male reproductive organs (Figure 1).
EWG test results — BPA is common contaminant in name-brand canned foods heavily consumed by women and infants
Canned Foods---Number of brands tested---Number of cans tested---Foods tested---BPA % detect Average BPA level* and range (ppb)
All foods 30 97 57% 7.9 (ND - 385)
Beans 3 6 baked beans 83% 9.7 (ND - 38)
Fruit 6 17 mixed fruit, cranberry sauce, peaches, pears, pineapple 35% 2.3 (ND - 27)
Infant formula 2 6 concentrated infant soy and milk-based formula 33% 2.4 (ND - 17)
Meal replacement 2 5 liquid meal replacements 40% 4.2 (ND - 66)
Milk products 3 evaporated milk 66% 3.5 (ND - 9)
Pasta 2 6 ravioli, spaghetti 100% 63.5 (16 - 247)
Soda 2 12 cola, diet cola 42% 1.7 (ND - 8)
Soup 5 19 beef stew, chicken noodle, chicken rice, chicken vegetable, tomato, vegetable 89% 57.6 (ND - 385)
Tuna 2 6 chunk lite, solid white 50% 9.6 (ND - 108)
Vegetable 8 17 corn, green beans, mixed vegetables, peas, tomatoes 41% 7.8 (ND - 330)
BPA concentrations are expressed in parts per billion (ppb) by weight (micrograms of BPA per kilogram of food).
* Average is the geometric mean. Non-detects considered to be 1/2 the detection limit (1 ppb) for purposes of this calculation.
Government assessments fail to consider BPA low-dose toxicity. As of December 2004, 94 of 115 peer-reviewed studies had confirmed BPA's toxicity at low levels of exposure. At some of the very lowest doses the chemical causes permanent alterations of breast and prostate cells the precede cancer, insulin resistance (a hallmark trait of Type II diabetes), and chromosomal damage linked to recurrent miscarriage and a wide range of birth defects including Down's syndrome (vom Saal 2005). Few chemicals have been found to consistently display such a diverse range of harm at such low doses.
Yet all of the most recent government reviews of bisphenol A have failed to set safety standards consistent with the chemical's low-dose toxicity. Each one either preceded the development of the low-dose literature, or heavily weighted industry-sponsored studies that are now known to have fundamental design flaws rendering them incapable of detecting BPA toxicity. U.S. safety reviews are described below:
The U.S. EPA established its generic safety standard for BPA (the reference dose, or RfD) in 1987, a decade before the BPA low-dose literature was established (EPA 1987). The vast majority of studies finding BPA toxic at low doses have been published since 1997, the year that pivotal studies showed BPA's ability to harm the prostate at levels far below what was thought safe (Nagel 1997; vom Saal et al. 1997). EPA's safety standard is 25 times the dose now known to cause birth defects in lab studies (50 ug/kg/d vs. 2 ug/kg/d), and has not been updated for 20 years.
The U.S. National Toxicology Program's 2001 assessment, which found BPA safe at low doses, relied heavily on industry-sponsored studies showing no low-dose BPA effects (NTP 2001). These studies are now known to have used animals resistant to the effects of estrogen-like chemicals such as BPA (vom Saal 2005). The NTP assessment considered studies published in 2000 or earlier. The six years following this review have seen the publication of dozens of low-dose BPA studies that substantially bolster the now near irrefutable evidence for low-dose effects.
FDA published estimates of infant and adult BPA exposures 10 years ago. Even though the Agency did not then and has not since assessed the low-dose toxicity of BPA, in 2005 an FDA official asserted, in response to questions from a California legislator considering a state BPA phase-out bill, that "...FDA sees no reason to change [its] long-held position that current [BPA] uses with food are safe" (FDA 2005). FDA makes this assertion even though the Agency has not yet established an Acceptable Daily Intake (ADI) for BPA, and has not even conducted the Agency's standard, basic toxicology study to determine a safe dose for humans (FDA 2007).
BPA's low dose toxicity. Companies began using BPA in metal can linings in the 1950s and 1960s (Schaefer 2004), fully twenty years after the chemical was first understood to be toxic (Dodds and Lawson, 1936 and 1938). These early warnings of toxicity were ignored or forgotten while companies steadily increased their reliance on BPA until it reached an annual U.S. production exceeding one billion pounds around 1990. In 1993 the chemical's signature toxic property, its ability to mimic estrogen, was accidentally discovered in a failed lab experiment (Krishnan et al. 1993), and the intervening years have witnessed the development of a body of low-dose science that has transformed our understanding of chemical toxicity.
Bisphenol A demonstrates the fallacy of nearly every long-standing tenet of government-style safety standards and traditional high-dose toxicology:
Low doses and toxicity. Where traditional toxicology asserts that higher doses confer greater harm, bisphenol A tests show that low doses can be the most toxic of all, below the radar screen of the body's compensatory detoxifying mechanisms, or below overtly toxic doses that destroy the tissues under study. In one investigation a low dose of BPA produced a 70% higher growth rate of prostate cancer cells in lab animals than did higher doses (Wetherill et al. 2002). In another study lower doses of BPA resulted in higher rates of breast cell growth that can precede cancer (Markey 2001). ("Low doses" are typically defined as those that produce tissue concentrations at or below those in the typical range of human exposures.)
Timing of the dose. While traditional methods set safety standards to control risks defined in adulthood, bisphenol A studies reveal that exposures at other times can confer far higher risks, especially in the womb and during early childhood. For example, recent studies show that prenatal exposure to BPA causes breast cancer in adult rats (Murray 2006), and causes genetic changes resulting in greater risk of prostate cancer in later life (Ho et al. 2006). In another study adult rats which had been dosed in the womb developed breast cancer in adulthood (Munoz-de-Toro 2005); these exposure levels during adulthood would not have caused cancer.
Genetic susceptibility. Traditional toxicology holds that a chemical's potency and risks are constant, regardless of who is exposed. Bisphenol A suggests a different truth: A person's genetics plays an important role in defining risks and health outcomes from exposures to toxic chemicals. For instance, studies suggest that for some but not all babies, BPA accumulates in amniotic fluid, suggesting differing innate capacities for excretion that would be defined by genetics (Yamada et al. 2002). A recent study of mammary gland development showed that animals exposed to BPA in utero are more likely to develop mammary tumors when they are exposed to carcinogenic chemicals later in life, compared to animals not previously exposed to BPA (Durando 2007). This study is one of many suggesting that early-life exposures to BPA may alter the expression or strength of genes to dramatically alter disease risk later in life.
Over the past year an average of four new BPA toxicity studies have been published in the peer-reviewed literature every month. New discoveries on BPA surface so routinely that the CERHR review document (CERHR 2006) describes fully 465 studies conducted primarily over the past 14 years. Among recent works:
A study showing that BPA exposures lead to an error in cell division called aneuploidy that causes spontaneous miscarriages, cancer, and birth defects in people, including Down Syndrome (Hunt 2003).
An investigation demonstrating that low doses of BPA spur both the formation and growth of fat cells, the two factors that drive obesity in humans (Masumo et al. 2002).
A study linking low doses of BPA to insulin resistance, a risk factor for Type II diabetes (Alonso-Magdalena 2006).
A preliminary investigation linking BPA exposures to recurrent miscarriage in a small group of Japanese women, made potentially pivotal by its concordance with lab studies of BPA-induced chromosome damage that could well cause miscarriage (Sugiura-Ogasawara 2005).
The unusually broad toxicity of BPA is explained by a prominent scientist as stemming from the fact that BPA can alter the behavior of over 200 genes — more than one percent of all human genes (Myers 2006). These genes control the growth and repair of nearly every organ and tissue in the body. Taken in its totality, the range of toxic effects linked to BPA is startlingly similar to the litany of human health problems on the rise or common across the population, including breast and prostate cancer, diabetes, obesity, infertility, and polycystic ovarian syndrome (Myers 2006).
Studies show that BPA is toxic to lab animals at doses overlapping with or very near to human exposures, and that the chemical causes toxic effects that are on the rise or very common in people. These disturbing facts raise questions about the extent to which current, widespread exposures to BPA are contributing to the burden of human disease.
Were the federal government to develop safety standards reflecting any of the more than 200 low-dose studies of BPA toxicity, the chemical would become the first widespread industrial compound with a government-recognized, harmful dose at such remarkably low levels that in some cases appear to overlap with human exposures. The science would fully justify a strict safety standard and would force industry to change food packaging to dramatically decrease the widespread BPA exposures to which they are currently subjecting the public.
FDA fails to protect the public. FDA is responsible for ensuring that food packaging chemicals like BPA are safe. In the case of BPA, the Agency has deemed the chemical safe even though its own exposure estimates for infants exceed doses shown to permanently harm the developing male reproductive system.
FDA does not restrict BPA levels in food. In the wake of a 1993 experiment proving that BPA disrupts estrogen levels, FDA tested 14 cans of infant formula and a few foods that adults eat, calculated exposures from these tests, and found them to be within safe levels (CERHR 2006). To make this determination the Agency compared the estimated exposures to "safe" doses far higher than those now known to cause permanent harm to lab animals.
Dr. George Pauli, at the time FDA's associate director for science and policy, offered this rationale: "FDA sees no reason at this time to ban or otherwise restrict the uses now in practice" (FDA 2005). Never mind that the Agency's estimated exposures for infants, at 15 to 24 ug/kg/d, exceed by a factor of up to 10 the dose shown to permanently alter prostate gland growth.
Bisphenol A is just one of hundreds of chemicals that pollute people - proof of critical need to reform our system of public health protections. Studies by European scientists show that BPA is just one of many chemicals that leach out of food can linings. Tests of just three can coatings found at least 23 different BPA-related chemicals leaching into food, all without legal limits (Schaefer 2004). Research shows these contaminants occur at levels that can dwarf better-known environmental pollutants that accumulate in food, like PCBs and DDT. One scientist writes that "Concentrations of [migrant chemicals like BPA] commonly exceed...pesticides by orders of magnitude; most of the migrating compounds are not even identified; and only a few have been tested for toxicity..." (Grob 1999).
FDA has tallied more than 1,000 indirect food additive chemicals in packaging and food processing, but food is just one of the many ways humans are exposed to industrial chemicals. EWG research reveals more than 200 pollutants in tap water supplies across the country; thousands of chemicals in cosmetics and personal care products; 470 industrial chemicals and pesticides in human tissues; and an average of 200 pollutants in each of 10 babies tested at the moment of birth. Nothing is known about the safety of the complex mixtures of low doses of a myriad of industrial chemicals in the human body.
The nation's system of public health protections from industrial chemicals like BPA are embodied in the Toxic Substances Control Act, a law passed in 1976 that is the only major environmental or public health statute that has never been updated. Under this law companies are not required to test chemicals for safety before they are sold and are not required to track whether their products end up in people at unsafe levels. As a result of this broken system, BPA is now one of the most widely used industrial chemicals, is found at unsafe levels in people, is allowed in unlimited quantities in a broad range of consumer products, and is entirely without safety standards. BPA gives irrefutable proof that our system of public health protections must be strengthened to protect children and others most vulnerable to chemical harm.
Part 2
Results — EWG's survey of BPA in canned food
Canned foods are thought to be the predominate route of BPA exposure (CERHR 2006). Numerous studies support this fact, including an investigation of BPA exposures for 257 young children in North Carolina and Ohio day care centers. Researchers collected samples of the air, water, dust, hand wipes and the daily diet and attributed 99 percent of children's daily BPA exposures to food (Wilson, Chuang et al. 2003; Wilson, Chuang et al. 2007). Despite this fact, very little canned food testing has been performed. Both the Plastics Industry and FDA have based their safety or exposure assessments for BPA on incredibly few canned food tests, fewer than 20 in both cases (FDA 1996; SPI 2007).
EWG tested foods and beverages from nearly 100 cans purchased in grocery stores in 3 states. EWG tested 28 different types of foods including canned fruits, vegetables, pasta, beans, infant formula, meal replacements and canned milk. We tested 1 to 6 samples of each type food. BPA levels varied from less the detection limit to a maximum level of 385 micrograms BPA per kilogram food (1 ug/kg is 1 part per billion). BPA test results for individual cans are shown at the end of this section.
EWG test results — BPA is common contaminant in name-brand canned foods heavily consumed by women and infants
Canned Foods Number of brands tested Number of cans tested Foods tested BPA % detect Average BPA level* and range (ppb)
All foods 30 97 57% 7.9 (ND - 385)
Beans 3 6 baked beans 83% 9.7 (ND - 38)
Fruit 6 17 mixed fruit, cranberry sauce, peaches, pears, pineapple 35% 2.3 (ND - 27)
Infant formula 2 6 concentrated infant soy and milk-based formula 33% 2.4 (ND - 17)
Meal replacement 2 5 liquid meal replacements 40% 4.2 (ND - 66)
Milk products 3 evaporated milk 66% 3.5 (ND - 9)
Pasta 2 6 ravioli, spaghetti 100% 63.5 (16 - 247)
Soda 2 12 cola, diet cola 42% 1.7 (ND - 8)
Soup 5 19 beef stew, chicken noodle, chicken rice, chicken vegetable, tomato, vegetable 89% 57.6 (ND - 385)
Tuna 2 6 chunk lite, solid white 50% 9.6 (ND - 108)
Vegetable 8 17 corn, green beans, mixed vegetables, peas, tomatoes 41% 7.8 (ND - 330)
BPA concentrations are expressed in parts per billion (ppb) by weight (micrograms of BPA per kilogram of food).
* Average is the geometric mean. Non-detects considered to be 1/2 the detection limit (1 ppb) for purposes of this calculation.
We found widespread contamination of BPA in canned foods. All six cans of spaghetti and ravioli tested contained measurable levels of BPA, averaging 63.5 parts per billion. Five of the six cans of baked beans examined had measurable levels of BPA, averaging 9.7 parts per billion. Two of six cans of infant formula tested contained BPA. The exposure that an infant might receive from canned formula, given his or her small size and limited food sources, makes the level of contamination in these cans particularly disturbing.
BPA is found in canned food around the world
Our study provides the most comprehensive U.S.-based examination of BPA in canned food available, but BPA contamination in food is a global concern. Below we show findings of other studies from around the world, as described in CERHR's review document for BPA (CERHR 2006).
Summary of BPA measurements in canned food from 9 previous studies
Food type Number of studies Location Total number of cans tested Percent of cans with BPA detected BPA range, ppb (ug/kg) EWG study: BPA range, ppb (ug/kg) References
Beverages 1 Austria 7 0% <0.9 - 3.4 2.4 - 8.2 [2]
Canned meat+ 3 New Zealand, UK 10 ~75% 8.6 - 89 NA [5, 6, 9]
Fruit 2 Austria, UK 6 >80% 5 - 38 2.2 - 27 [2, 5]
Fruit & vegetables 1 New Zealand 38 unavailable <20 - 24 NA [9]
Infant food 2 New Zealand, UK 10 30% <10 - 77 NA [5, 9]
Infant formula 3 US, UK, Taiwan 24 80% <0.002 - 113 10.9 - 17.1 [1, 5, 7]
Pasta 3 New Zealand, UK 10 >50% <7 - 130 16.2 - 247 [5, 6, 9]
Soup 3 New Zealand, UK 15 unavailable <2 - 39 8.6 - 385 [5, 6, 9]
Tuna 4 New Zealand, UK, Mexico, Austria 16 75% <7 - 109 80 - 108 [5, 8, 9,
10]
Vegetables 5 Austria, UK, Spain, US 34 >80% 4 - 76 8.9 - 330 [2, 3, 4, 5, 6]
+ Does not include tuna
References
U.S.: [1] Biles, J. E., McNeal, T. P. and Begley, T. H. Determination of bisphenol A migrating from epoxy can coatings to infant formula liquid concentrates. J Agric Food Chem 1997; 45: 4697-4700.
Austria: [2] Braunrath, R., Podlipna, D., Padlesak, S. and Cichna-Markl, M. Determination of bisphenol A in canned foods by immunoaffinity chromatography, HPLC, and fluorescence detection. J Agric Food Chem 2005; 53: 8911-7.
Spain: [3] Brotons, J. A., Olea-Serrano, M. F., Villalobos, M., Pedraza, V. and Olea, N. Xenoestrogens released from lacquer coatings in food cans. Environ Health Perspect 1995; 103: 608-12.
U.S.: [4] FDA. Cumulative Exposure Estimated for Bisphenol A (BPA), Individually for Adults and Infants from Its Use in Epoxy-Based Can Coatings and Polycarbonate (PC) Articles, verbal request of 10-23-95, memorandum to G. Diachenki, Ph.D, Division of Product Manufacture and Use, HGS-245, from Allan B. Bailey, Ph.D., Chemistry Review Branch, HFS-245. Department of Health and Human Services, Food and Drug Administration. Food and Drug Administration; 1996.
U.K.: [5] Goodson, A., Robin, H., Summerfield, W. and Cooper, I. Migration of bisphenol A from can coatings--effects of damage, storage conditions and heating. Food Addit Contam 2004; 21: 1015-26.
U.K.: [6] Goodson, A., Summerfield, W. and Cooper, I. Survey of bisphenol A and bisphenol F in canned foods. Food Addit Contam 2002; 19: 796-802.
Taiwan: [7] Kuo, H.-W. and Ding, W.-H. Trace determination of bisphenol A and phytoestrogens in infant formula powders by gas chromatography-mass spectometry. J Chromatogr A 2004; 1027: 67-74.
Mexico: [8] Mungu’a-L—pez , E. M., Gerardo-Lugo, S., Peralta, E., Bolumen, S. and Soto-Valdez, H. Migration of bisphenol A (BPA) from can coatings into a fatty-food simulant and tuna fish. Food Addit Contam 2005; 22: 892-8
New Zealand: [9] Thomson, B. M. and Grounds, P. R. Bisphenol A in canned foods in New Zealand: an exposure assessment. Food Addit Contam 2005; 22: 65-72.
BPA levels in individual cans - from EWG's test program of 97 cans of 30 name-brand foods
Type of canned food Specific food type State of purchase Bisphenol A (ppb)# Serving size (oz) + Average BPA exposure from single serving (ug/kg-d)*
Beans baked beans GA <2 4.1 ND
Beans baked beans GA 37.7 4.6 0.08
Beans baked beans CA 27.1 4.7 0.06
Beans baked beans CT 27 4.0 0.05
Beans baked beans CT 6.34 4.1 0.01
Beans baked beans CA 4.83 4.1 0.01
Fruit cranberry sauce CA <2 2.7 ND
Fruit cranberry sauce CT <2 2.7 ND
Fruit cranberry sauce GA <2 2.7 ND
Fruit mixed fruit CA <2 4.3 ND
Fruit mixed fruit CA <2 4.1 ND
Fruit mixed fruit CT <2 4.1 ND
Fruit mixed fruit GA <2 4.3 ND
Fruit mixed fruit GA <2 4.4 ND
Fruit mixed fruit CT 10.6 4.4 0.02
Fruit peaches GA <2 4.4 ND
Fruit peaches CT 7.43 4.2 0.01
Fruit pears CT <2 4.4 ND
Fruit pears CA 15.6 4.4 0.03
Fruit pears GA 14 4.3 0.03
Fruit pineapple GA <2 4.4 ND
Fruit pineapple CT 26.9 4.4 0.06
Fruit pineapple CA 2.2 4.0 0.00
Infant formula milk formula with iron CT <2 30.0 ND
Infant formula milk formula with iron GA <2 30.0 ND
Infant formula milk formula with iron CA 17.1 30.0 1.20
Infant formula milk formula with iron GA 10.9 30.0 0.76
Infant formula soy formula with iron CA <2 30.0 ND
Infant formula soy formula with iron CT <2 30.0 ND
Meal replacement chocolate shake CA <2 11.0 ND
Meal replacement chocolate shake CA <2 11.0 ND
Meal replacement chocolate shake CT <2 11.0 ND
Meal replacement chocolate shake GA 65.5 11.0 0.34
Meal replacement vanilla shake GA 19.3 11.0 0.10
Other evaporated milk CT <2 1.0 ND
Other evaporated milk GA 9 1.0 0.00
Other evaporated milk CA 4.83 1.0 0.00
Pasta ravioli CA 247 7.5 0.87
Pasta ravioli GA 220 7.5 0.78
Pasta ravioli CT 16.2 7.5 0.06
Pasta spaghetti CA 52.9 7.5 0.19
Pasta spaghetti GA 38.1 7.5 0.13
Pasta spaghetti CT 37.1 7.4 0.13
Soda cola CA <2 12.5 ND
Soda cola CT <2 8.4 ND
Soda cola CT <2 8.4 ND
Soda cola CA 4.19 12.5 0.02
Soda cola GA 3.35 12.5 0.02
Soda cola GA 2.41 8.4 0.01
Soda diet cola CA <2 12.5 ND
Soda diet cola CT <2 8.4 ND
Soda diet cola CT <2 8.4 ND
Soda diet cola GA <2 8.4 ND
Soda diet cola CA 8.21 12.5 0.05
Soda diet cola GA 2.74 12.5 0.02
Soup beef stew CT 26.9 9.4 0.12
Soup beef stew CA 19 9.4 0.08
Soup chicken broth CT 8.64 7.0 0.03
Soup chicken noodle soup GA <2 4.3 ND
Soup chicken noodle soup CT 385 7.2 1.32
Soup chicken noodle soup CT 184 4.2 0.37
Soup chicken noodle soup CA 83.3 4.3 0.17
Soup chicken rice soup GA 121 4.2 0.24
Soup chicken rice soup CT 104.4 4.2 0.21
Soup chicken rice soup CA 103 4.2 0.20
Soup chicken vegetable soup CA 122 9.5 0.55
Soup chicken vegetable soup CT 49.1 9.5 0.22
Soup noodle soup CA 191 4.4 0.40
Soup noodle soup GA 99.3 4.2 0.20
Soup other soup CT <15 7.1 ND
Soup tomato soup CA 176 4.3 0.36
Soup tomato soup CT 88.5 4.3 0.18
Soup tomato soup GA 78.2 4.3 0.16
Soup vegetable soup CA 79.6 9.2 0.35
Tuna chunk lite CA <2 2.4 ND
Tuna chunk lite CT 108 2.4 0.12
Tuna chunk lite CA 89.8 2.4 0.10
Tuna chunk lite GA 80 2.4 0.09
Tuna chunk white GA <2 2.4 ND
Tuna solid white CT <2 2.4 ND
Vegetable corn CT <2 4.4 ND
Vegetable corn GA <2 2.7 ND
Vegetable green beans CA <2 4.1 ND
Vegetable green beans GA 284 4.1 0.56
Vegetable green beans CT 209 4.1 0.41
Vegetable mixed vegetables CA <2 4.1 ND
Vegetable mixed vegetables CT <2 4.1 ND
Vegetable mixed vegetables CT <2 4.3 ND
Vegetable mixed vegetables GA <15 4.3 ND
Vegetable mixed vegetables GA 330 4.1 0.65
Vegetable mixed vegetables CA 225 4.3 0.46
Vegetable peas CT <2 4.3 ND
Vegetable peas CA 203.5 4.3 0.41
Vegetable peas GA 22.7 4.3 0.05
Vegetable tomatoes CA <2 2.2 ND
Vegetable tomatoes CT <2 4.1 ND
Vegetable tomatoes GA 8.94 2.2 0.01
Source: Chemical analyses of 97 canned foods by Southern Testing and Research Division of Microbac Laboratories, Inc., North Carolina.
# BPA concentrations are expressed in parts per billion (ppb) by weight (micrograms of BPA per kilogram of food)
+ Serving size as noted on can label.
* BPA exposure is expressed in ug/kg-d, or micrograms of BPA per kilogram of body weight per day. For comparison, numerous animal studies show toxic effects at 2 ug/kg/d and lower.
EWG estimated the BPA dose from single serving of food using the following assumptions: BPA calculations reflect a single adult serving, using label serving size and body weight of 60 kg (132 lbs); exposures for concentrated infant formula is calculated for exclusively formula-fed infant using average 3-month-old body weight (6 kg/13 lbs) and average daily formula ingestion (840 g/30 oz); formula is assumed diluted with water free of BPA.
BPA is toxic at low doses
Numerous studies indicate exposure to low levels of BPA causes a range of serious health effects in laboratory animals, particularly when exposures occur in utero (Maffini 2006). Below we list 21 key studies that indicate low-dose effects. Many of these were deemed by CERHR to be 'useful' for the purposes of evaluating BPA's low-dose effects on human health (CERHR 2006). The harmful doses defined by these studies are well below EPA's current safe dose for BPA of 50 ug/kg-day. And as shown on the table below, a pregnant woman's or infant's BPA dose from a single serving of food from many of the cans tested in our study would fall within a margin of 10 from the harmful effects shown in these studies.
Many studies confirm BPA's low-dose toxicity across a diverse range of toxic effects
Daily BPA exposure (ug/kg body weight-day) CERHR conclusion* Toxic effect Study details Reference % cans tested by EWG with single-serving BPA levels within a margin of 10 from harmful dose
0.0001 not included alterations in cell signalling pathways on the cell surface that control calcium eflux in cells in-vitro study which compared activity of BPA and other hormone disruptors Wozniak 2005 56.7 (all cans with detected BPA)
0.025 "very useful" persistent changes to breast tissue, predisposes cells to hormones and carcinogens fetal exposure, osmotic pumps, changes noted a 6 months of age Munoz-de-Toro 2005 55.7
0.025 "useful and shows tissue effects at extremely low dose levels" permanent changes to genital tract fetal exposure, osmotic pumps Markey 2005 55.7
0.2 utility "limited" decrease antioxidant enzymes adult exposure, oral Chitra 2003 47.4
0.25 utility "to be added" altered growth, cell size and lumen formation in mammary epithelium of mouse fetuses. exposure during pregnancy w/osmotic pumps Vandenberg 2007 45.4
2 "useful" increased prostate weight 30% fetal exposure, oral route Nagel 1997 20.6
2 "moderately useful" increased aggression at 8 weeks of life fetal exposure, oral route Kawai 2003 20.6
2.4 "useful", but non-traditional endpoint Decreased time from vaginal opening to first estrus, possibly earlier puberty fetal exposure, oral route Howdeshell 1999 17.5
2.4 "useful" lower bodyweight, increase of anogenital distance in both genders, signs of early puberty and longer estrus. fetal exposure, oral route Honma 2002 17.5
2.4 "adequate" decline in testicular testosterone fetal and neonatal exposure, gavage Akingbemi 2004 17.5
2.5 utility "to be added" breast cells predisposed to cancer fetal exposure, osmotic pumps Murray 2006 16.5
2.5 not included immune system impacts oral exposure Sawai 2003 16.5
10 utility "very useful" prostate cells more sensitive to hormones and cancer infant oral exposure, 3 day duration Ho 2006 2.1
10 utility "very useful" prostate cells more sensitive to hormones and cancer fetal exposure, oral route, short duration Timms 2005 2.1
10 not included insulin resistance develops in 2 days, chronic hyperinsulinemia at day 4 subcutaneous injection, short duration exposure Alonso-Magdalena 2006 2.1
10 "very useful" decreased maternal behaviors fetal and neonatal exposure, oral route Palanza 2002 2.1
20 not included damage to eggs and chromosomes fetal exposure, osmotic pumps Hunt 2003 0
20 not included damage to eggs fetal exposure, osmotic pumps Susiajro 2007 0
20 not included brain effects - disrupted neocortical development by accelerating neuronal differentiation and migration single injection Nakamura 2006 0
30 "...adequate for the evaluation process and gives cause for concern" reversed the normal sex differences in brain structure and behavior oral during gestation and lactation Kubo 2001 0
30 "suitable" hyperactivity oral Ishido 2004 0
50 EPA RfD EPA's 'safe exposure level, based on outdated, high dose studies and a 1000-fold margin of safety EPA 1998 0
*CERHR conclusion refers to the Center for Evaluation of Risks to Human Reproduction expert panel assessment of the utility of the study in the panel's review of BPA risks to human reproduction (CERHR 2006).
Statistics on percent cans with single servings that would yield human dose within a margin of 10 of the toxic dose are generated with the following assumptions: BPA calculations reflect a single adult serving, using label serving size and body weight of 60 kg (132 lbs); exposures for concentrated infant formula is calculated for exclusively formula-fed infant using average 3-month-old body weight (6 kg/13 lbs) and average daily formula ingestion (840 g/30 oz); formula is assumed diluted with water free of BPA.
Part 4
Human exposures to BPA approach or exceed toxic doses
A recent study from the Centers for Disease Control tested a demographically diverse group of almost 400 Americans for evidence of exposure to BPA and found that 95% of study participants had the chemical in their urine (Calafat 2005; Wolff 2007). BPA has been linked to a variety of health outcomes which are increasing in the United States and responsible for a major toll on our collective health. These include breast and prostate cancer, and infertility (Maffini 2006).
An analysis of CDC's body burden measurements shows that women are routinely exposed within a margin of 10 to doses that caused toxic effects in laboratory studies. The government typically mandates a 1,000- to 3,000-fold margin of safety between human exposures and levels found to harm lab animals. In the case of BPA, however, women routinely exceed this safety margin for 7 of the toxic doses from studies the CERHR has classified as appropriate for assessing human risks (see CERHR 2006 and Section 3 of this report). An analysis of CDC's data on women's exposures to BPA shows:
90% of all women are exposed to BPA at levels within a factor of 10 or less from doses shown to increase breast cancer risk and cause permanent changes in genital tract formation (see Section 3 for details). Scientists are debating the appropriate "effective dose" of BPA from the particular studies that measured these toxic effects, since BPA was delivered directly to the animals' bloodstream instead of through ingestion.
1.1% of all women are exposed to BPA within a margin of 10 of doses linked to early puberty.
3.1% of all women are exposed to BPA within a margin of 10 of doses linked to damage to the developing male reproductive system.
CDC data show that people are routinely exposed to unsafe levels of BPA
Source: EWG analysis of CDC measurements of BPA in urine from Calafat et al. (2005). Estimates assume 2 liters of urine excreted per day; and rely on linear interpolation between the percentiles of data provided in the study documentation, and linear extrapolation above the 95th percentile, using a best-fit estimation from the intercept at the 100th percentile of exposure.
Populations with unusual exposures are at special risk
Body burden studies indicate a fraction of the population is highly exposed to BPA. The most highly exposed people in the adult monitoring study excreted 6 times more BPA than the average participant (Calafat AM. 2005). A study of 7-year-old girls from 5 US cities found similar, if not slightly higher, exposures for children compared to adults (Wolff et al. 2007). Only summary results are available from the Wolff study, but they indicate an average exposure of 0.06 ug/kg-day, (CERHR 2006) and a maximum of 54.3 ppb (ug/L), 27 times higher than the median concentration. (Wolff 2007)
Since both studies collected samples at a single point in time it is difficult to know how much an individual's exposure varies from day to day. A few studies have collected 24-hour urine measurements over several days and found a high degree of variation in day-to-day exposure for individuals (Arakawa 2004).
Pre-natal and early life exposures. Studies have also documented BPA in fetal cord blood, amniotic fluid, and breast milk in women from industrialized countries, sometimes at higher concentrations than in maternal serum (Ikezuki, Tsutsumi et al. 2002; Schonfelder, Flick et al. 2002; Schonfelder, Wittfoht et al. 2002; Sun 2004; Irie et al. 2004; Kuruto-Niwa, Tateoka et al. 2007).
In laboratory animals BPA is rapidly passed to the developing fetus, and detected at higher concentrations in fetal than maternal blood (Schonfelder, Flick et al. 2002; Schonfelder, Wittfoht et al. 2002). Concern about daily pre- and post-natal exposures is heightened by the fact that detoxification mechanisms that rapidly deactivate and filter BPA from the body are not fully functional in the fetus and newborn. Most BPA is detoxified through a process known as glucuronidation, and the body's glucuronidation systems are not fully developed at birth (Schonfelder, Flick et al. 2002; Schonfelder, Wittfoht et al. 2002).
Takahashi exposed pregnant rats to BPA and found both the mean and maximum retention times of BPA in fetuses are longer than in maternal blood. (Takahashi and Oishi 2000) Hepatic glucuronidation activity in children aged 13 to 24 months was found to be 12- to 40-fold lower than in adults for five pharmaceutical drugs (Strassburg, Strassburg et al. 2002).
These findings provide evidence that exposure to BPA is pervasive and inclusive of the most vulnerable members of the population, namely the developing fetus, infant, and child. The body's immature detoxification systems result in greater exposure to the harmful form of BPA during infancy — a vulnerable period for brain and reproductive system development.
EWG's measurements of infant formula and various tests finding BPA leaching from polycarbonate baby bottles indicate that heightened pre-natal exposures might be followed by an intense period of dietary BPA exposure, resulting in much greater vulnerability for infants as opposed to children and adults.
Additional sources of BPA exposure in the human population
Canned food is a predominant, but not exclusive source of daily BPA exposure. BPA is found in many everyday products such as the hard clear plastic food containers — including baby bottles, baby toys, dental fillings and sealants, electronics, adhesives, paints and varnishes. BPA is found in a variety of other PVC plastics. Brominated BPA is a fire retardant with widespread use in the plastics used for electronics.
Polycarbonate plastics are rigid and clear or translucent, and often used for foods since they do not impart a plastic taste into food products. Polycarbonate plastics are often marked with the number 7. They are common in baby bottles, sippy toddler cups, Nalgene and other adult water bottles as well as plastics designed for longer-term food storage and microwave use. Water services using carboys also employ polycarbonate plastic. Polycarbonate is also made into disposable plastic tableware. Migration studies show a small degree of BPA leaching from plastics that are heated or abraded.
Another common source of BPA exposure is from tooth-colored dental fillings or sealants — which can contain up to 50 percent BPA (FDA 2004). Most exposure assessments consider these exposures to be intense but short lived since BPA is rapidly excreted from the body.
BPA is used in a variety of industrial products most of which result in little exposure for the general population. However worker exposures in these settings would be a particular concern for the smaller number of people with on-going, high level exposures. These might include plastics manufacturing for mobile phone housings, displays, computer parts, household electrical equipment, lamp fittings, automotive plastics, thermal paper and printing inks (CERHR 2006).
BPA is a building block for polycarbonate plastic and epoxy resins. BPA and related compounds leach from plastic and metal can linings into food and drinks — particularly after heating or as plastic ages — and from dental sealants.