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• W2041719197 abstract "The National Toxicology Program (NTP)1 established the NTP Center for the Evaluation of Risks to Human Reproduction (CERHR) in June 1998. The purpose of the CERHR is to provide timely, unbiased, scientifically sound evaluations of the potential for adverse effects on reproduction or development resulting from human exposures to substances in the environment. The NTP-CERHR is headquartered at NIEHS, Research Triangle Park, NC, and is staffed and administered by scientists and support personnel at NIEHS. Bisphenol A is a high-production volume chemical used in the production of epoxy resins, polyester resins, polysulfone resins, polyacrylate resins, polycarbonate plastics, and flame retardants. Polycarbonate plastics are used in food and drink packaging; resins are used as lacquers to coat metal products such as food cans, bottle tops, and water supply pipes. Some polymers used in dental sealants and tooth coatings contain bisphenol A. Exposure to the general population can occur through direct contact with bisphenol A or by exposure to food or drink that has been in contact with a material containing bisphenol A. CERHR selected bisphenol A for evaluation because of (1) high production volume; (2) widespread human exposure; (3) evidence of reproductive toxicity in laboratory animal studies; and (4) public concern for possible health effects from human exposures. Relevant literature on bisphenol A was identified from searches of the PubMed (Medline) and Toxline databases through February 2007 using the term “bisphenol” and the bisphenol A CAS RN (80-05-7). References were also identified from databases such as REPROTOX, HSDB, IRIS, and DART, from the bibliographies of the literature reviewed, by members of the expert panel, and in public comments. CERHR convened a 12-member, independent panel of government and non-government scientists to evaluate the scientific studies on the potential reproductive and developmental hazards of bisphenol A. The expert panel met publicly on March 5–7, 2007 and August 6–8, 2007. The Expert Panel Report on Bisphenol A is intended to (1) interpret the strength of scientific evidence that bisphenol A is a reproductive or developmental toxicant based on data from in vitro, animal, or human studies; (2) assess the extent of human exposures to include the general public, occupational groups, and other sub-populations; (3) provide objective and scientifically thorough assessments of the scientific evidence that adverse reproductive and developmental health effects may be associated with such exposures; and (4) identify knowledge gaps to help establish research and testing priorities to reduce uncertainties and increase confidence in future evaluations. This report has been reviewed by members of the expert panel and by CERHR staff scientists. Copies of this report have been provided to the CERHR Core Committee2 and will be made available to the public for comment. Following the public comment period, CERHR will prepare the NTP-CERHR Monograph on the Potential Human Reproductive and Developmental Effects of Bisphenol A. This monograph will include the NTP Brief, the Expert Panel Report, and all public comments received on the Expert Panel Report. The NTP-CERHR Monograph will be made publicly available and transmitted to appropriate health and regulatory agencies. Reports can be obtained from the web site (http://cerhr.niehs.nih.gov) or from: Michael D. Shelby, PhD, NIEHS EC-32, PO Box 12233, Research Triangle Park, NC 27709. E-mail: [email protected] Section 1 is based initially on secondary review sources. Primary study reports are addressed by the Expert Panel if they contain information that is highly relevant for determining the effect of exposure on developmental or reproductive toxicity or if the studies were released subsequent to the reviews. The CAS RN for bisphenol A is 80-05-7. Synonyms for bisphenol A listed in Chem IDplus (ChemIDplus, 2006) include: 2-(4,4′-Dihydroxydiphenyl)propane; 2,2-Bis(4-hydroxyphenyl)propane; 2,2-Bis(hydroxyphenyl)propane; 2,2-Bis(p-hydroxyphenyl)propane; 2,2-Bis-4′-hydroxyfenylpropan [Czech]; 2,2-Di(4-hydroxyphenyl)propane; 2,2-Di(4-phenylol)propane; 4,4′-(1-Methylethylidene)bisphenol; 4,4′-Bisphenol A; 4,4′-Dihydroxydiphenyl-2,2-propane; 4,4′-Dihydroxydiphenyldimethylmethane; 4,4′-Dihydroxydiphenylpropane; 4,4′-Isopropylidene diphenol; 4,4′-Isopropylidenebisphenol; 4,4′-Isopropylidene diphenol; Biphenol A; Bis(4-hydroxyphenyl) dimethylmethane; Bis(4-hydroxyphenyl)dimethylmethane; Bis(4-hydroxyphenyl)propane; Bisferol A [Czech]; Bisphenol. Bisphenol A; DIAN; Diano; Dimethyl bis(p-hydroxyphenyl)methane; Dimethylbis(p-hydroxyphenyl)methane; Dimethylmethylene-p,p′-diphenol; Diphenylolpropane; Ipognox 88; Isopropylidenebis(4-hydroxybenzene); Parabis A, Phenol; (1-methylethylidene)bis-, Phenol; 4,4′-(1-methylethylidene)bis-; Phenol, 4,4′-dimethylmethylenedi-; Phenol, 4,4′-isopropylidenedi-; Pluracol 245, Propane; 2,2-bis(p-hydroxyphenyl)-; Rikabanol; Ucar bisphenol A; Ucar bisphenol HP; beta,beta′-Bis(p-hydroxyphenyl)propane; beta-Di-p-hydroxyphenylpropane; p,p′-Bisphenol A; p,p′-Dihydroxydiphenyldimethylmethane; p,p′-Dihydroxydiphenylpropane; p,p′-Isopropylidenebisphenol; and p,p′-Isopropylidenediphenol. Bisphenol A has a molecular mass of 228.29 g/mol and a molecular formula of C15H1602 (European-Union, 2003). The structure for bisphenol A is shown in Figure 1. Structure for bisphenol A. Bisphenol A is a white solid with a mild phenolic odor (European-Union, 2003). Physicochemical properties are listed in Table 1. Purity of bisphenol A was reported at 99–99.8%, and common impurities observed were phenol and ortho and para isomers of bisphenol A [reviewed in (European-Union, 2003)]. Terasaki et al. (2004) used reversed phase chromatography and nuclear magnetic resonance spectroscopy to characterize the composition of 5 commercial bisphenol A samples. The nominal purity of the samples was 97 or 98%. Actual purities were 95.3 to >99%. Up to 15 contaminants were identified among which were: 4-hydroxyacetophenone; 4,4′-(1,3-dimethylbutylidene) bisphenol; p-cumylphenol; 4-hydroxyphenyl isobutyl methyl ketone; 2,4*-dibhydroxy-2,2-diphenylpropane; 2,4′-dibhydroxy-2,2-diphenylpropane; 2,4-bis(4-hydroxycumyl)phenol; 2,3-dihydro-3-(4′-hydroxyphenyl)-1,1,3-trimethyl-1H-inden-5-ol; 2-(4′-hydroxyphenol)-2,2,4-trimethylchroman; and 4-(4′-hydroxyphenol)-2,2,4-trimethylchroman (Terasaki et al., 2005). No information on trade names for bisphenol A was located. Measurement of bisphenol A in environmental and biologic samples can be affected by contamination with bisphenol A in plastic laboratory ware and in reagents (Tsukioka et al., 2004; Völkel et al., 2005). Accuracy is also affected by measurement technique, particularly at the very low concentrations that can now be measured. Enzyme-linked immunosorbent assay (ELISA) has poor correlation with the LC-ECD method and also the different ELISA kits correlate poorly with each other. ELISA methods may overestimate bisphenol A in biologic samples due to lack of specificity of the antibody and effects of the biologic matrix (Inoue et al., 2002; Fukata et al., 2006). Although high performance liquid chromatography (HPLC) with ultraviolet, fluorescence, or electrochemical detection can be sensitive to concentrations <0.5 ng/ml (Sajiki et al., 1999; Inoue et al., 2000; Kuroda et al., 2003; Sun et al., 2004), these methods are unable to make definitive identification of bisphenol A or bisphenol A glucuronides, because similar retention times may occur for the metabolites of other endogenous and exogenous compounds (Völkel et al., 2005). Use of LC-mass spectrometry (MS) with and without hydrolysis of bisphenol A glucuronide permits determination of free and total bisphenol A with a limit of quantification of 0.1 for MS (Sajiki et al., 1999) and 1 μg/L for MS/MS (Völkel et al., 2005). Gas chromatography (GC)/MS has been used with solid phase extraction after treatment with glucuronidase and derivatization to measure total bisphenol A with a limit of detection of 0.05 μg/L for MS (Tan and Mohd, 2003) and 0.1 μg/L for MS/MS (Calafat et al., 2005). Some of the variability in studies cited in this and subsequent sections may be due to differences in measurement techniques and to contamination. Bisphenol A glucuronidate can be an unstable product that can be degraded in acidic and basic pH solutions and can be hydrolyzed to free bisphenol A at neutral pH and room temperature in diluted rodent urine, placental and fetal tissue homogenates at room temperature. However, conjugates in urine are stable for at least 7 days when stored at −4°C and at least 180 days when stored at −70°C (Waechter et al., 2007; Ye et al., 2007). Bisphenol A is manufactured by the acid catalyzed condensation of phenol and acetone (SRI, 2004). In 1998, members of the Society of the Plastics Industry Bisphenol A Task Group [assumed manufacturers of bisphenol A] included Aristech Chemical Corporation, Bayer Corporation, Dow Chemical Company, and Shell Chemical Company (Staples et al., 1998). Current manufacturers of bisphenol A in the U.S. are Bayer MaterialScience, Dow Chemical Company, General Electric, Hexion Specialty Chemicals, and Sunoco Chemicals (SRI, 2004) (S. Hentges, public comments, February 2, 2007). There are currently six bisphenol A and four polycarbonate plants in the U.S. (S. Hentges, personal communication, October 30, 2006); three of four polycarbonate plants are located within bisphenol A plants. In 2000, there were 13 epoxy plants in the U.S., but was not clear if all of the plants manufactured bisphenol A-containing epoxy resins. In mid-2004, U.S. bisphenol A production volume was reported at 1.024 million metric tons [∼2.3 billion pounds] (SRI, 2004). A production volume of 7.26 billion g [16 million pounds] was reported for bisphenol A in 1991 (reviewed in HSDB, 2003). United States bisphenol A consumption was reported at 856,000 metric tons [∼1.9 billion pounds] in 2003 (SRI, 2004); 2003 consumption patterns included 619,000 metric tons [∼1.4 billion pounds] used in polycarbonate resins, 184,000 metric tons [∼406 million pounds] used in epoxy resins, and 53,000 metric tons [∼117 million pounds] used in other applications. In 1999 and 2003, it was reported that most bisphenol A produced in the U.S. was used in the manufacture of polycarbonate and epoxy resins and other products [reviewed in (Staples et al., 1998; SRI, 2004)]. Polycarbonate plastics may be used in the manufacture of compact discs, “solid and multi wall sheet in glazing applications and film,” food containers (e.g., milk, water, and infant bottles), and medical devices [reviewed in (European-Union, 2003)]. Bisphenol A may have been used at one time in Europe in polyvinyl chloride cling film and plastic bags, but that use is believed to have been discontinued (European Food Safety Authority, 2006). Contact with drinking water may occur through the use of polycarbonate for water pipes and epoxy-phenolic resins in surface coatings of drinking water storage tanks [reviewed by (European Food Safety Authority, 2006)]. Polycarbonate blends have been used to manufacture injected molded parts utilized in alarms, mobile phone housings, coil cores, displays, computer parts, household electrical equipment, lamp fittings, and power plugs. Automotive and related uses for polycarbonate blends include light reflectors and coverings, bumpers, radiator and ventilation grills, safety glazing, inside lights, and motorcycle shields and helmets. Epoxy resins are used in protective coatings, structural composites, electrical laminates, electrical applications, and adhesives. The European Union (2003) reported that smaller volumes of bisphenol A are used in production of phenoplast, phenolic, and unsaturated polyester resins, epoxy can coatings, polyvinyl chloride (PVC) plastic, alkoxylated bisphenol A, thermal paper, and polyols/polyurethane. Other uses reported for products manufactured from bisphenol A included protective window glazing, building materials, optical lenses, and development of dyes [reviewed in (Staples et al., 1998)]. A search of the National Library of Medicine Household Products Database (NLM, 2006) revealed that bisphenol A-based polymers are used in coatings, adhesives, and putties available to the general pubic for use in automobiles, home maintenance and repair, and hobbies, but only 3 epoxy products, used for crafts and hobbies, contain bisphenol A itself. Some polymers manufactured with bisphenol A are Food and Drug Administration (FDA)-approved for use in direct and indirect food additives and in dental materials, as reported in the Code of Federal Regulations (CFR) (FDA, 2006). In the CFR, bisphenol A is often referred to as 4,4′-isopropylidnediphenol. Polymers manufactured with bisphenol A are FDA-approved for use as anoxomers and in coatings, adhesives, single and repeated food contact surfaces, and tooth shade resin materials. The European Union (2003) noted that resins, polycarbonate plastics, and other products manufactured from bisphenol A can contain trace amounts of residual monomer and additional monomer may be generated during breakdown of polymer. The American Plastics Council reports that residual bisphenol A concentrations in polycarbonate plastics and epoxy resins are generally <50 ppm (S. Hentges, personal communication, October 30, 2006). Polymer hydrolysis can occur at elevated temperature or extreme pH. An example of potential human exposure is migration of bisphenol A from a food container into the food. Exposure to bisphenol A through food is discussed in detail in Section 1.2.3.2. Bisphenol A may be present in the environment as a result of direct releases from manufacturing or processing facilities, fugitive emission during processing and handling, or release of unreacted monomer from products (European-Union, 2003). According to the Toxics Release Inventory database, total environmental release of bisphenol A in 2004 was 181,768 pounds, with releases of 132,256 pounds to air, 3533 pounds to water, 172 pounds to underground injection, and 45,807 pounds to land (TRI, 2004). Bisphenol A released to the atmosphere is likely degraded by hydroxy radicals (European-Union, 2003). Half-life for the reaction between bisphenol A and hydroxy radicals was estimated at 0.2 days. It was also noted that photolysis and photodegradation of bisphenol A in the atmosphere is possible and photo-oxidation half-lives of 0.74–7.4 hr were estimated [reviewed in (Staples et al., 1998; European-Union, 2003)]. The European Union (2003) noted that because of its low volatility and relatively short half-life in the atmosphere, bisphenol A is not likely to enter the atmosphere in large amounts. Removal by precipitation and occurrence in rain water were thought likely to be negligible. Because of its short half-life in the atmosphere, bisphenol A is unlikely to be transported far from emission points. Based on vapor pressure and Henry constant (Table 1), the European Union (2003) and Staples et al. (1998) concluded that bisphenol A is of low volatility and not likely to be removed from water through volatilization. Both groups concluded that hydrolysis of bisphenol A in water is unlikely. However, there was disagreement on potential for photo-oxidation of bisphenol A in water. Based on physical and chemical properties, the European Union concluded that photolysis of bisphenol A in water is unlikely. Staples et al. (1998) noted that bisphenol A is able to absorb ultraviolet light, especially in a basic solution. Therefore, it was concluded that photolysis from surface water is possible, depending on conditions such as pH, turbidity, turbulence, and sunlight. Photo-oxidation half-life of bisphenol A in water was estimated at 66 hr to 160 days [reviewed in (Staples et al., 1998)]. Rapid biodegradation of bisphenol A from water was reported in the majority of studies reviewed by the European Union (2003) and Staples et al. (1998). A biodegradation half-life of 2.5–4 days was reported in a study measuring bisphenol A concentrations in surface waters near the receiving stream of a bisphenol A manufacturer [reviewed in (Staples et al., 1998)]. When the Staples et al. (1998) review was published, soil sorption constants had not been measured but were estimated at 314–1524. Based on such data, the European Union (2003) and Staples et al. (1998) concluded that bisphenol A adsorption to soils or sediments would be “modest” or “moderate.” Based on data for degradation of bisphenol A in water, the European Union (2003) predicted that bisphenol A would be degraded in soil and estimated a half-life of 30 days for degradation of bisphenol A in soil. Subsequent to the Staples et al. (1998) and European Union (2003) reviews, a study examining fate of 14C-bisphenol A in soils through laboratory soil degradation and batch adsorption tests was released by Fent et al. (2003). In that study, 14C-bisphenol A was dissipated and not detectable in 4 different soil types within 3 days. Soil distribution coefficients were determined at 636–931, and based on those values, the study authors concluded that bisphenol A has low mobility in soil. The study authors concluded that bisphenol A is not expected to be stable, mobile, or bioavailable from soils. In studies reviewed by the European Union (2003) and Staples et al. (1998), bioconcentration factors for fish were measured at 3.5–68 and were found to be lower than values estimated from the Kow. Both groups concluded that potential for bioconcentration of bisphenol A is low in fish. Higher bioconcentration factors (134–144) were determined for clams [reviewed in (European-Union, 2003)]. Two studies examining aggregate exposures in preschool age children in the U.S. used GC/MS to measure bisphenol A concentrations in environmental media (Wilson et al., 2003, 2006). In the first study (Wilson et al., 2003), bisphenol A concentrations were measured in air outside 2 day care centers and the homes of 9 children. Bisphenol A was detected in 9 of 13 outdoor air samples at <0.100–4.72 ng/m3 (mean concentration=2.53 ng/m3 at day care centers; 1.26 ng/m3 at home). In indoor air from day care centers and homes, bisphenol A was detected in 12 of 13 samples at <0.100–29 ng/m3 (mean concentration=6.38 ng/m3 at day care centers; 11.8 ng/m3 at home). At those same locations, bisphenol A was detected in all of 13 samples of floor dust at means (range) of 1.52–1.95 (0.567–3.26) ppm (μg/g) and play area soils at means (range) of 0.006–0.007 (0.004–0.014) ppm (μg/g). In the second study (Wilson et al., 2006), bisphenol A concentrations were measured inside and outside at least 222 homes and 29 daycare centers. Bisphenol A was detected in 31–44% of outdoor air samples from each location; concentrations ranged from <LOD (0.9) to 51.5 ng/m3. Medians were <limit of detection (LOD). Indoor air samples (45–73%) contained detectable concentrations of bisphenol A; concentrations were reported at <LOD (0.9)–193 ng/m3. Median values were <LOD–1.82 ng/m3. Bisphenol A was detected in 25–70% of dust samples; concentrations were reported at <LOD (20) to 707 ng/g. Median values were <LOD–30.8 ng/g. A second U.S. study used a GC/MS method to measure bisphenol A concentrations in dust from 1 office building and 3 homes and in air from 1 office building and 1 home (Rudel et al., 2001). Bisphenol A was detected in 3 of 6 dust samples (reporting limit >0.01 μg/extract) at concentrations of 0.25–0.48 μg/g dust. In indoor air samples collected from offices and residences, bisphenol A was detected in 3 of 6 samples (detection limit=∼0.5 ng/m3) at concentrations of 0.002–0.003 μg/m3. In another study using a GC/MS technique, bisphenol A concentrations in indoor air from 120 U.S. homes were below reporting limits (0.018 μg/m3) (Rudel et al., 2003). Median (range) bisphenol A concentration in dust in this study was 0.821 (<0.2–17.6) μg/g, with 86% of samples above the reporting limit. Limited information is available for bisphenol A concentrations in U.S. water (Table 2). In 1996 and/or 1997, mean bisphenol A concentrations were reported at 4–8 μg/L in surface water samples near 1 bisphenol A production site but bisphenol A was not detected (<1 μg/L) in surface water near 6 of 7 bisphenol A production sites in the U.S. (Staples et al., 2000). Bisphenol A was detected at a median concentration (in samples with detectable bisphenol A above the reporting limit of 0.09 μg/L) of 0.14 μg/L and a maximum concentration of 12 μg/L in 41.2% of 85 samples collected from U.S. streams in 1999 and 2000 (Kolpin, 2002). In 2001 and 2002, bisphenol A was not detected (<0.001 μg/L) in effluent from a wastewater treatment plant in Louisiana, and concentrations were not quantifiable [quantification limit not defined] in samples collected from surface waters in Louisiana and in drinking water at various stages of treatment at plants in Louisiana and Ontario, Canada (Boyd et al., 2003). In water samples collected in Europe and Japan from the 1970 s through 1989, bisphenol A concentrations were ≤1.9 μg/L and in most cases were ≤0.12 μg/L [reviewed in (European-Union, 2003)]. The European Union (2003) noted that the highest potential for human exposure to bisphenol A is through products that directly contact food. Examples of food contact materials that can contain bisphenol A include food and beverage containers with internal epoxy resin coatings and polycarbonate tableware and bottles, such as those used to feed infants. In addition to commercial food sources, infants consume breast milk. Calafat et al. (2006) reported a median bisphenol A concentration of ∼1.4 μg/L [as estimated from a graph] in milk from 32 women (Table 3). Bisphenol A was measured after enzymatic hydrolysis of conjugates. Ye et al. (2006) found measurable concentrations of bisphenol A in milk samples from 18 of 20 lactating women. Free bisphenol A was found in samples from 12 women. The median total bisphenol concentration in milk was 1.1 μg/L (range: undetectable to 7.3 μg/L). The median free bisphenol A concentration was 0.4 μg/L (range: undetectable to 6.3 μg/L). Sun et al. (2004) used an HPLC method to measure bisphenol A concentrations in milk from 23 healthy lactating Japanese women. Bisphenol A concentrations ranged from 0.28–0.97 μg/L, and the mean±SD concentration was reported at 0.61±0.20 μg/L. No correlations were observed between bisphenol A and triglyceride concentrations in milk. Values from 6 milk samples were compared to maternal and umbilical blood samples reported previously in a study by Kuroda et al. (2003). Bisphenol A values were higher in milk, and the milk/serum ratio was reported at 1.3. Bisphenol A values in milk were comparable to those in umbilical cord serum. [It was not clear whether milk and serum samples were obtained from the same volunteers in the two studies.] Studies have measured migration of bisphenol A from polycarbonate infant bottles or containers into foods or food simulants. Results of those studies are summarized in Table 4. Analyses for bisphenol A were conducted by GC/MS or HPLC. The European Union (2003) group noted that in many cases bisphenol A concentrations were below the detection limit in food simulants. When bisphenol A was detected, concentrations were typically ≤50 μg/L in simulants exposed to infant bottles and ≤5 μg/kg in simulants exposed to polycarbonate tableware. An exception is one study that reported bisphenol A concentrations at up to ∼192 μg/L in a 10% ethanol food simulant and 654 μg/L in a corn oil simulant (Onn Wong et al., 2005). In the study, cut pieces of bottles were incubated, and the study authors acknowledged that bisphenol A could have migrated from the cut edges. [The Expert Panel notes that incubations were at 70 or 100°C for 240 hr, representing conditions not anticipated for normal use of baby bottles.] One study conducted with actual infant food (formula and fruit juice) reported no detectable bisphenol A (Mountfort et al., 1997). Some studies examining the effects of repeated use of polycarbonate items noted increased leaching of bisphenol A with repeated use (Earls, 2000; Brede et al., 2003; CSL, 2004). It was suggested that the increase in bisphenol A migration was caused by damage to the polymer during use. Results from other reports suggested that leaching of bisphenol A decreased with repeated use, and it was speculated that available bisphenol A was present at the surface of the product and therefore removed by washing (Biles et al., 1997b; Kawamura et al., 1999; Haighton et al., 2002; European Union, 2003). One study (Kawamura et al., 1999) showed higher concentrations of bisphenol A in simulants exposed to products that had been recalled because of unacceptable residual concentrations of bisphenol A and other compounds. The study by Biles et al. (1997b) demonstrated that infant bottles exposed to 50 or 95% ethanol at 65°C for 240 hr leached bisphenol A at concentrations exceeding residual monomer concentrations, and it was suggested that hydrolysis of the polymer had occurred. High molecular weight, heat-cured bisphenol A-based epoxy resins are used as protective linings in cans for food and beverages and may be used in wine storage vats (European-Union, 2003). Residual bisphenol A monomer can migrate from the coatings to foods or beverages contained within cans. Studies were conducted to measure actual concentrations of bisphenol A in commercially available foods or to measure concentrations of bisphenol A leaching from can linings into food simulants. Because the actual measurement of bisphenol A concentrations in canned foods represents the most realistic situation, the CERHR review will focus on those data. Studies conducted with simulants will not be reviewed, with the exception of one study by Howe et al. (1998) that was considered by the FDA (1996) in their estimates of bisphenol A intake. Bisphenol A concentrations detected in infant foods are summarized in Table 5, and bisphenol A concentrations detected in non-infant foods are summarized in Table 6. With the exception of isolated cases in which bisphenol A concentrations were measured at up to ∼0.8 mg/kg food, most measurements were below 0.1 mg/kg. The European Union also noted an extraction study conducted with an epoxy resin that is occasionally used to line wine vats. Based on that study, a worst-case scenario of 0.65 mg/L bisphenol A in wine was used. The European Union noted that the value represents a very worst-case exposure scenario but decided to use that number in risk estimates because no other value was available. [The Expert Panel notes that a study of bisphenol A in wine (Brenn-Struckhofova and Cichna-Markl, 2006) identified a maximum concentration of 2.1 μg/L (Table 6).] In one study, empty cans were filled with soup, beef, evaporated milk, carrots, or 10% ethanol (Goodson et al., 2004). The cans were then sealed, processed at 5, 20, or 40°C, and sampled at 1 or 10 days or 1, 3, or 9 months. Half the cans processed according to each condition were dented. It was determined that 80–100% of the bisphenol A migrated to food immediately after processing, and that bisphenol A concentrations did not change during storage or as a result of denting. The study authors concluded that most migration occurred during can processing. Boiling the cans or heating to 230°C did not increase migration of bisphenol A, but that finding appears to contrast with findings of others. Kang et al. (2003) examined the effects of temperature, duration of heating, glucose, sodium, and oil on migration of bisphenol A from cans. In cans filled with water, heating to 121°C compared to 105°C increased migration of bisphenol A but the duration of heating had no significant effect. Compared to cans filled with water, increased amounts of bisphenol A migrated from cans filled with 1–10% sodium chloride, 5–20% glucose, or vegetable oils and heated to 121°C. Takao et al. (2002) reported increased leaching of bisphenol A from cans into water when the cans were heated to ≥80°C. A study examining aggregate exposures of U.S. preschool age children measured bisphenol A concentrations in liquid food and solid food served to the children at home and at child care centers (Wilson et al., 2003). Duplicate plates of food served to nine children were collected over a 48-hr period. GC/MS analyses were conducted on four liquid food samples and four solid food samples from the child care center and nine liquid food samples and nine solid food samples from home. Bisphenol A was detected in all solid food samples, three liquid food samples from the child care center, and two liquid food samples from the home. Concentrations of bisphenol A ranged from <0.100–1.16 ng/g [μg/kg] in liquid foods and from 0.172–4.19 ng/g [μg/kg] in solid food. The study examining aggregate exposures of U.S. preschool age children was repeated with a larger sample and again measured bisphenol A concentrations in liquid food and solid food served to the children at home and at child care centers (Wilson et al., 2006). Bisphenol A concentrations were measured by GC/MS in food served over a 48-hr period to at least 238 children at home and 49 children at daycare centers. Bisphenol A was detected in 83–100% of solid food samples; concentrations were reported at <LOD (0.8) to 192 ng/g [μg/kg]. Sixty-nine to 80% of liquid food contained detectable concentrations of bisphenol A; concentrations were reported at <LOD (0.3)–17.0 ng/mL in liquid food. Data were also collected for hand wipes of 193 children at daycare centers and 60 children at home. Bisphenol A was detected in 94–100% of handwipe samples; concentrations ranged from <LOD [not defined] to 46.6 ng/cm2. Bisphenol A was detected in 85–89% of food preparation surface wipes from homes; concentrations were reported at <LOD [not defin" @default.
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• W2041719197 title "NTP-CERHR expert panel report on the reproductive and developmental toxicity of bisphenol A" @default.
• W2041719197 cites W1488973437 @default.
• W2041719197 cites W1542274612 @default.
• W2041719197 cites W1543402833 @default.
• W2041719197 cites W1543950566 @default.
• W2041719197 cites W1572243376 @default.
• W2041719197 cites W1665186530 @default.
• W2041719197 cites W1863544056 @default.
• W2041719197 cites W1919564391 @default.
• W2041719197 cites W1964288917 @default.
• W2041719197 cites W1964818491 @default.
• W2041719197 cites W1965691830 @default.
• W2041719197 cites W1966071231 @default.
• W2041719197 cites W1966198506 @default.
• W2041719197 cites W1966287514 @default.
• W2041719197 cites W1966871799 @default.
• W2041719197 cites W1967546850 @default.
• W2041719197 cites W1968078123 @default.
• W2041719197 cites W1968614586 @default.
• W2041719197 cites W1968877966 @default.
• W2041719197 cites W1968900944 @default.
• W2041719197 cites W1969785163 @default.
• W2041719197 cites W1970505374 @default.
• W2041719197 cites W1970858934 @default.
• W2041719197 cites W1971500946 @default.
• W2041719197 cites W1971914348 @default.
• W2041719197 cites W1971947104 @default.
• W2041719197 cites W1972047961 @default.
• W2041719197 cites W1973556480 @default.
• W2041719197 cites W1973847024 @default.
• W2041719197 cites W1974949724 @default.
• W2041719197 cites W1975062839 @default.
• W2041719197 cites W1975204728 @default.
• W2041719197 cites W1975804302 @default.
• W2041719197 cites W1976578309 @default.
• W2041719197 cites W1976740823 @default.
• W2041719197 cites W1978076833 @default.
• W2041719197 cites W1978082040 @default.
• W2041719197 cites W1978662324 @default.
• W2041719197 cites W1979440858 @default.
• W2041719197 cites W1979443612 @default.
• W2041719197 cites W1980368019 @default.
• W2041719197 cites W1980383923 @default.
• W2041719197 cites W1981454226 @default.
• W2041719197 cites W1981546766 @default.
• W2041719197 cites W1981993170 @default.
• W2041719197 cites W1982377908 @default.
• W2041719197 cites W1982469906 @default.
• W2041719197 cites W1982477373 @default.
• W2041719197 cites W1982546336 @default.
• W2041719197 cites W1982630982 @default.
• W2041719197 cites W1982942271 @default.
• W2041719197 cites W1983295104 @default.
• W2041719197 cites W1984569506 @default.
• W2041719197 cites W1984673012 @default.
• W2041719197 cites W1985071502 @default.
• W2041719197 cites W1985433964 @default.
• W2041719197 cites W1985569861 @default.
• W2041719197 cites W1985941840 @default.
• W2041719197 cites W1986138749 @default.
• W2041719197 cites W1986955479 @default.
• W2041719197 cites W1987033364 @default.
• W2041719197 cites W1987538361 @default.
• W2041719197 cites W1987836585 @default.
• W2041719197 cites W1988172495 @default.
• W2041719197 cites W1988230359 @default.
• W2041719197 cites W1988538574 @default.
• W2041719197 cites W1990207997 @default.
• W2041719197 cites W1991299939 @default.
• W2041719197 cites W1992136235 @default.
• W2041719197 cites W1992241432 @default.
• W2041719197 cites W1992316644 @default.
• W2041719197 cites W1992629360 @default.
• W2041719197 cites W1992995039 @default.
• W2041719197 cites W1993210636 @default.
• W2041719197 cites W1993269979 @default.
• W2041719197 cites W1993352525 @default.
• W2041719197 cites W1993433827 @default.
• W2041719197 cites W1993539670 @default.
• W2041719197 cites W1994048261 @default.
• W2041719197 cites W1994136133 @default.
• W2041719197 cites W1994976609 @default.

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