- Email: [email protected]
Letter to the editor (Wright-Walters et al., 2011)
Science of the Total Environment 450–451 (2013) 369–371
Contents lists available at SciVerse ScienceDirect
Science of the Total Environment journal homepage: www.elsevier.com/locate/scitotenv
Letter to the editor (Wright-Walters et al., 2011)
Dear Sir/Madam: We have read with interest the recent paper updating the aquatic hazard assessment of Bisphenol A (Wright-Walters et al., 2011). The paper developed a “new” predicted no effect concentration (PNEC) for Bisphenol A (BPA) of 0.06 μg/L for long term aquatic exposure to freshwater organisms. This new PNEC was calculated using the species sensitivity distribution (SSD) HC5 (lower 5th percentile hazard concentration) method of van der Hoeven (2001) with a large set of acute and chronic studies taken from published literature and unpublished sources. The new PNEC is considerably lower than other SSD-based HC5 values derived for BPA for use as a PNEC (Staples et al., 2008; EC, 2010). The HC5 values calculated by Staples et al. (2008) and EC (2010) are 18 and 7.5 μg/L, respectively. EC (2010) used a further assessment factor of 5 to arrive at a PNEC of 1.5 μg/L, while neither Staples et al. (2008) nor Wright-Walters et al. (2011) applied an assessment factor. Although different models were used, the differences between the HC5 values calculated by Staples et al. (2008), EC (2010) and Wright-Walters et al. (2011) are largely due to the use of different datasets. Wright-Walters et al. (2011) conducted literature searches to identify potentially relevant studies and also reportedly assessed the quality of each study. The resulting dataset is shown in Table 2 of the paper and includes 61 studies and 94 no observed effect concentrations (NOEC). Unfortunately, the dataset that resulted from this process and was used by Wright-Walters et al. (2011) to derive the PNEC is fraught with errors and omits a number of important studies. The result of the errors and omissions in the dataset is that the “new” PNEC calculated by Wright-Walters et al. (2011) is incorrect and should not be used to assess the hazard of BPA. The dataset assembled by Wright-Walters et al. (2011) includes values that do not exist in the specified studies. NOEC for Hydra vulgaris, Gammarus pulex, and Chironomus riparius of 0.002, 0.01 and 0.078 μg/L from Pascoe et al. (2002) and Watts et al. (2001, 2003) were cited by Wright-Walters et al. (2011), but these values are not in any of the published papers. Acute data were improperly included in the chronic toxicity dataset even though valid chronic data were available. For example, the Wright-Walters et al. (2011) dataset included a 96-h NOEC of 1400 μg/L from an acute lethality study with Chironomus tentans (Sayers, 2005), and an extended acute 14-d NOEC of 3200 μg/L with zebrafish (Bayer AG, 1999). Instead, the dataset should have included the valid chronic studies with the midge C. riparius and zebrafish that do exist for these species (Watts et al., 2003; Segner et al., 2003a). Studies were improperly included that lacked sufficient documentation to score their validity using procedures based on Klimisch et al. (1997). The studies reported by Fraunhofer (2000) and Segner et al. 0048-9697/$ – see front matter © 2012 Elsevier B.V. All rights reserved. doi:10.1016/j.scitotenv.2012.05.055
(2003b) with zebrafish, and Bowmer and Borst (1999) with carp are only summaries or abstracts that lack sufficient documentation of methodologies, control performance, statistical analyses, analytical chemistry measurements, and quality control results to assess their validity. Without adequate documentation of these aspects of each study, Klimisch scores of “4” must be assigned to them. Only studies with Klimisch scores of “1” or “2” should be used in hazard assessment. Studies with Klimisch scores of “3” (not valid) or “4” (unassignable due to insufficient documentation) generally should not be used in a hazard assessment. A number of poorly designed studies, such that the results reported cannot be properly interpreted, were included by Wright-Walters et al. (2011). Studies with the ramshorn snail Marisa cornuarietis reported by Oehlmann et al. (2000, 2006) should receive Klimisch scores of “3”, not valid, due to critical shortcomings in their design and conduct. As explained in a critical review by Dietrich et al. (2006) and in the European Union (EU) risk assessment (EC, 2010), these studies used pseudoreplication, had a high and varying density of test organisms, used improper statistics and, in some cases, lacked analytical verification of test concentrations. Because of these concerns and because of a general lack of information about the proper husbandry and life history of Marisa snails, a series of studies were conducted by Forbes et al. (Aufderheide et al., 2006; Selck et al., 2006; Forbes et al., 2007a, 2007b, 2008). The husbandry and life history information were used to aid in the design of the toxicity studies. The results from these fully valid studies with M. cornuarietis by Forbes et al. (validity scores of “1”) were excluded by Wright-Walters et al. (2011) but should be used to assess the chronic toxicity of BPA to Marisa snails. Forbes et al. (2008) reported a lowest NOEC of 25 μg/L for BPA in a 328 day lifecycle study with M. cornuarietis. Similarly, studies with the African clawed frog Xenopus laevis reported by Kloas et al. (1999) and Levy et al. (2004) used improper experimental design, employed incorrect statistical methods, and had other concerns that are documented by Pickford et al. (2003). Pickford et al. (2003) conducted studies with the same species using a robust study design, proper statistical analysis, measurement of test concentrations, and followed Good Laboratory Practices (GLP). Pickford et al. (2003) reported 90-d NOEC of 500 μg/L for several mortality, growth and development endpoints with X. laevis. In addition, the Wright-Walters et al. (2011) dataset included a study with brown trout by Lahnsteiner et al. (2005) that only examined non-apical endpoints related to sperm quality. As reviewed in the EU risk assessment (EC, 2010), the Lahnsteiner et al. (2005) study suffered from lack of replication, very small sample sizes, unclear experimental design, use of wild-caught fish, lack of husbandry conditions, unjustified endpoints, and lack of confirmation of sexual maturity of the fish, which caused the EU to assign a Klimisch score of “3” or not valid. None of the endpoints related to sperm quality reported by the authors were linked to any apical endpoint related to reproduction and thus are not useful for an assessment of long term chronic toxicity. While long term tests assessing reproduction are not available for brown trout, life-cycle tests are available for three other species of
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Letter to the Editor
fish. AIST (2007) reported a 1.5 generation NOEC of 247 μg/L with Japanese medaka. Caunter (2000) reported a lowest NOEC of 16 μg/L in a multigeneration test with fathead minnow. Segner et al. (2003a) reported an EC50 of 1370 μg/L based on reproductive success in a life cycle study with zebrafish. In addition to the errors and omissions in the Wright-Walters et al. (2011) dataset described above, the authors made improper use of valid studies. The intent of the paper was to assess the hazard of BPA using a species sensitivity distribution (SSD) approach (van der Hoeven, 2001) and, therefore, a dataset of species-specific NOEC is needed. For each valid study, the lowest consistent and treatmentrelated NOEC among apical endpoints related to mortality, growth and development, and reproduction should be identified (EC, 2010; Staples et al., 2008). If more than one valid study exists for a species, the longest duration study should be used to represent that species. Thus, there should be one long-term NOEC for each species used in the SSD-based assessment. Wright-Walters et al. (2011) included multiple NOECs from each of numerous studies and included more than one study for several species. Doing so gives improper weight both to those studies with multiple NOECs and to those species with multiple studies. The SSD-based calculation method used by Wright-Walters et al. (2011) is the method developed by van der Hoeven (2001). The van der Hoeven (2001) paper states that the method “…can be applied from sample size 19 upwards.” Since this is a method to calculate a species sensitivity distribution, this statement means that 19 or more species are needed to apply this method. As documented in the hazard assessments reported by EC (2010), and Staples et al. (2008), there are valid chronic toxicity studies available for approximately 16 freshwater species representing 10 different taxonomic groups. Thus, the sample size is too small to use the van der Hoeven (2001) method to calculate an SSD-based HC5 value for use as a PNEC for BPA. There are other statistical methods available to calculate SSD-based HC5 values and these have been successfully used to do so (EC, 2010; RIVM, 2004; Staples et al., 2008). The exact SSD-based HC5 value that is calculated will be influenced both by the model that is chosen and the dataset that is modeled. The choice of the SSD model requires that the user understand and follow the underlying requirements of the model. The specific aquatic toxicity dataset used with the SSD model to calculate HC5 values for use as PNEC should be assembled so that only valid studies are included, that each valid study has a lowest NOEC based on apical endpoints, and that each genus/species has a representative NOEC. Because of the numerous errors contained in the dataset used by Wright-Walters et al. (2011), their omission of other high quality relevant studies, and their inappropriate use of the van der Hoeven SSD modeling method, their “new” PNEC should not be used to assess the long term aquatic hazard of BPA. References AIST. AIST risk assessment document series no. 4 bisphenol A. Tsukuba, Ibaraki, Japan: National Institute of Advanced Industrial Science and Technology (AIST), Research Center for Chemical Risk Management; 2007. November, 2007. Aufderheide J, Warbritton R, Pounds N, File-Emperador S, Staples C, Caspers N, et al. Effects of husbandry parameters on the life-history traits of the apple snail, Marisa cornuarietis: effects of temperature, photoperiod, and population density. Invertebr Biol 2006;125:9-20. Bayer AG. Fish, prolonged toxicity test (Brachydanio rerio) 14 day study of bisphenol A. Study number 707 A/98 F1, Leverkusen, Germany; 1999. Bowmer T, Borst B. Environmental risk assessment of endocrine active substances — a reality? International Symposium on Environmental Endocrine Disruptors 1999. Extended Abstract, December 9-11, 1999. Kobe, Japan; 1999. p. 85–8. Caunter JE. Bisphenol A: multigeneration study with fathead minnow (Pimephales promelas). Report no. BL6878/B. Brixham, Devon, UK: Brixham Environmental Laboratory, AstraZeneca UK Ltd.; 2000. Dietrich DR, O'Brien E, Hoffmann S, Balaguer P, Nicolas J-C, Seinen W, et al. Effects of BPA in snails. Environ Health Perspect 2006;114:A340–1. EC (European Commission). Updated European Union risk assessment report; 4,4'-isopropylidenediphenol (bisphenol-A); CAS number: 80-05-7; EINECS number:
201-245-8; environment addendum of February 2008. 2010. http://esis.jrc.ec.europa. eu. (accessed June 5, 2012). Forbes VE, Selck H, Palmqvist A, Aufderheide J, Warbritton R, Pounds N, et al. Does bisphenol A induce superfeminization in Marisa cornuarietis? Part I: intra- and inter-laboratory variability in test endpoints. Ecotoxicol Environ Saf 2007a;66: 309–18. Forbes VE, Aufderheide J, Warbritton R, van der Hoeven N, Caspers N. Does bisphenol A induce superfeminization in Marisa cornuarietis? Part II: toxicity test results and requirements for statistical power analyses. Ecotoxicol Environ Saf 2007b;66: 319–25. Forbes VE, Warbritton R, Aufderheide J, van der Hoeven N, Caspers N. Effects of bisphenol A on fecundity, egg hatchability, and juvenile growth of Marisa cornuarietis. Environ Toxicol Chem 2008;27:2332–40. Fraunhofer (Fraunhofer Institute of Environmental Chemistry and Ecotoxicology). Der Einfluss von Xeno-oestrogenen auf den Lebenszyklus von Fischen. Annual Report 2000, Schmallenberg, Germany; 2000. p. 32–3. Klimisch H-J, Andreae M, Tillmann U. A systematic approach for evaluating the quality of experimental toxicological and ecotoxicological data. Regul Toxicol Pharmacol 1997;25:1–5. Kloas W, Lutz I, Einspanier R. Amphibians as a model to study endocrine disruptors: II. Estrogenic activity of environmental chemicals in vitro and in vivo. Sci Total Environ 1999;225:59–68. Lahnsteiner F, Berger B, Kletzl M, Weismann T. Effect of bisphenol A on maturation and quality of semen and eggs in the brown trout, Salmo trutta f. fario. Aquat Toxicol 2005;75:213–24. Levy G, Lutz I, Kruger A, Kloas W. Bisphenol A induces feminization in Xenopus laevis tadpoles. Environ Res 2004;94:102–11. Oehlmann J, Schulte-Oehlmann U, Tillmann M, Markert B. Effects of endocrine disruptors on prosobranch snails (Mollusca: Gastropoda) in the laboratory. Part I: bisphenol A and octylphenol. Ecotoxicology 2000;9:383–97. Oehlmann J, Schulte-Oehlmann U, Bachmann J, Oetken M, Lutz I, Kloas W, et al. Bisphenol A induces superfeminization in the ramshorn snail Marisa cornuarietis (Gastropoda: Prosobranchia) at environmentally-relevant concentrations. Environ Health Perspect 2006;114(Supplement 1):127–33. Pascoe D, Carroll K, Karntanut W, Watts MM. Toxicity of 17-ethinylestradiol and bisphenol A to the freshwater cnidarian Hydra vulgaris. Arch Environ Contam Toxicol 2002;43:56–63. Pickford DB, Hetheridge MJ, Caunter JE, Hall AT, Hutchinson TH. Assessing chronic toxicity of bisphenol A to larvae of the African clawed frog (Xenopus laevis) in a flow-through exposure system. Chemosphere 2003;53:223–35. RIVM (The Netherlands National Institute of Public Health and the Environment). ETX 2.0. Bilthoven, The Netherlands; 2004. Sayers LE. Bisphenol A (BPA) — acute toxicity to midges (Chironomus tentans) under flow-through conditions. Report no. 13796.6107. Wareham, MA, USA: Springborn Smithers Laboratories, Inc.; 2005. Segner H, Navas JM, Schaefers C, Wenzel A. Potencies of estrogenic compounds in in vitro screening assays and in life cycle tests with zebrafish in vivo. Ecotoxicol Environ Saf 2003a;54:315–22. Segner H, Caroll K, Fenske M, Janssen CT, Maack CG, Pascoe A. Identification of endocrine disrupting effects in aquatic vertebrates and invertebrates: report from the European IDEA project. Ecotoxicol Environ Saf 2003b;54: 302–14. Selck H, Aufderheide J, Pounds N, Staples C, Caspers N, Forbes V. Effects of food type, feeding frequency, and temperature on juvenile survival and growth of Marisa cornuarietis (Mollusca: Gastropods). Invertebr Biol 2006;125: 106–16. Staples CA, Woodburn KB, Klecka GM, Mihaich EM, Hall AT, Ortego L, et al. Comparison of four species sensitivity distribution methods to calculate predicted no effect concentrations for bisphenol A. Hum Ecol Risk Assess 2008;14: 455–78. van der Hoeven N. Estimating the 5-percentile of the species sensitivity distributions without any assumptions about the distribution. Ecotoxicology 2001;10: 25–34. Watts MM, Pascoe D, Carroll K. Survival and precopulatory behavior of Gammarus pulex (L.) exposed to two xenoestrogens. Water Res 2001;35:2347–52. Watts MM, Pascoe D, Carroll K. Exposure to 17α-ethinylestradiol and bisphenol A — effects on larval moulting and mouthpart structure of Chironomus riparius. Ecotoxicol Environ Saf 2003;54:207–15. Wright-Walters M, Volz C, Talbott E, Davis D. An updated weight of evidence approach to the aquatic hazard assessment of Bisphenol A and the derivation a new predicted no effect concentration (Pnec) using a non-parametric methodology. Sci Total Environ 2011;409:676–85.
Steven Hentges American Chemistry Council, Washington, DC Norbert Caspers Currenta, Leverkusen, Germany Gary M. Klecka The Dow Chemical Company, Midland, MI
Letter to the Editor
371
Ellen M. Mihaich
Charles A. Staples
ER2, on behalf of SABIC Innovative Plastics, Durham, NC
Assessment Technologies, Keswick, VA
Lisa Ortego
10 October 2011
DABT, Bayer CropScience, Research Triangle Park, NC
Contents lists available at SciVerse ScienceDirect
Science of the Total Environment journal homepage: www.elsevier.com/locate/scitotenv
Letter to the editor (Wright-Walters et al., 2011)
Dear Sir/Madam: We have read with interest the recent paper updating the aquatic hazard assessment of Bisphenol A (Wright-Walters et al., 2011). The paper developed a “new” predicted no effect concentration (PNEC) for Bisphenol A (BPA) of 0.06 μg/L for long term aquatic exposure to freshwater organisms. This new PNEC was calculated using the species sensitivity distribution (SSD) HC5 (lower 5th percentile hazard concentration) method of van der Hoeven (2001) with a large set of acute and chronic studies taken from published literature and unpublished sources. The new PNEC is considerably lower than other SSD-based HC5 values derived for BPA for use as a PNEC (Staples et al., 2008; EC, 2010). The HC5 values calculated by Staples et al. (2008) and EC (2010) are 18 and 7.5 μg/L, respectively. EC (2010) used a further assessment factor of 5 to arrive at a PNEC of 1.5 μg/L, while neither Staples et al. (2008) nor Wright-Walters et al. (2011) applied an assessment factor. Although different models were used, the differences between the HC5 values calculated by Staples et al. (2008), EC (2010) and Wright-Walters et al. (2011) are largely due to the use of different datasets. Wright-Walters et al. (2011) conducted literature searches to identify potentially relevant studies and also reportedly assessed the quality of each study. The resulting dataset is shown in Table 2 of the paper and includes 61 studies and 94 no observed effect concentrations (NOEC). Unfortunately, the dataset that resulted from this process and was used by Wright-Walters et al. (2011) to derive the PNEC is fraught with errors and omits a number of important studies. The result of the errors and omissions in the dataset is that the “new” PNEC calculated by Wright-Walters et al. (2011) is incorrect and should not be used to assess the hazard of BPA. The dataset assembled by Wright-Walters et al. (2011) includes values that do not exist in the specified studies. NOEC for Hydra vulgaris, Gammarus pulex, and Chironomus riparius of 0.002, 0.01 and 0.078 μg/L from Pascoe et al. (2002) and Watts et al. (2001, 2003) were cited by Wright-Walters et al. (2011), but these values are not in any of the published papers. Acute data were improperly included in the chronic toxicity dataset even though valid chronic data were available. For example, the Wright-Walters et al. (2011) dataset included a 96-h NOEC of 1400 μg/L from an acute lethality study with Chironomus tentans (Sayers, 2005), and an extended acute 14-d NOEC of 3200 μg/L with zebrafish (Bayer AG, 1999). Instead, the dataset should have included the valid chronic studies with the midge C. riparius and zebrafish that do exist for these species (Watts et al., 2003; Segner et al., 2003a). Studies were improperly included that lacked sufficient documentation to score their validity using procedures based on Klimisch et al. (1997). The studies reported by Fraunhofer (2000) and Segner et al. 0048-9697/$ – see front matter © 2012 Elsevier B.V. All rights reserved. doi:10.1016/j.scitotenv.2012.05.055
(2003b) with zebrafish, and Bowmer and Borst (1999) with carp are only summaries or abstracts that lack sufficient documentation of methodologies, control performance, statistical analyses, analytical chemistry measurements, and quality control results to assess their validity. Without adequate documentation of these aspects of each study, Klimisch scores of “4” must be assigned to them. Only studies with Klimisch scores of “1” or “2” should be used in hazard assessment. Studies with Klimisch scores of “3” (not valid) or “4” (unassignable due to insufficient documentation) generally should not be used in a hazard assessment. A number of poorly designed studies, such that the results reported cannot be properly interpreted, were included by Wright-Walters et al. (2011). Studies with the ramshorn snail Marisa cornuarietis reported by Oehlmann et al. (2000, 2006) should receive Klimisch scores of “3”, not valid, due to critical shortcomings in their design and conduct. As explained in a critical review by Dietrich et al. (2006) and in the European Union (EU) risk assessment (EC, 2010), these studies used pseudoreplication, had a high and varying density of test organisms, used improper statistics and, in some cases, lacked analytical verification of test concentrations. Because of these concerns and because of a general lack of information about the proper husbandry and life history of Marisa snails, a series of studies were conducted by Forbes et al. (Aufderheide et al., 2006; Selck et al., 2006; Forbes et al., 2007a, 2007b, 2008). The husbandry and life history information were used to aid in the design of the toxicity studies. The results from these fully valid studies with M. cornuarietis by Forbes et al. (validity scores of “1”) were excluded by Wright-Walters et al. (2011) but should be used to assess the chronic toxicity of BPA to Marisa snails. Forbes et al. (2008) reported a lowest NOEC of 25 μg/L for BPA in a 328 day lifecycle study with M. cornuarietis. Similarly, studies with the African clawed frog Xenopus laevis reported by Kloas et al. (1999) and Levy et al. (2004) used improper experimental design, employed incorrect statistical methods, and had other concerns that are documented by Pickford et al. (2003). Pickford et al. (2003) conducted studies with the same species using a robust study design, proper statistical analysis, measurement of test concentrations, and followed Good Laboratory Practices (GLP). Pickford et al. (2003) reported 90-d NOEC of 500 μg/L for several mortality, growth and development endpoints with X. laevis. In addition, the Wright-Walters et al. (2011) dataset included a study with brown trout by Lahnsteiner et al. (2005) that only examined non-apical endpoints related to sperm quality. As reviewed in the EU risk assessment (EC, 2010), the Lahnsteiner et al. (2005) study suffered from lack of replication, very small sample sizes, unclear experimental design, use of wild-caught fish, lack of husbandry conditions, unjustified endpoints, and lack of confirmation of sexual maturity of the fish, which caused the EU to assign a Klimisch score of “3” or not valid. None of the endpoints related to sperm quality reported by the authors were linked to any apical endpoint related to reproduction and thus are not useful for an assessment of long term chronic toxicity. While long term tests assessing reproduction are not available for brown trout, life-cycle tests are available for three other species of
370
Letter to the Editor
fish. AIST (2007) reported a 1.5 generation NOEC of 247 μg/L with Japanese medaka. Caunter (2000) reported a lowest NOEC of 16 μg/L in a multigeneration test with fathead minnow. Segner et al. (2003a) reported an EC50 of 1370 μg/L based on reproductive success in a life cycle study with zebrafish. In addition to the errors and omissions in the Wright-Walters et al. (2011) dataset described above, the authors made improper use of valid studies. The intent of the paper was to assess the hazard of BPA using a species sensitivity distribution (SSD) approach (van der Hoeven, 2001) and, therefore, a dataset of species-specific NOEC is needed. For each valid study, the lowest consistent and treatmentrelated NOEC among apical endpoints related to mortality, growth and development, and reproduction should be identified (EC, 2010; Staples et al., 2008). If more than one valid study exists for a species, the longest duration study should be used to represent that species. Thus, there should be one long-term NOEC for each species used in the SSD-based assessment. Wright-Walters et al. (2011) included multiple NOECs from each of numerous studies and included more than one study for several species. Doing so gives improper weight both to those studies with multiple NOECs and to those species with multiple studies. The SSD-based calculation method used by Wright-Walters et al. (2011) is the method developed by van der Hoeven (2001). The van der Hoeven (2001) paper states that the method “…can be applied from sample size 19 upwards.” Since this is a method to calculate a species sensitivity distribution, this statement means that 19 or more species are needed to apply this method. As documented in the hazard assessments reported by EC (2010), and Staples et al. (2008), there are valid chronic toxicity studies available for approximately 16 freshwater species representing 10 different taxonomic groups. Thus, the sample size is too small to use the van der Hoeven (2001) method to calculate an SSD-based HC5 value for use as a PNEC for BPA. There are other statistical methods available to calculate SSD-based HC5 values and these have been successfully used to do so (EC, 2010; RIVM, 2004; Staples et al., 2008). The exact SSD-based HC5 value that is calculated will be influenced both by the model that is chosen and the dataset that is modeled. The choice of the SSD model requires that the user understand and follow the underlying requirements of the model. The specific aquatic toxicity dataset used with the SSD model to calculate HC5 values for use as PNEC should be assembled so that only valid studies are included, that each valid study has a lowest NOEC based on apical endpoints, and that each genus/species has a representative NOEC. Because of the numerous errors contained in the dataset used by Wright-Walters et al. (2011), their omission of other high quality relevant studies, and their inappropriate use of the van der Hoeven SSD modeling method, their “new” PNEC should not be used to assess the long term aquatic hazard of BPA. References AIST. AIST risk assessment document series no. 4 bisphenol A. Tsukuba, Ibaraki, Japan: National Institute of Advanced Industrial Science and Technology (AIST), Research Center for Chemical Risk Management; 2007. November, 2007. Aufderheide J, Warbritton R, Pounds N, File-Emperador S, Staples C, Caspers N, et al. Effects of husbandry parameters on the life-history traits of the apple snail, Marisa cornuarietis: effects of temperature, photoperiod, and population density. Invertebr Biol 2006;125:9-20. Bayer AG. Fish, prolonged toxicity test (Brachydanio rerio) 14 day study of bisphenol A. Study number 707 A/98 F1, Leverkusen, Germany; 1999. Bowmer T, Borst B. Environmental risk assessment of endocrine active substances — a reality? International Symposium on Environmental Endocrine Disruptors 1999. Extended Abstract, December 9-11, 1999. Kobe, Japan; 1999. p. 85–8. Caunter JE. Bisphenol A: multigeneration study with fathead minnow (Pimephales promelas). Report no. BL6878/B. Brixham, Devon, UK: Brixham Environmental Laboratory, AstraZeneca UK Ltd.; 2000. Dietrich DR, O'Brien E, Hoffmann S, Balaguer P, Nicolas J-C, Seinen W, et al. Effects of BPA in snails. Environ Health Perspect 2006;114:A340–1. EC (European Commission). Updated European Union risk assessment report; 4,4'-isopropylidenediphenol (bisphenol-A); CAS number: 80-05-7; EINECS number:
201-245-8; environment addendum of February 2008. 2010. http://esis.jrc.ec.europa. eu. (accessed June 5, 2012). Forbes VE, Selck H, Palmqvist A, Aufderheide J, Warbritton R, Pounds N, et al. Does bisphenol A induce superfeminization in Marisa cornuarietis? Part I: intra- and inter-laboratory variability in test endpoints. Ecotoxicol Environ Saf 2007a;66: 309–18. Forbes VE, Aufderheide J, Warbritton R, van der Hoeven N, Caspers N. Does bisphenol A induce superfeminization in Marisa cornuarietis? Part II: toxicity test results and requirements for statistical power analyses. Ecotoxicol Environ Saf 2007b;66: 319–25. Forbes VE, Warbritton R, Aufderheide J, van der Hoeven N, Caspers N. Effects of bisphenol A on fecundity, egg hatchability, and juvenile growth of Marisa cornuarietis. Environ Toxicol Chem 2008;27:2332–40. Fraunhofer (Fraunhofer Institute of Environmental Chemistry and Ecotoxicology). Der Einfluss von Xeno-oestrogenen auf den Lebenszyklus von Fischen. Annual Report 2000, Schmallenberg, Germany; 2000. p. 32–3. Klimisch H-J, Andreae M, Tillmann U. A systematic approach for evaluating the quality of experimental toxicological and ecotoxicological data. Regul Toxicol Pharmacol 1997;25:1–5. Kloas W, Lutz I, Einspanier R. Amphibians as a model to study endocrine disruptors: II. Estrogenic activity of environmental chemicals in vitro and in vivo. Sci Total Environ 1999;225:59–68. Lahnsteiner F, Berger B, Kletzl M, Weismann T. Effect of bisphenol A on maturation and quality of semen and eggs in the brown trout, Salmo trutta f. fario. Aquat Toxicol 2005;75:213–24. Levy G, Lutz I, Kruger A, Kloas W. Bisphenol A induces feminization in Xenopus laevis tadpoles. Environ Res 2004;94:102–11. Oehlmann J, Schulte-Oehlmann U, Tillmann M, Markert B. Effects of endocrine disruptors on prosobranch snails (Mollusca: Gastropoda) in the laboratory. Part I: bisphenol A and octylphenol. Ecotoxicology 2000;9:383–97. Oehlmann J, Schulte-Oehlmann U, Bachmann J, Oetken M, Lutz I, Kloas W, et al. Bisphenol A induces superfeminization in the ramshorn snail Marisa cornuarietis (Gastropoda: Prosobranchia) at environmentally-relevant concentrations. Environ Health Perspect 2006;114(Supplement 1):127–33. Pascoe D, Carroll K, Karntanut W, Watts MM. Toxicity of 17-ethinylestradiol and bisphenol A to the freshwater cnidarian Hydra vulgaris. Arch Environ Contam Toxicol 2002;43:56–63. Pickford DB, Hetheridge MJ, Caunter JE, Hall AT, Hutchinson TH. Assessing chronic toxicity of bisphenol A to larvae of the African clawed frog (Xenopus laevis) in a flow-through exposure system. Chemosphere 2003;53:223–35. RIVM (The Netherlands National Institute of Public Health and the Environment). ETX 2.0. Bilthoven, The Netherlands; 2004. Sayers LE. Bisphenol A (BPA) — acute toxicity to midges (Chironomus tentans) under flow-through conditions. Report no. 13796.6107. Wareham, MA, USA: Springborn Smithers Laboratories, Inc.; 2005. Segner H, Navas JM, Schaefers C, Wenzel A. Potencies of estrogenic compounds in in vitro screening assays and in life cycle tests with zebrafish in vivo. Ecotoxicol Environ Saf 2003a;54:315–22. Segner H, Caroll K, Fenske M, Janssen CT, Maack CG, Pascoe A. Identification of endocrine disrupting effects in aquatic vertebrates and invertebrates: report from the European IDEA project. Ecotoxicol Environ Saf 2003b;54: 302–14. Selck H, Aufderheide J, Pounds N, Staples C, Caspers N, Forbes V. Effects of food type, feeding frequency, and temperature on juvenile survival and growth of Marisa cornuarietis (Mollusca: Gastropods). Invertebr Biol 2006;125: 106–16. Staples CA, Woodburn KB, Klecka GM, Mihaich EM, Hall AT, Ortego L, et al. Comparison of four species sensitivity distribution methods to calculate predicted no effect concentrations for bisphenol A. Hum Ecol Risk Assess 2008;14: 455–78. van der Hoeven N. Estimating the 5-percentile of the species sensitivity distributions without any assumptions about the distribution. Ecotoxicology 2001;10: 25–34. Watts MM, Pascoe D, Carroll K. Survival and precopulatory behavior of Gammarus pulex (L.) exposed to two xenoestrogens. Water Res 2001;35:2347–52. Watts MM, Pascoe D, Carroll K. Exposure to 17α-ethinylestradiol and bisphenol A — effects on larval moulting and mouthpart structure of Chironomus riparius. Ecotoxicol Environ Saf 2003;54:207–15. Wright-Walters M, Volz C, Talbott E, Davis D. An updated weight of evidence approach to the aquatic hazard assessment of Bisphenol A and the derivation a new predicted no effect concentration (Pnec) using a non-parametric methodology. Sci Total Environ 2011;409:676–85.
Steven Hentges American Chemistry Council, Washington, DC Norbert Caspers Currenta, Leverkusen, Germany Gary M. Klecka The Dow Chemical Company, Midland, MI
Letter to the Editor
371
Ellen M. Mihaich
Charles A. Staples
ER2, on behalf of SABIC Innovative Plastics, Durham, NC
Assessment Technologies, Keswick, VA
Lisa Ortego
10 October 2011
DABT, Bayer CropScience, Research Triangle Park, NC