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• W2335163225 abstract "Vol. 124, No. 3 CorrespondenceOpen AccessComment on “Effects of in Utero Exposure to Arsenic during the Second Half of Gestation on Reproductive End Points and Metabolic Parameters in Female CD-1 Mice” Amy L. Williams and John M. DeSesso Amy L. Williams †Address correspondence to A.L. Williams, Exponent, Inc., 1800 Diagonal Rd., Ste. 500, Alexandria, VA 22314 USA. E-mail: E-mail Address: [email protected] Search for more papers by this author and John M. DeSesso Search for more papers by this author Published:1 March 2016https://doi.org/10.1289/ehp.1511031AboutSectionsPDF ToolsDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InReddit Rodriguez et al. recently reported that the adult female offspring of pregnant CD-1 mice exposed to 10 ppb or 42.5 ppm arsenic (As) exhibited reproductive and metabolic effects. These findings are not consistent with those of others working in this field and did not show a dose response. As such, we urge caution against drawing conclusions based on this single study.Rodriguez et al. reported that on postnatal day 21, female offspring in the 10-ppb and 42.5-ppm dose groups were approximately 11% and 7% heavier, respectively, than controls. At 6 months of age, the treated female offspring were ≥ 22% (the exact percentages are unclear from the study report) heavier than controls. The study authors mention data from other investigators using C57BL6/J mice showing no effects of gestational As exposure on offspring body weight (Ramsey et al. 2013; Kozul-Horvath et al. 2012). Other studies using a similar exposure paradigm also reported no effects on body weight of the female offspring of C3H mice (Waalkes et al. 2003, 2004), C57BL6/J mice (Markowski et al. 2011, 2012), or Tg.AC mice (Tokar et al. 2010).The authors suggest that discrepancies between their results and those of others may be due to differences in the genetic background of the mice in the various studies. However, Waalkes et al. (2006) conducted a study in pregnant CD-1 mice exposed to 0 or 85 ppm sodium arsenite from gestational day (GD) 8 to GD18 with no effects of treatment on female offspring body weight. In another study (Tokar et al. 2011) involving whole-life exposure (from preconception into adulthood) of CD-1 mice to 6, 12, or 24 ppm sodium arsenite, body weights of treated mice were similar to those of controls at all time points assessed. It is also interesting to note that controls in the study by Tokar et al. (2011) weighed considerably more (42.4 g at 25 weeks of age) than controls in the Rodriguez et al. study (approximately 34.4 g at 26 weeks of age).The reason for this discrepancy between the findings of Rodriguez et al. and those of other investigators is not known but may relate to differences in diet or husbandry. Alternatively, it is possible that the controls in the study by Rodriguez et al. are unusually small for their age, such that the observed effect of treatment may be a statistical anomaly; this could explain why a dose-related difference was not observed.Rodriguez et al. also reported that both doses of As were associated with early vaginal opening; again, no dose response was evident. The authors mention the results of two other studies in their discussion—both of which showed delays in puberty rather than early onset (Reilly et al. 2014; Davila-Esqueda et al. 2012). We identified two other studies that examined vaginal opening with gestational-only As exposure. Markowski et al. (2012) exposed pregnant C57BL6/J mice to 0, 8, 25, or 80 ppm sodium arsenite from GD4 until birth with no effects on the onset of puberty. Gandhi et al. (2012) exposed pregnant albino rats to 0, 1.5, 3, or 4.5 mg As/kg/day from GD8 until birth; again, no effects on vaginal opening were observed.The onset of puberty is positively correlated with body weight (Carney et al. 2004). Unfortunately, Rodriguez et al. did not report the mean weights at vaginal opening; therefore, we do not know if the early vaginal opening in the As-treated groups may have been a function of the increased body weights. However, animals in the 10-ppb and 42.5-ppm groups weighed more than controls and thus were likely to reach puberty earlier than controls.In closing, the findings of Rodriguez et al. with regard to body weight and pubertal effects conflict with those of other investigators. Until other investigators can replicate the results reported by Rodriguez et al., we believe these findings should be viewed with extreme caution.Financial support for this analysis was provided in part by the Arsenic Science Task Force. The analysis and conclusions presented in this letter are those of the authors.ReferencesCarney EW, Zablotny CL, Marty MS, Crissman JW, Anderson P, Woolhiser Met al.. 2004. The effects of feed restriction during in utero and postnatal development in rats.Toxicol Sci 82(1):237-249, PMID:15310860. Crossref, Medline, Google ScholarDavila-Esqueda ME, Jiménez-Capdeville ME, Delgado JM, De la Cruz E, Aradillas-García C, Jiménez-Suárez Vet al.. 2012. Effects of arsenic exposure during the pre- and postnatal development on the puberty of female offspring.Exp Toxicol Pathol 64(1–2):25-30, doi:10.1016/j.etp.2010.06.00120580540. Crossref, Medline, Google ScholarGandhi DN, Panchal GM, Patel KG. 2012. Developmental and neurobehavioural toxicity study of arsenic on rats following gestational exposure.Indian J Exp Biol 50(2):147-155, PMID:22670478. Medline, Google ScholarKozul-Horvath CD, Zandbergen F, Jackson BP, Enelow RI, Hamilton JW. 2012. 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In utero exposure to low dose arsenic via drinking water impairs early life lung mechanics in mice.BMC Pharmacol Toxicol 14:13, doi:10.1186/2050-6511-14-1323419080. Crossref, Medline, Google ScholarReilly MP, Saca JC, Hamilton A, Solano RF, Rivera JR, Whitehouse-Innis Wet al.. 2014. Prepubertal exposure to arsenic(III) suppresses circulating insulin-like growth factor-1 (IGF-1) delaying sexual maturation in female rats.Reprod Toxicol 44:41-49, doi:10.1016/j.reprotox.2013.09.00524090629. Crossref, Medline, Google ScholarTokar EJ, Diwan BA, Waalkes MP. 2010. Arsenic exposure in utero and nonepidermal proliferative reponse in adulthood in Tg.AC mice.Int J Toxicol 29(3):291-296, doi:10.1177/109158181036280420448261. Crossref, Medline, Google ScholarTokar EJ, Diwan BA, Ward JM, Delker DA, Waalkes MP. 2011. Carcinogenic effects of “whole life” exposure to inorganic arsenic in CD1 mice.Toxicol Sci 119(1):73-83, doi:10.1093/toxsci/kfq31520937726. Crossref, Medline, Google ScholarWaalkes MP, Liu J, Ward JM, Powell DA, Diwan BA. 2006. Urogenital carcinogenesis in female CD1 mice induced by in utero arsenic exposure is exacerbated by postnatal diethylstilbestrol treatment.Cancer Res 66(3):1337-1345, doi:10.1158/0008-5472.CAN-05-353016452187. Crossref, Medline, Google ScholarWaalkes MP, Ward JM, Diwan BA. 2004. Induction of tumors of the liver, lung, ovary and adrenal in adult mice after brief maternal gestational exposure to inorganic arsenic: promotional effects of postnatal phorbol ester exposure on hepatic and pulmonary, but not dermal cancers.Carcinogenesis 25(1):133-141, doi:10.1093/carcin/bgg18114514661. Crossref, Medline, Google ScholarWaalkes MP, Ward JM, Liu J, Diwan BA. 2003. Transplacental carcinogenicity of inorganic arsenic in the drinking water: induction of hepatic, ovarian, pulmonary, and adrenal tumors in mice.Toxicol Appl Pharmacol 186(1):7-17, doi:10.1016/S0041-008X(02)00022-412583988. Crossref, Medline, Google ScholarFiguresReferencesRelatedDetails Vol. 124, No. 3 March 2016Metrics About Article Metrics Publication History Originally published1 March 2016Published in print1 March 2016 Financial disclosuresPDF download License information EHP is an open-access journal published with support from the National Institute of Environmental Health Sciences, National Institutes of Health. All content is public domain unless otherwise noted. Note to readers with disabilities EHP strives to ensure that all journal content is accessible to all readers. However, some figures and Supplemental Material published in EHP articles may not conform to 508 standards due to the complexity of the information being presented. If you need assistance accessing journal content, please contact [email protected]. Our staff will work with you to assess and meet your accessibility needs within 3 working days." @default.
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