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• W2410009112 abstract "Vol. 124, No. 6 CorrespondenceOpen AccessComment on “Effects of Arsenite during Fetal Development on Energy Metabolism and Susceptibility to Diet-Induced Fatty Liver Diseases in Male Mice” and “Mechanisms Underlying Latent Disease Risk Associated with Early-Life Arsenic Exposure: Current Trends and Scientific Gaps” Paul A. Fowler, Amanda J. Drake, Peter J. O’Shaughnessy, Siladitya Bhattacharya, Andrea Raab, Kevin D. Sinclair, Jörg Feldmann, and Andrew A. Meharg Paul A. Fowler †Address correspondence to P.A. Fowler, Institute of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen, AB25 2ZD, United Kingdom. E-mail: E-mail Address: [email protected] Institute of Medical Sciences, University of Aberdeen, Aberdeen, United Kingdom Search for more papers by this author , Amanda J. Drake University/BHF Centre for Cardiovascular Science, University of Edinburgh, Queen’s Medical Research Institute, Edinburgh, United Kingdom Search for more papers by this author , Peter J. O’Shaughnessy Institute of Biodiversity, Animal Health and Comparative Medicine, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, United Kingdom Search for more papers by this author , Siladitya Bhattacharya Institute of Applied Health Sciences, University of Aberdeen, Aberdeen, United Kingdom Search for more papers by this author , Andrea Raab TESLA (Trace Element Speciation Laboratory) and Marine Biodiscovery Laboratory, University of Aberdeen, Aberdeen, United Kingdom Search for more papers by this author , Kevin D. Sinclair School of Biosciences, Sutton Bonington Campus, University of Nottingham, Loughborough, United Kingdom Search for more papers by this author , Jörg Feldmann TESLA (Trace Element Speciation Laboratory) and Marine Biodiscovery Laboratory, University of Aberdeen, Aberdeen, United Kingdom Search for more papers by this author , and Andrew A. Meharg Institute for Global Food Security, Queen’s University Belfast, Belfast, United Kingdom Search for more papers by this author Published:1 June 2016https://doi.org/10.1289/ehp.1611345Cited by:1AboutSectionsPDF ToolsDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InReddit We were very interested to read the excellent article and commentary on arsenic and health, with respect to prenatal exposures, metabolic health, and underlying mechanisms, by Ditzel et al. and Bailey et al. For many years there have been growing concerns as knowledge accumulates about the long-term consequences of early-life influences on adult health (Fleming et al. 2015), including environmental programming resulting from prenatal exposure to arsenic (Farzan et al. 2013). These concerns rightly extend to metabolic consequences for the offspring (Ashley-Martin et al. 2015) and also encompass epigenetic modifications as a result of developmental exposures to arsenic and other metals (Bailey and Fry 2014).The elephant in the room, however, is the paucity of knowledge about what is happening to the human fetus early in gestation. A great deal of emphasis is placed on levels of toxicants in maternal urine or plasma, and on levels in the offspring at term (usually in cord blood), which is then often mislabeled as “fetal.”Last year we published a study of 55 normally progressing, electively terminated second-trimester human fetuses where changes in fetal hepatic cobalt levels were traced through vitamin B12 to changes in one-carbon metabolism and alterations in DNA methylation (Drake et al. 2015). We also characterized hepatic concentrations of essential and nonessential elements. Maternal smoking was validated by measuring circulating fetal cotinine, and we were surprised to find no increase in the number of fetal livers with cadmium levels above limits of detection when the mother smoked (only 5 of 55 fetuses had hepatic levels of cadmium above limits of detection, irrespective of smoke exposure) (Drake et al. 2015), despite a known increase in maternal cadmium levels with smoking (Sikorski et al. 1988). This clearly demonstrates the importance of studying fetal toxicant burden in our own species rather than simply making assumptions from animal models.Relevant to Ditzel et al. and Bailey et al., we also published fetal hepatic arsenic concentrations and found levels above limits of detection in 39 of 55 fetuses, with a median arsenic concentration of 39.8 ng/g dry liver weight (Drake et al. 2015). As with cadmium, maternal smoking did not significantly alter fetal hepatic levels of arsenic, and arsenic concentrations did not change between 11 and 21 weeks of gestation. These kinds of “real-life” human fetal data are essential to improve our understanding of the risks to the developing human, the points during gestation when those risks are most acute, and the key underlying mechanisms.Editor’s note: In accordance with journal policy, Ditzel et al. and Fry et al. were asked whether they wanted to respond to this letter. Neither group chose to do so.The authors declare they have no actual or potential competing financial interests.ReferencesAshley-Martin J, Dodds L, Arbuckle TE, Ettinger AS, Shapiro GD, Fisher Met al.. 2015. Maternal blood metal levels and fetal markers of metabolic function.Environ Res 136:27-34, doi:10.1016/j.envres.2014.10.02425460617. Crossref, Medline, Google ScholarBailey KA, Fry RC. 2014. Arsenic-associated changes to the epigenome: what are the functional consequences?Curr Environ Health Rep 1:22-34, doi:10.1007/s40572-013-0002-824860721. Crossref, Medline, Google ScholarDrake AJ, O’Shaughnessy PJ, Bhattacharya S, Monteiro A, Kerrigan D, Goetz Set al.. 2015. In utero exposure to cigarette chemicals induces sex-specific disruption of one-carbon metabolism and DNA methylation in the human fetal liver.BMC Med 13:18, doi:10.1186/s12916-014-0251-x25630355. Crossref, Medline, Google ScholarFarzan SF, Karagas MR, Chen Y. 2013. In utero and early life arsenic exposure in relation to long-term health and disease.Toxicol Appl Pharmacol 272(2):384-390, doi:10.1016/j.taap.2013.06.03023859881. Crossref, Medline, Google ScholarFleming TP, Velazquez MA, Eckert JJ. 2015. Embryos, DOHaD and David Barker.J Dev Orig Health Dis 6(5):377-383, doi:10.1017/S204017441500110525952250. Crossref, Medline, Google ScholarSikorski R, Radomański T, Paszkowski T, Skoda J. 1988. Smoking during pregnancy and the perinatal cadmium burden.J Perinat Med 16(3):225-231, PMID: 3210108. Crossref, Medline, Google ScholarFiguresReferencesRelatedDetailsCited by Treviño L and Katz T (2017) Endocrine Disruptors and Developmental Origins of Nonalcoholic Fatty Liver Disease, Endocrinology, 10.1210/en.2017-00887, 159:1, (20-31), Online publication date: 1-Jan-2018. Vol. 124, No. 6 June 2016Metrics About Article Metrics Publication History Originally published1 June 2016Published in print1 June 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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