Abstract
Purpose of Review
This review summarizes studies highlighting perfluoroalkyl substances (PFAS) and their effects on the placenta, pregnancy outcomes, and child health. It highlights human population-based associations as well as in vitro-based experimental data to inform an understanding of the molecular mechanisms underlying these health effects. Among the mechanisms by which PFAS may induce toxicity is via their interaction with the peroxisome proliferator-activated receptors (PPARs), nuclear receptors that regulate lipid metabolism and placental functions important to healthy pregnancies, as well as fetal and child development.
Recent Findings
In utero exposure to prevalent environmental contaminants such as PFAS is associated with negative health outcomes during pregnancy, birth outcomes, and later in life. Specifically, PFAS have been associated with increased incidence of gestational diabetes, childhood obesity, preeclampsia, and fetal growth restriction. In terms of placental molecular mechanisms underlying these associations, studies demonstrate that PFAS interfere with trophoblast lipid homeostasis, inflammation, and invasion. Moreover these effects could be mediated in part by the interaction between PFAS and PPARs, as well as other biological mechanisms.
Summary
This review summarizes how PFAS, critical environmental contaminants, may contribute to diseases of pregnancy as well as early and later child health.
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References
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Burton GJ, Jauniaux E. Pathophysiology of placental-derived fetal growth restriction. Am J Obstet Gynecol. 2018;218(2s):S745–s61.
Tetro N, Moushaev S, Rubinchik-Stern M, Eyal S. The placental barrier: the gate and the fate in drug distribution. Pharm Res. 2018;35(4):71.
Zheng T, Zhang J, Sommer K, Bassig BA, Zhang X, Braun J, et al. Effects of environmental exposures on fetal and childhood growth trajectories. Ann Glob Health. 2016;82(1):41–99.
Sajid M, Ilyas M. PTFE-coated non-stick cookware and toxicity concerns: a perspective. Environ Sci Pollut Res Int. 2017;24(30):23436–40.
Renner R. Canada eyes limits on nonstick chemicals. Environ Sci Technol. 2006;40(16):4818.
Kovarova J, Svobodova Z. Perfluorinated compounds: occurrence and risk profile. Neuro Endocrinol Lett. 2008;29(5):599–608.
Rayne S, Forest K. Perfluoroalkyl sulfonic and carboxylic acids: a critical review of physicochemical properties, levels and patterns in waters and wastewaters, and treatment methods. J Environ Sci Health A Tox Hazard Subst Environ Eng. 2009;44(12):1145–99.
Huang Q, Chen Q. Mediating roles of PPARs in the effects of environmental chemicals on sex steroids. PPAR Res. 2017;2017:3203161.
Kleszczynski K, Skladanowski AC. Mechanism of cytotoxic action of perfluorinated acids. I. Alteration in plasma membrane potential and intracellular pH level. Toxicol Appl Pharmacol. 2009;234(3):300–5.
Kleszczynski K, Stepnowski P, Skladanowski AC. Mechanism of cytotoxic action of perfluorinated acids II. Disruption of mitochondrial bioenergetics. Toxicol Appl Pharmacol. 2009;235(2):182–90.
Kleszczynski K, Skladanowski AC. Mechanism of cytotoxic action of perfluorinated acids. III. Disturbance in Ca(2)+ homeostasis. Toxicol Appl Pharmacol. 2011;251(2):163–8.
•• DeWitt JC, Blossom SJ, Schaider LA. Exposure to per-fluoroalkyl and polyfluoroalkyl substances leads to immunotoxicity: epidemiological and toxicological evidence. J Exp Sci Environ Epidemiol. 2019;29(2):148–56 This review provides a detailed description of the immunosupressive effects of PFAS. This effects are demonstrated across both in vivo and in vitro studies.
Abbott BD, Wolf CJ, Das KP, Zehr RD, Schmid JE, Lindstrom AB, et al. Developmental toxicity of perfluorooctane sulfonate (PFOS) is not dependent on expression of peroxisome proliferator activated receptor-alpha (PPAR alpha) in the mouse. Reprod Toxicol (Elmsford, NY). 2009;27(3–4):258–65.
Abbott BD, Wood CR, Watkins AM, Tatum-Gibbs K, Das KP, Lau C. Effects of perfluorooctanoic acid (PFOA) on expression of peroxisome proliferator-activated receptors (PPAR) and nuclear receptor-regulated genes in fetal and postnatal CD-1 mouse tissues. Reprod Toxicol (Elmsford, NY). 2012;33(4):491–505.
Cwinn MA, Jones SP, Kennedy SW. Exposure to perfluorooctane sulfonate or fenofibrate causes PPAR-alpha dependent transcriptional responses in chicken embryo hepatocytes. Comp Biochem Physiol Toxicol Pharmacol. 2008;148(2):165–71.
Jiang Q, Lust RM, DeWitt JC. Perfluorooctanoic acid induced-developmental cardiotoxicity: are peroxisome proliferator activated receptor alpha (PPARalpha) and bone morphorgenic protein 2 (BMP2) pathways involved? J Toxicol Environ Health Part A. 2013;76(11):635–50.
Mattsson A, Karrman A, Pinto R, Brunstrom B. Metabolic profiling of chicken embryos exposed to perfluorooctanoic acid (PFOA) and agonists to peroxisome proliferator-activated receptors. PLoS One. 2015;10(12):e0143780.
Ren H, Vallanat B, Nelson DM, Yeung LW, Guruge KS, Lam PK, et al. Evidence for the involvement of xenobiotic-responsive nuclear receptors in transcriptional effects upon perfluoroalkyl acid exposure in diverse species. Reprod Toxicol (Elmsford, NY). 2009;27(3–4):266–77.
Takacs ML, Abbott BD. Activation of mouse and human peroxisome proliferator-activated receptors (alpha, beta/delta, gamma) by perfluorooctanoic acid and perfluorooctane sulfonate. Toxicol Sci. 2007;95(1):108–17.
Tsang H, Cheung TY, Kodithuwakku SP, Chai J, Yeung WS, Wong CK, et al. Perfluorooctanoate suppresses spheroid attachment on endometrial epithelial cells through peroxisome proliferator-activated receptor alpha and down-regulation of Wnt signaling. Reprod Toxicol (Elmsford, NY). 2013;42:164–71.
Watkins AM, Wood CR, Lin MT, Abbott BD. The effects of perfluorinated chemicals on adipocyte differentiation in vitro. Mol Cell Endocrinol. 2015;400:90–101.
Yamamoto J, Yamane T, Oishi Y, Kobayashi-Hattori K. Perfluorooctanoic acid binds to peroxisome proliferator-activated receptor gamma and promotes adipocyte differentiation in 3T3-L1 adipocytes. Biosci Biotechnol Biochem. 2015;79(4):636–9.
Zhao M, Jiang Q, Geng M, Zhu L, Xia Y, Khanal A, et al. The role of PPAR alpha in perfluorooctanoic acid induced developmental cardiotoxicity and l-carnitine mediated protection—results of in ovo gene silencing. Environ Toxicol Pharmacol. 2017;56:136–44.
Han L, Shen W-J, Bittner S, Kraemer FB, Azhar S. PPARs: regulators of metabolism and as therapeutic targets in cardiovascular disease. Part II: PPAR-β/δ and PPAR-γ. Futur Cardiol. 2017;13(3):279–96.
Nadra K, Quignodon L, Sardella C, Joye E, Mucciolo A, Chrast R, et al. PPARgamma in placental angiogenesis. Endocrinology. 2010;151(10):4969–81.
Fournier T, Tsatsaris V, Handschuh K, Evain-Brion D. PPARs and the placenta. Placenta. 2007;28(2–3):65–76.
Lendvai A, Deutsch MJ, Plosch T, Ensenauer R. The peroxisome proliferator-activated receptors under epigenetic control in placental metabolism and fetal development. Am J Physiol Endocrinol Metab. 2016;310(10):E797–810.
Qiao L, Wattez JS, Lee S, Guo Z, Schaack J, Hay WW Jr, et al. Knockout maternal adiponectin increases fetal growth in mice: potential role for trophoblast IGFBP-1. Diabetologia. 2016;59(11):2417–25.
Tarrade A, Schoonjans K, Guibourdenche J, Bidart JM, Vidaud M, Auwerx J, et al. PPAR gamma/RXR alpha heterodimers are involved in human CG beta synthesis and human trophoblast differentiation. Endocrinology. 2001;142(10):4504–14.
Holdsworth-Carson SJ, Lim R, Mitton A, Whitehead C, Rice GE, Permezel M, et al. Peroxisome proliferator-activated receptors are altered in pathologies of the human placenta: gestational diabetes mellitus, intrauterine growth restriction and preeclampsia. Placenta. 2010;31(3):222–9.
Wen X, Baker AA, Klaassen CD, Corton JC, Richardson JR, Aleksunes LM. Hepatic carboxylesterases are differentially regulated in PPARalpha-null mice treated with perfluorooctanoic acid. Toxicology. 2019;416:15–22.
Bjork JA, Butenhoff JL, Wallace KB. Multiplicity of nuclear receptor activation by PFOA and PFOS in primary human and rodent hepatocytes. Toxicology. 2011;288(1–3):8–17.
Shoaff J, Papandonatos GD, Calafat AM, Chen A, Lanphear BP, Ehrlich S, et al. Prenatal exposure to perfluoroalkyl substances: infant birth weight and early life growth. Environ Epidemiol. 2018;2(2):e010.
Rappazzo KM, Coffman E, Hines EP. Exposure to perfluorinated alkyl substances and health outcomes in children: a systematic review of the epidemiologic literature. Int J Environ Res Public Health. 2017;14(7):691.
Ballesteros V, Costa O, Iniguez C, Fletcher T, Ballester F, Lopez-Espinosa MJ. Exposure to perfluoroalkyl substances and thyroid function in pregnant women and children: a systematic review of epidemiologic studies. Environ Int. 2017;99:15–28.
Bach CC, Bech BH, Brix N, Nohr EA, Bonde JP, Henriksen TB. Perfluoroalkyl and polyfluoroalkyl substances and human fetal growth: a systematic review. Crit Rev Toxicol. 2015;45(1):53–67.
Leddy MA, Power ML, Schulkin J. The impact of maternal obesity on maternal and fetal health. Rev Obstet Gynecol. 2008;1(4):170–8.
Heindel JJ, Blumberg B. Environmental obesogens: mechanisms and controversies. Annu Rev Pharmacol Toxicol. 2019;59:89–106.
Mack LR, Tomich PG. Gestational diabetes: diagnosis, classification, and clinical care. Obstet Gynecol Clin N Am. 2017;44(2):207–17.
Rahman ML, Zhang C, Smarr MM, Lee S, Honda M, Kannan K, et al. Persistent organic pollutants and gestational diabetes: a multi-center prospective cohort study of healthy US women. Environ Int. 2019;124:249–58.
Jensen RC, Glintborg D, Timmermann CAG, Nielsen F, Kyhl HB, Andersen HR, et al. Perfluoroalkyl substances and glycemic status in pregnant Danish women: the Odense child cohort. Environ Int. 2018;116:101–7.
Gao Y, She R, Sha W. Gestational diabetes mellitus is associated with decreased adipose and placenta peroxisome proliferator-activator receptor gamma expression in a Chinese population. Oncotarget. 2017;8(69):113928–37.
Rong C, Cui X, Chen J, Qian Y, Jia R, Hu Y. DNA methylation profiles in placenta and its association with gestational diabetes mellitus. Exp Clin Endocrinol Diabetes. 2015;123(5):282–8.
Hales CM, Carroll MD, Fryar CD, Ogden CL. Prevalence of obesity among adults and youth: United States, 2015-2016. NCHS Data Brief. 2017;(288):1–8.
Tang-Peronard JL, Heitmann BL, Andersen HR, Steuerwald U, Grandjean P, Weihe P, et al. Association between prenatal polychlorinated biphenyl exposure and obesity development at ages 5 and 7 y: a prospective cohort study of 656 children from the Faroe Islands. Am J Clin Nutr. 2014;99(1):5–13.
Henriquez-Hernandez LA, Luzardo OP, Valeron PF, Zumbado M, Serra-Majem L, Camacho M, et al. Persistent organic pollutants and risk of diabetes and obesity on healthy adults: results from a cross-sectional study in Spain. Sci Total Environ. 2017;607–608:1096–102.
Donat-Vargas C, Gea A, Sayon-Orea C, Carlos S, Martinez-Gonzalez MA, Bes-Rastrollo M. Association between dietary intakes of PCBs and the risk of obesity: the SUN project. J Epidemiol Community Health. 2014;68(9):834–41.
•• Mora AM, Oken E, Rifas-Shiman SL, Webster TF, Gillman MW, Calafat AM, et al. Prenatal exposure to perfluoroalkyl substances and adiposity in early and mid-childhood. Environ Health Perspect. 2017;125(3):467–73 This study examines the association of PFAS concentrations in plasma during pregnancy with child health outcomes in the Project Viva cohort in Massachusettes. PFAS concentrations during pregnancy were associated with child adiposity at 3 and 8 years old in the Project Viva cohort in Massachusettes.
Chen Q, Zhang X, Zhao Y, Lu W, Wu J, Zhao S, et al. Prenatal exposure to perfluorobutanesulfonic acid and childhood adiposity: a prospective birth cohort study in Shanghai, China. Chemosphere. 2019;226:17–23.
Braun JM, Chen A, Romano ME, Calafat AM, Webster GM, Yolton K, et al. Prenatal perfluoroalkyl substance exposure and child adiposity at 8 years of age: the HOME study. Obesity (Silver Spring). 2016;24(1):231–7.
Starling AP, Adgate JL, Hamman RF, Kechris K, Calafat AM, Dabelea D. Prenatal exposure to per- and polyfluoroalkyl substances and infant growth and adiposity: the Healthy Start Study. Environ Int. 2019;131:104983.
Hartman TJ, Calafat AM, Holmes AK, Marcus M, Northstone K, Flanders WD, et al. Prenatal exposure to perfluoroalkyl substances and body fatness in girls. Childhood Obes (Print). 2017;13(3):222–30.
Manzano-Salgado CB, Casas M, Lopez-Espinosa MJ, Ballester F, Iniguez C, Martinez D, et al. Prenatal exposure to perfluoroalkyl substances and cardiometabolic risk in children from the Spanish INMA Birth Cohort Study. Environ Health Perspect. 2017;125(9):097018.
Li X, Ycaza J, Blumberg B. The environmental obesogen tributyltin chloride acts via peroxisome proliferator activated receptor gamma to induce adipogenesis in murine 3T3-L1 preadipocytes. J Steroid Biochem Mol Biol. 2011;127(1–2):9–15.
Burton GJ, Fowden AL, Thornburg KL. Placental origins of chronic disease. Physiol Rev. 2016;96(4):1509–65.
Gorrochategui E, Perez-Albaladejo E, Casas J, Lacorte S, Porte C. Perfluorinated chemicals: differential toxicity, inhibition of aromatase activity and alteration of cellular lipids in human placental cells. Toxicol Appl Pharmacol. 2014;277(2):124–30.
Kor EDA, 許穎達. The effects of perfluorooctane sulfonate on placenta: modulation of placental lipid homeostasis. Pokfulam, Hong Kong: The University of Hong Kong; 2016.
Spratlen M, Perera F, Lederman SA, Robinson M, Kannan K, Herbstman J, et al. The association between Perfluoroalkyl substances and lipids in cord blood. J Clin Endocrinol Metab. 2020;105(1):43–54.
Kennedy GL Jr, Butenhoff JL, Olsen GW, O'Connor JC, Seacat AM, Perkins RG, et al. The toxicology of perfluorooctanoate. Crit Rev Toxicol. 2004;34(4):351–84.
Hirschmugl B, Desoye G, Catalano P, Klymiuk I, Scharnagl H, Payr S, et al. Maternal obesity modulates intracellular lipid turnover in the human term placenta. Int J Obes (2005). 2017;41(2):317–23.
Calabuig-Navarro V, Haghiac M, Minium J, Glazebrook P, Ranasinghe GC, Hoppel C, et al. Effect of maternal obesity on placental lipid metabolism. Endocrinology. 2017;158(8):2543–55.
Szabo AJ. Transferred maternal fatty acids stimulate fetal adipogenesis and lead to neonatal and adult obesity. Med Hypotheses. 2019;122:82–8.
Park H-J, Choi J-M. Sex-specific regulation of immune responses by PPARs. Exp Mol Med. 2017;49(8):e364-e.
Benz V, Kintscher U, Foryst-Ludwig A. Sex-specific differences in type 2 diabetes mellitus and dyslipidemia therapy: PPAR agonists. Handb Exp Pharmacol. 2012;214:387–410.
Jalouli M, Carlsson L, Ameen C, Linden D, Ljungberg A, Michalik L, et al. Sex difference in hepatic peroxisome proliferator-activated receptor alpha expression: influence of pituitary and gonadal hormones. Endocrinology. 2003;144(1):101–9.
Yoon M. PPARalpha in obesity: sex difference and estrogen involvement. PPAR Res. 2010;2010:1–16.
Sedlmeier EM, Brunner S, Much D, Pagel P, Ulbrich SE, Meyer HH, et al. Human placental transcriptome shows sexually dimorphic gene expression and responsiveness to maternal dietary n-3 long-chain polyunsaturated fatty acid intervention during pregnancy. BMC Genomics. 2014;15:941.
Cox LA, Li C, Glenn JP, Lange K, Spradling KD, Nathanielsz PW, et al. Expression of the placental transcriptome in maternal nutrient reduction in baboons is dependent on fetal sex. J Nutr. 2013;143(11):1698–708.
Belbasis L, Savvidou MD, Kanu C, Evangelou E, Tzoulaki I. Birth weight in relation to health and disease in later life: an umbrella review of systematic reviews and meta-analyses. BMC Med. 2016;14(1):147.
Ashley-Martin J, Dodds L, Arbuckle TE, Bouchard MF, Fisher M, Morriset AS, et al. Maternal concentrations of perfluoroalkyl substances and fetal markers of metabolic function and birth weight. Am J Epidemiol. 2017;185(3):185–93.
Darrow LA, Stein CR, Steenland K. Serum perfluorooctanoic acid and perfluorooctane sulfonate concentrations in relation to birth outcomes in the Mid-Ohio Valley, 2005-2010. Environ Health Perspect. 2013;121(10):1207–13.
Stein CR, Savitz DA, Dougan M. Serum levels of perfluorooctanoic acid and perfluorooctane sulfonate and pregnancy outcome. Am J Epidemiol. 2009;170(7):837–46.
Washino N, Saijo Y, Sasaki S, Kato S, Ban S, Konishi K, et al. Correlations between prenatal exposure to perfluorinated chemicals and reduced fetal growth. Environ Health Perspect. 2009;117(4):660–7.
Abbott BD, Wolf CJ, Schmid JE, Das KP, Zehr RD, Helfant L, et al. Perfluorooctanoic acid induced developmental toxicity in the mouse is dependent on expression of peroxisome proliferator activated receptor-alpha. Toxicol Sci. 2007;98(2):571–81.
Conley JM, Lambright CS, Evans N, Strynar MJ, McCord J, McIntyre BS, et al. Adverse maternal, fetal, and postnatal effects of hexafluoropropylene oxide dimer acid (GenX) from oral gestational exposure in Sprague-Dawley rats. Environ Health Perspect. 2019;127(3):37008.
Blake BE, Cope HA, Hall SM, Keys RD, Mahler BW, McCord J, et al. Evaluation of maternal, embryo, and placental effects in CD-1 mice following gestational exposure to Perfluorooctanoic acid (PFOA) or hexafluoropropylene oxide dimer acid (HFPO-DA or GenX). Environ Health Perspect. 2020;128(2):27006.
Gombos I, Bacso Z, Detre C, Nagy H, Goda K, Andrasfalvy M, et al. Cholesterol sensitivity of detergent resistance: a rapid flow cytometric test for detecting constitutive or induced raft association of membrane proteins. Cytometry Part A. 2004;61(2):117–26.
Fournier T, Handschuh K, Tsatsaris V, Evain-Brion D. Involvement of PPARgamma in human trophoblast invasion. Placenta. 2007;28(Suppl A):S76–81.
Diaz M, Bassols J, Lopez-Bermejo A, Gomez-Roig MD, de Zegher F, Ibanez L. Placental expression of peroxisome proliferator-activated receptor gamma (PPARgamma): relation to placental and fetal growth. J Clin Endocrinol Metab. 2012;97(8):E1468–72.
Phipps E, Prasanna D, Brima W, Jim B. Preeclampsia: updates in pathogenesis, definitions, and guidelines. Clin J Am Soc Nephrol. 2016;11(6):1102–13.
Duley L. The global impact of pre-eclampsia and eclampsia. Semin Perinatol. 2009;33(3):130–7.
Millar LK, Wing DA, Leung AS, Koonings PP, Montoro MN, Mestman JH. Low birth weight and preeclampsia in pregnancies complicated by hyperthyroidism. Obstet Gynecol. 1994;84(6):946–9.
Odegard RA, Vatten LJ, Nilsen ST, Salvesen KA, Austgulen R. Preeclampsia and fetal growth. Obstet Gynecol. 2000;96(6):950–5.
Backes CH, Markham K, Moorehead P, Cordero L, Nankervis CA, Giannone PJ. Maternal preeclampsia and neonatal outcomes. J Pregnancy. 2011;2011:214365.
•• Ganss R. Maternal metabolism and vascular adaptation in pregnancy: The PPAR link. Trends Endocrinol Metab. 2017;28(1):73–84 This review details how placental PPAR is involved in diseases of pregnancy. This review focuses on metabolic and vascular changes disorders such as GDM and preeclampsia, respectively.
Kang JH, Song H, Yoon JA, Park DY, Kim SH, Lee KJ, et al. Preeclampsia leads to dysregulation of various signaling pathways in placenta. J Hypertens. 2011;29(5):928–36.
Wikström S, Lindh CH, Shu H, Bornehag C-G. Early pregnancy serum levels of perfluoroalkyl substances and risk of preeclampsia in Swedish women. Sci Rep. 2019;9(1):9179.
• Huang R, Chen Q, Zhang L, Luo K, Chen L, Zhao S, et al. Prenatal exposure to perfluoroalkyl and polyfluoroalkyl substances and the risk of hypertensive disorders of pregnancy. Environ Health. 2019;18(1):5 This study highlights the correlation between PFAS exposure, quantified in cord blood plasma, and the incidence of preeclampsia.
Evain-Brion D, Fournier T, Therond P, Tarrade A, Pavan L. Pathogenesis of pre-eclampsia: role of gamma PPAR in trophoblast invasion. Bull Acad Natl Med. 2002;186(2):409–18 discussion 18-20.
Nishimura K, Nakano N, Chowdhury VS, Kaneto M, Torii M, Hattori MA, et al. Effect of PPARbeta/delta agonist on the placentation and embryo-fetal development in rats. Birth Defects Res B Dev Reprod Toxicol. 2013;98(2):164–9.
Martinez N, Kurtz M, Capobianco E, Higa R, White V, Jawerbaum A. PPARalpha agonists regulate lipid metabolism and nitric oxide production and prevent placental overgrowth in term placentas from diabetic rats. J Mol Endocrinol. 2011;47(1):1–12.
•• Szilagyi JT, Freedman AN, Kepper SL, Keshava AM, Bangma JT, Fry RC. Per- and polyfluoroalkyl substances (PFAS) differentially inhibit placental trophoblast migration and invasion in vitro. Toxicol Sci. 2020;175(2):210–9 This study demonstrates that PFOS, PFOA, and GenX decrease extravillous trophoblast mobility and inflamatory signaling. This study supports the epidemiological observations that PFAS exposure is associated with the incidence of preeclampsia.
Meher A, Sundrani D, Joshi S. Maternal nutrition influences angiogenesis in the placenta through peroxisome proliferator activated receptors: a novel hypothesis. Mol Reprod Dev. 2015;82(10):726–34.
Torres-Espinola FJ, Altmae S, Segura MT, Jerez A, Anjos T, Chisaguano M, et al. Maternal PPARG Pro12Ala polymorphism is associated with infant's neurodevelopmental outcomes at 18 months of age. Early Hum Dev. 2015;91(8):457–62.
Schmidt A, Morales-Prieto DM, Pastuschek J, Frohlich K, Markert UR. Only humans have human placentas: molecular differences between mice and humans. J Reprod Immunol. 2015;108:65–71.
Fry RC, Bangma J, Szilagyi J, Rager JE. Developing novel in vitro methods for the risk assessment of developmental and placental toxicants in the environment. Toxicol Appl Pharmacol. 2019;378:114635.
Kudo N, Kawashima Y. Fish oil-feeding prevents perfluorooctanoic acid-induced fatty liver in mice. Toxicol Appl Pharmacol. 1997;145(2):285–93.
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Szilagyi, J.T., Avula, V. & Fry, R.C. Perfluoroalkyl Substances (PFAS) and Their Effects on the Placenta, Pregnancy, and Child Development: a Potential Mechanistic Role for Placental Peroxisome Proliferator–Activated Receptors (PPARs). Curr Envir Health Rpt 7, 222–230 (2020). https://doi.org/10.1007/s40572-020-00279-0
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DOI: https://doi.org/10.1007/s40572-020-00279-0