Skip to main content

Endocrine-Disrupting Chemical Exposure and Later-Onset Diseases

  • Chapter
  • First Online:
Early-life Environmental Exposure and Disease
  • 323 Accesses

Abstract

The ‘developmental origins of health and disease’ (DOHaD) suggests that early-life stress can affect the risk of later-onset diseases, while the potential mechanisms remain largely unknown. Epigenetics is defined as changes in gene expression that occur without changes in DNA sequence and can be transmitted to offspring. Increasing evidence has suggested that epigenetic regulation might be involved in developmental programming of late-onset pathologies. Here, we review current understandings of the relationship between early-life exposure of several endocrine-disrupting chemicals (EDCs) and later-life diseases, as well as potential epigenetic mechanisms.

This is a preview of subscription content, log in via an institution to check access.

Access this chapter

Chapter
USD 29.95
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
eBook
USD 119.00
Price excludes VAT (USA)
  • Available as EPUB and PDF
  • Read on any device
  • Instant download
  • Own it forever
Softcover Book
USD 159.99
Price excludes VAT (USA)
  • Compact, lightweight edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info
Hardcover Book
USD 159.99
Price excludes VAT (USA)
  • Durable hardcover edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info

Tax calculation will be finalised at checkout

Purchases are for personal use only

Institutional subscriptions

References

  1. Goyal D, Limesand SW, Goyal R (2019) Epigenetic responses and the developmental origins of health and disease. J Endocrinol 242(1):T105–T119

    CAS  PubMed  Google Scholar 

  2. Vaiserman A (2014) Early-life exposure to endocrine disrupting chemicals and later-life health outcomes: an epigenetic bridge? Aging Dis 5(6):419–429

    PubMed  PubMed Central  Google Scholar 

  3. Bollati V, Baccarelli A (2010) Environmental epigenetics. Heredity (Edinb) 105(1):105–112

    CAS  Google Scholar 

  4. Calafat AM, Weuve J, Ye X, Jia LT, Hu H, Ringer S et al (2009) Exposure to bisphenol A and other phenols in neonatal intensive care unit premature infants. Environ Health Perspect 117(4):639–644

    CAS  PubMed  Google Scholar 

  5. Doherty LF, Bromer JG, Zhou Y, Aldad TS, Taylor HS (2010) In utero exposure to diethylstilbestrol (DES) or bisphenol-A (BPA) increases EZH2 expression in the mammary gland: an epigenetic mechanism linking endocrine disruptors to breast cancer. Horm Cancer 1(3):146–155

    CAS  PubMed  PubMed Central  Google Scholar 

  6. Veiga-Lopez A, Luense LJ, Christenson LK, Padmanabhan V (2013) Developmental programming: gestational bisphenol-A treatment alters trajectory of fetal ovarian gene expression. Endocrinology 154(5):1873–1884

    CAS  PubMed  PubMed Central  Google Scholar 

  7. Abi Salloum B, Steckler TL, Herkimer C, Lee JS, Padmanabhan V (2013) Developmental programming: impact of prenatal exposure to bisphenol-A and methoxychlor on steroid feedbacks in sheep. Toxicol Appl Pharmacol 268(3):300–308

    CAS  PubMed  Google Scholar 

  8. Ho SM, Tang WY, Belmonte de Frausto J, Prins GS (2006) Developmental exposure to estradiol and bisphenol A increases susceptibility to prostate carcinogenesis and epigenetically regulates phosphodiesterase type 4 variant 4. Cancer Res 66(11):5624–5632

    CAS  PubMed  PubMed Central  Google Scholar 

  9. Lite C, Ahmed S, Santosh W, Seetharaman B (2019) Prenatal exposure to bisphenol-A altered miRNA-224 and protein expression of aromatase in ovarian granulosa cells concomitant with elevated serum estradiol levels in F1 adult offspring. J Biochem Mol Toxicol 33(6):e22317

    PubMed  Google Scholar 

  10. Prins GS, Tang WY, Belmonte J, Ho SM (2008) Perinatal exposure to oestradiol and bisphenol A alters the prostate epigenome and increases susceptibility to carcinogenesis. Basic Clin Pharmacol Toxicol 102(2):134–138

    CAS  PubMed  PubMed Central  Google Scholar 

  11. Woodruff TJ, Zota AR, Schwartz JM (2011) Environmental chemicals in pregnant women in the United States: NHANES 2003–2004. Environ Health Perspect 119(6):878–885

    PubMed  PubMed Central  Google Scholar 

  12. Braun JM, Kalkbrenner AE, Just AC, Yolton K, Calafat AM, Sjodin A et al (2014) Gestational exposure to endocrine-disrupting chemicals and reciprocal social, repetitive, and stereotypic behaviors in 4- and 5-year-old children: the HOME study. Environ Health Perspect 122(5):513–520

    CAS  PubMed  PubMed Central  Google Scholar 

  13. Olsen GW, Burris JM, Ehresman DJ, Froehlich JW, Seacat AM, Butenhoff JL et al (2007) Half-life of serum elimination of perfluorooctanesulfonate, perfluorohexanesulfonate, and perfluorooctanoate in retired fluorochemical production workers. Environ Health Perspect 115(9):1298–1305

    CAS  PubMed  PubMed Central  Google Scholar 

  14. Sunderland EM, Hu XC, Dassuncao C, Tokranov AK, Wagner CC, Allen JG (2019) A review of the pathways of human exposure to poly- and perfluoroalkyl substances (PFASs) and present understanding of health effects. J Expo Sci Environ Epidemiol 29(2):131–147

    CAS  PubMed  Google Scholar 

  15. Post GB, Cohn PD, Cooper KR (2012) Perfluorooctanoic acid (PFOA), an emerging drinking water contaminant: a critical review of recent literature. Environ Res 116:93–117

    CAS  PubMed  Google Scholar 

  16. Johnson PI, Sutton P, Atchley DS, Koustas E, Lam J, Sen S et al (2014) The navigation guide – evidence-based medicine meets environmental health: systematic review of human evidence for PFOA effects on fetal growth. Environ Health Perspect 122(10):1028–1039

    PubMed  PubMed Central  Google Scholar 

  17. Koustas E, Lam J, Sutton P, Johnson PI, Atchley DS, Sen S et al (2014) The navigation guide – evidence-based medicine meets environmental health: systematic review of nonhuman evidence for PFOA effects on fetal growth. Environ Health Perspect 122(10):1015–1027

    CAS  PubMed  PubMed Central  Google Scholar 

  18. Jaddoe VW, de Jonge LL, Hofman A, Franco OH, Steegers EA, Gaillard R (2014) First trimester fetal growth restriction and cardiovascular risk factors in school age children: population based cohort study. BMJ 348:g14

    PubMed  PubMed Central  Google Scholar 

  19. Perng W, Hajj H, Belfort MB, Rifas-Shiman SL, Kramer MS, Gillman MW et al (2016) Birth size, early life weight gain, and midchildhood cardiometabolic health. J Pediatr 173:122–130. e121

    PubMed  PubMed Central  Google Scholar 

  20. Braun JM, Chen A, Romano ME, Calafat AM, Webster GM, Yolton K et al (2016) Prenatal perfluoroalkyl substance exposure and child adiposity at 8 years of age: the HOME study. Obesity (Silver Spring) 24(1):231–237

    CAS  Google Scholar 

  21. Hoyer BB, Ramlau-Hansen CH, Vrijheid M, Valvi D, Pedersen HS, Zviezdai V et al (2015) Anthropometry in 5- to 9-year-old Greenlandic and Ukrainian children in relation to prenatal exposure to perfluorinated alkyl substances. Environ Health Perspect 123(8):841–846

    PubMed  PubMed Central  Google Scholar 

  22. Barry V, Darrow LA, Klein M, Winquist A, Steenland K (2014) Early life perfluorooctanoic acid (PFOA) exposure and overweight and obesity risk in adulthood in a community with elevated exposure. Environ Res 132:62–69

    CAS  PubMed  Google Scholar 

  23. Consales C, Toft G, Leter G, Bonde JP, Uccelli R, Pacchierotti F et al (2016) Exposure to persistent organic pollutants and sperm DNA methylation changes in Arctic and European populations. Environ Mol Mutagen 57(3):200–209

    CAS  PubMed  Google Scholar 

  24. Leter G, Consales C, Eleuteri P, Uccelli R, Specht IO, Toft G et al (2014) Exposure to perfluoroalkyl substances and sperm DNA global methylation in Arctic and European populations. Environ Mol Mutagen 55(7):591–600

    CAS  PubMed  Google Scholar 

  25. Guerrero-Preston R, Goldman LR, Brebi-Mieville P, Ili-Gangas C, Lebron C, Witter FR et al (2010) Global DNA hypomethylation is associated with in utero exposure to cotinine and perfluorinated alkyl compounds. Epigenetics 5(6):539–546

    CAS  PubMed  PubMed Central  Google Scholar 

  26. Watkins DJ, Wellenius GA, Butler RA, Bartell SM, Fletcher T, Kelsey KT (2014) Associations between serum perfluoroalkyl acids and LINE-1 DNA methylation. Environ Int 63:71–76

    CAS  PubMed  Google Scholar 

  27. Fletcher T, Galloway TS, Melzer D, Holcroft P, Cipelli R, Pilling LC et al (2013) Associations between PFOA, PFOS and changes in the expression of genes involved in cholesterol metabolism in humans. Environ Int 57–58:2–10

    PubMed  Google Scholar 

  28. Vanden Heuvel JP, Thompson JT, Frame SR, Gillies PJ (2006) Differential activation of nuclear receptors by perfluorinated fatty acid analogs and natural fatty acids: a comparison of human, mouse, and rat peroxisome proliferator-activated receptor-alpha, -beta, and -gamma, liver X receptor-beta, and retinoid X receptor-alpha. Toxicol Sci 92(2):476–489

    Google Scholar 

  29. Taxvig C, Dreisig K, Boberg J, Nellemann C, Schelde AB, Pedersen D et al (2012) Differential effects of environmental chemicals and food contaminants on adipogenesis, biomarker release and PPARgamma activation. Mol Cell Endocrinol 361(1–2):106–115

    CAS  PubMed  Google Scholar 

  30. Bastos Sales L, Kamstra JH, Cenijn PH, van Rijt LS, Hamers T, Legler J (2013) Effects of endocrine disrupting chemicals on in vitro global DNA methylation and adipocyte differentiation. Toxicol in Vitro 27(6):1634–1643

    CAS  PubMed  Google Scholar 

  31. Wang CF, Tian Y (2015) Reproductive endocrine-disrupting effects of triclosan: population exposure, present evidence and potential mechanisms. Environ Pollut 206:195–201

    CAS  PubMed  Google Scholar 

  32. Sandborgh-Englund G, Adolfsson-Erici M, Odham G, Ekstrand J (2006) Pharmacokinetics of triclosan following oral ingestion in humans. J Toxicol Environ Health A 69(20):1861–1873

    CAS  PubMed  Google Scholar 

  33. Allmyr M, Adolfsson-Erici M, McLachlan MS, Sandborgh-Englund G (2006) Triclosan in plasma and milk from Swedish nursing mothers and their exposure via personal care products. Sci Total Environ 372(1):87–93

    CAS  PubMed  Google Scholar 

  34. Wang X, Chen X, Feng X, Chang F, Chen M, Xia Y et al (2015) Triclosan causes spontaneous abortion accompanied by decline of estrogen sulfotransferase activity in humans and mice. Sci Rep 5:18252

    CAS  PubMed  PubMed Central  Google Scholar 

  35. Calafat AM, Ye X, Wong LY, Reidy JA, Needham LL (2008) Urinary concentrations of triclosan in the U.S. population: 2003–2004. Environ Health Perspect 116(3):303–307

    CAS  PubMed  Google Scholar 

  36. Yin J, Wei L, Shi Y, Zhang J, Wu Q, Shao B (2016) Chinese population exposure to triclosan and triclocarban as measured via human urine and nails. Environ Geochem Health 38(5):1125–1135

    CAS  PubMed  Google Scholar 

  37. Heffernan AL, Baduel C, Toms LM, Calafat AM, Ye X, Hobson P et al (2015) Use of pooled samples to assess human exposure to parabens, benzophenone-3 and triclosan in Queensland, Australia. Environ Int 85:77–83

    CAS  PubMed  PubMed Central  Google Scholar 

  38. Cheng W, Yang S, Liang F, Wang W, Zhou R, Li Y et al (2019) Low-dose exposure to triclosan disrupted osteogenic differentiation of mouse embryonic stem cells via BMP/ERK/Smad/Runx-2 signalling pathway. Food Chem Toxicol 127:1–10

    CAS  PubMed  Google Scholar 

  39. Du G, Yu M, Wang L, Hu W, Song L, Lu C et al (2018) Transcriptome and DNA Methylome dynamics during Triclosan-induced cardiomyocyte differentiation toxicity. Stem Cells Int 2018:8608327

    PubMed  PubMed Central  Google Scholar 

  40. Ma Y, Zang L, Wang D, Jiang J, Wang C, Wang X et al (2019) Effects of miR-181a-5p abnormal expression on zebrafish (Danio rerio) vascular development following triclosan exposure. Chemosphere 223:523–535

    CAS  PubMed  Google Scholar 

  41. Harley KG, Berger KP, Kogut K, Parra K, Lustig RH, Greenspan LC et al (2019) Association of phthalates, parabens and phenols found in personal care products with pubertal timing in girls and boys. Hum Reprod 34(1):109–117

    CAS  PubMed  Google Scholar 

  42. Bertelsen RJ, Longnecker MP, Lovik M, Calafat AM, Carlsen KH, London SJ et al (2013) Triclosan exposure and allergic sensitization in Norwegian children. Allergy 68(1):84–91

    CAS  PubMed  Google Scholar 

  43. Xue J, Wu Q, Sakthivel S, Pavithran PV, Vasukutty JR, Kannan K (2015) Urinary levels of endocrine-disrupting chemicals, including bisphenols, bisphenol a diglycidyl ethers, benzophenones, parabens, and triclosan in obese and non-obese Indian children. Environ Res 137:120–128

    CAS  PubMed  Google Scholar 

  44. Li S, Zhao J, Wang G, Zhu Y, Rabito F, Krousel-Wood M et al (2015) Urinary triclosan concentrations are inversely associated with body mass index and waist circumference in the US general population: experience in NHANES 2003–2010. Int J Hyg Environ Health 218(4):401–406

    CAS  PubMed  PubMed Central  Google Scholar 

  45. Buser MC, Murray HE, Scinicariello F (2014) Association of urinary phenols with increased body weight measures and obesity in children and adolescents. J Pediatr 165(4):744–749

    CAS  PubMed  Google Scholar 

  46. Gyllenberg D, Sourander A, Surcel HM, Hinkka-Yli-Salomaki S, McKeague IW, Brown AS (2016) Hypothyroxinemia during gestation and offspring schizophrenia in a national birth cohort. Biol Psychiatry 79(12):962–970

    CAS  PubMed  Google Scholar 

  47. Gorr MW, Velten M, Nelin TD, Youtz DJ, Sun Q, Wold LE (2014) Early life exposure to air pollution induces adult cardiac dysfunction. Am J Physiol Heart Circ Physiol 307(9):H1353–H1360

    CAS  PubMed  PubMed Central  Google Scholar 

  48. Rosa MJ, Hair GM, Just AC, Kloog I, Svensson K, Pizano-Zarate ML et al (2019) Identifying critical windows of prenatal particulate matter (PM2.5) exposure and early childhood blood pressure. Environ Res 182:109073

    PubMed  Google Scholar 

  49. Melody SM, Ford JB, Wills K, Venn A, Johnston FH (2019) Maternal exposure to fine particulate matter from a large coal mine fire is associated with gestational diabetes mellitus: a prospective cohort study. Environ Res:108956

    Google Scholar 

  50. Hectors TL, Vanparys C, van der Ven K, Martens GA, Jorens PG, Van Gaal LF et al (2011) Environmental pollutants and type 2 diabetes: a review of mechanisms that can disrupt beta cell function. Diabetologia 54(6):1273–1290

    CAS  PubMed  Google Scholar 

  51. West NA, Crume TL, Maligie MA, Dabelea D (2011) Cardiovascular risk factors in children exposed to maternal diabetes in utero. Diabetologia 54(3):504–507

    CAS  PubMed  Google Scholar 

  52. Barker DJ (2007) The origins of the developmental origins theory. J Intern Med 261(5):412–417

    CAS  PubMed  Google Scholar 

  53. Grandjean P, Barouki R, Bellinger DC, Casteleyn L, Chadwick LH, Cordier S et al (2015) Life-long implications of developmental exposure to environmental stressors: new perspectives. Endocrinology 156(10):3408–3415

    CAS  PubMed  PubMed Central  Google Scholar 

  54. Wu X, Zhang Y (2017) TET-mediated active DNA demethylation: mechanism, function and beyond. Nat Rev Genet 18(9):517–534

    CAS  PubMed  Google Scholar 

  55. Bernstein BE, Meissner A, Lander ES (2007) The mammalian epigenome. Cell 128(4):669–681

    CAS  PubMed  Google Scholar 

  56. Jefferson WN, Chevalier DM, Phelps JY, Cantor AM, Padilla-Banks E, Newbold RR et al (2013) Persistently altered epigenetic marks in the mouse uterus after neonatal estrogen exposure. Mol Endocrinol 27(10):1666–1677

    CAS  PubMed  PubMed Central  Google Scholar 

  57. Kurian JR, Louis S, Keen KL, Wolfe A, Terasawa E, Levine JE (2016) The Methylcytosine dioxygenase ten-eleven Translocase-2 (tet2) enables elevated GnRH gene expression and maintenance of male reproductive function. Endocrinology 157(9):3588–3603

    CAS  PubMed  PubMed Central  Google Scholar 

  58. Dolinoy DC, Huang D, Jirtle RL (2007) Maternal nutrient supplementation counteracts bisphenol A-induced DNA hypomethylation in early development. Proc Natl Acad Sci U S A 104(32):13056–13061

    CAS  PubMed  PubMed Central  Google Scholar 

  59. Greathouse KL, Bredfeldt T, Everitt JI, Lin K, Berry T, Kannan K et al (2012) Environmental estrogens differentially engage the histone methyltransferase EZH2 to increase risk of uterine tumorigenesis. Mol Cancer Res 10(4):546–557

    CAS  PubMed  Google Scholar 

  60. Wang Q, Trevino LS, Wong RL, Medvedovic M, Chen J, Ho SM et al (2016) Reprogramming of the epigenome by MLL1 links early-life environmental exposures to prostate cancer risk. Mol Endocrinol 30(8):856–871

    CAS  PubMed  PubMed Central  Google Scholar 

  61. Esteban J, Serrano-Macia M, Sanchez-Perez I, Alonso-Magdalena P, Pellin MC, Garcia-Arevalo M et al (2019) In utero exposure to bisphenol-A disrupts key elements of retinoid system in male mice offspring. Food Chem Toxicol 126:142–151

    CAS  PubMed  Google Scholar 

  62. Faulk C, Kim JH, Jones TR, McEachin RC, Nahar MS, Dolinoy DC et al (2015) Bisphenol A-associated alterations in genome-wide DNA methylation and gene expression patterns reveal sequence-dependent and non-monotonic effects in human fetal liver. Environ Epigenet 1(1):dvv006

    PubMed  PubMed Central  Google Scholar 

  63. DeBenedictis B, Guan H, Yang K (2016) Prenatal exposure to bisphenol A disrupts mouse fetal liver maturation in a sex-specific manner. J Cell Biochem 117(2):344–350

    CAS  PubMed  Google Scholar 

  64. Nahar MS, Kim JH, Sartor MA, Dolinoy DC (2014) Bisphenol A-associated alterations in the expression and epigenetic regulation of genes encoding xenobiotic metabolizing enzymes in human fetal liver. Environ Mol Mutagen 55(3):184–195

    CAS  PubMed  Google Scholar 

  65. Doshi T, Mehta SS, Dighe V, Balasinor N, Vanage G (2011) Hypermethylation of estrogen receptor promoter region in adult testis of rats exposed neonatally to bisphenol A. Toxicology 289(2–3):74–82

    CAS  PubMed  Google Scholar 

Download references

Acknowledgments

This study was supported by the National Natural Science Foundation of China (81402706), the Natural Science Foundation of Jiangsu Province (BK20181366).

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to Guizhen Du .

Editor information

Editors and Affiliations

Rights and permissions

Reprints and permissions

Copyright information

© 2020 Springer Nature Singapore Pte Ltd.

About this chapter

Check for updates. Verify currency and authenticity via CrossMark

Cite this chapter

Wu, D., Du, G. (2020). Endocrine-Disrupting Chemical Exposure and Later-Onset Diseases. In: Xia, Y. (eds) Early-life Environmental Exposure and Disease. Springer, Singapore. https://doi.org/10.1007/978-981-15-3797-4_11

Download citation

Publish with us

Policies and ethics