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Environmental monitoring and the developmental origins of health and disease

Published online by Cambridge University Press:  27 May 2019

Douglas Lopes Almeida Open the ORCID record for Douglas Lopes Almeida [Opens in a new window] ,
Audrei Pavanello ,
Lucas Paulo Saavedra ,
Tais Susane Pereira ,
Marialba Avezum Alves de Castro-Prado  and
Paulo Cezar de Freitas Mathias
Douglas Lopes Almeida*
Affiliation:
Laboratory of Secretion Cell Biology, Department of Biotechnology, Genetics and Cell Biology, State University of Maringá, Maringá, Brazil
Audrei Pavanello
Affiliation:
Laboratory of Secretion Cell Biology, Department of Biotechnology, Genetics and Cell Biology, State University of Maringá, Maringá, Brazil
Lucas Paulo Saavedra
Affiliation:
Laboratory of Secretion Cell Biology, Department of Biotechnology, Genetics and Cell Biology, State University of Maringá, Maringá, Brazil
Tais Susane Pereira
Affiliation:
Laboratory of Mutagenesis, Department of Biotechnology, Genetics and Cell Biology, State University of Maringá, Maringá, Brazil
Marialba Avezum Alves de Castro-Prado
Affiliation:
Laboratory of Mutagenesis, Department of Biotechnology, Genetics and Cell Biology, State University of Maringá, Maringá, Brazil
Paulo Cezar de Freitas Mathias
Affiliation:
Laboratory of Secretion Cell Biology, Department of Biotechnology, Genetics and Cell Biology, State University of Maringá, Maringá, Brazil
*
Address for correspondence: Douglas Lopes Almeida, Department of Biotechnology, Cell Biology and Genetics, State University of Maringá, 5790 Av. Colombo, Sala 19, Maringá, PR, 87020-900, Brazil. Email: [email protected]
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Abstract

Early-life chronic exposure to environmental contaminants, such as bisphenol-A, particulate matter air pollution, organophosphorus pesticides, and pharmaceutical drugs, among others, may affect central tissues, such as the hypothalamus, and peripheral tissues, such as the endocrine pancreas, causing inflammation and apoptosis with severe implications to the metabolism. The Developmental Origins of Health and Disease (DOHaD) concept articulates events in developmental phases of life, such as intrauterine, lactation, and adolescence, to later-life metabolism and health. These developmental phases are more susceptible to environmental changes, such as those caused by environmental contaminants, which may predispose individuals to obesity, metabolic syndrome, and chronic noncommunicable diseases later in life. Alterations in the epigenome are explored as an underlying mechanism to the programming effects on metabolism, as the expression of key genes related with central and peripheral metabolic functions may be altered in response to environmental disturbances. Studies show that environmental contaminants may affect gene expressions in mammals, especially when exposed to during the developmental phases of life, leading to metabolic disorders in adulthood. In this review, we discuss the current obesity epidemics, the DOHaD concept, pollutants’ toxicology, environmental control, and the role of environmental contaminants in the central and peripheral programming of obesity and metabolic syndrome. Improving environmental monitoring may directly affect the quality of life of the population and help protect the future generations from metabolic diseases.

Keywords

DOHaDenvironmental contaminantsmetabolic programmingobesitymetabolic syndrome
Type
Review
Information
Journal of Developmental Origins of Health and Disease , Volume 10 , Issue 6 , December 2019 , pp. 608 - 615
Copyright
© Cambridge University Press and the International Society for Developmental Origins of Health and Disease 2019 

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References

Giroux, E. Epidemiology and the bio-statistical theory of disease: a challenging perspective. Theor Med Bioeth. 2015; 36, 175–195.CrossRefGoogle ScholarPubMed
Omran, AR. The epidemiologic transition. A theory of the epidemiology of population change. Milbank Mem Fund Q. 1971; 49, 509–538.CrossRefGoogle ScholarPubMed
Samson, SL, Garber, AJ. Metabolic syndrome. Endocrinol Metab Clin North Am. 2014; 43, 1–23.CrossRefGoogle ScholarPubMed
Sherling, DH, Perumareddi, P, Hennekens, CH. Metabolic syndrome. J Cardiovasc Pharmacol Ther. 2017; 22, 365–367.CrossRefGoogle ScholarPubMed
Suzuki, K. The developing world of DOHaD. J Dev Orig Health Dis. 2017; 9, 266–269.CrossRefGoogle ScholarPubMed
Hales, CN, Barker, DJ. Type 2 (non-insulin-dependent) diabetes mellitus: the thrifty phenotype hypothesis. Diabetologia. 1992; 35, 595–601.CrossRefGoogle ScholarPubMed
McMillen, IC, Robinson, JS. Developmental origins of the metabolic syndrome: prediction, plasticity, and programming. Physiol Rev. 2005; 85, 571–633.CrossRefGoogle ScholarPubMed
Plagemann, A, Harder, T, Schellong, K, Schulz, S, Stupin, JH. Early postnatal life as a critical time window for determination of long-term metabolic health. Best Pract Res Clin Endocrinol Metab. 2012; 26, 641–653.CrossRefGoogle ScholarPubMed
Ashley-Martin, J, Levy, AR, Arbuckle, TE, et al. Maternal exposure to metals and persistent pollutants and cord blood immune system biomarkers. Environ Health. 2015; 14, 52.CrossRefGoogle ScholarPubMed
Harrison, J, Dawson, L. Occupational health: meeting the challenges of the next 20 years. Saf Health Work. 2016; 7, 143–149.CrossRefGoogle ScholarPubMed
Fabricio, G, Malta, A, Chango, A, De Freitas Mathias, PC. Environmental contaminants and pancreatic beta-cells. J Clin Res Pediatr Endocrinol. 2016; 8, 257–263.CrossRefGoogle ScholarPubMed
Signorelli, SS, Ferrante, M. [Editorial] Environmental and occupational risk factors associated with different pathological conditions. Mol Med Rep. 2017; 15, 3315–3316.CrossRefGoogle ScholarPubMed
Fruh, SM. Obesity: risk factors, complications, and strategies for sustainable long-term weight management. J Am Assoc Nurse Pract. 2017; 29, S3–S14.Google ScholarPubMed
Apovian, CM. Obesity: definition, comorbidities, causes, and burden. Am J Manag Care. 2016; 22, s176–s185.Google ScholarPubMed
Seidell, JC, Halberstadt, J. The global burden of obesity and the challenges of prevention. Ann Nutr Metab. 2015; 66, 7–12.CrossRefGoogle ScholarPubMed
Flegal, KM, Kruszon-Moran, D, Carroll, MD, Fryar, CD, Ogden, CL. Trends in obesity among adults in the United States, 2005 to 2014. JAMA. 2016; 315, 2284–2291.CrossRefGoogle ScholarPubMed
Jimenez-Cruz, A, Bacardi-Gascon, M. Obesity in Latin America: the need for a comprehensive approach. Nutr Hosp. 2015; 31, 2334–2335.Google ScholarPubMed
Kinge, JM, Strand, BH, Vollset, SE, Skirbekk, V. Educational inequalities in obesity and gross domestic product: evidence from 70 countries. J Epidemiol Community Health. 2015; 69, 1141–1146.CrossRefGoogle ScholarPubMed
Rtveladze, K, Marsh, T, Webber, L, et al. Health and economic burden of obesity in Brazil. PLoS One. 2013; 8, e68785.CrossRefGoogle Scholar
Gluckman, PD, Hanson, M, Zimmet, P, Forrester, T. Losing the war against obesity: the need for a developmental perspective. Sci Transl Med. 2011; 3, 93cm19.CrossRefGoogle ScholarPubMed
Husemann, BJ. Obesity: an innately incurable disease? Obes Surg. 1999; 9, 244–249.CrossRefGoogle ScholarPubMed
Barker, DJ, Bull, AR, Osmond, C, Simmonds, SJ. Fetal and placental size and risk of hypertension in adult life. BMJ. 1990; 301, 259–262.CrossRefGoogle ScholarPubMed
Lumey, LH. Decreased birthweights in infants after maternal in utero exposure to the Dutch famine of 1944-1945. Paediatr Perinat Epidemiol. 1992; 6, 240–253.CrossRefGoogle ScholarPubMed
Ravelli, AC, van der Meulen, JH, Michels, RP, et al. Glucose tolerance in adults after prenatal exposure to famine. Lancet. 1998; 351, 173–177.CrossRefGoogle Scholar
Cleal, JK, Poore, KR, Boullin, JP, et al. Mismatched pre- and postnatal nutrition leads to cardiovascular dysfunction and altered renal function in adulthood. Proc Natl Acad Sci U S A. 2007; 104, 9529–9533.CrossRefGoogle ScholarPubMed
Veena, SR, Wills, AK, Fisher, DJ, et al. Early life factors and type 2 diabetes in south India: Do the associations change with age? J Diabetes. 2009; 1, 218–226.CrossRefGoogle ScholarPubMed
Cureau, FV, Duarte, P, dos Santos, DL, Reichert, FF, Clustering of risk factors for noncommunicable diseases in Brazilian adolescents: prevalence and correlates. J Phys Act Health. 2014; 11, 942–949.CrossRefGoogle ScholarPubMed
Metges, CC. Early nutrition and later obesity: animal models provide insights into mechanisms. Adv Exp Med Biol. 2009; 646, 105–112.CrossRefGoogle ScholarPubMed
Gluckman, PD, Hanson, MA. Developmental and epigenetic pathways to obesity: an evolutionary-developmental perspective. Int J Obes (Lond). 2008; 32, S62–S71.CrossRefGoogle Scholar
Wu, Z, Puigserver, P, Spiegelman, BM. Transcriptional activation of adipogenesis. Curr Opin Cell Biol. 1999; 11, 689–694.CrossRefGoogle ScholarPubMed
de Oliveira, JC, Gomes, RM, Miranda, RA, et al. Protein restriction during the last third of pregnancy malprograms the neuroendocrine axes to induce metabolic syndrome in adult male rat offspring. Endocrinology. 2016; 157, 1799–1812.CrossRefGoogle ScholarPubMed
de Oliveira, JC, Lisboa, PC, de Moura, EG, et al. Poor pubertal protein nutrition disturbs glucose-induced insulin secretion process in pancreatic islets and programs rats in adulthood to increase fat accumulation. J Endocrinol. 2013; 216, 195–206.CrossRefGoogle ScholarPubMed
Li, L, Law, C, Lo Conte, R, Power, C. Intergenerational influences on childhood body mass index: the effect of parental body mass index trajectories. Am J Clin Nutr. 2009; 89, 551–557.CrossRefGoogle ScholarPubMed
Ng, SF, Lin, RC, Laybutt, DR, et al. Chronic high-fat diet in fathers programs beta-cell dysfunction in female rat offspring. Nature. 2010; 467, 963–966.CrossRefGoogle ScholarPubMed
Montague, CT, Farooqi, IS, Whitehead, JP, et al. Congenital leptin deficiency is associated with severe early-onset obesity in humans. Nature. 1997; 387, 903–908.CrossRefGoogle ScholarPubMed
Frayling, TM, Timpson, NJ, Weedon, MN, et al. A common variant in the FTO gene is associated with body mass index and predisposes to childhood and adult obesity. Science. 2007; 316, 889–894.CrossRefGoogle ScholarPubMed
Willyard, C. Heritability: the family roots of obesity. Nature. 2014; 508, S58–60.CrossRefGoogle ScholarPubMed
Godfrey, KM, Lillycrop, KA, Burdge, GC, Gluckman, PD, Hanson, MA. Epigenetic mechanisms and the mismatch concept of the developmental origins of health and disease. Pediatr Res. 2007; 61, 5R–10R.CrossRefGoogle ScholarPubMed
Fleming, TP, Velazquez, MA, Eckert, JJ, Embryos, DOHaD and David Barker. J Dev Orig Health Dis. 2015; 6, 377–383.CrossRefGoogle ScholarPubMed
Cahoon, EK, Nadirov, EA, Polanskaya, ON, et al. Risk of thyroid nodules in residents of Belarus exposed to Chernobyl fallout as children and adolescents. J Clin Endocrinol Metab. 2017; 40, 2207–2217.CrossRefGoogle Scholar
Pizzo, F, Benfenati, E. In silico models for Repeated-Dose Toxicity (RDT): prediction of the No Observed Adverse Effect Level (NOAEL) and Lowest Observed Adverse Effect Level (LOAEL) for drugs. Methods Mol Biol. 2016; 1425, 163–176.CrossRefGoogle Scholar
Valcke, M, Bouchard, M. Determination of no-observed effect level (NOEL)-biomarker equivalents to interpret biomonitoring data for organophosphorus pesticides in children. Environ Health. 2009; 8, 5.CrossRefGoogle ScholarPubMed
Mehrpour, O, Karrari, P, Zamani, N, Tsatsakis, AM, Abdollahi, M. Occupational exposure to pesticides and consequences on male semen and fertility: a review. Toxicol Lett. 2014; 230, 146–156.CrossRefGoogle ScholarPubMed
Guven, M, Bayram, F, Unluhizarci, K, Kelestimur, F. Endocrine changes in patients with acute organophosphate poisoning. Hum Exp Toxicol. 1999; 18, 598–601.CrossRefGoogle ScholarPubMed
Korsak, RJ, Sato, MM. Effects of chronic organophosphate pesticide exposure on the central nervous system. Clin Toxicol. 1977; 11, 83–95.CrossRefGoogle ScholarPubMed
Ribeiro, TA, Prates, KV, Pavanello, A, et al. Acephate exposure during a perinatal life program to type 2 diabetes. Toxicology. 2016; 372, 12–21.CrossRefGoogle ScholarPubMed
How, V, Hashim, Z, Ismail, P, et al. Exploring cancer development in adulthood: cholinesterase depression and genotoxic effect from chronic exposure to organophosphate pesticides among rural farm children. J Agromedicine. 2014; 19, 35–43.CrossRefGoogle ScholarPubMed
Geens, T, Aerts, D, Berthot, C, et al. A review of dietary and non-dietary exposure to bisphenol-A. Food Chem Toxicol. 2012; 50, 3725–3740.CrossRefGoogle ScholarPubMed
Gould, JC, Leonard, LS, Maness, SC, et al. Bisphenol A interacts with the estrogen receptor alpha in a distinct manner from estradiol. Mol Cell Endocrinol. 1998; 142, 203–214.CrossRefGoogle Scholar
Paulose, T, Speroni, L, Sonnenschein, C, Soto, AM. Estrogens in the wrong place at the wrong time: Fetal BPA exposure and mammary cancer. Reprod Toxicol. 2015; 54, 58–65.CrossRefGoogle Scholar
Resolução n°41. Brasil, Ministério da Saúde, 2011.Google Scholar
Fiordelisi, A, Piscitelli, P, Trimarco, B, et al. The mechanisms of air pollution and particulate matter in cardiovascular diseases. Heart Fail Rev. 2017; 22, 337–347.CrossRefGoogle ScholarPubMed
Mukherjee, A, Agrawal, M. A global perspective of fine particulate matter pollution and its health effects. Rev Environ Contam Toxicol. 2017; 244, 5–51.Google Scholar
Zhao, H, Yang, B, Xu, J, Chen, DM, Xiao, CL. PM2.5-induced alterations of cell cycle associated gene expression in lung cancer cells and rat lung tissues. Environ Toxicol Pharmacol. 2017; 52, 77–82.CrossRefGoogle ScholarPubMed
Dumax-Vorzet, AF, Tate, M, Walmsley, R, Elder, RH, Povey, AC. Cytotoxicity and genotoxicity of urban particulate matter in mammalian cells. Mutagenesis. 2015; 30, 621–633.CrossRefGoogle ScholarPubMed
Lai, CH, Huang, HB, Chang, YC, et al. Exposure to fine particulate matter causes oxidative and methylated DNA damage in young adults: a longitudinal study. Sci Total Environ. 2017; 598, 289–296.CrossRefGoogle ScholarPubMed
Puckowski, A, Mioduszewska, K, Lukaszewicz, P, et al. Bioaccumulation and analytics of pharmaceutical residues in the environment: a review. J Pharm Biomed Anal. 2016; 127, 232–255.CrossRefGoogle ScholarPubMed
Cardoso, O, Porcher, JM, Sanchez, W. Factory-discharged pharmaceuticals could be a relevant source of aquatic environment contamination: review of evidence and need for knowledge. Chemosphere. 2014; 115, 20–30.CrossRefGoogle ScholarPubMed
Barra Caracciolo, A, Topp, E, Grenni, P. Pharmaceuticals in the environment: biodegradation and effects on natural microbial communities. A review. J Pharm Biomed Anal. 2015; 106, 25–36.CrossRefGoogle ScholarPubMed
da Silva, BS, Rovaris, DL, Bonotto, RM, et al. The influence on DNA damage of glycaemic parameters, oral antidiabetic drugs and polymorphisms of genes involved in the DNA repair system. Mutagenesis. 2013; 28, 525–30.CrossRefGoogle ScholarPubMed
Sant’Anna, JR, Yajima, JP, Rosada, LJ, et al. Metformin’s performance in in vitro and in vivo genetic toxicology studies. Exp Biol Med (Maywood). 2013; 238, 803–810.CrossRefGoogle ScholarPubMed
Harishankar, MK, Logeshwaran, S, Sujeevan, S, et al. Genotoxicity evaluation of metformin and glimepiride by micronucleus assay in exfoliated urothelial cells of type 2 diabetes mellitus patients. Food Chem Toxicol. 2015; 83, 146–150.CrossRefGoogle ScholarPubMed
Amador, RR, Longo, JP, Lacava, ZG, Dorea, JG, Almeida Santos, MdeFM. Metformin (dimethyl-biguanide) induced DNA damage in mammalian cells. Genet Mol Biol. 2012; 35, 153–158.CrossRefGoogle ScholarPubMed
Morais, JF, Sant’Anna, JR, Pereira, TS, et al. Genotoxic investigation of a thiazolidinedione PPARgamma agonist using the in vitro micronucleus test and the in vivo homozygotization assay. Mutagenesis. 2016; 31, 417–424.CrossRefGoogle ScholarPubMed
Baillie-Hamilton, PF. Chemical toxins: a hypothesis to explain the global obesity epidemic. J Altern Complement Med. 2002; 8, 185–192.CrossRefGoogle ScholarPubMed
Jobst, KA, You are what you eat: stress, survival anxiety, the environment, and chemical “obesogens”. J Altern Complement Med. 2002; 8, 101–102.CrossRefGoogle ScholarPubMed
de Git, KC, Adan, RA. Leptin resistance in diet-induced obesity: the role of hypothalamic inflammation. Obes Rev. 2015; 16, 207–224.CrossRefGoogle ScholarPubMed
den Hartigh, LJ, Lame, MW, Ham, W, et al. Endotoxin and polycyclic aromatic hydrocarbons in ambient fine particulate matter from Fresno, California initiate human monocyte inflammatory responses mediated by reactive oxygen species. Toxicol In Vitro. 2010; 24, 1993–2002.CrossRefGoogle ScholarPubMed
Regnier, SM, Sargis, RM. Adipocytes under assault: environmental disruption of adipose physiology. Biochim Biophys Acta. 2014; 1842, 520–533.CrossRefGoogle ScholarPubMed
Li, W, Dorans, KS, Wilker, EH, et al. Residential proximity to major roadways, fine particulate matter, and adiposity: The Framingham heart study. Obesity (Silver Spring). 2016; 24, 2593–2599.CrossRefGoogle ScholarPubMed
Li, C, McDonald, TJ, Wu, G, Nijland, MJ, Nathanielsz, PW. Intrauterine growth restriction alters term fetal baboon hypothalamic appetitive peptide balance. J Endocrinol. 2013; 217, 275–282.CrossRefGoogle ScholarPubMed
Plagemann, A, Harder, T, Brunn, M, et al. Hypothalamic proopiomelanocortin promoter methylation becomes altered by early overfeeding: an epigenetic model of obesity and the metabolic syndrome. J Physiol. 2009; 587, 4963–4976.CrossRefGoogle ScholarPubMed
Haugen, AC, Schug, TT, Collman, G, Heindel, JJ. Evolution of DOHaD: the impact of environmental health sciences. J Dev Orig Health Dis. 2015; 6, 55–64.CrossRefGoogle ScholarPubMed
Calderon-Garciduenas, L, Calderon-Garciduenas, A, Torres-Jardon, R, et al. Air pollution and your brain: what do you need to know right now. Prim Health Care Res Dev. 2015; 16, 329–345.CrossRefGoogle Scholar
Fang, Z, Zhu, Q, Gu, T, et al. Anti-androgenic effects of bisphenol-A on spatial memory and synaptic plasticity of the hippocampus in mice. Horm Behav. 2017; 93, 151–158.CrossRefGoogle ScholarPubMed
Chen, X, Wang, Y, Xu, F, et al. The rapid effect of Bisphenol-A on long-term potentiation in Hippocampus involves estrogen receptors and ERK activation. Neural Plast. 2017; 2017, 5196958.CrossRefGoogle ScholarPubMed
Wang, C, Niu, R, Zhu, Y, et al. Changes in memory and synaptic plasticity induced in male rats after maternal exposure to bisphenol A. Toxicology. 2014; 322, 51–60.CrossRefGoogle ScholarPubMed
Cao, J, Mickens, JA, McCaffrey, KA, et al. Exposure alters sexually dimorphic gene expression in the postnatal rat hypothalamus. Neurotoxicology. 2012; 33, 23–36.CrossRefGoogle ScholarPubMed
Tait, S, Ricceri, L, Venerosi, A, et al. Long-term effects on hypothalamic neuropeptides after developmental exposure to chlorpyrifos in mice. Environ Health Perspect. 2009; 117, 112–116.CrossRefGoogle ScholarPubMed
Naseh, M, Vatanparast, J. Enhanced expression of hypothalamic nitric oxide synthase in rats developmentally exposed to organophosphates. Brain Res. 2014; 1579, 10–19.CrossRefGoogle ScholarPubMed
Wang, Y, Zhang, Y, Ji, L, et al. Prenatal and postnatal exposure to organophosphate pesticides and childhood neurodevelopment in Shandong, China. Environ Int. 2017; 108, 119–126.CrossRefGoogle ScholarPubMed
Ilagan, Y, Mamillapalli, R, Goetz, LG, Kayani, J, Taylor, HS. Bisphenol-A exposure in utero programs a sexually dimorphic estrogenic state of hepatic metabolic gene expression. Reprod Toxicol. 2017; 71, 84–94.CrossRefGoogle ScholarPubMed
Lapworth, DJ, Baran, N, Stuart, ME, Ward, RS. Emerging organic contaminants in groundwater: a review of sources, fate and occurrence. Environ Pollut. 2012; 163, 287–303.CrossRefGoogle ScholarPubMed
Gervin, K, Nordeng, H, Ystrom, E, Reichborn-Kjennerud, T, Lyle, R. Long-term prenatal exposure to paracetamol is associated with DNA methylation differences in children diagnosed with ADHD. Clin Epigenetics. 2017; 9, 77.CrossRefGoogle ScholarPubMed
Ystrom, E, Gustavson, K, Brandlistuen, RE, et al. Prenatal exposure to acetaminophen and risk of ADHD. Pediatrics. 2017; 140, e20163840.CrossRefGoogle ScholarPubMed
Liew, Z, Ritz, B, Virk, J, Olsen, J. Maternal use of acetaminophen during pregnancy and risk of autism spectrum disorders in childhood: a Danish national birth cohort study. Autism Res. 2016; 9, 951–958.CrossRefGoogle ScholarPubMed
Aoi, T. Biology of lung cancer: genetic mutation, epithelial-mesenchymal transition, and cancer stem cells. Gen Thorac Cardiovasc Surg. 2016; 64, 517–523.CrossRefGoogle ScholarPubMed
Zhang, X, Wallace, AD, Du, P, et al. Genome-wide study of DNA methylation alterations in response to diazinon exposure in vitro. Environ Toxicol Pharmacol. 2012; 34, 959–968.CrossRefGoogle ScholarPubMed
Anway, MD, Cupp, AS, Uzumcu, M, Skinner, MK. Epigenetic transgenerational actions of endocrine disruptors and male fertility. Science. 2005; 308, 1466–1469.CrossRefGoogle ScholarPubMed
Akhter, A, Rahaman, M, Suzuki, RT, Murono, Y, Tokumoto, T. Next-generation and further transgenerational effects of bisphenol A on zebrafish reproductive tissues. Heliyon. 2018; 4, e00788.CrossRefGoogle ScholarPubMed
Adamkovicova, M, Toman, R, Martiniakova, M, et al. Sperm motility and morphology changes in rats exposed to cadmium and diazinon. Reprod Biol Endocrinol. 2016; 14, 42.CrossRefGoogle ScholarPubMed
Sundaram, R, Mumford, SL, Buck Louis, GM. Couples’ body composition and time-to-pregnancy. Hum Reprod. 2017; 32, 662–668.CrossRefGoogle ScholarPubMed
Jerrett, M, McConnell, R, Wolch, J, et al. Traffic-related air pollution and obesity formation in children: a longitudinal, multilevel analysis. Environ Health. 2014; 13, 49.CrossRefGoogle ScholarPubMed
Li, J, Li, WX, Bai, C, Song, Y. Particulate matter-induced epigenetic changes and lung cancer. Clin Respir J. 2017; 11, 539–546.CrossRefGoogle ScholarPubMed
Catalanotto, C, Cogoni, C, Zardo, G. MicroRNA in control of gene expression: an overview of nuclear functions. Int J Mol Sci. 2016; 17, pii: E1712.CrossRefGoogle ScholarPubMed
Tanwar, V, Gorr, MW, Velten, M, et al. In utero particulate matter exposure produces heart failure, electrical remodeling, and epigenetic changes at adulthood. J Am Heart Assoc. 2017; 6, pii: e005796.CrossRefGoogle ScholarPubMed
Puddu, A, Sanguineti, R, Mach, F, et al. Update on the protective molecular pathways improving pancreatic beta-cell dysfunction. Mediators Inflamm. 2013; 2013, 750540.CrossRefGoogle ScholarPubMed
Zhou, JY, Xu, B, Li, L. A new role for an old drug: metformin targets MicroRNAs in treating diabetes and cancer. Drug Dev Res. 2015; 76, 263–269.CrossRefGoogle ScholarPubMed
Salomaki, H, Vahatalo, LH, Laurila, K, et al. Prenatal metformin exposure in mice programs the metabolic phenotype of the offspring during a high fat diet at adulthood. PLoS One. 2013; 8, e56594.CrossRefGoogle ScholarPubMed