Advanced SearchSearch Tips
Environmental Pollutants and Epigenetics
facebook(new window)  Pirnt(new window) E-mail(new window) Excel Download
 Title & Authors
Environmental Pollutants and Epigenetics
Park, Sung-Kyun; Lee, Sun-Dong;
  PDF(new window)
Since Barker found associations between low birth weight and several chronic diseases later in life, the hypothesis of fetal origins of adult disease (aka, Barker Hypothesis) and epigenetics have been emerging as a new paradigm for geneenvironment interaction of chronic disease. Epigenetics is the study of heritable changes in gene silencing that occur without any change in DNA sequence. Gene expression can be regulated by several epigenetic mechanisms, including DNA methylation and histone modifications, which may be associated with chronic conditions, such as cancers, cardiovascular disease, and type-2 diabetes. One carbon metabolism which involves the transfer of a methyl group catalyzed by DNA methyltransferase is an important mechanism by which DNA methylation occurs in promoter regions and/or repetitive elements of the genome. Environmental factors may induce epigenetic modification through production of reactive oxygen species, alteration of methyltransferase activity, and/or interference with methyl donors. In this review, we introduce recent studies of epigenetic modification and environmental factors, such as heavy metals, environmental hormones, air pollution, diet and psychosocial stress. We also discuss epigenetic perspectives of early life environmental exposure and late life disease occurrence.
environment;epigenetics;DNA methylation;histone modification;one-carbon metabolism;
 Cited by
최근 보건의료분야에서 활발하게 연구되고 있는 "Epigenetics"란 무엇인가? -기본개념 및 기전을 중심으로-,이선동;박성균;고성규;신헌태;김명동;

대한예방한의학회지, 2010. vol.14. 2, pp.1-12
환경성 발암 기전에서 유전자-환경 상호작용의 역할,한소희;이경무;

한국환경보건학회지, 2010. vol.36. 1, pp.1-13 crossref(new window)
The Role of Gene-environment Interaction in Environmental Carcinogenesis, Korean Journal of Environmental Health Sciences, 2010, 36, 1, 1  crossref(new windwow)
Barker, D. J., Eriksson, J. G., Forsen, T. and Osmond, C. : Fetal origins of adult disease: s trength of effects and biological basis. International Journal of Epidemiology, 31(6), 1235-1239, 2002 crossref(new window)

Barker, D. J. : In utero programming of chronic disease. Clinical Science (Lond), 95(2), 115-128, 1998 crossref(new window)

Tang, W. Y. and Ho, S. M. : Epigenetic reprogramming and imprinting in origins of disease. Reviews in Endocrine & Metabolic Disorders, 8(2), 173-182, 2007 crossref(new window)

Barker, D. J. : Fetal origins of coronary heart disease. British Medical Journal, 311(6998), 171-174, 1995 crossref(new window)

Barker, D. J., Osmond, C., Golding, J., Kuh, D.,Wadsworth, M. E. : Growth in utero, blood pressure in childhood and adult life, and mortality from cardiovascular disease. British Medical Journal, 298(6673), 564-567, 1989 crossref(new window)

Hales, C. N., Barker, D. J., Clark, P. M., Cox, L. J.,Fall, C. and Osmond, C., et al. : Fetal and infant growth and impaired glucose tolerance at age 64. British Medical Journal, 303(6809), 1019-1022, 1991 crossref(new window)

Bolin, C. M., Basha, R, Cox, D., Zawia, N. H., Maloney,B., Lahiri, D. K., et al. : Exposure to lead and the developmental origin of oxidative DNA damage in the aging brain. FASEB Journal, 20(6), 788-790, 2006

Dolinoy, D. C., Huang, D. and Jirtle, R. L. : Maternal nutrient supplementation counteracts bisphenol A-induced DNA hypomethylation in early development. Proceedings of the National Academy of Sciences of the United States of America, 104(32), 13056-13061, 2007 crossref(new window)

Krause, E. T., Honarmand, M., Wetzel, J. and Naguib, M. : Early fasting is long lasting: differences in early nutritional conditions reappear under stressful conditions in adult female zebra finches. Public Library of Science ONE, 4(3), e5015-0000, 2009

Wu, J., Basha, M. R., Brock, B., Cox, D. P., Cardozo-Pelaez, F. and McPherson, C. A, et al. : Alzheimer's disease (AD)-like pathology in aged monkeys after infantile exposure to environmental metal lead (Pb): evidence for a developmental origin and environmentallink for AD. Journal of Neuroscience, 28(1), 3-9, 2008 crossref(new window)

Gluckman, P. D., Hanson, M. A., Cooper, C., Thornburg, K. L. : Effect of in utero and early-life conditions on adult health and disease. New England Journal of Medicine, 359(1), 61-73, 2008 crossref(new window)

Waggoner, D. : Mechanisms of disease: epigenesis. Seminars in Pediatric Neurology, 14(1), 7-14, 2007 crossref(new window)

Waterland, R. A. and Michels, K. B. : Epigenetic epidemiology of the developmental origins hypothesis. Annual Review of Nutrition, 27, 363-388, 2007 crossref(new window)

Esteller, M. : Epigenetics in cancer. New England Journal of Medicine, 358(11), 1148-1159, 2008 crossref(new window)

Lopez, J., Percharde, M., Coley, H. M., Webb, A. and Crook, T. : The context and potential of epigenetics in oncology. British Journal of Cancer, 100(4), 571- 577, 2009 crossref(new window)

Yoo, C. B. and Jones, P. A. : Epigenetic therapy of cancer: past, present and future. Nature Reviews Drug Discovery, 5(1), 37-50, 2006 crossref(new window)

Simmons, R. A. : Developmental origins of beta-cell failure in type 2 diabetes: the role of epigenetic mechanisms. Pediatric Research, 61(5 Pt 2), 64R-67R, 2007 crossref(new window)

Campion, J., Milagro, F. I. and Martinez. J. A. :Individuality and epigenetics in obesity. Obes Rev, 10(4), 383-392, 2009 crossref(new window)

Zawia, N. H., Lahiri, D. K., Cardozo-Pelaez, F. : Epigenetics, oxidative stress, and Alzheimer disease. Free Radical Biology & Medicine, 46(9), 1241-1249, 2009 crossref(new window)

Schanen, N. C. : Epigenetics of autism spectrum disorders. Human Molecular Genetics, 15 Spec No 2, R138-50, 2006 crossref(new window)

Steinke, J. W., Rich, S. S. and Borish, L. : 5. Genetics of allergic disease. Journal of Allergy and Clinical Immunology, 121(2 Suppl), S384-7; quiz S416, 2008

Foley, D. L., Craig, J. M., Morley, R., Olsson, C. A.,Dwyer, T. and Smith, K., et al. : Prospects for epigenetic epigenetic epidemiology. American Journal of Epidemiology, 169(4), 389-400, 2009 crossref(new window)

Holliday, R. : Epigenetics: a historical overview. Epigenetics, 1(2), 76-80, 2006 crossref(new window)

Allis, C. D., Jenuwein, T., Reinberg, D. Overview and Concepts. In: Allis, C. D., Jenuwein, T., Reinberg, D., Caparros, M.-L, eds. Epigenetics. New York: Cold Spring Harbor Laboratory Press, 2007

Robertson, K. D., Wolffe, A. P. : DNA methylation in health and disease. Nature Reviews Genetics, 1(1), 11-19, 2000 crossref(new window)

Slotkin, R. K., Martienssen R. : Transposable elements and the epigenetic regulation of the genome. Nature Reviews Genetics, 8(4), 272-285, 2007 crossref(new window)

Zeisel, S. H. : Importance of methyl donors during reproduction. American Journal of Clinical Nutrition, 89(2), 673S-677S, 2009 crossref(new window)

Vickers, M. H., Gluckman, P. D., Coveny, A. H.,Hofman, P. L., Cutfield, W. S., Gertler, A., et al. :Neonatal leptin treatment reverses developmental programming. Endocrinology, 146(10), 4211-4216, 2005 crossref(new window)

Waterland, R. A, Jirtle, R. L. : Transposable elements:targets for early nutritional effects on epigenetic gene regulation. Molecular and Cellular Biology, 23(15), 5293-5300, 2003 crossref(new window)

Santos, F., Hendrich, B., Reik, W., Dean, W. : Dynamic reprogramming of DNA methylation in the early mouse embryo. Developmental Biology, 241(1), 172-182, 2002 crossref(new window)

Kaneko-Ishino, T., Kohda, T., Ono, R. and Ishino, F. : hypothesis: the necessity of a monoallelic gene expression mechanism in mammalian development. Cytogenetic and Genome Research, 113(1-4), 24-30, 2006 crossref(new window)

Bird, A. : Perceptions of epigenetics. Nature, 447(7143), 396-398, 2007 crossref(new window)

Kaati, G., Bygren, L. O. and Edvinsson, S. : Cardiovascular and diabetes mortality determined by nutrition during parents' and grandparents' slow growth period. European Journal of Human Genetics, 10(11), 682-688, 2002 crossref(new window)

Cheng, R. Y., Hockman, T., Crawford, E., Anderson, L. M. and Shiao, Y. H. : Epigenetic and gene expression changes related to transgenerational carcinogenesis. Molecular Carcinogenesis, 40(1), 1-11, 2004 crossref(new window)

Anway, M. D., Leathers, C. and Skinner, M. K. :Endocrine disruptor vinclozolin induced epigenetic transgenerational adult-onset disease. Endocrinology, 147(12), 5515-5523, 2006 crossref(new window)

Ercal, N., Gurer-Orhan, H., Aykin-Burns, N. : Toxic metals and oxidative stress part I: mechanisms involved in metal-induced oxidative damage. Current Topics in Medicinal Chemistry, 1(6), 529-539, 2001 crossref(new window)

Bindhumol, V., Chitra, K. C. and Mathur, P. P. : Bisphenol A induces reactive oxygen species gener ation in the liver of male rats. Toxicology, 188(2-3), 117-124, 2003 crossref(new window)

Brook, R. D., Franklin, B., Cascio, W., Hong, Y.,Howard, G., Lipsett, M., et al. : Air pollution and cardiovascular disease: a statement for healthcare professionals from the Expert Panel on Population and Prevention Science of the American Heart Association. Circulation, 109(21), 2655-2671, 2004 crossref(new window)

Franco, R., Schoneveld, O., Georgakilas, A. G. and Panayiotidis, M. I. Oxidative stress, DNA methylation and carcinogenesis. Cancer Letters, 266(1), 6-11, 2008 crossref(new window)

Xu, Y., Wang, Y., Zheng, Q., Li, X., Li, B., Jin, Y.,et al. : Association of oxidative stress with arsenic methylation in chronic arsenic-exposed children and adults. Toxicology and Applied Pharmacology, 232(1), 142-149, 2008 crossref(new window)

Prins, G. S., Tang, W. Y., Belmonte, J., Ho and S.M. Perinatal exposure to oestradiol and bisphenol A alters the prostate epigenome and increases susceptibility to carcinogenesis. Basic Clin Pharmacol Toxicol, 102(2), 134-138, 2008 crossref(new window)

Valinluck, V., Tsai, H. H., Rogstad, D. K., Burdzy, A., Bird, A., Sowers, L. C. : Oxidative damage to methyl-CpG sequences inhibits the binding of the methyl-CpG binding domain (MBD) of methyl-CpG binding protein 2 (MeCP2). Nucleic Acids Research, 32(14), 4100-4108, 2004 crossref(new window)

Poirier, L. A., Vlasova, T. I. : The prospective role of abnormal methyl metabolism in cadmium toxicity. Environmental Health Perspectives, 110 Suppl 5, 793-795, 2002 crossref(new window)

Reichard, J. F., Schnekenburger, M. and Puga, A. : Long term low-dose arsenic exposure induces loss of DNA methylation. Biochemical and Biophysical Research Communications, 352(1), 188-192, 2007 crossref(new window)

Takiguchi, M., Achanzar, W. E, Qu, W., Li, G. and Waalkes, M. P. : Effects of cadmium on DNA-(Cytosine-5) methyltransferase activity and DNA methylation status during cadmium-induced cellular transformation. Experimental Cell Research, 286(2), 355-365, 2003 crossref(new window)

Chanda, S., Dasgupta, U. B., Guhamazumder, D.,Gupta, M., Chaudhuri, U. and Lahiri, S., et al. :DNA hypermethylation of promoter of gene p53 and p16 in arsenic-exposed people with and without malignancy. Toxicological Science, 89(2), 431-437, 2006 crossref(new window)

Goering, P. L., Aposhian, H. V., Mass, M. J., Cebrian, M., Beck, B. D.,Waalkes, M. P. : The enigma of arsenic carcinogenesis: role of metabolism. Toxicological Science, 49(1), 5-14, 1999 crossref(new window)

Sutherland, J. E., Costa, M. : Epigenetics and the environment. Annals of the New York Academy of Sciences, 983, 151-160, 2003 crossref(new window)

ATSDR. Toxicological profile for cadmium. Atlanta, GA: U.S. Department of Health & Human Services, 1999

Waalkes, M. P. : Cadmium carcinogenesis in review. Journal of Inorganic Biochemistry, 79(1-4), 241-244, 2000 crossref(new window)

Huang, D., Zhang, Y., Qi, Y., Chen, C. and Ji, W. :Global DNA hypomethylation, rather than reactive oxygen species (ROS), a potential facilitator of cadmium- stimulated K562 cell proliferation. Toxicology Letters, 179(1), 43-47, 2008 crossref(new window)

Jiang, G., Xu, L., Song, S., Zhu, C., Wu, Q. and Zhang. L., et al. : Effects of long-term low-dose cadmium exposure on genomic DNA methylation in human embryo lung fibroblast cells. Toxicology, 244(1), 49-55, 2008 crossref(new window)

Benbrahim-Tallaa, L., Waterland, R. A., Dill, A. L.,Webber, M. M. and Waalkes, M. P. : Tumor suppressor gene inactivation during cadmium-induced malignant transformation of human prostate cells correlates with overexpression of de novo DNA methyltransferase. Environmental Health Perspectives, 115(10), 1454-1459, 2007

Benbrahim-Tallaa, L., Waterland, R. A., Styblo, M.,Achanzar, W. E., Webber, M. M. and Waalkes, M.P. : Molecular events associated with arsenicinduced malignant transformation of human prostatic epithelial cells: aberrant genomic DNA methylation and K-ras oncogene activation. Toxicology and Applied Pharmacology, 206(3), 288-298, 2005 crossref(new window)

Chen, H., Liu, J., Zhao, C. Q,, Diwan, B. A., Merrick,B. A. and Waalkes, M. P. : Association of cmyc overexpression and hyperproliferation with arsenite- induced malignant transformation. Toxicology and Applied Pharmacology, 175(3), 260-268, 2001 crossref(new window)

Sciandrello, G., Caradonna, F., Mauro, M. and Barbata, G. : Arsenic-induced DNA hypomethylation affects chromosomal instability in mammalian cells. Carcinogenesis, 25(3), 413-417, 2004 crossref(new window)

Chai, C. Y., Huang, Y. C., Hung, W. C., Kang, W.Y. and Chen, W. T. : Arsenic salts induced autophagic cell death and hypermethylation of DAPK promoter in SV-40 immortalized human uroepithelial cells. Toxicology Letters, 173(1), 48-56, 2007 crossref(new window)

Chen, W. T., Hung, W. C., Kang, W. Y., Huang, Y.C. and Chai, C. Y. : Urothelial carcinomas arising in arsenic-contaminated areas are associated with hypermethylation of the gene promoter of the deathassociated protein kinase. Histopathology, 51(6), 785-792, 2007 crossref(new window)

Cui, X., Wakai, T., Shirai, Y., Hatakeyama, K. and Hirano, S. : Chronic oral exposure to inorganic arsenate interferes with methylation status of p16INK4a and RASSF1A and induces lung cancer in A/J mice. Toxicological Science, 91(2), 372-381, 2006 crossref(new window)

Zhang, A. H., Bin, H. H., Pan, X. L., Xi and X. G.. :Analysis of p16 gene mutation, deletion and methylation in patients with arseniasis produced by indoor unventilated-stove coal usage in Guizhou, China. Journal of Toxicology and Environmental Health, 70(11), 970-975, 2007 crossref(new window)

Ramirez, T., Brocher, J., Stopper, H. and Hock, R. :Sodium arsenite modulates histone acetylation, histone deacetylase activity and HMGN protein dynamics in human cells. Chromosoma, 117(2), 147-157, 2008 crossref(new window)

Pilsner, J. R., Liu, X., Ahsan, H., Ilievski, V., Slavkovich, V. and Levy, D., et al. : Genomic methylation of peripheral blood leukocyte DNA: influences of arsenic and folate in Bangladeshi adults. American Journal of Clinical Nutrition, 86(4), 1179-1186, 2007

Pilsner, J. R., Liu, X., Ahsan, H., Ilievski, V., Slavkovich, V. and Levy, D., et al. : Folate deficiency, hyperhomocysteinemia, low urinary creatinine, and hypomethylation of leukocyte DNA are risk factors for arsenic-induced skin lesions. Environmental Health Perspectives, 117(2), 254-260, 2009 crossref(new window)

Kanduc, D., Rossiello, M. R., Aresta, A., Cavazza, C., Quagliariello, E. and Farber, E. : Transitory DNA hypomethylation during liver cell proliferation induced by a single dose of lead nitrate. Archives of Biochemistry and Biophysics, 286(1), 212-216, 1991 crossref(new window)

Rossiello, M. R., Aresta, A. M., Prisco, M. and Kanduc, D. : DNA hypomethylation during liver cell proliferation induced by a single dose of lead nitrate. Bollettino Societa Italiana Biologia Sperimentale, 67(12), 993-997, 1991

Basha, M. R., Wei, W., Bakheet, S. A., Benitez, N.,Siddiqi, H. K. and Ge, Y. W., et al. : The fetal basis of amyloidogenesis: exposure to lead and latent overexpression of amyloid precursor protein and beta-amyloid in the aging brain. Journal of Neuroscience, 25(4), 823-829, 2005 crossref(new window)

Pilsner, J. R., Hu, H., Ettinger, A., S\acute{a}nchez, B. N.,Wright, R. O., Cantonwine, D., et al. : Inf luence o f Prenatal Lead Exposure on Genomic Methylation of Cord Blood DNA. Environmental Health Perspectives, (in press), 2009 crossref(new window)

Ji, W., Yang, L., Yu, L., Yuan, J., Hu, D. and Zhang, W., et al. : Epigenetic silencing of O6-methylguanine DNA methyltransferase gene in NiS-transformed cells. Carcinogenesis, 29(6), 1267-1275, 2008 crossref(new window)

Ke, Q., Davidson, T., Chen, H., Kluz, T. and Costa, M. : Alterations of histone modifications and transgene silencing by nickel chloride. Carcinogenesis, 27(7), 1481-1488, 2006 crossref(new window)

Lee, Y. W., Klein, C. B., Kargacin, B., Salnikow, K., Kitahara, J. and Dowjat. K., et al. : Carcinogenic nickel silences gene expression by chromatin condensation and DNA methylation: a new model for epigenetic carcinogens. Molecular and Cellular Biology, 15(5), 2547-2557, 1995

Kondo, K., Takahashi, Y., Hirose, Y., Nagao, T.,Tsuyuguchi, M. and Hashimoto, M., et al. : The reduced expression and aberrant methylation of p16(INK4a) in chromate workers with lung cancer. Lung Cancer, 53(3), 295-302, 2006 crossref(new window)

Schnekenburger, M., Talaska, G. and Puga, A. : Chromium cross-links histone deacetylase 1-DNA methyltransferase 1 complexes to chromatin, inhibiting histone-remodeling marks critical for transcriptional activation. Molecular and Cellular Biology, 27(20), 7089-7101, 2007 crossref(new window)

NTP, CERHR. NTP-CERHR Monograph on the potential human reproductive and developmental effects of bisphenol A. National Institutes of Health 2008

Maffini, M. V., Rubin, B. S., Sonnenschein, C. and Soto, A. M. : Endocrine disruptors and reproductive health: the case of bisphenol-A. Molecular and Cellular Endocrinology, 254-255, 179-186, 2006 crossref(new window)

Welshons, W. V., Nagel, S. C. and vom Saal, F. S. :Large effects from small exposures. III. Endocrine mechanisms mediating effects of bisphenol A at levels of human exposure. Endocrinology, 147(6 Suppl), S56-69, 2006 crossref(new window)

Ho, S. M., Tang, W. Y., Belmonte, de Frausto, J. and Prins, G. S. : Developmental exposure to estradiol and bisphenol A increases susceptibility to prostate carcinogenesis and epigenetically regulates phosphodiesterase type 4 variant 4. Cancer Research, 66(11), 5624-5632, 2006 crossref(new window)

Rubin, M. M. : Antenatal exposure to DES: lessons learned...future concerns. Obstetrical & Gynecological Survey, 62(8), 548-555, 2007 crossref(new window)

84Li, S., Hansman, R., Newbold, R., Davis, B., McLachlan, J. A. and Barrett, J. C. : Neonatal diethylstilbestrol exposure induces persistent elevation of c-fos expression and hypomethylation in its exon-4 in mouse uterus. Molecular Carcinogenesis, 38(2), 78-84, 2003 crossref(new window)

Li, S., Washburn, K. A., Moore, R., Uno, T., Teng, C. and Newbold, R. R., et al. : Developmental exposure to diethylstilbestrol elicits demethylation of estrogen-responsive lactoferrin gene in mouse uterus. Cancer Research, 57(19), 4356-4359, 1997

Sato, K., Fukata, H., Kogo, Y., Ohgane, J., Shiota, K. and Mori, C. : Neonatal exposure to diethylstilbestrol alters the expression of DNA methyltransferases and methylation of genomic DNA in the epididymis of mice. Endocrine Journal, 53(3), 331-337, 2006 crossref(new window)

Tang, W. Y., Newbold, R., Mardilovich, K., Jefferson, W., Cheng, R. Y. and Medvedovic, M., et al. :Persistent hypomethylation in the promoter of nucleosomal binding protein 1 (Nsbp1) correlates with overexpression of Nsbp1 in mouse uteri neonatally exposed to diethylstilbestrol or genistein. Endocrinology, 149(12), 5922-5931, 2008 crossref(new window)

Newbold, R. R., Padilla-Banks, E. and Jefferson, W.N. : Adverse effects of the model environmental estrogen diethylstilbestrol are transmitted to subsequent generations. Endocrinology, 147(6 Suppl), S11-7, 2006 crossref(new window)

Anway, M. D., Cupp, A. S., Uzumcu, M. and Skinner, M. K. : Epigenetic transgenerational actions of endocrine disruptors and male fertility. Science, 308(5727), 1466-1469, 2005 crossref(new window)

Crews, D., Gore, A. C., Hsu, T. S., Dangleben, N.L., Spinetta, M. and Schallert, T., et al. : Transgenerational epigenetic imprints on mate preference. Proceedings of the National Academy of Sciences of the United States of America, 104(14), 5942-5946, 2007 crossref(new window)

Rusiecki, J. A., Baccarelli, A., Bollati, V., Tarantini, L., Moore, L. E. and Bonefeld-Jorgensen, E. C. :Global DNA hypomethylation is associated with high serum-persistent organic pollutants in Greenlandic Inuit. Environmental Health Perspectives, 116(11), 1547-1552, 2008 crossref(new window)

Bunger, M. K., Glover, E., Moran, S. M., Walisser, J. A., Lahvis, G. P. and Hsu, E. L., et al. : Abnormal liver development and resistance to 2,3,7,8-tetrachlorodibenzo-p-dioxin toxicity in mice carrying a mutation in the DNA-binding domain of the aryl hydrocarbon receptor. Toxicological Science, 106(1), 83-92, 2008 crossref(new window)

Okey, A. B. : An aryl hydrocarbon receptor odyssey to the shores of toxicology: the Deichmann Lecture, International Congress of Toxicology-XI. Toxicological Science, 98(1), 5-38, 2007 crossref(new window)

Wu, Q., Ohsako, S., Ishimura, R., Suzuki, and J. S.,Tohyama, C. : Exposure of mouse preimplantation embryos to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) alters the methylation status o f imprinted genes H19 and Igf2. Biology of Reproduction, 70(6), 1790-1797, 2004 crossref(new window)

Schwartz, J. : Air pollution and children's health. Pediatrics, 113(4 Suppl), 1037-1043, 2004

Baccarelli, A., Wright, R. O., Bollati, V., Tarantini, L., Litonjua, A. A. and Suh, H. H., et al. : Rapid DNA methylation changes after exposure to traffic particles. American Journal of Respiratory and Critical Care Medicine, 179(7), 572-578, 2009 crossref(new window)

Perera, F., Tang, W. Y., Herbstman, J., Tang, D.,Levin, L. and Miller, R., et al. : R elation of DNA methylation of 5'-CpG island of ACSL3 to transplacental exposure to airborne polycyclic aromatic hydrocarbons and childhood asthma. Public Library of Science ONE, 4(2), e4488, 2009 crossref(new window)

Tarantini, L., Bonzini, M., Apostoli, P., Pegoraro, V., Bollati, V. and Marinelli. B, et al. : E f f ects o f particulate matter on genomic DNA methylation content and iNOS promoter methylation. Environmental Environmental Health Perspectives, 117(2), 217-222, 2009 crossref(new window)

Belinsky, S. A., Snow, S. S., Nikula, K. J., Finch, G.L., Tellez, C. S. and Palmisano, W. A. : Aberrant CpG island methylation of the p16(INK4a) and estrogen receptor genes in rat lung tumors induced by particulate carcinogens. Carcinogenesis, 23(2), 335-339, 2002 crossref(new window)

Park, S. K., O'Neill, M. S., Vokonas, P. S., Sparrow, D., Spiro, A., 3rd and Tucker, K. L., et al. :Traffic-related particles are associated with elevated homocysteine: the VA normative aging study. American Journal of Respiratory and Critical Care Medicine, 178(3), 283-289, 2008 crossref(new window)

Cobiac, L. : Epigenomics and nutrition. Forum of Nutrition, 60, 31-41, 2007 crossref(new window)

Gallou-Kabani, C., Vige, A., Gross, M. S. and Junien, C. : Nutri-epigenomics: lifelong remodelling of our epigenomes by nutritional and metabolic factors and beyond. Clinical Chemistry and Laboratory Medicine, 45(3), 321-327, 2007 crossref(new window)

Baccarelli, A., Cassano, P. A., Litonjua, A., Park, S.K., Suh, H. and Sparrow, D., et al. : Cardiac autonomic dysfunction: effects from particulate air pollution and protection by dietary methyl nutrients and metabolic polymorphisms. Circulation, 117(14), 1802-1809, 2008 crossref(new window)

Fish, E. W., Shahrokh, D., Bagot, R., Caldji, C.,Bredy, T. and Szyf, M., et al. : Epigenetic programming of stress responses through variations in maternal care. Annals of the New York Academy of Sciences, 1036, 167-180, 2004 crossref(new window)

Szyf, M., Weaver, I., Meaney, M. : Maternal care, the epigenome and phenotypic differences in behavior. Reproductive Toxicology, 24(1), 9-19, 2007 crossref(new window)