294
38. Clemons GP, Sisler H. Localization of the site of action of a fungitoxic benomyl derivative.
Pestic Biochem Physiol. 1971;1(1):32–43.
39. O’Malley M. The regulatory evaluation of the skin effects of pesticides. In: Hayes’ handbook
of pesticide toxicology. Amsterdam: Elsevier; 2010. p. 701–87.
40. Mahajan R, Blair A, Coble J, Lynch CF, Hoppin JA, Sandler DP, et al. Carbaryl exposure and
incident cancer in the Agricultural Health Study. Int J Cancer. 2007;121(8):1799–805.
41. Singh S, Singh N, Kumar V, Datta S, Wani AB, Singh D, et al. Toxicity, monitoring and biodegradation of the fungicide carbendazim. Environ Chem Lett. 2016;14(3):317–29.
42. Vialaton D, Pilichowski J-F, Baglio D, Paya-Perez A, Larsen B, Richard C. Phototransformation
of propiconazole in aqueous media. J Agric Food Chem. 2001;49(11):5377–82.
43. Heindel JJ, Blumberg B, Cave M, Machtinger R, Mantovani A, Mendez MA, et al. Metabolism
disrupting chemicals and metabolic disorders. Reprod Toxicol. 2017;68:3–33.
44. Heindel JJ, Balbus J, Birnbaum L, Brune-Drisse MN, Grandjean P, Gray K, et al.
Developmental origins of health and disease: integrating environmental influences.
Endocrinology. 2015;156(10):3416–21.
45. Newbold RR, Padilla-Banks E, Jefferson WN. Adverse effects of the model environmental estrogen diethylstilbestrol are transmitted to subsequent generations. Endocrinology.
2006;147(6):s11–s7.
46. Newbold RR, Padilla-Banks E, Snyder RJ, Jefferson WN. Perinatal exposure to environmental estrogens and the development of obesity. Mol Nutr Food Res. 2007;51(7):912–7.
47. Smith CJ, Ryckman KK. Epigenetic and developmental influences on the risk of obesity,
diabetes, and metabolic syndrome. Diabete Metab Syndr Obes: Target Ther. 2015;8:295.
48. Stel J, Legler J. The role of epigenetics in the latent effects of early life exposure to obesogenic endocrine disrupting chemicals. Endocrinology. 2015;156(10):3466–72.
49. Treviño LS, Wang Q, Walker CL. Phosphorylation of epigenetic “readers, writers and erasers”: implications for developmental reprogramming and the epigenetic basis for health and
disease. Prog Biophys Mol Biol. 2015;118(1–2):8–13.
50. Holbrook JD. An epigenetic escape route. Trends Genet. 2015;31(1):2–4.
51. Martínez JA, Milagro FI, Claycombe KJ, Schalinske KL. Epigenetics in adipose tissue, obesity, weight loss, and diabetes. Adv Nutr. 2014;5(1):71–81.
52. Wadhwa PD, Buss C, Entringer S, Swanson JM, editors. Developmental origins of health
and disease: brief history of the approach and current focus on epigenetic mechanisms. In:
Seminars in reproductive medicine. New York: Thieme Medical Publishers; 2009.
53. Scarpato R, Migliore L, Angotzi G, Fedi A, Miligi L, Loprieno N. Cytogenetic monitoring of
a group of Italian floriculturists: no evidence of DNA damage related to pesticide exposure.
Mutat Res Genet Toxicol. 1996;367(2):73–82.
54. Oesch F, Herrero ME, Hengstler JG, Lohmann M, Arand M. Metabolic detoxification: implications for thresholds. Toxicol Pathol. 2000;28(3):382–7.
55. Hodgson E, Levi PE. Textbook of modern toxicology. Oxford: Elsevier; 1987.
56. Abass K, Turpeinen M, Rautio A, Hakkola J, Pelkonen O. Metabolism of pesticides by human
cytochrome P450 enzymes in vitro–a survey. In: Insecticides—advances in integrated pest
management. Croatia: InTech; 2012. p. 165–94.
57. Ho S-M, Cheong A, Adgent MA, Veevers J, Suen AA, Tam NN, et al. Environmental factors, epigenetics, and developmental origin of reproductive disorders. Reprod Toxicol. 2017;
68:85–104.
58. Rhodes CJ. Type 2 diabetes-a matter of ß-cell life and death? Science. 2005;307(5708):380–4.
59. Kahn S. The relative contributions of insulin resistance and beta-cell dysfunction to the
pathophysiology of type 2 diabetes. Diabetologia. 2003;46(1):3–19.
60. Alonso-Magdalena P, Quesada I, Nadal A. Endocrine disruptors in the etiology of type 2
diabetes mellitus. Nat Rev Endocrinol. 2011;7(6):346.
61. Utzschneider KM, Van de Lagemaat A, Faulenbach MV, Goedecke JH, Carr DB, Boyko EJ,
et al. Insulin resistance is the best predictor of the metabolic syndrome in subjects with a firstdegree relative with type 2 diabetes. Obesity. 2010;18(9):1781–7.
S. Kamal et al.
38. Clemons GP, Sisler H. Localization of the site of action of a fungitoxic benomyl derivative.
Pestic Biochem Physiol. 1971;1(1):32–43.
39. O’Malley M. The regulatory evaluation of the skin effects of pesticides. In: Hayes’ handbook
of pesticide toxicology. Amsterdam: Elsevier; 2010. p. 701–87.
40. Mahajan R, Blair A, Coble J, Lynch CF, Hoppin JA, Sandler DP, et al. Carbaryl exposure and
incident cancer in the Agricultural Health Study. Int J Cancer. 2007;121(8):1799–805.
41. Singh S, Singh N, Kumar V, Datta S, Wani AB, Singh D, et al. Toxicity, monitoring and biodegradation of the fungicide carbendazim. Environ Chem Lett. 2016;14(3):317–29.
42. Vialaton D, Pilichowski J-F, Baglio D, Paya-Perez A, Larsen B, Richard C. Phototransformation
of propiconazole in aqueous media. J Agric Food Chem. 2001;49(11):5377–82.
43. Heindel JJ, Blumberg B, Cave M, Machtinger R, Mantovani A, Mendez MA, et al. Metabolism
disrupting chemicals and metabolic disorders. Reprod Toxicol. 2017;68:3–33.
44. Heindel JJ, Balbus J, Birnbaum L, Brune-Drisse MN, Grandjean P, Gray K, et al.
Developmental origins of health and disease: integrating environmental influences.
Endocrinology. 2015;156(10):3416–21.
45. Newbold RR, Padilla-Banks E, Jefferson WN. Adverse effects of the model environmental estrogen diethylstilbestrol are transmitted to subsequent generations. Endocrinology.
2006;147(6):s11–s7.
46. Newbold RR, Padilla-Banks E, Snyder RJ, Jefferson WN. Perinatal exposure to environmental estrogens and the development of obesity. Mol Nutr Food Res. 2007;51(7):912–7.
47. Smith CJ, Ryckman KK. Epigenetic and developmental influences on the risk of obesity,
diabetes, and metabolic syndrome. Diabete Metab Syndr Obes: Target Ther. 2015;8:295.
48. Stel J, Legler J. The role of epigenetics in the latent effects of early life exposure to obesogenic endocrine disrupting chemicals. Endocrinology. 2015;156(10):3466–72.
49. Treviño LS, Wang Q, Walker CL. Phosphorylation of epigenetic “readers, writers and erasers”: implications for developmental reprogramming and the epigenetic basis for health and
disease. Prog Biophys Mol Biol. 2015;118(1–2):8–13.
50. Holbrook JD. An epigenetic escape route. Trends Genet. 2015;31(1):2–4.
51. Martínez JA, Milagro FI, Claycombe KJ, Schalinske KL. Epigenetics in adipose tissue, obesity, weight loss, and diabetes. Adv Nutr. 2014;5(1):71–81.
52. Wadhwa PD, Buss C, Entringer S, Swanson JM, editors. Developmental origins of health
and disease: brief history of the approach and current focus on epigenetic mechanisms. In:
Seminars in reproductive medicine. New York: Thieme Medical Publishers; 2009.
53. Scarpato R, Migliore L, Angotzi G, Fedi A, Miligi L, Loprieno N. Cytogenetic monitoring of
a group of Italian floriculturists: no evidence of DNA damage related to pesticide exposure.
Mutat Res Genet Toxicol. 1996;367(2):73–82.
54. Oesch F, Herrero ME, Hengstler JG, Lohmann M, Arand M. Metabolic detoxification: implications for thresholds. Toxicol Pathol. 2000;28(3):382–7.
55. Hodgson E, Levi PE. Textbook of modern toxicology. Oxford: Elsevier; 1987.
56. Abass K, Turpeinen M, Rautio A, Hakkola J, Pelkonen O. Metabolism of pesticides by human
cytochrome P450 enzymes in vitro–a survey. In: Insecticides—advances in integrated pest
management. Croatia: InTech; 2012. p. 165–94.
57. Ho S-M, Cheong A, Adgent MA, Veevers J, Suen AA, Tam NN, et al. Environmental factors, epigenetics, and developmental origin of reproductive disorders. Reprod Toxicol. 2017;
68:85–104.
58. Rhodes CJ. Type 2 diabetes-a matter of ß-cell life and death? Science. 2005;307(5708):380–4.
59. Kahn S. The relative contributions of insulin resistance and beta-cell dysfunction to the
pathophysiology of type 2 diabetes. Diabetologia. 2003;46(1):3–19.
60. Alonso-Magdalena P, Quesada I, Nadal A. Endocrine disruptors in the etiology of type 2
diabetes mellitus. Nat Rev Endocrinol. 2011;7(6):346.
61. Utzschneider KM, Van de Lagemaat A, Faulenbach MV, Goedecke JH, Carr DB, Boyko EJ,
et al. Insulin resistance is the best predictor of the metabolic syndrome in subjects with a firstdegree relative with type 2 diabetes. Obesity. 2010;18(9):1781–7.
S. Kamal et al.