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完整後設資料紀錄
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.advisor | 陳保中 | |
dc.contributor.author | Yu-Chuan Chen | en |
dc.contributor.author | 陳郁荃 | zh_TW |
dc.date.accessioned | 2021-06-13T15:39:39Z | - |
dc.date.available | 2017-08-09 | |
dc.date.copyright | 2011-10-03 | |
dc.date.issued | 2011 | |
dc.date.submitted | 2011-08-10 | |
dc.identifier.citation | Reference 1
1. Grandjean P. and Landrigan P.J. Developmental neurotoxicity of industrial chemicals. Lancet 2006; 368(9553): 2167-78. 2. Takser L., Mergler D., Hellier G., Sahuquillo J., and Huel G. Manganese, monoamine metabolite levels at birth, and child psychomotor development. Neurotoxicology 2003; 24(4-5): 667-74. 3. Su F.C., Liao H.F., Hwang Y.H., Hsieh W.S., Wu H.C., Jeng S.F., Su Y.N., and Chen P.C. In utero exposure to manganese and psychomotor development at the age of six months. Journal of Occupational Safety and Health 2007; 15: 204-217. 4. Claus Henn B., Ettinger A.S., Schwartz J., Tellez-Rojo M.M., Lamadrid-Figueroa H., Hernandez-Avila M., Schnaas L., Amarasiriwardena C., Bellinger D.C., Hu H., and Wright R.O. Early postnatal blood manganese levels and children's neurodevelopment. Epidemiology 2010; 21(4): 433-9. 5. Landrigan P.J., Whitworth R.H., Baloh R.W., Staehling N.W., Barthel W.F., and Rosenblum B.F. Neuropsychological dysfunction in children with chronic low-level lead absorption. Lancet 1975; 1(7909): 708-12. 6. Needleman H.L., Gunnoe C., Leviton A., Reed R., Peresie H., Maher C., and Barrett P. Deficits in psychologic and classroom performance of children with elevated dentine lead levels. N Engl J Med 1979; 300(13): 689-95. 7. CDC (Centers for Disease Control and Prevention), Preventing lead exposure in young children: a housing-based approach to primary prevention of lead poisoning. CDC 1991; available from http://www.cdc.gov/nceh/lead/publications/PrimaryPreventionDocument.pdf. 8. Canfield R.L., Henderson C.R., Jr., Cory-Slechta D.A., Cox C., Jusko T.A., and Lanphear B.P. Intellectual impairment in children with blood lead concentrations below 10 microg per deciliter. N Engl J Med 2003; 348(16): 1517-26. 9. Bellinger D.C. Very low lead exposures and children's neurodevelopment. Curr Opin Pediatr 2008; 20(2): 172-7. 10. Jedrychowski W., Perera F.P., Jankowski J., Mrozek-Budzyn D., Mroz E., Flak E., Edwards S., Skarupa A., and Lisowska-Miszczyk I. Very low prenatal exposure to lead and mental development of children in infancy and early childhood: Krakow prospective cohort study. Neuroepidemiology 2009; 32(4): 270-8. 11. Dong J. and Su S.Y. The association between arsenic and children's intelligence: a meta-analysis. Biol Trace Elem Res 2009; 129(1-3): 88-93. 12. Kjellstrom T., Kennedy P., Wallis S., Stewart A., Friberg L., and Lind B. Physical and mental development of children with prenatal exposure to mercury from fish. Stage II: interviews and psychological tests at age 6. National Swedish Environmental Protection Board 1989: report 3642. 13. Grandjean P., Weihe P., White R.F., Debes F., Araki S., Yokoyama K., Murata K., Sorensen N., Dahl R., and Jorgensen P.J. Cognitive deficit in 7-year-old children with prenatal exposure to methylmercury. Neurotoxicol Teratol 1997; 19(6): 417-28. 14. Gao Y., Yan C.H., Tian Y., Wang Y., Xie H.F., Zhou X., Yu X.D., Yu X.G., Tong S., Zhou Q.X., and Shen X.M. Prenatal exposure to mercury and neurobehavioral development of neonates in Zhoushan City, China. Environ Res 2007; 105(3): 390-9. 15. Chandra A.V., Ali M.M., Saxena D.K., and Murthy R.C. Behavioral and neurochemical changes in rats simultaneously exposed to manganese and lead. Arch Toxicol 1981; 49(1): 49-56. 16. Chandra S.V., Murthy R.C., Saxena D.K., and Lal B. Effects of pre- and postnatal combined exposure to Pb and Mn on brain development in rats. Ind Health 1983; 21(4): 273-9. 17. Kim Y., Kim B.N., Hong Y.C., Shin M.S., Yoo H.J., Kim J.W., Bhang S.Y., and Cho S.C. Co-exposure to environmental lead and manganese affects the intelligence of school-aged children. Neurotoxicology 2009; 30(4): 564-71. 18. Liu J.-H., Wu H.-C., Chen P.-C., Guo L.Y.-L., and Hwang Y.-H. Concentration distributions of elements in umbilical cord blood in Taiwan. Taiwan journal of public health 2009; 28(5): 420-435. 19. Wang T., Su C., Liao H., Lin L., Chou K., and Lin S. The standardization of the Comprehensive Developmental Inventory for Infants and Toddlers. Psychol Test 1998: 19-46 [in Chinese; English abstract]. 20. Liao H.F., Wang T.M., Yao G., and Lee W.T. Concurrent validity of the Comprehensive Developmental Inventory for Infants and Toddlers with the Bayley Scales of Infant Development-II in preterm infants. J Formos Med Assoc 2005; 104(10): 731-7. 21. Liao H.F. and Pan Y.L. Test-retest and inter-rater reliability for the Comprehensive Developmental Inventory for Infants and Toddlers diagnostic and screening tests. Early Hum Dev 2005; 81(11): 927-37. 22. Carlson D., Labarba R., Sclafani J., and Bowers C. Cognitive and motor development in infants of adolescent mothers: A longitudinal analysis. . Int J Behav 1985; 9: 1-13. 23. Bradley R.H., Caldwell B.M., Rock S.L., Ramey C.T., Barnard K.E., Gray C., Hammond M.A., Mitchell S., Gottfried A.W., Siegel L., and Johnson D.L. Home environment and cognitive development in the 1st 3 years of life-a collaborative study involving 6 sites and 3 ethnic-groups in north America. . Dev Psychol 1989; 25: 217-235. 24. Bradley R.H., Burchinal M., and Casey P.H. Early intervention: The moderating role of the home environment. Applied Developmental Science 2001; 5(1): 2-8. 25. Bradley R.H. and Caldwell B.M. The relation of infants' home environments to achievement test performance in first grade: a follow-up study. Child Dev 1984; 55(3): 803-9. 26. Zota A.R., Ettinger A.S., Bouchard M., Amarasiriwardena C.J., Schwartz J., Hu H., and Wright R.O. Maternal blood manganese levels and infant birth weight. Epidemiology 2009; 20(3): 367-73. 27. Abdelouahab N., Huel G., Suvorov A., Foliguet B., Goua V., Debotte G., Sahuquillo J., Charles M.A., and Takser L. Monoamine oxidase activity in placenta in relation to manganese, cadmium, lead, and mercury at delivery. Neurotoxicol Teratol 2010; 32(2): 256-61. 28. Jones E.A., Wright J.M., Rice G., Buckley B.T., Magsumbol M.S., Barr D.B., and Williams B.L. Metal exposures in an inner-city neonatal population. Environ Int 2010; 36(7): 649-54. 29. Takser L., Mergler D., and Lafond J. Very low level environmental exposure to lead and prolactin levels during pregnancy. Neurotoxicol Teratol 2005; 27(3): 505-8. 30. Hwang Y.H., Ko Y., Chiang C.D., Hsu S.P., Lee Y.H., Yu C.H., Chiou C.H., Wang J.D., and Chuang H.Y. Transition of cord blood lead level, 1985-2002, in the Taipei area and its determinants after the cease of leaded gasoline use. Environ Res 2004; 96(3): 274-82. 31. Chen J.J., Master Thesis: Characteristics of metals elements in both gasoline and engine exhaust,Department of Environmental Engineering, Cheng-Kung University 2002. 32. Lin Y.Y., Leon Guo Y.L., Chen P.C., Liu J.H., Wu H.C., and Hwang Y.H. Associations between petrol-station density and manganese and lead in the cord blood of newborns living in Taiwan. Environ Res 2011; 111(2): 260-5. 33. Jiang C.B., Yeh C.Y., Lee H.C., Chen M.J., Hung F.Y., Fang S.S., and Chien L.C. Mercury concentration in meconium and risk assessment of fish consumption among pregnant women in Taiwan. Sci Total Environ 2010; 408(3): 518-23. 34. Han B., Jeng W.L., Chen R.Y., Fang G.T., Hung T.C., and Tseng R.J. Estimation of target hazard quotients and potential health risks for metals by consumption of seafood in Taiwan. Arch Environ Contam Toxicol 1998; 35(4): 711-20. 35. Ericson J.E., Crinella F.M., Clarke-Stewart K.A., Allhusen V.D., Chan T., and Robertson R.T. Prenatal manganese levels linked to childhood behavioral disinhibition. Neurotoxicol Teratol 2007; 29(2): 181-7. 36. Menezes-Filho J.A., Novaes Cde O., Moreira J.C., Sarcinelli P.N., and Mergler D. Elevated manganese and cognitive performance in school-aged children and their mothers. Environ Res 2011; 111(1): 156-63. 37. Lanphear B.P., Hornung R., Khoury J., Yolton K., Baghurst P., Bellinger D.C., Canfield R.L., Dietrich K.N., Bornschein R., Greene T., Rothenberg S.J., Needleman H.L., Schnaas L., Wasserman G., Graziano J., and Roberts R. Low-level environmental lead exposure and children's intellectual function: an international pooled analysis. Environ Health Perspect 2005; 113(7): 894-9. 38. Herrmann M., King K., and Weitzman M. Prenatal tobacco smoke and postnatal secondhand smoke exposure and child neurodevelopment. Curr Opin Pediatr 2008; 20(2): 184-90. 39. ATSDR (Agency for Toxic Substances and Disease Registry). Toxicological profile for mercury. ATSDR 1999. 40. Davidson P.W., Myers G.J., Cox C., Axtell C., Shamlaye C., Sloane-Reeves J., Cernichiari E., Needham L., Choi A., Wang Y., Berlin M., and Clarkson T.W. Effects of prenatal and postnatal methylmercury exposure from fish consumption on neurodevelopment: outcomes at 66 months of age in the Seychelles Child Development Study. JAMA 1998; 280(8): 701-7. References 2 1. Amended final report on the safety assessment of polyacrylamide and acrylamide residues in cosmetics. Int J Toxicol 2005; 24(Suppl 2): 21-50. 2. Smith C.J., Perfetti T.A., Rumple M.A., Rodgman A., and Doolittle D.J. 'IARC group 2A Carcinogens' reported in cigarette mainstream smoke. Food Chem Toxicol 2000; 38(4): 371-383. 3. Tareke E., Rydberg P., Karlsson P., Eriksson S., and Tornqvist M. Analysis of acrylamide, a carcinogen formed in heated foodstuffs. J Agric Food Chem 2002; 50(17): 4998-5006. 4. Mottram D.S., Wedzicha B.L., and Dodson A.T. Acrylamide is formed in the Maillard reaction. Nature 2002; 419(6906): 448-449. 5. Stadler R.H., Blank I., Varga N., Robert F., Hau J., Guy P.A., Robert M.C., and Riediker S. Acrylamide from Maillard reaction products. Nature 2002; 419(6906): 449-450. 6. Sharp D. Acrylamide in food. Lancet 2003; 361(9355): 361-362. 7. WHO (World Health Organisation). FAO/WHO Consultation of the health implications of acrylamide in food. Summary report of a meetingheld in Geneva. WHO 2002; available from http://ntp.niehs.nih.gov/ntp/htdocs/Chem_Background/ExSumPdf/Acrylamide.pdf. 8. Shipp A., Lawrence G., Gentry R., McDonald T., Bartow H., Bounds J., Macdonald N., Clewell H., Allen B., and Van Landingham C. Acrylamide: review of toxicity data and dose-response analyses for cancer and noncancer effects. Crit Rev Toxicol 2006; 36(6-7): 481-608. 9. IARC (International Agency for Research on Cancer). IARC monographs on the evaluation of the carcinogenic risk of chemicals to humans. Some industrial chemicals -acrylamide. IARC 1994: 389-433. 10. WHO (World Health Organisation). Summary and conclusions of the sixty-fourth meeting of the Joint FAO/WHO Expert Committee on Food Additives (JECFA). WHO 2005; available from http://www.who.int/entity/ipcs/food/jecfa/summaries/summary_report_64_final.pdf. 11. Sickles D.W., Stone J.D., and Friedman M.A. Fast axonal transport: a site of acrylamide neurotoxicity? Neurotoxicology 2002; 23(2): 223-51. 12. LoPachin R.M., Ross J.F., and Lehning E.J. Nerve terminals as the primary site of acrylamide action: a hypothesis. Neurotoxicology 2002; 23(1): 43-59. 13. Rice J.M. The carcinogenicity of acrylamide. Mutat Res 2005; 580(1-2): 3-20. 14. Johnson K.A., Gorzinski S.J., Bodner K.M., Campbell R.A., Wolf C.H., Friedman M.A., and Mast R.W. Chronic toxicity and oncogenicity study on acrylamide incorporated in the drinking water of Fischer 344 rats. Toxicol Appl Pharmacol 1986; 85(2): 154-68. 15. Friedman M.A., Dulak L.H., and Stedham M.A. A lifetime oncogenicity study in rats with acrylamide. Fundam Appl Toxicol 1995; 27(1): 95-105. 16. Larsson S.C., Akesson A., and Wolk A. Long-term dietary acrylamide intake and breast cancer risk in a prospective cohort of Swedish women. Am J Epidemiol 2009; 169(3): 376-381. 17. Pelucchi C., Galeone C., Levi F., Negri E., Franceschi S., Talamini R., Bosetti C., Giacosa A., and La Vecchia C. Dietary acrylamide and human cancer. Int J Cancer 2006; 118(2): 467-471. 18. Mucci L.A. and Wilson K.M. Acrylamide intake through diet and human cancer risk. J Agric Food Chem 2008; 56(15): 6013-6019. 19. Yousef M.I. and El-Demerdash F.M. Acrylamide-induced oxidative stress and biochemical perturbations in rats. Toxicology 2006; 219(1-3): 133-41. 20. Totani N., Yawata M., Ojiri Y., and Fujioka Y. Effects of trace acrylamide intake in Wistar rats. J Oleo Sci 2007; 56(9): 501-6. 21. Lin C.Y., Lin Y.C., Kuo H.K., Hwang J.J., Lin J.L., Chen P.C., and Lin L.Y. Association among acrylamide, blood insulin, and insulin resistance in adults. Diabetes Care 2009; 32(12): 2206-11. 22. Boettcher M.I., Schettgen T., Kutting B., Pischetsrieder M., and Angerer J. Mercapturic acids of acrylamide and glycidamide as biomarkers of the internal exposure to acrylamide in the general population. Mutat Res 2005; 580(1-2): 167-76. 23. Fennell T.R., Sumner S.C., Snyder R.W., Burgess J., Spicer R., Bridson W.E., and Friedman M.A. Metabolism and hemoglobin adduct formation of acrylamide in humans. Toxicol Sci 2005; 85(1): 447-59. 24. Huang Y.F., Wu K.Y., Liou S.H., Uang S.N., Chen C.C., Shih W.C., Lee S.C., Huang C.C., and Chen M.L. Biological monitoring for occupational acrylamide exposure from acrylamide production workers. Int Arch Occup Environ Health 2011; 84(3): 303-13. 25. Hartmann E.C., Boettcher M.I., Bolt H.M., Drexler H., and Angerer J. N-Acetyl-S-(1-carbamoyl-2-hydroxy-ethyl)-L-cysteine (iso-GAMA) a further product of human metabolism of acrylamide: comparison with the simultaneously excreted other mercaptuic acids. Arch Toxicol 2009; 83(7): 731-734. 26. Boettcher M.I. and Angerer J. Determination of the major mercapturic acids of acrylamide and glycidamide in human urine by LC-ESI-MS/MS. J Chromatogr B Analyt Technol Biomed Life Sci 2005; 824(1-2): 283-94. 27. Huang C.C., Li C.M., Wu C.F., Jao S.P., and Wu K.Y. Analysis of urinary N-acetyl-S-(propionamide)-cysteine as a biomarker for the assessment of acrylamide exposure in smokers. Environ Res 2007; 104(3): 346-51. 28. Urban M., Kavvadias D., Riedel K., Scherer G., and Tricker A.R. Urinary mercapturic acids and a hemoglobin adduct for the dosimetry of acrylamide exposure in smokers and nonsmokers. Inhal Toxicol 2006; 18(10): 831-9. 29. Heudorf U., Hartmann E., and Angerer J. Acrylamide in children--exposure assessment via urinary acrylamide metabolites as biomarkers. Int J Hyg Environ Health 2009; 212(2): 135-41. 30. Dybing E., Farmer P.B., Andersen M., Fennell T.R., Lalljie S.P., Muller D.J., Olin S., Petersen B.J., Schlatter J., Scholz G., Scimeca J.A., Slimani N., Tornqvist M., Tuijtelaars S., and Verger P. Human exposure and internal dose assessments of acrylamide in food. Food Chem Toxicol 2005; 43(3): 365-410. 31. Tsai C.W., Kuo C.C., Wu C.F., Chien K.L., Wu V.C., Chen M.F., Sung F.C., and Su T.C. Associations of renal vascular resistance with albuminuria in adolescents and young adults. Nephrol Dial Transplant 2011. 32. Kopp E.K., Sieber M., Kellert M., and Dekant W. Rapid and sensitive HILIC-ESI-MS/MS quantitation of polar metabolites of acrylamide in human urine using column switching with an online trap column. J Agric Food Chem 2008; 56(21): 9828-34. 33. Fennell T.R., Sumner S.C., Snyder R.W., Burgess J., and Friedman M.A. Kinetics of elimination of urinary metabolites of acrylamide in humans. Toxicol Sci 2006; 93(2): 256-267. 34. Niessen W.M.A., Liquid chromatography-mass spectrometry. CRC/Taylor & Francis 2006: 310. 35. Huang Y.S., Wong P., Blache D., Barbeau A., and Davignon J. Tissue lipids in acute acrylamide intoxicated rats. Can J Neurol Sci 1982; 9(2): 181-4. 36. Wallace T.M., Levy J.C., and Matthews D.R. Use and abuse of HOMA modeling. Diabetes Care 2004; 27(6): 1487-95. 37. Fennell T.R. and Friedman M.A. Comparison of acrylamide metabolism in humans and rodents. Adv Exp Med Biol 2005; 561: 109-16. 38. Boettcher M.I., Bolt H.M., Drexler H., and Angerer J. Excretion of mercapturic acids of acrylamide and glycidamide in human urine after single oral administration of deuterium-labelled acrylamide. Arch Toxicol 2006; 80(2): 55-61. 39. Fuhr U., Boettcher M.I., Kinzig-Schippers M., Weyer A., Jetter A., Lazar A., Taubert D., Tomalik-Scharte D., Pournara P., Jakob V., Harlfinger S., Klaassen T., Berkessel A., Angerer J., Sorgel F., and Schomig E. Toxicokinetics of acrylamide in humans after ingestion of a defined dose in a test meal to improve risk assessment for acrylamide carcinogenicity. Cancer Epidemiol Biomarkers Prev 2006; 15(2): 266-71. 40. Hartmann E.C., Boettcher M.I., Bolt H.M., Drexler H., and Angerer J. N-Acetyl-S-(1-carbamoyl-2-hydroxy-ethyl)-L-cysteine (iso-GAMA) a further product of human metabolism of acrylamide: comparison with the simultaneously excreted other mercaptuic acids. Arch Toxicol 2009; 83(7): 731-4. 41. Kopp E.K. and Dekant W. Toxicokinetics of acrylamide in rats and humans following single oral administration of low doses. Toxicol Appl Pharmacol 2009; 235(2): 135-42. 42. Bjellaas T., Janak K., Lundanes E., Kronberg L., and Becher G. Determination and quantification of urinary metabolites after dietary exposure to acrylamide. Xenobiotica 2005; 35(10-11): 1003-18. 43. Boettcher M.I., Bolt H.M., and Angerer J. Acrylamide exposure via the diet: influence of fasting on urinary mercapturic acid metabolite excretion in humans. Arch Toxicol 2006; 80(12): 817-9. 44. Bjellaas T., Stolen L.H., Haugen M., Paulsen J.E., Alexander J., Lundanes E., and Becher G. Urinary acrylamide metabolites as biomarkers for short-term dietary exposure to acrylamide. Food Chem Toxicol 2007; 45(6): 1020-6. 45. Hartmann E.C., Boettcher M.I., Schettgen T., Fromme H., Drexler H., and Angerer J. Hemoglobin adducts and mercapturic acid excretion of acrylamide and glycidamide in one study population. J Agric Food Chem 2008; 56(15): 6061-8. 46. Yu S., Son F., Yu J., Zhao X., Yu L., Li G., and Xie K. Acrylamide alters cytoskeletal protein level in rat sciatic nerves. Neurochem Res 2006; 31(10): 1197-204. 47. Facchini F.S., Hollenbeck C.B., Jeppesen J., Chen Y.D., and Reaven G.M. Insulin resistance and cigarette smoking. Lancet 1992; 339(8802): 1128-30. 48. Odland L., Romert L., Clemedson C., and Walum E. Glutathione content, glutathione transferase activity and lipid peroxidation in acrylamide-treated neuroblastoma N1E 115 cells. Toxicol In Vitro 1994; 8(2): 263-7. | |
dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/37706 | - |
dc.description.abstract | 中文摘要一
研究背景與目的:錳、鉛、砷與汞為常見具有神經毒之金屬。然而,於妊娠時期暴露低劑量神經毒性金屬與其孩童往後神經行為發展之相關性目前仍不清楚。因此,本研究目的為探討妊娠時期神經毒性金屬暴露與其孩童兩歲神經行為發展之相關性。 材料與方法:本研究之230位足月單胞胎個案選自台北出生世代追蹤研究(Taiwan Birth Panel Study),於孩童兩歲大時進行嬰幼兒綜合發展測驗(Comprehensive Developmental Inventory for Infants and Toddlers, CDIIT),以評估其認知、語言、動作(含粗大動作及精細動作)、社會與自理能力之發展。以Agilent 7500C型感應耦合電漿質譜儀(ICP-MS)測量臍帶血中金屬濃度,並使用複迴歸來探討神經毒性金屬暴露與神經行為發展之關係。 結果:臍帶血之錳、鉛、砷與汞中位數濃度分別為47.90 μg/L、11.41 μg/L、4.05 μg/L與12.17 μg/L。在調整母親年齡、孩童性別、環境二手菸暴露與家庭物理環境評估後,錳濃度較高的組別其認知與語言發展商數(developmental quotients)較低(β = -4.72, SE = 2.16, P = 0.029; β = -3.91, SE = 1.87, P = 0.038),鉛濃度較高的組別其認知與社會發展商數較低(β = -5.21, SE = 2.18, P = 0.018; β = -6.36, SE = 2.50, P = 0.012)。在多金屬分析下,錳濃度與鉛濃度都較高的組別,其認知、語言與社會的發展商數則更低(β = -7.48, SE = 2.67, P = 0.006; β = -7.62, SE = 3.18, P = 0.018; β = -7.29, SE = 2.76, P = 0.009; β = -7.57, SE = 3.65, P = 0.039)。 結論:妊娠時期暴露較高濃度的金屬鉛或錳,其孩童兩歲神經行為發展較差;若共同暴露到較高濃度的鉛與錳,對其神經行為發展則會有加乘之交互作用。 中文摘要二 研究背景與目的:丙烯醯胺具神經毒性且被國際癌症研究署(IARC)歸類為人類可能致癌物質。近年來,於香菸的主流菸與高溫長時間烹煮碳水化合物含量較高的食品中皆發現含有較高濃度之丙烯醯胺。研究指出比起成年人,兒童與年輕族群可能會因飲食習慣不同而攝取較多的丙烯醯胺。由於目前針對兒童與年輕族群暴露丙烯醯胺的內在劑量評估較缺乏,而丙烯醯胺與人體內生化值改變之關係,尤其是在醣類與酯質恆定方面目前也仍不清楚。因此,本研究目的為分析青少年與青年尿中丙烯醯胺代謝物(N-acetyl-S-(propionamide)-cysteine, AAMA)濃度,並探討其分布與生化值變化之關係。 材料與方法:本研究選自1992至2000年台灣省中小學生尿液篩檢陽性者,且於2006至2008年接受追蹤檢查與問卷訪談的台北地區個案,並於追蹤時收集個案尿液與血液檢體進行分析,使用極致液相層析-串聯質譜儀(UHPLC-MS/MS)分析尿液中丙烯醯胺主要代謝物濃度。 結果:本研究共納入800位年齡介於12至30歲之個案,其尿中AAMA之中位數濃度為56.51 μg/L,經由尿中肌酸酐校正後之中位數濃度為39.37μg/g creatinine。女性、體重過輕者、高家庭收入者與抽菸者有較高之AAMA濃度。速食、咖啡與甜食的攝取頻率沒有顯著改變AAMA的濃度。在調整性別、年齡、家庭收入、身體質量指數、抽菸、喝酒、肥肉攝取頻率、高血糖和高血壓後,AAMA與血清中三酸甘油脂的濃度(per log10 unit: β = -0.05, SE = 0.02, P = 0.009)和球蛋白的濃度(per log10 unit: β = -0.09, SE = 0.03, P = 0.003)呈現負相關。 結論:於青少年與青年族群中,抽菸為丙烯醯胺暴露的主要貢獻因子,且尿中丙烯醯胺代謝物濃度與血清中三酸甘油脂和球蛋白呈負相關,但仍需要更多長期或動物研究來釐清其相關之生理代謝機制。 | zh_TW |
dc.description.abstract | Abstract 1
Background and objective: Manganese, lead, arsenic and mercury are common neurotoxic metals in the environment. Nonetheless, the association between prenatal exposure to low-dose neurotoxic metals and neurodevelopment in children were not clear. The objective of this study is to explore the association between in utero exposure to environmental neurotoxic metals and neurodevelopment at 2 years of age. Methods: The population of this study was from the Taiwan Birth Panel Study. To prevent confounding factors, we finally included 230 pairs of non-smoking mothers without any occupational exposure and their singleton full-term children. The information during pregnancy was obtained by a structured questionnaire and manganese, lead, arsenic and mercury levels in umbilical cord blood was analyzed by using inductive couple plasma - mass spectrometry. We used Comprehensive Developmental Inventory for Infants and Toddlers (CDIIT) to evaluate child developmental status at 2 years of age and examined the association between in utero exposure to environmental metals in umbilical cord blood and neurodevelopment by linear regression models. Results: The median concentrations of manganese, lead, arsenic and mercury in cord blood were 47.90 μg/L (17.88 - 106.85), 11.41 μg/L (0.16 - 43.22), 4.05 μg/L (1.50 - 12.88) and 12.17 μg/L (1.53 - 64.87) in this study, respectively. After adjusting for maternal age, infant gender, environmental tobacco smoke during pregnancy and after delivery, Home Observation for Measurement of the Environment, arsenic and mercury levels in cord blood and the group of manganese levels ≥ 75th percentile and lead levels ≥ 75th percentile in umbilical cord blood had a significantly adverse association with the whole, cognitive, language and social developmental quotients of CDIIT (β = -7.48, SE = 2.67, P = 0.006; β = -7.62, SE = 3.18, P = 0.018; β = -7.29, SE = 2.76, P = 0.009; β = -7.57, SE = 3.65, P = 0.039, respectively). Conclusions: In utero exposure to environmental manganese and lead may have an adverse association with neurodevelopment at 2 years of age. And there is an interaction effect between manganese and lead in cord blood. Abstract 2 Background and objective: Acrylamide, a neurotoxicant and probable human carcinogen, has been found in certain foods by high-temperature processing and in the mainstream of cigarette smoke. The dietary intakes of acrylamide in children and young populations were relatively higher than in adults, but few studies focused on the assessment of internal dose in this population. The effect of acrylamide exposure related to biochemistry changes, especially in glucose and lipid homeostasis, in human is still not clear. The objective of this study was to explore the acrylamide exposure and biochemistry changes among adolescents and young adults. Methods: The population of this study was recruited from the urine screening project conducted by Chinese Foundation of Health for school-age students from 1992 to 2000 in Taiwan. From 2006 to 2008, we invited these subjects who had been studied in Taipei to conduct a urine screening and complete questionnaires about lifestyles. We used ultra performance liquid chromatography – tandem mass spectrometry to analyze the N-acetyl-S-(propionamide)-cysteine (AAMA) which was the major and noninvasive biomarker in urine to assess the exposure of acrylamide levels. Subjects with urine creatinine levels below 0.3 g/L or over 3 g/L were excluded. Half of detection limit would be regarded as the AAMA levels in urine if the AAMA levels were lower than the limits of detection. Results: The mean (range) age of 800 subjects was 21.3 (12-30) years old and the median (range) levels of AAMA were 56.51 (< LOD-1012.78) μg/L and 39.37 (0.14-718.80) μg/g creatinine. Females, current smokers and subjects with low BMI and higher household income had higher AAMA levels. There were no significant AAMA level differences in different intake frequency of fast-food, coffee and sweet food. After adjusting for confounders (sex, age, BMI, current number of cigarettes, alcohol intake status, household income, fatty meat consumption, hyperglycemia and hypertension), each 1-unit increase in log AAMA was associated with a decrease in serum triglyceride (β = -0.05, SE = 0.02, P = 0.009) and globulin (β = -0.09, SE = 0.03, P = 0.003). Conclusion: Cigarette smoking is the major contributor to the overall acrylamide exposure among adolescents and young adults. Acrylamide exposure may have an inverse association with serum triglycerides and globulin, and this effect is still needed to be clarified by further longitudinal and animal studies. | en |
dc.description.provenance | Made available in DSpace on 2021-06-13T15:39:39Z (GMT). No. of bitstreams: 1 ntu-100-R98841015-1.pdf: 1288887 bytes, checksum: 924fca7e2b28e73916d2a953be33ab5c (MD5) Previous issue date: 2011 | en |
dc.description.tableofcontents | Contents 1
中文摘要........................................................................i Abstract.......................................................................ii Figure of contents..............................................................v Table of contents..............................................................vi Introduction....................................................................1 Material and Methods............................................................3 Study design and population.....................................................3 Measurement of metals...........................................................4 Comprehensive Developmental Inventory for Infants and Toddlers (CDIIT)..........4 Home Observation for Measurement of the Environment Inventory (HOME Inventory)..5 Statistical analysis............................................................6 Results.........................................................................8 Discussion......................................................................9 Conclusion.....................................................................14 Reference......................................................................15 Appendix 1.....................................................................26 Contents 2 中文摘要........................................................................i Abstract.......................................................................ii Figure of contents..............................................................v Table of contents..............................................................vi Introduction...................................................................29 Materials and methods..........................................................33 Study population and data collection...........................................33 Measurement of main acrylamide metabolite in urine.............................33 Chemicals and reagents.........................................................33 Sample preparation.............................................................34 Instrument analysis............................................................35 Evaluation of matrix effect and extraction efficiency of sample pretreatment...36 Method validation and quantification...........................................37 Biochemical data...............................................................38 Statistical analysis...........................................................38 Results........................................................................40 Method performance, matrix effect, recovery and method validation..............40 Levels of AAMA in urine among adolescents and young adults.....................40 AAMA levels and biochemistry changes among adolescents and young adults........41 Discussion.....................................................................43 Conclusion.....................................................................48 References.....................................................................49 Appendix 1.....................................................................71 Appendix 2.....................................................................72 Appendix 3.....................................................................74 Appendix 4.....................................................................75 | |
dc.language.iso | en | |
dc.title | 一、妊娠時期環境鉛錳暴露與其孩童兩歲行為發展之相關性
二、青少年與青年尿中丙烯醯胺代謝物分布與生化值變化之關係 | zh_TW |
dc.title | 1. In Utero Exposure to Environmental Lead and Manganese and Neurodevelopment at 2 Years of Age
2. Distribution of Acrylamide Urinary Metabolite in Relation to Biochemistry Changes in Adolescents and Young Adults | en |
dc.type | Thesis | |
dc.date.schoolyear | 99-2 | |
dc.description.degree | 碩士 | |
dc.contributor.oralexamcommittee | 黃耀輝,蘇大成,吳焜裕 | |
dc.subject.keyword | 1. 兒童,妊娠時期暴露,神經行為發展,神經毒性金屬,2. 丙烯醯胺,丙烯醯胺尿液代謝物,菸,三酸甘油脂,球蛋白, | zh_TW |
dc.subject.keyword | 1. Children,In utero exposure,Neurodevelopment,Neurotoxic metals,2. Acrylamide,N-acetyl-S-(propionamide)-cysteine (AAMA),Cigarette smoke,triglyceride,globulin, | en |
dc.relation.page | 75 | |
dc.rights.note | 有償授權 | |
dc.date.accepted | 2011-08-10 | |
dc.contributor.author-college | 公共衛生學院 | zh_TW |
dc.contributor.author-dept | 職業醫學與工業衛生研究所 | zh_TW |
顯示於系所單位: | 職業醫學與工業衛生研究所 |
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