(34.228.41.66) 您好!臺灣時間:2018/12/12 19:56
字體大小: 字級放大   字級縮小   預設字形  
回查詢結果

詳目顯示:::

我願授權國圖
本論文永久網址: 
line
研究生:張光億
研究生(外文):Kuang-Yi Chang
論文名稱:嫘縈絲廠男性勞工二硫化碳暴露與其配偶懷孕所需時間研究;嫘縈絲廠男性勞工二硫化碳暴露與生殖內分泌研究
論文名稱(外文):Time to Pregnancy Study in Male Workers Exposed to Carbon Disulfide in the Rayon Industry;Reproductive Endocrine Study in Male Workers Exposed to Carbon Disulfide in the Rayon Industry
指導教授:陳保中陳保中引用關係
學位類別:碩士
校院名稱:國立臺灣大學
系所名稱:職業醫學與工業衛生研究所
學門:醫藥衛生學門
學類:公共衛生學類
論文出版年:2004
畢業學年度:92
語文別:英文
論文頁數:74
中文關鍵詞:黃體生成素受孕所需時間二硫化碳男性睪固酮生育能力濾泡刺激素抑制素B
外文關鍵詞:testosteronetime to pregnancyinhibin Bfollicle stimulating hormoneluetinizing hormonefecundabilitymalecarbon disulfide
相關次數:
  • 被引用被引用:3
  • 點閱點閱:480
  • 評分評分:系統版面圖檔系統版面圖檔系統版面圖檔系統版面圖檔系統版面圖檔
  • 下載下載:0
  • 收藏至我的研究室書目清單書目收藏:0
第一部分
此研究目的為評估暴露於二硫化碳(carbon disulfide)下是否對男性受孕力有所影響。受孕力研究以回溯性研究設計,評估男性暴露於二硫化碳下是否會延長其配偶受孕所需時間(time to pregnancy),共有五十六位男性 員工加入此研究,並直接暴露於二硫化碳,因此將五十六對夫婦共有150孕次作為研究族群並將其暴露分組及計算暴露年資,而等待受孕的時間定義為在懷孕前,也就是開始於最後一次月經週期來潮前及之前持續停止避孕的一段時間,利用家訪方式訪問每一位參與研究的男性員工及其配偶,以清楚測量每次懷孕受孕所需時間;藉以探討其配偶受孕所需時間是否延長,二硫化碳暴露評估使用先前空氣採樣資料進行暴露分組,最後分別使用discrete Cox迴歸統計模式進行分析。
分析結果顯示相對於不曾暴露於二硫化碳的孕次,暴露10年以上者有較低的生育能力密度比 (FDR=0.47; 95% CI: 0.23 to 0.93),且暴露濃度大於30 ppm也有較低的生育能力密度比 (FDR=0.58; 95% CI: 0.26 to 1.29) 但是並無達到統計顯著意義。若同時暴露30 ppm且時間持續暴露10年以上生育能力密度比則有顯著的下降 (FDR=0.42; 95% CI: 0.19 to 0.93). 結果顯示出暴露於二硫化碳對男性生育能力有顯著影響,而長期且高濃度暴露其生育力下降的趨勢較為明顯。

第二部分
此研究目的為評估縲縈絲製造廠男性員工暴露於二硫化碳下是否對其生殖荷爾蒙造成影響。此研究為一橫斷性研究,研究對象為五十三位在台灣某縲縈絲製造廠中不同工作環境工作至少超過三個月之男性。在這五十三位男性員工中,皆直接暴露於二硫化碳,二硫化碳之暴露評估是使用先前空氣以及個人採樣資料進行暴露分組,並計算暴露年資以及累積暴露值 (暴露濃度×年資);對照組部份來自另兩間無暴露於二硫化碳的工廠,共一百零六位男性員工。男性生殖荷爾蒙是由免疫螢光分析方式來測定血清中的濾泡刺激素 (follicle stimulating hormone)、黃體生成素 (luetinizing hormone) 及睪固酮 (testosterone)、抑制素B (inhibin B)。藉以探討暴露二硫化碳是否改變男性生殖荷爾蒙, 進一步了解其對生殖系統的影響。統計分析方式以General linear model分析。
分析結果顯示在年齡分層後比較未曾暴露以及其他暴露分組,在濾泡刺激素、黃體生成素及睪固酮三種荷爾蒙方面並無顯著差異;而在高暴露組部分相對於低暴露以及對照組部分,抑制素B則是有顯著的昇高。研究結果表示縲縈絲男性勞工暴露於二硫化碳下,對於生殖荷爾蒙有非臨床症狀的影響,但是對於真正的危害機制仍須更進一步的研究探討。



part I
The aim of study was to estimate whether exposed to carbon disulfide (CS2) has an impact on couple fecundability. For couple fecundability used a retrospective cohort in design. A total of 56 male workers in the rayon industry were recruited. We used time to pregnancy (TTP) as a measure of couple fecundability, which was defined as the duration between the dates of discontinuing contraceptive procedures and beginning of last menstrual period before pregnancy, and used a structured questionnaire to interview each male worker and his spouse. We conducted the exposure assessment of CS2 using previously air-sampling data. Finally, we analyzed the data of TTP using the discrete Cox’s proportional hazards model. The pregnancies with the employment of 10 years or more had a lower fecundability density ratio (FDR=0.47; 95% CI: 0.23 to 0.93) and those exposed more than 30 ppm had a lower ratio (FDR=0.58; 95% CI: 0.26 to 1.29) compared to those before the employment. Furthermore, workers exposed more than 30 ppm and their employment of 10 years or more were associated with a decreased fecundability density ratio (FDR=0.42; 95% CI: 0.19 to 0.93). The results showed that the exposure to CS2 had a significant effect on male fecundability, especially for those with the CS2 exposure of long duration and high concentration.

part II
The objective of the study was to estimate whether exposed to carbon disulfide (CS2) has an impact on male reproductive endocrine. The study was a cross-sectional study in design. The study population consisted of 53 male workers with the continuous work in the rayon manufacturing factory at least three months. All 53 workers from the department of a viscose rayon factory with potentially direct exposure to CS2, and 106 male workers in other factories were recruited as the exposed groups and non-exposed group. We conducted the exposure assessment of CS2 using previously air-sampling data, including area and personal sampling. We calculated not only cumulative potential exposure dose from information on the total number of years working with CS2 but also cumulative index (ppm×years). The level of serum follicle stimulating hormone (FSH), luetinizing hormone (LH), total testosterone, and inhibin B were used to determine by enzyme-linked immunosorbent assay (ELISA). Finally, we analyzed the data of reproductive endocrine using the General linear models.
The exposure group of serum FSH, LH, and testosterone were no significant association with exposure after age stratified. However, the serum inhibin B was significantly increased with high exposure. We found the potential effects of exposure CS2 induced subclinical alterations in male reproductive endocrine. Furthermore, the CS2 damage on reproductive endocrine mechanism is still a question that we need to clarify.


part I
摘要 3
Abstract 4
Contents 5
List of Tables 6
List of Figures 7
Introduction 8
A Review of Literature 9
Material and Methods 15
Study population 15
Exposure assessment 15
Questionnaire interview 16
Statistical analysis 17
Results 18
Discussion 25
References 29

part II
摘要 3
Abstract 4
Contents 6
List of Tables 7
List of Figures 8
Introduction 9
Material and Methods 11
Study population 11
Exposure assessment 11
Hormone assay 12
Statistical analysis 13
Results 14
Discussion 26
Reference 33
Appendix 36



part I
(1) Beauchamp RO Jr, Bus JS, Popp JA. A critical review of the literature on carbon disulfide toxicity. Critical Reviews in Toxicology 1983; 11(3):169-278.
(2) Reinhardt F, Drexler H, Bickel A, Claus D, Angerer J, Ulm K et al. Neurotoxicity of long-term low level exposure to carbon disulphide: Results of questionnaire, clinical neurological examination and neuropsychological testing. International Archives of Occupational and Environmental Health 1997; 69(5):332-338.
(3) Cassitto MG, Camerino D, Imbriani M, Contardi T, Masera L, Gilioli R. Carbon-Disulfid(e and the Central-Nervous-System - A 15-Year Neurobehavioral Surveillance of An Exposed Population. Environmental Research 1993; 63(2):252-263.
(4) Jhun HJ, Yim SH, Kim R, Paek D. Heart-rate variability of carbon disulfide-poisoned subjects in Korea. International Archives of Occupational and Environmental Health 2003; 76(2):156-160.
(5) Korinth G, Goen T, Ulm K, Hardt R, Hubmann M, Drexler H. Cardiovascular function of workers exposed to carbon disulphide. International Archives of Occupational and Environmental Health 2003; 76(1):81-85.
(6) Vanhoorne M, Debacquer D, Barbier F. Epidemiologic-Study of Gastrointestinal and Liver Effects of Carbon-Disulfide. International Archives of Occupational and Environmental Health 1992; 63(8):517-523.
(7) Zhou SY, Liang YX, Chen ZQ, Wang YL. Effects of occupational exposure to low-level carbon disulfide (CS2) on menstruation and pregnancy. Industrial Health 1988; 26(4):203-214.
(8) Cai SX, Bao YS. Placental transfer, secretion into mother milk of carbon disulphide and the effects on maternal function of female viscose rayon workers. Industrial Health 1981; 19(1):15-29.
(9) Tsai ML, Chang JH, Huang BM, Liu MY. In vivo exposure to carbon disulfide increases the contraction frequency of pregnant rat uteri through an indirect pathway. Life Sciences 2000; 66(3):201-208.
(10) Saillenfait AM, Bonnet P, de Ceaurriz J. Effects of inhalation exposure to carbon disulfide and its combination with hydrogen sulfide on embryonal and fetal development in rats. Toxicology Letters 1989; 48(1):57-66.
(11) Bao YS. [Effect of carbon disulfide on human embryo and fetal development]. Zhonghua Yi Xue Za Zhi 1984; 64(4):217-221.
(12) Zenick H, Blackburn K, Hope E, Baldwin D. An evaluation of the copulatory, endocrinologic, and spermatotoxic effects of carbon disulfide in the rat. Toxicology and Applied Pharmacology 1984; 73(2):275-283.
(13) Tepe SJ, Zenick H. The effects of carbon disulfide on the reproductive system of the male rat. Toxicology 1984; 32(1):47-56.
(14) Kumar S, Patel KG, Gautam AK, Agarwal K, Shah BA, Saiyed HN. Detection of germ cell genotoxic potential of carbon disulphide using sperm head shape abnormality test. Human & Experimental Toxicology 1999; 18(12):731-734.
(15) Le JY, Fu XM. Human sperm chromosome analysis--study on human sperm chromosome mutagenesis induced by carbon disulfide. Biomedical & Environmental Sciences 1996; 9(1):37-40.
(16) Meyer CR. Semen quality in workers exposed to carbon disulfide compared to a control group from the same plant. Journal of Occupational Medicine 1981; 23(6):435-439.
(17) Wagar G, Tolonen M, Stenman UH, Helpio E. Endocrinologic studies in men exposed occupationally to carbon disulfide. Journal of Toxicology and Environmental Health 1981; 7(3-4):363-371.
(18) Wagar G, Tolonen M, Tanner P, Helpio E. Serum gonadotropins and testosterone in men occupationally exposed to carbon disulfide. Journal of Toxicology and Environmental Health 2004; 11(4-6):691-701.
(19) Wang C, Bi Y, Tan X, Yan J. Serum sex hormone and urinary metabolites of male workers exposed to carbon disulfide. Wei Sheng Yen Chiu/Journal of Hygiene Research 1999; 28(3):132-133.
(20) Vanhoorne M, Comhaire F, Debacquer D. Epidemiologic-Study of the Effects of Carbon-Disulfide on Male-Sexuality and Reproduction. Archives of Environmental Health 1994; 49(4):273-278.
(21) Vanhoorne M, Vermeulen A, Debacquer D. Epidemiologic-Study of Endocrinologic Effects of Carbon-Disulfide. Archives of Environmental Health 1993; 48(5):370-375.
(22) Takebayashi T, Omae K, Ishizuka C, Nomiyama T, Sakurai H. Cross sectional observation of the effects of carbon disulphide on the nervous system, endocrine system, and subjective symptoms in rayon manufacturing workers. Occupational and Environmental Medicine 1998; 55(7):473-479.
(23) Takebayashi T, Nishiwaki Y, Nomiyama T, Uemura T, Yamauchi T, Tanaka S et al. Lack of relationship between occupational exposure to carbon disulfide and endocrine dysfunction: A six-year cohort study of the Japanese rayon workers. Journal of Occupational Health 2003; 45(2):111-118.
(24) Donna Day Baird, Allen J.Wilcox, Clarice R.Weinberg. Use of time to pregnancy to study environmental exposures. American Journal of Epidemiology 1986; 124(3):470-480.
(25) Joffe M. Time to pregnancy: A measure of reproductive function in either sex. Occupational and Environmental Medicine 1997; 54(5):289-295.
(26) Tomeo CA, Rich-Edwards JW, Michels KB, Berkey CS, Hunter DJ, Frazier AL et al. Reproducibility and validity of maternal recall of pregnancy-related events. Epidemiology 1999; 10(6):774-777.
(27) Chang SJ, Shih TS, Chou TC, Chen CJ, Chang HY, Sung FC. Hearing loss in workers exposed to carbon disulfide and noise. Environmental Health Perspectives 2003; 111(13):1620-1624.
(28) Shih TS, Chou TC, Chang HY, Wu CC, Wang PY. Accumulation of urinary 2-thiothiazolidine-4-carboxylic acid (TTCA) among workers occupationally exposed to carbon disulfide for 1 week. Science of the Total Environment 2003; 308(1-3):37-47.
(29) Sallmen M, Lindbohm ML, Anttila A, Taskinen H, Hemminki K. Time to pregnancy among the wives of men occupationally exposed to lead. Epidemiology 2000; 11(2):141-147.
(30) Chen PC, Hsieh GY, Wang JD, Cheng TJ. Prolonged time to pregnancy in female workers exposed to ethylene glycol ethers in semiconductor manufacturing. Epidemiology 2002; 13(2):191-196.
(31) Scheike TH, Jensen TK. A discrete survival model with random effects: An application to time to pregnancy. Biometrics 1997; 53(1):318-329.
(32) Weinberg CR, Baird DD, Wilcox AJ. Sources of Bias in Studies of Time to Pregnancy. Statistics in Medicine 1994; 13(5-7):671-681.
(33) Hassan MAM, Killick SR. Effect of male age on fertility: evidence for the decline in male fertility with increasing age. Fertility and Sterility 2003; 79:1520-1527.
(34) Juhl M, Andersen AMN, Gronbaek M, Olsen J. Moderate alcohol consumption and waiting time to pregnancy. Human Reproduction 2001; 16(12):2705-2709.
(35) Bolumar F, Olsen J, Boldsen J, Karmaus W, Fletcher T, FigaTalamanca I et al. Smoking reduces fecundity: A European multicenter study on infertility and subfecundity. American Journal of Epidemiology 1996; 143(6):578-587.

part II
(1) Reinhardt F, Drexler H, Bickel A, Claus D, Angerer J, Ulm K et al. Neurotoxicity of long-term low level exposure to carbon disulphide: Results of questionnaire, clinical neurological examination and neuropsychological testing. International Archives of Occupational and Environmental Health 1997; 69(5):332-338.
(2) Cassitto MG, Camerino D, Imbriani M, Contardi T, Masera L, Gilioli R. Carbon-Disulfide and the Central-Nervous-System - A 15-Year Neurobehavioral Surveillance of An Exposed Population. Environmental Research 1993; 63(2):252-263.
(3) Vanhoorne M, DeRouck A, Bacquer D. Epidemiological study of the systemic ophthalmological effects of carbon disulfide. Archives of Environmental Health 1996; 51(3):181-188.
(4) Vanhoorne M, Debacquer D, Barbier F. Epidemiologic-Study of Gastrointestinal and Liver Effects of Carbon-Disulfide. International Archives of Occupational and Environmental Health 1992; 63(8):517-523.
(5) Zhou SY., Liang YX., Chen ZQ., Wang YL. Effects of occupational exposure to low-level carbon disulfide (CS2) on menstruation and pregnancy. Industrial Health 1988; 26(4):203-214.
(6) Cai SX., Bao YS. Placental transfer, secretion into mother milk of carbon disulphide and the effects on maternal function of female viscose rayon workers. Industrial Health 1981; 19(1):15-29.
(7) Tepe SJ., Zenick H. The effects of carbon disulfide on the reproductive system of the male rat. Toxicology 1984; 32(1):47-56.
(8) Tsai ML, Chang JH, Huang BM, Liu MY. In vivo exposure to carbon disulfide increases the contraction frequency of pregnant rat uteri through an indirect pathway. Life Sciences 2000; 66(3):201-208.
(9) Bao YS. [Effect of carbon disulfide on human embryo and fetal development]. Zhonghua Yi Xue Za Zhi 1984; 64(4):217-221.
(10) Zenick H., Blackburn K., Hope E., Baldwin D. An evaluation of the copulatory, endocrinologic, and spermatotoxic effects of carbon disulfide in the rat. Toxicology and Applied Pharmacology 1984; 73(2):275-283.
(11) Kumar S, Patel KG, Gautam AK, Agarwal K, Shah BA, Saiyed HN. Detection of germ cell genotoxic potential of carbon disulphide using sperm head shape abnormality test. Human & Experimental Toxicology 1999; 18(12):731-734.
(12) Vanhoorne M, Comhaire F, Debacquer D. Epidemiologic-Study of the Effects of Carbon-Disulfide on Male-Sexuality and Reproduction. Archives of Environmental Health 1994; 49(4):273-278.
(13) Wagar G., Tolonen M., Stenman UH., Helpio E. Endocrinologic studies in men exposed occupationally to carbon disulfide. Journal of Toxicology and Environmental Health 1981; 7(3-4):363-371.
(14) Wagar G., Tolonen M., Tanner P., Helpio E. Serum gonadotropins and testosterone in men occupationally exposed to carbon disulfide. Journal of Toxicology and Environmental Health 2004; 11(4-6):691-701.
(15) Vanhoorne M, Vermeulen A, Debacquer D. Epidemiologic-Study of Endocrinologic Effects of Carbon-Disulfide. Archives of Environmental Health 1993; 48(5):370-375.
(16) Takebayashi T, Omae K, Ishizuka C, Nomiyama T, Sakurai H. Cross sectional observation of the effects of carbon disulphide on the nervous system, endocrine system, and subjective symptoms in rayon manufacturing workers. Occupational and Environmental Medicine 1998; 55(7):473-479.
(17) Takebayashi T, Nishiwaki Y, Nomiyama T, Uemura T, Yamauchi T, Tanaka S et al. Lack of relationship between occupational exposure to carbon disulfide and endocrine dysfunction: A six-year cohort study of the Japanese rayon workers. Journal of Occupational Health 2003; 45(2):111-118.
(18) Yalti S., Gurbuz B., Ficicioglu C. Serum levels of inhibin B in men and their relationship with gonadal hormones, testicular volume, testicular biopsy results and sperm parameters. Journal of Obstetrics and Gynaecology 2002; 22(6):649-654.
(19) Andersson AM. Inhibin B in the assessment of seminiferous tubular function. Best Practice & Research Clinical Endocrinology & Metabolism 2000; 14(3):389-397.
(20) Chang SJ, Shih TS, Chou TC, Chen CJ, Chang HY, Sung FC. Hearing loss in workers exposed to carbon disulfide and noise. Environmental Health Perspectives 2003; 111(13):1620-1624.
(21) Groome N, Obrien M. Immunoassays for Inhibin and Its Subunits - Further Applications of the Synthetic Peptide Approach. Journal of Immunological Methods 1993; 165(2):167-176.
(22) Groome NP, Illingworth PJ, OBrien M, Pai R, Rodger FE, Mather JP et al. Measurement of dimeric inhibin B throughout the human menstrual cycle. Journal of Clinical Endocrinology and Metabolism 1996; 81(4):1401-1405.
(23) Simon D, Preziosi P, Barrettconnor E, Roger M, Saintpaul M, Nahoul K et al. The Influence of Aging on Plasma Sex-Hormones in Men - the Telecom-Study. American Journal of Epidemiology 1992; 135(7):783-791.
(24) Pierik FH, Vreeburg JTM, Stijnen T, de Jong FH, Weber RFA. Serum inhibin B as a marker of spermatogenesis. Journal of Clinical Endocrinology and Metabolism 1998; 83(9):3110-3114.
(25) Hipler UC, Hochheim B, Knoll B, Tittelbach J, Schreiber G. Serum inhibin B as a marker for spermatogenesis. Archives of Andrology 2001; 46(3):217-222.
(26) Anawalt BD, Bebb RA, Matsumoto AM, Groome NP, Illingworth PJ, McNeilly AS et al. Serum inhibin B levels reflect sertoli cell function in normal men and men with testicular dysfunction. Journal of Clinical Endocrinology and Metabolism 1996; 81(9):3341-3345.




QRCODE
 
 
 
 
 
                                                                                                                                                                                                                                                                                                                                                                                                               
第一頁 上一頁 下一頁 最後一頁 top
系統版面圖檔 系統版面圖檔