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研究生:黃美蘭
研究生(外文):Huang, Mei-Lan
論文名稱:氯乙烯單體製造廠及儲運業工人生物標記之探討
論文名稱(外文):Biological Markers in VCM Workers at Manufacturing and Transportation Plants
指導教授:鄭尊仁鄭尊仁引用關係
指導教授(外文):Tsun-Jen Cheng
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:1997
畢業學年度:85
語文別:中文
論文頁數:140
中文關鍵詞:氯乙烯單體二氯乙烷肝功能檢查腹部超音波檢查姊妹染色分體交換基因型 (CYP2E1GSTT1GSTM1ALDH2)
外文關鍵詞:Vinyl Chloride Monomer (VCM)12-Ethylenechloride (EDC)Liver DamageAbdominal Ultrasonography (US)Sister Chromatid Exchanges (SCEs)Genotyping (CYP2E1GSTT1GSTM1ALDH2)
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摘 要聚氯乙烯(PVC)是塑膠工業重要原料,研究顯示氯乙烯單體(VCM)是
一種具有肝毒性的致癌物,可引起肝血管肉瘤、肝硬化、脾腫大、肝功能
指標異常及基因毒性;VCM或EDC皆可能經由細胞色素P-450 2E1(CYP 2E1)
或麩胺基硫轉移(GSTs)活化成親電子性的中間產物2-chloroethene
oxide (CEO) 和 chloroacetaldehyde (CAA) (研究顯示此兩種物質都可
能造成肝危害及基因危害)或是再經由GSTs 和乙醛脫氫(ALDH)代謝排出
體外。但過去的研究大多集中於聚氯乙烯工人。事實上,VCM製造廠及運
輸業工人也可能暴露於產物氯乙烯單體(VCM)或原料二氯乙烷(EDC)。所以
本研究針對台灣地區VCM製造廠及運輸業工人進行肝臟危害探討,研究對
象包括三家VCM製造廠及二家VCM運輸業272名現職男性員工,依據環境及
個人採樣濃度配合工人目前工作職務及工作所在區域分為高氯乙烯且高二
氯乙烷暴露組(high VCM and high EDC group)、高氯乙烯低二氯乙烷暴
露組(high VCM and low EDC group)、高二氯乙烷低氯乙烯暴露組(high
EDC and low VCM group)、低氯乙烯或二氯乙烷暴露組(low VCM and
low EDC group)及極低氯乙烯或二氯乙烷暴露對照組(minimal VCM and
minimal EDC group)等五組以及並推估工人累積暴露VCM及EDC劑量而以中
間數分四組。肝功能是以天門冬酸胺基(AST)、氨基丙酸轉胺基(ALT)
及丙麩氨轉(r-GT)等酵素異常率來作指標。此外,並收集40名男性現
職員工全血進行姊妹染色分體交換(SCEs)實驗,SCEs採用標準方法進行周
邊淋巴球培養及染色,由一位實驗者於顯微鏡下計數。CYP 2E1、 GST M1
、 GST T1、以及ALDH2基因多形性則利用聚合鍊鎖反應 (PCR) 及RFLP
之方法測定,另外收集個人基本資料、詳細工作史、腹部超音波檢查及其
它影響肝臟機能因素包括B型肝炎抗原、C型肝炎抗體、飲酒、身體質量指
數(BMI)及其它影響SCE因素包括抽煙等。結果顯示AST及ALT異常率於VCM
高暴露工人較高,同樣AST及ALT異常率於EDC高暴露工人也高;腹部超音
波肝臟實質病變、肝硬化或脾腫大於累積高暴露組異常率可能較高;此外
SCEs上升與VCM之暴露有關,而ALDH2基因型在氯乙烯代謝解毒的途徑上可
能扮演重要的角色。本研究顯示,VCM、EDC洩料人員、廢水廢氣處理員、
司機以及設備維修人員,其VCM或EDC暴露量可能與肝功能異常及基因毒性
有關,應進一步環境測定及健康追蹤來釐清暴露與肝病變及基因毒性之相
關。關鍵詞:聚氯乙烯、氯乙烯單體、二氯乙烷、肝功能檢查、腹部超音
波檢查、 姊妹染色分體交換、細胞色素P-450 2E1(CYP 2E1)、麩
胺基硫轉移(GSTs)、 乙醛脫氫(ALDH)
Abstract Vinyl chloride monomer (VCM), an important
material for plastic industry, is hepatotoxic as well as
carcinogenic in human. Previous studies focused on workers
engaged in vinyl chloride polr-merization. However, workers from
VCM manufacturing or transportation may be exposed to VCM or
1,2-ethylenedichloride (EDC), which both can damage liver cells
and cause genetic toxicity. In vivo, VCM or EDC is metabolized
by cytochrome P450 2E1 (CYP2E1) or glutathione S-transferases
(GST) to form chloroethylene (CEO) an oroactetaldehyde (CAA),
both electrophilic metabolites, which may either cause genetic
toxicity or damage liver cells or are further metabolized and
detoxified by GST and aldehyde dehydrogenase (ALDH2). To
determine if liver damage and genetic toxicity is associated
with VCM or EDC exposures. 272 male workers in three VCM
manufacturing plants and two VCM transportation plants were
included for this study. The frequency of sister chromatid
exchanges (SCEs) in peripheral blood lymphocytes from 40 male
workers were measured and the genotypes, CYP2E1, GSTT1, GSTM1,
and ALDH2, were determined by PCR and RFLP on peripheral white
blood cell DNA. Those who were exposed to VCM or EDC were
classified into high VCM and high EDC group、high VCM and low
EDC group、high EDC and low VCM group、low VCM and low EDC group
and minimal VCM and mimnimal EDC group based on their job
titles, work-sites, and the airborne EDC or VCM concentration.
The medical examination included detailed occupational history,
abdominal ultrasonography (US), AST, ALT, GGT, HBsAg, anti-HCV,
driok status, cigarette smoking, and medications. The analysis
showed AST, ALT and SCEs were statistically significant
different between groups after adjusting other possible
confounders, and ALDH2 variants (DD) significantly increased the
frequency of SCEs. We conclude that elevation of ALT and
frequency of SCEs may be associated with current exposure to VCM
or EDC, US might be a useful tool to find the chronic effect of
VCM and EDC exposures and ALDH2 may be as determinant of SCEs in
VCM workers. Key Words: Vinyl chloride monomer (VCM),
1,2-ethylenedichloride (EDC), liver damage, abdominal
ultrasonography (US), genetic toxicity, sister
chromatid exchanges (SCEs), cytochrome P450 2E1 (CYP2E1),
glutathione S-transferase (GST), aldehyde dehydrogenase (ALDH2)
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