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題名:臺灣地品氯乙烯暴露工人之慢性肝臟疾病--病例對照研究
書刊名:勞工安全衛生研究季刊
作者:翁瑞宏陳保中杜宗禮王榮德鄭尊仁
作者(外文):Wong, Ruey-hongChen, Pau-chungDu, Chung-liWang, Jung-derCheng, Tsun-jen
出版日期:2001
卷期:9:4
頁次:頁368-383
主題關鍵詞:氯乙烯B型肝炎病毒感染慢性肝臟疾病Vinyl chlorideHepatitis B virus infectionChronic liver diseases
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     我們先前的研究顯示作業員工暴露於高濃度的氯乙烯,發生肝癌死亡的危險性較高;不過B型肝炎病毒感染(HBV)是臺灣地區慢性肝臟疾病的主要原因之一,而肝炎病毒感染在氯乙烯暴露所導致的慢性肝臟疾病中所扮演的角色目前仍不清楚。因此本研究利用病例對照研究法,來了解氯乙烯累積暴露增加是否具有較高的慢性肝臟疾病危險性,並且探討氮乙烯暴露與B型肝炎病毒感染,是否對氯乙烯工人的慢性肝臟疾病具有交互作用存在。以年齡及工廠別進行配對,共收集78名病例組與216名對照組氯乙烯暴露工人,所有研究對象皆接受詳細的問卷訪視,內容包括飲酒及吸菸習慣、詳細工作史以及家族疾病史。在控制其他相關因子後,以條件對數複迴歸模式(conditional logistic regression)進行配對危險對比值分析,結果顯示1970-1979年代第一次進廠的工人 (matched odd sratio,ORm=1.07),以及1970年以前第一次進廠的工人(ORm=1.09)在HBsAg陰性之病例對照組中,相較於1980年代進廠的工人,並未對慢性肝臟疾病具有統計上的顯著危險性,然而在HBsAg陽性之病例對照組中,1970-1979年代第一次進廠的工人相較於1980年代進廠的工人,對於慢性肝臟疾病的危險性升至1.62倍,而1970年以前第一次進廠的工人則更具有統計上的顯著危險性(ORm=5.14,95%C.I.=2.59-7.69)。因此氯乙烯暴露可能會加強B型肝炎病毒感染所導致慢性肝臟疾病。
     Our previous study showed that workers exposed to vinyl chloride monomer (VCM) may develop higher risk of liver cancer. Since hepatitis B virus (HBV) infection is the major cause of chronic liver diseases in Taiwan, the role of chronic hepatitis infection in VCM related chronic liver diseases remains unclear. Therefore, we designed a case-control study to investigate whether there is an elevated risk on chronic liver damage in workers with high level of vinyl chloride exposure, and whether there is an interaction between vinyl chloride exposure and HBV infection on chronic liver damage. A total of 78 cases and 216 matched controls were recruited for the analysis. Case-control pairs were matched on age and place of employment. History of alcohol consumption, smoking, detailed occupation, and familial history of liver diseases were obtained by interviewer-administered questionnaires. After adjusting for other confounders, HBsAg negative VCM workers who were first employed during 1970 - 1979 (matched odds ratio, OPm = 1.07); or those were employed prior to 1970 (ORm =1.09), did not have a higher risk developing chronic liver disease, as compared to those employed al~er 1980. Further, HBsAg positive VCM workers who were first employed during 1970 - 1979 had a 1.62-fold of risk, whereas HBsAg carriers who were first employed before 1970 had a significantly higher risk (ORm = 5.14, 95% C.I. = 2.59 - 7.69). We concluded that VCM exposure may potentiate the HBV-induced chronic liver diseases.
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