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吕嘉春, 宾晓农, 纪卫东, 施侣元, 周亦武, 吴中亮, 陈家堃. 镍、铬等金属与非职业暴露人群肺癌的关系[J]. 中国公共卫生, 2003, 19(5): 513-515.
引用本文: 吕嘉春, 宾晓农, 纪卫东, 施侣元, 周亦武, 吴中亮, 陈家堃. 镍、铬等金属与非职业暴露人群肺癌的关系[J]. 中国公共卫生, 2003, 19(5): 513-515.
LU Jia-chun, BIN Xiao-nong, JI Wei-dong, . Study on relationship between metal like nickel, chromium, and development of lung cancer in non-occupational population[J]. Chinese Journal of Public Health, 2003, 19(5): 513-515.
Citation: LU Jia-chun, BIN Xiao-nong, JI Wei-dong, . Study on relationship between metal like nickel, chromium, and development of lung cancer in non-occupational population[J]. Chinese Journal of Public Health, 2003, 19(5): 513-515.

镍、铬等金属与非职业暴露人群肺癌的关系

Study on relationship between metal like nickel, chromium, and development of lung cancer in non-occupational population

  • 摘要:
      目的   研究镍、铬等金属毒物在非职业暴露人群肺癌发生中的作用.
      方法   收集无金属类毒物职业接触史、经手术切除的肺癌组织55例, 肺良性病变或意外死亡者的正常肺组织23例, 用感耦等离子体-原子发射光谱仪(ICP-AES)检测肺组织中镉(Cd)、铬(Cr)、镍(Ni)、铅(Pb)、铍(Be)、砷(As)等金属和类金属毒物的含量, 按吸烟史和细胞类型进行分层分析; 并用硫化镍和苯并(a)芘-C, 8, 二醇-90环氧化物(BPDE)诱导正常人气管上皮细胞系发生恶性转化的癌变模型, 检测转化细胞经裸鼠成瘤组织的金属类毒物的含量.
      结果   在肺组织中可检出多种金属类毒物, 在肺癌组织中镍和铬的含量分别为(10.5172±26739)和(7.6906±3.1012)μg/g干肺组织, 显著高于正常肺组织的镍、铬含量(4.1218±2.1752)和(4.1244±2.7538)μg/g干肺组织, t值分别为10.14和5.04, P < 0.01.按吸烟和细胞类型分层, 吸烟者肺组织中的镍、铬含量皆高于非吸烟者, P < 0.05;肺鳞癌中镍的含量(12.5609±2.3455)μg/g干肺组织高于肺腺癌(8.2377±2.7828)μg/g干肺组织, t=6.25, P < 0.01.在用硫化镍和BPDE诱导正常人气管上皮细胞系发生恶性转化经裸鼠成瘤的癌组织中, 硫化镍诱导组的镍含量(21.00μg/g·干瘤组织) 是BPDE(4.88μg/g·干瘤组织) 诱导组的413倍.
      结论   镍、铬等金属类毒物是肺癌的危险因素, 吸烟是接触金属类毒物的重要非职业性暴露途径。

     

    Abstract:
      Objective   Nickel, chromium, and other metal poisons are confirmed as chemical carcinogens to human.The effects of nickel, chromium and other metal poisons on the development of human lung cancer are investigated.
      Methods   55 lung cancer patients tumor specimens and 23 normal lung tissues from benign lung lesion cases and accidental deaths are collected.The metal poisons like cadmium(Cd), chromium(Cr), nickel(Ni), lead(Pb), beryllium(Be), and metalloid arsenic(As) are detected by Inductively Coupled Plasms-Atomic Emission Spectrometry(ICP-A ES).The specimens are stratified by cell types and smoking status.These metal poisons are also detected in tumorous tissues from nude mice inoculated with human bronchial epithelial cells which are transformed by sulfide nickel(NiS)and BPDE(anti-Benzo(a)pyrene diol-epoxide) in vitro.
      Results   Some kinds of metal poisons are determined in the lung tissues of general population.Ni content is higher in lung cancer specimens than that in normal lungs(10.5172±2.6739)μg/g dried lung tissue(mean+/-SD)versus(4.121 8±2.175 2)μg/g, t=10.14, P < 0.01.Similar tendency is found in Cr content, i.e.(7.690 6±3.101 2)μg/g versus(4.124 4±2.753 8)μg/g t=5.04, P < 0.01.In smokers, Ni and Cr content are higher than that in non-smokers, P < 0.05.In squamous cell carcinoma, Ni content is higher than that of adenocarcinoma(12.560 9±2.345 5)μg/g versus(8.237 7±2.782 8)μg/g, t=6.25, P < 0.01.Transformation of human bronchial epithelial cells are induced by sulfide nickel(NiS)and BPDE in vitro.The transformed cells were injected to nude mice, and grow as tumorous tissues.Nickel content in nude mice's tumor from NiS treated cells is 4.3 times higher than that from BPDE transformed cells(21.00μg/g versus 4.88μg/g dried tumor tissue).
      Conclusion   Nickel, chromium and other metal poisons are the risk factors of human lung cancer.Smoking is an important un-occupational exposure to metal poisons.

     

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