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1.
目的探讨镉对作业工人尿镉、尿β2-微球蛋白和视黄醇结合蛋白的影响。方法用原子吸收法检测尿镉和空气中镉水平,用ELISA方法测定尿β2-微球蛋白和视黄醇结合蛋白。结果受检对象中尿镉水平(ug/g肌酐)的分布情况是:0~有86人,2-有145人,3-有182人,4~有159人,〉5有80人。其中2人不仅尿镉超标而且β2-微球蛋白达到慢性轻度镉中毒水平。工作场所空气中镉浓度0.005—0.16mg/m^3,样品超标率33.3%。结论镉作业可引起部分接触者尿镉和尿β2-微球蛋白水平发生改变,是评价镉毒性作用的重要指标。 相似文献
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镉作业工人健康损害的调查分析 总被引:1,自引:0,他引:1
目的了解镉作业工人的职业病危害情况。方法对某企业熔炼车间工作场所进行职业卫生学调查,33名镉作业工人进行尿镉与尿β2-微球蛋白测定。结果工作场所18个检测样品中12个超标,浇注岗位镉的8h时间加权浓度超标77.2倍,短时间接触浓度超标226倍。33名镉作业工人尿镉连续两次以上超过5μmol/mol肌酐者共有27例,且同时伴有尿β2-微球蛋白超过9.4μmol/mol肌酐7例。27名尿镉超标的工人两年后复查尿镉、尿β2-微球蛋白无明显变化。结论镉在人体内代谢周期长,因此,尿镉水平与肾功能损伤程度及可逆性仍需进一步跟踪研究更长时间。对镉作业者应加强防护。 相似文献
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目的:探讨慢性职业性镉中毒的早期诊断指标.方法:以职业接触镉工人144人为接触组和未接触镉且体检未见异常的员工114人为研究对象,分别检测尿中镉(Cd)、α,-微球蛋白(α-MG)、β2-微球蛋白(β2-MG)、视黄醇结合蛋白(RBP)、N-乙酰-β-D-氨基葡萄糖苷酶(NAG)、碱性磷酸酶(AKP)、Υ-谷氨酰基转移酶(GGT)的含量,应用SPSS10.0软件进行统计学分析.结果:镉作业工人尿镉含量在各接触组中均增高,尿α1-MG、β2-MG、RBP在接触2、3组中增高,与对照组相比有显著性差异(P<0.05),且随着接触时间的延长呈上升趋势;各接触组尿GGT、NAG活性均明显高于对照组(P<0.05).结论:尿镉、α1-MG、β2-MG、RBP、GGT、NAG可作为慢性职业性镉中毒的早期诊断指标. 相似文献
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检查镉作业工人134人,发现65人有不同程度的干性鼻炎、萎缩性鼻炎、鼻中镉粘膜糜烂、鼻衄、嗅觉减退或丧失等鼻部改变,伴有随工龄的增加而加重的趋。对照组为非镉作业的动力处工人113人,仅11人有轻度的鼻部改变。两者差异甚为显著。本文提示长期接触较高浓度的镉会造成不同程度的各种鼻部损害。 相似文献
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镉是一种有害环境污染物,在自然界不易降解,机体内半衰期长达16~33a,生产过程及环境中的镉可经呼吸道和消化道进入机体,通过血液向肾脏、肝脏、骨骼等器官分布,产生多系统、多器官的毒性损害[1]。在工业上应用十分广泛,如金属镉及含镉合金冶炼、焊接、镍-镉电池制造、颜料制造、金属表层镀镉等。本次分析的7例病例均为江苏省镇江市某焊料有限公司的工人。公司产品为各种钎焊材料。1主要生产流程及车间基本情况1.1主要生产流程熔炼→挤压→拉丝→切丝(或制环)→包装→进库。其中熔炼的分流程:合料→搅拌→浇注→脱模→剪锭→掼锭→磨锭。“熔… 相似文献
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镉作业工人肾损伤血镉临界值的研究 总被引:1,自引:0,他引:1
本文调查了我省某矿务局68名镉作业工人尿蛋白、尿β_2-MG、尿镉、血镉水平的变化。结果发现,尿镉与肾损害并无关系;血镉与尿蛋白、尿β_2-MG相关。通过时血镉与尿蛋白、尿β_2-MG的回归分析,我们认为引起镉作业工人轻度肾损伤的血镉临界值为5.43μg/L,当血镉浓度大于16.9μg/L时,可能产生比较严重的肾损伤。 相似文献
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铬、镉作业工人尿γ-GT同功酶变化的研究 总被引:1,自引:1,他引:1
本文调查了98名铬(Cr)作业工人和58名镉(Cd)作业工人尿中γ-GT同功酶的变化。在Cr作业工人中,当受检者尿蛋白和尿民β_2-MG均在正常范围内时,尿γ-GT、γ-GTⅠ和γ-GTⅡ活性已开始显著高于对照组,随肾损害程度加重,尿γ-GT、γ-GTⅠ和γ-GTⅡ活性呈明显的升高趋势,但γ-GTⅠ/γ-GTⅡ与对照组比较均未见显著变化;这似可提示尿γ-GT总酶和同功酶均可作为检测铬性肾损害较灵敏的指标,这对早期诊断和防治佑性肾损害有一定的理论意义和实用参考价值。在Cd作业工人中,所有Cd作业工人尿中γ-GT、γ-GTⅠ、γ-GTⅡ均超出正常值上限;随肾损伤程度的加重,尿γ-GT、γ-GTⅠ明显升高,而且γ-GTⅠ/γ-GTⅡ呈下降趋势,在重度肾损伤的Cd作业工人中,尿γ-GTⅠ/γ-GTⅡ由正常的6.02下降到3.73;结果提示,尿γ-GT可能作为Cd接触者健康监测的一个敏感指标;尿γ-GTⅠ/γ-GTⅡ的变化似与Cd作业工人肾损伤程度有密切关系,其机理值得进一步研究。 相似文献
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铅对肾脏有毒性作用,动物实验证实铅主要影响肾近曲小管~[1]。而铅作业工人的肾损害是一个长期慢性的变化过程,临床表现潜隐,早期不易发现。近年来尿酶在肾脏损伤监测中的应用价值受到了重视。 相似文献
10.
目的了解镉作业工人的职业危害状况。方法对江苏省某镍镉电池生产企业进行职业卫生学调查,并对镉作业工人进行尿镉水平检测。结果个体采样的8个含镉作业岗位空气中镉及其化合物时间加权平均浓度(TWA)有6个岗位超过职业卫生接触限值。1 177名镉作业工人中有18例尿镉水平超标。尿镉超标工人所在岗位空气中镉及其化合物短时间接触浓度(STEL)与时间加权平均浓度(TWA)均超过国家标准限值。不同工龄镉作业工人尿镉水平比较,差异有统计学意义(P<0.05)。结论企业应降低工作场所空气中镉的浓度,减少作业工人的接触时间,将镉对人体的损害降到最低。 相似文献
11.
C G Elinder C Edling E Lindberg B K?gedal O Vesterberg 《British journal of industrial medicine》1985,42(11):754-760
Cadmium induced renal effects were examined in 60 workers (58 men, 2 women) previously exposed to cadmium. Tubular damage in the form of beta 2-microglobulinuria was found in 40%, and urinary albumin and orosomucoid increased significantly with increasing urinary cadmium and increasing relative clearance of beta 2-microglobulin. It is suggested that increased albumin excretion is secondary to the tubular damage. In no case was typical glomerular proteinuria found that could be related to cadmium. Histories of renal stones were more common among the workers with high urinary cadmium concentrations. The glomerular filtration rate was measured in 17 of the workers who had pronounced tubular dysfunction. The average glomerular filtration rate for these men was less than the age adjusted predicted value (mean = 84%). Furthermore, there was a significant (p less than 0.05) correlation (r = -0.47) between tubular reabsorption loss and a decreased glomerular filtration rate. 相似文献
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C G Elinder C Edling E Lindberg B K?gedal O Vesterberg 《Occupational and environmental medicine》1985,42(11):754-760
Cadmium induced renal effects were examined in 60 workers (58 men, 2 women) previously exposed to cadmium. Tubular damage in the form of beta 2-microglobulinuria was found in 40%, and urinary albumin and orosomucoid increased significantly with increasing urinary cadmium and increasing relative clearance of beta 2-microglobulin. It is suggested that increased albumin excretion is secondary to the tubular damage. In no case was typical glomerular proteinuria found that could be related to cadmium. Histories of renal stones were more common among the workers with high urinary cadmium concentrations. The glomerular filtration rate was measured in 17 of the workers who had pronounced tubular dysfunction. The average glomerular filtration rate for these men was less than the age adjusted predicted value (mean = 84%). Furthermore, there was a significant (p less than 0.05) correlation (r = -0.47) between tubular reabsorption loss and a decreased glomerular filtration rate. 相似文献
13.
镉接触工人体内血清性激素水平的变化 总被引:3,自引:0,他引:3
目的 探讨镉接触工人体内血清性激素水平的变化及其机制。方法 选取南方某冶炼厂镉接触工人及当地健康男性为调查对象,经空气采样测定各车间空气中镉的浓度,用原子吸收分光光度法测定尿镉,并经肌酐校正作为调查对象体内镉负荷的生物标记物;同时测定工人体内性激素水平,并进行镉接触的剂量-效应评定。结果 在控制年龄等混杂因素后,血清睾酮水平随镉接触水平的增高而呈升高趋势,其中尿镉为10.9-21.9μmol/mol肌酐及>21.9μmol/mol肌酐组的睾酮水平分别为:13.00nmol/L和11.37nmol/L,与0.0-2.2μmol/mol肌酐组的9.31nmol/L比较,差异有显著性;电解车间及尿镉>21.9μmol/mol肌酐组人的血清黄体生成素水平分别为4.11U/T和4.32U/L,显著同于对照组的2.52U/L和尿镉0.0-2.2μmol/mol肌酐组的2.64U/L。结论 镉接触能引起工人血清性激素水平的变化。 相似文献
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Cadmium induced renal tubular effects were examined in 65 female workers in a factory manufacturing nickel cadmium batteries. Urinary beta 2-microglobulin (beta 2m), urinary N-acetyl-D-glucosaminidase activity (NAG), and serum creatinine and serum urea concentrations were used to assess the renal effects. Of the four measures, only urinary NAG and urinary beta 2m showed a strong positive correlation with blood cadmium concentrations (r = 0.49 and 0.43 respectively); NAG showed a weaker correlation with urinary cadmium concentrations (r = 0.35). Urinary beta 2m has weak correlation with urinary cadmium (r = 0.04). Only urinary NAG showed a significant deterioration in renal function among the exposed group. NAG detects the largest proportion of abnormalities among the exposed group. Abnormal urinary beta 2m is detected in only 15.4% of the workers, half of whom have blood cadmium above 10 micrograms/l. The proportion of abnormalities detected by urinary NAG differs significantly from the proportion of abnormalities detected by urinary beta 2m (p less than 0.01). The age adjusted mean urinary NAG excretion showed a significant rise with urinary cadmium of above 3 micrograms/g creatinine. Urinary beta 2m failed to show any significant rise. With blood cadmium concentrations, the age adjusted mean urinary NAG excretion showed a rise from 1 microgram/l of blood cadmium followed by a plateau between blood cadmium concentrations of 3-10 micrograms/l. No significant rise in mean urinary excretion in beta 2m was seen until blood cadmium concentrations exceeded 10 micrograms/l. 相似文献
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Cadmium induced renal tubular effects were examined in 65 female workers in a factory manufacturing nickel cadmium batteries. Urinary beta 2-microglobulin (beta 2m), urinary N-acetyl-D-glucosaminidase activity (NAG), and serum creatinine and serum urea concentrations were used to assess the renal effects. Of the four measures, only urinary NAG and urinary beta 2m showed a strong positive correlation with blood cadmium concentrations (r = 0.49 and 0.43 respectively); NAG showed a weaker correlation with urinary cadmium concentrations (r = 0.35). Urinary beta 2m has weak correlation with urinary cadmium (r = 0.04). Only urinary NAG showed a significant deterioration in renal function among the exposed group. NAG detects the largest proportion of abnormalities among the exposed group. Abnormal urinary beta 2m is detected in only 15.4% of the workers, half of whom have blood cadmium above 10 micrograms/l. The proportion of abnormalities detected by urinary NAG differs significantly from the proportion of abnormalities detected by urinary beta 2m (p less than 0.01). The age adjusted mean urinary NAG excretion showed a significant rise with urinary cadmium of above 3 micrograms/g creatinine. Urinary beta 2m failed to show any significant rise. With blood cadmium concentrations, the age adjusted mean urinary NAG excretion showed a rise from 1 microgram/l of blood cadmium followed by a plateau between blood cadmium concentrations of 3-10 micrograms/l. No significant rise in mean urinary excretion in beta 2m was seen until blood cadmium concentrations exceeded 10 micrograms/l. 相似文献
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The health effects of occupational exposure to cadmium were studied in a group of 902 workers employed for at least one year in a Swedish battery factory between 1931 and 1982. Data on air cadmium concentrations for different periods were combined with company employment records to obtain individual cumulative exposure estimates. A questionnaire including questions on the occurrence of kidney stones was sent to all 601 living workers and to the next of kin of 267 of the deceased workers. The response rate was 88%. 73 workers reported renal calculi that appeared after initial employment. A dose-response relation was found between cumulative exposure to cadmium and age standardised cumulative incidence. Incidence rate ratios (IRRs) were then computed for three exposure categories (< 250, 250- < 5000, and 5000 micrograms/m3 x years) standardised for calendar time, age, and smoking with the low exposure group as reference level. The IRRs were 1.0, 1.6 [95% confidence interval (95% CI) 0.7-3.4], and 3.0 (95% CI 1.3-6.8) respectively. beta 2 Microglobulin measurements were available for 33 workers who formed stones; 13 of these workers had tubular proteinuria (beta 2 microglobulin > or = 34 micrograms/mmole creatinine)--that is, a prevalence of 39%. There was also an indication of a steeper dose-response relation among workers with tubular proteinuria. 相似文献
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对长期接触低浓度氨工人血氨和血清ALT进行测定,以探讨长期接氨对肝功能的影响。结果表明长期低浓度氨接触可使肝功能出现轻微异常,脱离氨作业环境后,肝功能可逐步恢复正常。 相似文献
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镉接触工人尿镉含量水平影响因素分析 总被引:1,自引:0,他引:1
目的分析镉接触工人尿镉含量的影响因素。方法选取深圳市3家镍-镉电池厂镉接触工人375名为接触组,另选取153名未接触镉的上岗前工人作为对照组,分析两组人群的尿镉含量水平,同时对3间镍-镉电池厂工作场所进行职业卫生学调查。结果工作场所空气中氧化镉短时间接触浓度平均为0.027 mg/m3,超标率为37.0%;接触组尿镉含量为(3.36±2.43)μmol/molCr,明显高于对照组[(2.09±1.74)μmol/molCr](P<0.01),接触组女性尿镉含量为(3.68±2.92)μmol/molCr,明显高于男性接触组[(2.76±2.21)μmol/molCr](P<0.01);高浓度组尿镉含量[(3.79±3.41)μmol/molCr]明显高于低浓度组[(2.82±2.12)μmol/molCr](P<0.01),高浓度接触组尿镉异常率(21.9%)也高于低浓度接触组(7.7%)(P<0.01);多元线性回归分析结果显示,工龄、工种(接触浓度)、年龄、性别与尿镉含量的相关系数依次为0.559、0.266、0.233和0.092(均P<0.05)。结论工龄增加、工作场所氧化镉浓度超标是尿镉增高的主要危险因素,降低氧化镉浓度至职业接触限值以下和减少接触时间是预防慢性镉中毒的关键。 相似文献