职业性镉接触工人尿镉含量的影响因素

目的分析镉接触工人的尿镉含量的影响因素。方法选取无锡某电池厂的镉接触工人437名为接触组,另选取782名未接触镉的工人作为对照组,分析2组人群的尿镉含量水平,同时对此镍镉电池厂进行劳动卫生学调查。结果工作场所中镉及其化合物的短时间接触浓度范围为0．002～3．058mg／m3,超标率为87．5％。接触组尿镉含量（中位数1．4300μmol／mol肌酐）明显高于对照组（中位数0．7300μmol／mol肌酐）,高浓度接触组的尿镉含量（中位数1．7500μmol／mol肌酐）明显高于低浓度接触组（中位数1．2450μmol／mol肌酐）,高浓度接触组的尿镉异常率（6．40％）也明显高于低浓度接触组（2．14％）。对照组和接触组中女性尿镉含量明显高于男性;多元线性回归分析结果显示,车间空气中镉暴露水平、工龄和年龄与尿镉含量的相关系数依次为0．851、0．630和0．038。结论工作场所中镉及其化合物浓度超标、工龄的增加是尿镉含量升高的主要因素,降低工作场所空气中镉及其化合物的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。     

某电池厂镉作业女工尿镉水平调查

目的了解某电池厂镉作业女工的尿镉水平。方法了解生产车间空气中的镉及其化合物的浓度；检测镉作业女工的尿镉含量，并与当地健康人的尿镉水平进行比较。结果①生产车间空气中镉及其化合物浓度的检测结果均符合国家职业卫生接触限值。②尿镉超标女工63人，达28．8％。③各工种尿镉水平均有不同程度的超标。④调查组的尿镉水平明显高于对照组，差异有统计学意义（P〈0．01）。⑤工龄〉2年组的尿镉超标率明显高于工龄≤2年组，差异有统计学意义（P〈0．01）。结论该电池厂镉作业女工的尿镉水平显示不同程度的超标，应加强对镉作业工人的职业卫生教育，纠正不良卫生行为。     

基准剂量在镉接触人群骨效应研究中的应用

目的通过镉接触人群流行病学研究，估测环境镉接触引起人群骨质疏松的基准剂量。方法镉污染区居住的居民为接触组，非污染区居民为对照组。尿镉（UCd）、血镉（BCd）为接触生物标记物；代表骨质疏松的Z评分为效应生物标记物。结果污染区人群尿镉、血镉水平均明显高于对照地区（P〈0．05），且高污染医人群尿镉、血镉水平明显高于中污染区（P〈0．05）。与5μg/gCr组相比，各人群尿镉水平、血镉水平最高组的骨密度均明显降低，差异有统计学意义（P〈0．05）。人群随着体内镉接触水平的升高，骨质疏松的患病率均随之明显升高，有统计学意义（P〈0．05）并有线性关系（P〈0．05）。计算得到基准剂量（BMD），推出基准剂量的95％低限水平（BMDL）。镉所引起的骨质疏松指标的尿镉BMDL值高于镉致肾功能不全指标的BMDL值。结论高剂量镉能引起人群骨质疏松，但时间上晚于镉致肾功能不全的损害。基准剂量是一种值得应用的新方法。     

镉作业女工外周血红细胞参数分析

目的了解职业性镉接触对女性外周血红细胞相关参数的影响。方法对219名镉作业女工的尿镉及外周血进行检测，比较接触组与对照组间红细胞相关参数红细胞计数（RBC）、血红蛋白含量（HGB）、红细胞比积（HCT）、红细胞平均容积（MCV）、红细胞平均血红蛋白量（MCH）、红细胞平均血红蛋白浓度（MCHC）及红细胞体积分布宽度（RDW）的差异。结果①以尿镉含量分组，低镉组几何均数为1．47（0．3～5．0）μg/gCr、高镉组尿为11．43（5．2～51．4）μg／gCr；②低镉组HGB、HCT、MCH和MCHC明显低于对照组，而RDW明显高于对照组，差异均有统计学意义（P〈0．05；P〈0．01）；高镉组各项红细胞参数与对照组比较差异均有统计学意义（P〈0．05；P〈0．01）；高镉组MCHC和RDW与低镉组比较差异均有统计学意义（P〈0．05）。结论镉可导致作业女工的红细胞相关参数发生改变。     

镉接触工人尿镉含量水平影响因素分析

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。     

人血浆抗金属硫蛋白抗体与镉致肾损伤易感性的关系

目的研究人血浆抗金属硫蛋白扰体（anit-MT Ab）与职业镉接触所致肾功能损伤的关系。方法选择某镉冶炼厂男性作业工人为研究对象，进行接触评定和效应评定，以尿镉（UCd）、血镉（BCd）和职业镉摄入（TTCd）为接触指标，尿β2-微球蛋白（Uβ2-MG）、尿N-乙酰-β-D-氨基葡萄糖苷酶（UNAG）、尿白蛋白（UALB）作为镉敛肾损伤的效应标志物。酶联免疫吸附法（EHSA）检测血浆中anti-MT Ab滴度。结果职业镉接触组中UCd（3．16μg／g Cr）、血镉（9．28βg/L）、Uβ2-MC（81．17βg/g Cr）、UALB（7．03mg／gCr）水平明显高于对照组，随着职业镉接触水平升高，Uβ2-MG、UNAG和UALB含帚和异常发生率明显升高。对照组与接触组间anti-MT Ab滴度的差异无统计学意义（P〉0．05）。anti-MT Ab滴度并不随接触剂晕增加而增加，与血镉、UCd和TIEd间无明显联系（P〉0．05）。拄接触组中anti-MT Ab与UNAG和Uβ2-MG呈正相关，相关系数分别为0．302和0．218（P〈0．05）。相同机体镉负荷下，anti-MT Ab高滴度人群较低滴度人群更易出现肾小管损伤，比值比为4．200。结论职业性镉接触与肾功能损害间存在剂量一反应关系，而与血浆anti-MT Ab间无明显关联。镉接触人群中血浆anti-MT Ab高水平者更容易出现肾脏损伤。     

血镉和尿镉含量与鼻和鼻旁窦病变的关系

血镉和尿镉含量与鼻和鼻旁窦病变的关系ＪｕｄｉｔｈＳｈａｈａｍ本文研究者在评价镍镉电池厂接触高浓度镉工人的血镉和尿镉含量与鼻旁窦Ｘ线异常之间的关系。作者调查了一家镍镉电池厂接触高浓度镉和镍的１０６名工人。男性６７人（６３％），平均年龄４０．５±１０．９...     

沈阳市镉污染区居民尿镉及骨密度调查

目的通过检测脱离环境镉接触人群的尿镉及骨密度，探讨镉致肾损伤的远期效应与骨密度的关系。方法选择在镉污染区连续居住20年以上的居民为调查对象，应用GMY-1型单光子骨密度吸收仪，测量其桡骨远端骨密度（BMD）；用原子吸收分光光度法检测该人群的尿镉（UCd）水平。结果污染区居民的尿镉水平显著高于对照组（P〈0．05），并随着镉污染程度的增加而增高；BMD随着UCd水平的增加而下降，接触组与对照组差异有统计学意义（P〈0．05）。结论长期脱离镉污染环境后，体内镉仍处于一个较高水平，并影响骨代谢导致骨密度下降。     

某镉电池厂镉作业女性32人尿镉及血清中性激素的水平

目的了解镉作业女工尿镉及血清中性激素水平改变的影响因素并初步探讨其机制。方法 2010年11月,选取某镉电池工厂镉作业女工100名作为接触组,按工作场所空气中镉含量的水平分成高、低2个接触浓度组;并选取来自同一家工厂未接触镉作业的50名女工作为对照组,测定3组人群的尿镉、促卵泡刺激素（FSH）、促黄体生成素（LH）及雌二醇（E2）的水平并进行统计分析。结果 2个接触组尿镉含量和异常率均明显高于对照组,差异有统计学意义（P〈0.05,P〈0.01）;高浓度接触组工人在月经周期中的月经期血清中FSH水平和E2水平均低于对照组,差异均有统计学意义（P〈0.01）;增殖期血清中LH水平低于对照组,差异有统计学意义（P〈0.01）;分泌期血清中LH和E2水平均低于对照组,差异均有统计学意义（P〈0.01）。结论在该研究的条件下,工作场所中氧化镉浓度超标是导致尿镉水平升高的主要危险因素;镉暴露可能对下丘脑-垂体-卵巢轴的性激素分泌功能造成影响,从而对女性工人的生殖系统产生内分泌干扰作用。     

金属硫蛋白基因亚型表达在镉接触中作为生物标志物的研究

目的探讨人外周血淋巴细胞（HPBIs）中金属硫蛋白（MT）基因业型的表达在镉接触中作为生物标志物的可行性。方法选择职业接触镉的人群，进行接触评定和效应评定，分离淋巴细胞，用RT-PCR测定MT基因亚型的表达水平。结果接触组工人的MT-1A、1E、1F、1X和MT-2A mRNA表达水平明显高于对照组，差异有统计学意义（P〈0．05）。随血镉水平增高，MT-1A1E、1F、1X和MT-2A mRNA表达水平都明显增高（P〈0．05）。随尿镉水平增高，MT-1A、1E、1F、1X和MT-2A mRNA表达水平有升高趋势，且MT-1A和MT-2A mRNA表达水平明显升高（P〈0．05）。MT-1A、1E、1F、1X和MT-2A mRNA表达水平与血镉水平明显相关（P〈0．05），同时MT-1A、1F、MT-2A mRNA表达水平与尿镉水平明显相关（P〈0．05）。血镉与MT-1E、MT-1F、MT-1X、MT-2A mRNA基础表达水平存在剂量-效应关系；血镉、β2-MG和尿金属硫蛋白（UMT）与MT-1A基础表达水平存在剂量-效应关系。结论HPBLs中MT基因亚型的表达可作为镉接触性生物标志物，其中MT-1A还可作为镉致肾毒性的效应性生物标志物。     

云南省大型矿企职工尿中铅和镉的检测结果

目的了解云南省某大型矿企职工尿铅、尿镉超标情况,为评价职工健康状况提供依据。方法收集该矿企11个分厂职工尿液,应用岛津6300原子吸收分光光度计分别进行尿铅和尿镉检测。结果 3 841名职工进行尿铅检测,有227例的尿铅含量异常,尿铅异常百分率为5.91%,尿铅含量范围为0.34～3.64μmol/L。异常者中有59%尿铅结果在"观察对象"值2倍以下。有3个分厂职工的尿铅平均异常百分率偏高,分别为23.33%、20.35%、12.5%。对2 442名职工进行尿镉检测,有11例尿镉含量超过0.04μmol/L,尿镉异常百分率为0.45%,尿镉含量范围为0.042～0.52μmol/L。结论部分分厂职工尿铅、尿镉异常百分率偏高,需加强作业工人的职业病防护和定期进行职业健康检查。     

镉接触工人尿镉血镉与尿β_2MG RPB含量的跟踪研究

目的:跟踪调查镉接触工人停止接触镉后尿镉、血镉的变化及肾功能损害情况,寻找镉接触指标与肾功能损害指标的关系,初步探讨职业性镉引起的肾功能特点及规律。方法:选择深圳某镍镉电池厂29名镉中毒观察对象(尿镉连续2次超过5μmol/mol肌酐)为研究对象,分析尿镉、血镉含量与尿β2-微球蛋白(β2MG)、尿视黄醇结合蛋白(RPB)排出量的关系;并通过跟踪研究他们在停止接触镉1年后,接触指标(尿镉、血镉)及肾功能损害指标的变化的规律。结果:镉中毒观察对象在停止接触1年后,尿镉由(7.16±2.81)μmol/mol肌酐下降至(7.03±2.84)μmol/mol肌酐,尿镉含量下降没有显著性差异(P>0.05);血镉明显下降,由(5.8±1.81)μg/L下降至(3.5±1.24)μg/L,有显著性差异(P<0.01);尿β2-微球蛋白含量(中位数)由1.19μmol/mol肌酐上升至1.21μmol/mol肌酐,尿视黄醇结合蛋白含量(中位数)由0.39μmol/mol肌酐上升至0.42μmol/mol肌酐,统计学秩和检验结果显示均没有显著性差异(P>0.05)。尿镉与血镉存在明显的线性正相关,相关系数(r)为0.721,(P<0.01),回归分析得出的方程为:y=1.132x+3.656,(y代表尿镉,x代表血镉)。尿镉、血镉与尿β2-微球蛋白含量的相关系数分别为0.321,0.346,统计学上均没有显著性相关(P>0.05)。结论:职业性镉中毒观察对象停止接触镉1年后,血镉明显下降,尿镉含量下降不明显,尿镉与血镉存在线性正相关,尿β2-微球蛋白、尿视黄醇结合蛋白含量总体水平变化不显著,但有个别仍可以出现肾功能异常,镉对肾功能损害存在明显个体差异性。     

Renal tubular function of workers exposed to low levels of cadmium

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.     

Renal tubular function of workers exposed to low levels of cadmium.

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.     

Cadmium in blood and urine related to present and past exposure. A study of workers in an alkaline battery factory

Blood and urinary cadmium concentrations together with cadmium in air concentrations from the breathing zone of 18 male workers in an alkaline battery factory were determined at regular intervals for 11 consecutive weeks. Nine of the workers examined were smokers and nine non-smokers. Smokers and non-smokers did not differ in age or years of employment. Cadmium in air concentrations varied, but no definite trend was observed. The concentrations of cadmium in the blood and urine were found to be stable. Exposure to airborne cadmium was identical for smokers and non-smokers but average cadmium concentrations in the blood and urine of smokers were approximately twice as high as those in non-smokers. For the whole group, urinary cadmium was significantly correlated with years of employment, but no correlation was found between blood cadmium concentrations and exposure. For non-smokers, the correlation between cadmium in blood and years of employment was statistically significant (p less than 0.001). This finding indicated that blood concentrations of cadmium reflect body burden in non-smokers at current low exposure levels.     

Cadmium in blood and urine related to present and past exposure. A study of workers in an alkaline battery factory.

Blood and urinary cadmium concentrations together with cadmium in air concentrations from the breathing zone of 18 male workers in an alkaline battery factory were determined at regular intervals for 11 consecutive weeks. Nine of the workers examined were smokers and nine non-smokers. Smokers and non-smokers did not differ in age or years of employment. Cadmium in air concentrations varied, but no definite trend was observed. The concentrations of cadmium in the blood and urine were found to be stable. Exposure to airborne cadmium was identical for smokers and non-smokers but average cadmium concentrations in the blood and urine of smokers were approximately twice as high as those in non-smokers. For the whole group, urinary cadmium was significantly correlated with years of employment, but no correlation was found between blood cadmium concentrations and exposure. For non-smokers, the correlation between cadmium in blood and years of employment was statistically significant (p less than 0.001). This finding indicated that blood concentrations of cadmium reflect body burden in non-smokers at current low exposure levels.     

镉电池厂职业性慢性镉中毒发病情况分析

目的探讨镉电池厂职业性慢性镉中毒发病情况,尿镉、尿视黄醇结合蛋白（RBP）和尿＆微球蛋白（β2MG）与工龄的关系,为镉中毒的防治提供科学依据。方法回顾分析45例职业性慢性镉中毒病例,采用职业卫生学调查、工作场所职业病危害因素现场检测和职业健康检查进行综合分析。结果工作场所空气中镉浓度0．001～0．848mg／m^3,超过《工作场所有害因素职业接触限值》GBZ2．1—2007的要求;45例病例中,RBP与β2MG含量有直线相关关系,尿镉与RBP、β2MG及工龄之间均无直线相关关系;镉电池厂中毒病例并发肾结石的机率高。结论职业性慢性镉中毒病例RBP的诊断意义更大,β2MG诊断值有待降低。应加强镉的职业危害防治,用其他电池代替镉电池生产,从源头控制职业危害。     

低浓度镉暴露对工人肾功能及体液中铁和锌水平的影响

[目的]探讨通过呼吸道职业性接触镉的情况下,工人体液中铁和锌的水平与镉肾毒作用间的相互关系。[方法]随机抽取镉接触工人103人和对照组人员36人,分别测定镉接触标志物[血镉（blood cadmium,BCd）和尿镉（urinary cadmium,UCd）]、镉肾毒性的效应标志物[尿β2-微球蛋白（urinary β2-microglobulin,Uβ2-MG）、尿白蛋白（urinary albumin,UALB）和尿N-乙酰-β-D-氨基葡萄糖苷酶（urinary N-acetyl-β-D-glucosaminidase,UNAG）]和反映铁状态的生物标志物[血红蛋白（Hb）、血清铁蛋白（serum ferritin,SF）和血清转铁蛋白受体（serum transferrin receptor,sTfR）],测定血锌和尿锌来反映体液中锌水平,并分析这些标志物间的相互关系。[结果]镉接触工人的血镉、尿镉均明显增高,尿β2-MG和UALB均高于对照组,尿NAG、β2-MG和UALB均随尿镉水平的增高而增高,存在剂量-效应关系,Hb含量和SF低于对照组,贫血患病率高于对照组。接触组血锌和尿锌含量与对照组的差异无统计学意义,但是尿锌与尿镉和血镉间均呈正相关关系,尿镉高的工人尿锌浓度高于尿镉低的工人。[结论]职业性镉接触能引起体内铁储存量下降和贫血患病率增高,在体内镉蓄积到一定程度时,会引起尿锌排泄增加。     

Renal Effects of Cadmium Intake of a Japanese General Population in Two Areas Unpolluted by Cadmium

Renal effects of cadmium exposure (i.e., in food products) on people living in two areas unpolluted by cadmium in Japan were investigated. The population comprised 875 inhabitants (i.e., 346 males and 529 females) and 635 inhabitants (i.e., 222 males and 413 females), all of whom in each area were 50+ y of age. The authors used urinary cadmium concentration as an indicator of internal dose, and total urinary protein, β₂-microglobulin, and N-acetyl-β-glucosaminidase were indicators of renal dysfunction. The authors used multiple-regression and logistic-regression analyses to study the relationship between urinary cadmium excretion and the above indicators of renal dysfunction. In the two geographic areas, both analyses revealed that urinary cadmium concentrations were associated significantly with indicators of renal dysfunction. The results suggest that renal dysfunction is related significantly with environmental cadmium exposure in areas of Japan that are not polluted by cadmium.