镉作业工人尿镉增高7例报告

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…     

镉作业工人的肾脏功能变化

对镉作业工人的肾脏损害进行了探讨,结果表明尿镉低于临界值（5.05μg/gCr),尿中β2-MG、AKP、LDH已显著高于对照组;尿镉高于临界值,尿中β2-MG、AKP、LDH、γ-GT、NAG均升高,建议将β2-MG、AKP、LDH联合应用作为镉作业工人早期检测指标。     

江苏省某镍镉电池生产企业镉作业工人尿镉水平调查

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。     

应用尿微量蛋白联合尿酶测定CS2作业工人肾损伤

二硫化碳 ( CS2 )是一种用途广泛的有机溶剂 ,主要接触场所在粘胶纤维生产过程中。接触 CS2 引起的主要危害通常是心血管系统和眼等感觉器官[1,2 ] 。近年来 ,也有文献报道长期接触 CS2 的作业工人有可能导致肾脏病变。目前尿微量蛋白联合尿酶的测定 ,已广泛用于多种疾病的继发早期肾损害检测。本文通过定量检测尿中微量蛋白 ,包括 :尿微量白蛋白( m Alb)、免疫球蛋白 ( Ig G)、联合尿酶 ( NAG)等 ,探讨其在接触 CS2 作业工人肾损害中的临床价值 ,以确定是否可将上述指标用于 CS2 接触人群的职业性健康监护。1　材料与方法1 .1　对象…     

镉作业工人尿镉含量水平的调查

目的调查镉职业接触者尿镉含量水平。方法对广东省两家镉电池厂作业环境进行卫生学的调查及对587名接镉作业工人的尿镉进行分析,并与103名对照组相比较。结果作业现场20个点的氧化镉浓度测定中,平均浓度为0.077mg/m3,测定点浓度超标率为45%,平均超标2.85倍,最高浓度超标为35.50倍;接触组尿镉为(6.48±2.52)μmol/molCr,明显高于对照组的(2.96±1.26)μmol/molCr(P<0.01),尿镉增高的人数为226名,占38.50%,明显高于对照组的9.71%(P<0.01);工龄大于3年的工人尿镉超标人数比例增加;〗尿镉与血镉之间存在正相关关系(r=0.51,P<0.01),特别是当尿镉含量大于5μmol/molCr时,这种相关程度更高(r=0.63,P<0.01)。结论镉职业接触者尿镉含量增高,其含量水平随着接触时间的增加而增加。加强工作场所的职业病防治是降低职业危害的关键。     

镉作业工人尿镉和血常规检查结果分析

选择某镍镉电池企业进行在岗期间职业健康检查的241名镉作业工人作为接触组,以当地无职业性镉接触史的96名受检者作为对照组,测定尿镉、尿β2-微球蛋白、白细胞(WBC)、中性粒细胞(NE)、淋巴细胞(LY)、红细胞(RBC)、血红蛋白(Hb)、红细胞压积(HTC)、红细胞分布宽度(RDW)、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),并对两组检测结果进行比较。结果显示,接触组负极拉浆、负极制片、负极点焊、卷绕、装配、封口岗位的镉作业工人尿镉、HTC、MCV、RDW、MCH与对照组比较差异有统计学意义。提示该企业镉危害严重,作业工人的镉负荷量较高,应采取措施预防镉中毒。     

镉作业工人尿镉和尿蛋白变化的检测分析

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。     

镉作业工人健康损害的调查分析

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。     

某锌粉厂镉作业工人血镉、尿镉、尿β2-微球蛋白动态观察

目的 探讨低剂量接触工人尿镉(urinary cadmium,UCd)、血镉(blood cadminm,BCd)及尿β₂-微球蛋白((urinary β₂-microgloblin,Uβ₂-MG)的变化。 方法 检测某锌粉加工厂作业场所空气镉浓度,连续7年对接触工人进行UCd、BCd、Uβ₂-MG检查。 结果 接触BCd[7.05(3.50,11.80)μg/g],高于对照组[2.84(0.92,7.76)μg/g],差异有统计学意义(P＜0.05);UCd、BCd超标率、脂肪肝检出率分别为24.1%、56.6%和39.8%,高于对照组(8.9%、33.3%和22.2%),差异有统计学意义(P＜0.05);观察7年,接触组UCd、BCd和Uβ₂-MG M值分别波动于2.74(1.68,4.29)～4.42(2.88,6.17)μg/gCr、3.78(2.08,5.80)～10.23(3.55,14.54)μg/g、250.0(128.6,449.2)～436.0(366.0,500.4)μg/gCr之间,年度间总体比较,差异有统计学意义(P＜0.01);超标率波动于15.6%～41.1%、35.7%～71.4%、2.4%～27.4%,年度间总体比较,差异有统计学意义(P＜0.01);UCd水平超标构成比年度间差异无统计学意义(P＞0.05)。 结论 接触低浓度Cd可影响镉作业工人UCd、BCd、Uβ₂-MG水平,UCd、BCd、Uβ₂-MG水平处于波动状态。     

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。     

Metallothionein in cadmium-exposed workers

A radioimmunoassay for human metallothionein (Mt) was utilized to measure urinary Mt in cadmium-exposed and nonexposed workers. Workers in an environment of high concentration had higher Mt levels than those in an environment of lower Cd concentration. Control groups had lower Mt levels than either exposed group. Additional urinary proteins were measured in order to assess functional renal status. Mt concentration in urine was similar in individuals with and without renal damage. Mt concentration in urine was found to correlate with urinary Cd level, a correlation (r) of 0.94 being obtained between log Cd in urine and log Mt in urine. Additionally, a correlation of 0.82 was obtained between log Cd in blood and log Mt in urine.     

Dose-response relations between urinary cadmium and tubular proteinuria in cadmium-exposed workers

Cadmium in urine reflects the body burden in cadmium-exposed individuals. Urinary β2-microglobulin is frequently used as a marker of tubular proteinuria with an arbitrarily chosen value (34 μg/mmole creatinine) as the cut-off limit. Both this cut-off level and a lower limit (25 μg/mmole creatinine) were used in a study of the relationship between urinary cadmium and β₂-microglobulin in 561 cadmium-exposed battery workers. There was a clear dose-response relation between the urinary cadmium level and the prevalence of tubular proteinuria ranging from 0.8% in the lowest exposure group, excreting less than 1 nmole cadmium/mmole creatinine, to 46.4% (50.0 for the lower cut-off level) in the highest exposure group with a mean urinary cadmium of 15 nmole/mmole creatinine. The relation between urinary cadmium and tubular proteinuria was also assessed using probit analysis. There was a 10% response at a urinary cadmium of 3 nmole/mmole creatinine. The impact of age on the dose-response relation was explored in two age groups with the cut-off point at 60 years of age, showing a 10% prevalence of tubular proteinuria at urinary cadmium levels of 1.5 nmole/mmole creatinine in this older age group and 5.0 nmole/mmole creatinine in the category under 60 years of age. The study thus indicates that the present health-based limit (10 nmole/mmole creatinine) proposed by the World Health Organization (WHO) is too high and it is suggested that a new limit should be set to 3 nmole/mmole creatinine.     

Characterization of the proteinuria in cadmium-exposed workers

Summary The concentration of several protein (₂-microglobulin, orosomucoid, albumin, transferrin) and of total amino acids was determined in the urine of 18 cadmium-exposed workers and in a group of matched nonexposed workers. The results were compared with the electrophoretic pattern of urinary proteins on agarose gel.Ten of the cadmium-exposed workers had an abnormal electrophoretic pattern, eight of them excreted larger quantities of high and low molecular weight proteins, and the other two showed only an increased excretion of high molecular weight proteins. An increased ₂-microglobulin excretion was found in five workers with a normal urinary protein electrophoresis whereas only the urine of three exposed workers were found to be normal. We have confirmed a previous observation that in the majority of the cadmium-exposed workers with an abnormal electrophoretic pattern or an increased total proteinuria, not only low molecular weight proteins (₂-microglobulin) are excreted in greater amount but also high molecular weight proteins such as albumin and transferrin.Furthermore, in cadmium-exposed workers proteinuria is more closely related to the concentrations of albumin and orosomucoid in urine than that of ₂-microglobulin. The change in urinary concentration of total amino acids was less marked than that of protein. The determination of both low and high molecular weight proteins ought to be recommended for detecting renal damage due to cadmium.     

Prevalence of hypertension among cadmium-exposed workers

In a retrospective study of 311 male workers in an alkaline battery factory, the relationship between exposure to cadmium oxide and hypertension has been investigated. Blood pressure measurements, taken by the same physician, were available for a 30-yr period. When age-matched groups of hypertensive and normotensive workers were compared, employment time was significantly longer (P = .0109) in the hypertensive group. This indicates a possible relationship between exposure to cadmium oxide and the development of hypertension.     

Mortality of cadmium-exposed workers. A five-year update

A cohort mortality study of cadmium-exposed workers initially followed to the end of 1979 has been updated for a further five years. The update has confirmed the findings of the original study with a significant excess risk from bronchitis related to intensity of exposure, although over the five-year period the excess mortality was no longer significant, a finding suggesting that the risk from bronchitis may now be declining in this cohort. In contrast, there is now a stronger indication of a excess risk from lung cancer related to intensity of exposure, significant for both the total and the five-year periods. There was again no increased risk from prostatic cancer, and from this and other studies it appears unlikely that cadmium, in the concentrations encountered in this and other recent studies, acts as a prostatic carcinogen. As in the initial study, there was no significant excess risk from hypertensive disease, nor any suggestion of an increased risk from cerebrovascular or renal disease.     

镉接触对749名工人健康影响的随访观察

目的 分析镉镍电池生产企业工人尿镉水平升高的危险因素,了解镉接触对他们健康的影响。
方法 选取2011年新乡市某电池生产企业参加体检的749人为研究对象,对他们进行问卷调查,检测其尿镉水平。分析不同尿镉水平与血常规、肺功能、尿常规、血压、肝功能等指标的关系。并在2014年对270位工人进行随访。
结果 2011年749名工人尿镉水平为（8.89±4.00）μg/g Cr,尿镉超标率（尿镉≥ 5 μg/g Cr）为64.0%（479/749）。女性作业工人尿镉水平为（9.35±4.00）μg/g Cr,高于男性的（8.36±3.94）μg/g Cr,差异有统计学意义（P < 0.01）。随着尿镉水平升高,工人肺功能、血压、肝功能、B超、胸片异常率亦随之升高（P < 0.05）。经多元线性回归分析,性别（β_女vs.男=0.680,P < 0.01）、年龄（β=0.048,P < 0.05）、工龄（β=0.114,P < 0.01）、接触水平（β_中vs.低=3.030,β_高vs.低=4.661,P < 0.01）是尿镉水平升高的影响因素,所得回归方程的R2=0.242,整体的F=47.519（P < 0.01）。2014年随访发现,270名工人尿镉超标率为70.0%,其中β₂-微球蛋白、血常规、血压和胸片检查的异常率均高于2011年（P < 0.05）。
结论 长时间镉接触可对职业工人血压、肝功能、肺功能等健康指标产生一定影响,须重点关注。
     

某铅锌矿79例镉作业者健康情况调查报告

本文报告某铅锌矿镉作业者79例的健康检查结果。部分作业者有头晕、四肢发麻、关节酸痛、膝反射减弱、牙齿黄染、肢端挛缩等症状和体征。实验室检查,近1/3作业者尿镉升高,尿β_2-M增高占31.6%,尿总蛋白升高占13.9%。结果表明,该矿镉作业者中,部分人已有过量镉接触及镉吸收,少数人有轻度肾小管功能改变,极少数人有轻度肾小球功能改变。因此,该矿须进一步加强防护措施,继续对作业者进行随访观察。     

Determinants of lung cancer risk among cadmium-exposed workers.

Workers at a cadmium recovery plant in Globe, Colorado, showed an increased risk of lung cancer, which some investigators have attributed to cadmium exposure. We conducted a cohort mortality analysis of this work force and a case-control analysis of the lung cancer cases within this work force in order to assess the probable causes of the lung cancer excess. The Globe plant began as a lead smelter about 1886, switched to arsenic production in 1920, and became a cadmium metal production facility in 1926. Cadmium, arsenic, and cigarette smoking are three potential lung carcinogens found in this workplace. Industrial hygiene data collected from 1943 onward served as the basis for the National Institute for Occupational Safety and Health (NIOSH)-derived exposure algorithm that assigned cadmium exposure estimates to employees based on their work area in the plant and calendar time. Few exposure data existed for substances other than cadmium. Feedstock ore concentrations were used as a surrogate measure of air arsenic levels. The arsenic content of the fines used as feedstock prior to 1940 was considerably higher than that of the fines used after 1940. Smoking histories had been obtained previously for 45% of the workers. A case-control analysis of the 25 cases of lung cancer known to have occurred among these workers through 1982 was conducted using three controls per case, matched by closest data of hire and age at hire. Potential causal agents for lung cancer included cadmium exposure, cigarette smoking, and arsenic exposure. Exposure variables for each case and control included estimated cumulative cadmium exposure in milligram-years per cubic meter, cigarette smoking history, and plant arsenic exposure status at the time of hire. Estimated cumulative cadmium exposures of cases and controls did not differ overall or within the date-of-hire strata. Cases were more than eight times more likely to have been cigarette smokers than were controls. Lung cancer risk in this workplace was more closely related to the period of hire, not to the cumulative cadmium exposure. The period of hire appears to be a surrogate for arsenic exposure as related to feedstock. The measures used here seem to indicate that exposure to arsenic and cigarette particulates, rather than to cadmium particulates, may have caused the increased rate of lung cancer of these workers.     

职业性镉接触人群泌尿、血液、呼吸系统相关指标的变化

目的 分析职业性镉接触人群泌尿、血液、呼吸系统相关指标的变化。 方法 比较某镍镉电池厂镉接触人群(n=100)与无镉接触对照人群(n=81)尿镉、尿β₂-微球蛋白、血红蛋白、红细胞、白细胞、血小板、FEV₁/FVC(第1 s用力呼气容积/用力肺活量)的差异。 结果 该厂工人作业环境中镉浓度超过国家标准。接触组尿镉超标率(25%, 25/100)显著高于对照组(2.47%, 2/81)(P<0.001),尿镉、β₂-微球蛋白水平显著高于对照组(P<0.05),血红蛋白显著低于对照组(P<0.05)。接触组和对照组之间红细胞、白细胞、血小板、FEV₁/FVC差异无统计学意义(P>0.05)。 结论 镍镉电池厂镉接触会使尿镉、β₂-微球蛋白值增加,并导致贫血。     

Hexamitiasis in cadmium-exposed mice.

Mortality was observed in 4- to 5-week-old Swiss Webster mice exposed to 300 or 3 ppm cadmium as cadmium chloride in the drinking water. Mice receiving 300 ppm cadium suffered 26% mortality as compared with 7% of those on the low cadmium dose. Death did not occur in control mice. Clinical signs and histopathology established Hexamita muris as the causative agent. Cadmium lesions were not observed. It is suggested that mortality due to hexamitiasis resulted from synergism between cadmium and H muris.