小型蓄电池厂铅危害调查分析

本文对九江市某小型蓄电池厂劳动卫生状况及铅对工人健康危害进行了调查分析。该厂主要职业危害因素是生产性铅尘、铅烟。生产设备简陋、无隔离通风防护措施，造成了各生产工序的交叉污染。车间空气的粉尘浓度较高，铅尘浓度０．９３￣４．８０ｍｇ／ｍ＾３，铅烟浓度０．０５￣０．６６ｍｇ／ｍ＾３，球磨工序是主要的铅污染源，粉尘浓度高达４．８０ｍｇ／ｍ＾３，超过国家卫生标准９５倍。２５名接触铅作业工人中，４人被诊断为轻     

某铅冶炼厂铅危害调查分析

本文对甘肃安西某铅冶炼厂劳动卫生状况及铅对工人健康危害进行调查分析。主要职业危害因素是生产性铅尘、铅烟。生产设备简陋、无隔离通风防护措施,造成各生产工序的交叉污染。车间空气的粉尘浓度较高,铝尘浓度０．３９０～１．０４５ｍｇ／ｍ＾３,铅烟浓度０．０２４～０．４７２ｍｇ／ｍ＾３,破碎工序是主要的铅污染源,粉尘浓度 １．０４５ｍｇ／ｍ＾３,超过国家卫生标准１９．９倍。３９名接触作业工人中,２０人被诊断为     

某镍矿采,选,炼生产的劳动卫生学调查

报告了某镍矿劳动卫生问题现场调查和环境监测的结果。该矿主要职业危害因素是生产性粉尘、镍及其他化学物所致空气污染、噪声以及高气温与热辐射。粉尘中游离二氧化硅含量４．５０％～２５．９５％。采矿车间和冶炼车间干燥工段粉尘浓度较高，大部分样品浓度超过１０ｍｇ／ｍ３。总的看来，空气镍浓度与粉尘浓度大致平行。空气镍水平的次序为冶炼车间＞选矿车间＞采矿车间；在冶炼车间有１８个样品浓度超过１ｍｇ／ｍ３。在汽修车间和矿内居民区大气中镍平均浓度也分别达到了０．００４６ｍｇ／ｍ３和０．００５６ｍｇ／ｍ３。空气中检出了钴和铬，但浓度低。仅在冶炼车间检出了二氧化硫，其浓度波动剧烈。在３４个作业点测量了噪声，采矿车间和选矿车间噪声平均声级达到１００ｄＢ（Ａ）和９１ｄＢ（Ａ）。就改善劳动卫生条件提出了几项措施建议。     

牡丹江市某化工厂草酸对工人健康影响的调查研究

经监测，牡丹江市某化工厂草酸生产车间空气中草酸平均浓度为０．６６～１．７８ｍｇ／ｍ＾３，分别有２／５５个样品超过２ｍｇ／ｍ＾３与相当于２ｍｇ／ｍ＾３水平，体检结果该作业工人除咽痛症状与对照组比较有显著差异（Ｐ＜０．０５）外，其它体证两组间均无明显差异。当车间空气中划酸浓度波动于１ｍｇ／ｍ＾３左右，不超过２ｍｇ／ｍ＾３时，可以认为是比较安全的，建议我国车间空气中草酸卫生标准以不超过２ｍｇ／ｍ＾３为宜     

氢醌作业工人的健康调查及分析

本文报导了某化学厂接触氢醌（ＨＱ）生产的工人健康状况及ＨＱ的接触水平，ＨＱ生产车间空气中ＨＱ平均几何浓度为０．３７２ｍｇ／ｍ３．ＴＷＡ为０．２１６ｍｇ／ｍ３，其中以包装工段为最高，依次为后处理、还原、氧化工段。接触工人除视力、肺功能、血小板与对照组相比略有降低外，其他症状、体征（除晶体）、免疫指标、造血功能、肝功能、肾功能等无异常改变。     

超高压静电空气离子化集尘箱治理铬酸酐粉尖的应用研究

该厂一氧化碳催化剂车间混料岗位在混料、下料时产生大量铬酸酐粉尘。为了消除粉尘危害，我们设计了超高压静电空气离子化集尘箱，使混料岗位工人操作地点呼吸带粉尘浓度由７２．６ｍｇ／ｍ￣３下降为１０．５ｍｇ／ｍ￣３，除尘率为８５．５％，下料口旁１ｍ高处粉尘浓度由１４８．８ｍｇ／ｍ￣３下降为９．７ｍｇ／ｍ￣３，除尘率为９３．４％，未加超高压静电时集尘箱排风口粉尘浓度为２６３．９ｍｇ／ｍ￣３，加高压后下降为１５．９ｍｇ／ｍ￣３，除尘率为９４％；厂房中空气负离子浓度由１２×１０￣４／ｍ￣３增加为５．７×１０￣９个／ｍ￣３。结果表明超高压静电空气离子化集尘箱除尘净化空气效果明显。     

砂轮制作工人接尘剂量—反应关系的研究

本文收集了某砂轮厂１９７３￣１９９１年粉尘测定资料，以及６１６例接尘者职业性体检资料。所研究的６１６例中，接尘者５７１例，尘肺患者４５例，采用寿命表法研究了砂轮作业工人接尘剂量与反应的关系，估算接尘３０年尘肺发病率小于１％时，砂轮粉尘浓度不超过７．５２ｍｇ／ｍ＾３，作者建议砂轮粉尘容许浓度为５ｍｇ／ｍ＾３为宜。     

聚丙烯腈纤维粉尘作业场所劳动卫生学调查

对３个聚丙烯腈纤维生产，加工厂的１０个岗位进行了粉尘浓度监测，共测得样品７１个，平均浓度为１．６５ｍｇ／ｍ＾２（０．２７～８．８８ｍｇ／ｍ＾３）对６个岗位进行了个体接触水平测定，监测样品１８个，其时间加权平均浓度为１．２８ｍｇ／ｍ＾３（０．２７～４．２４ｍｇ／ｍ＾３）并结合我国现有经济，技术情况，动物实验研究和健康体检结果，提出车间空气中聚丙烯腈纤维粉尘最高容许浓度为４ｍｇ／ｍ＾３时间加权平均容许     

车间空气中麻尘（亚麻,黄麻和苎麻）卫生标准研制

根据现场卫生学调查、流行病学调查、动物实验、体外实验及剂量－反应关系的资料，并参考国外接触限值制订了麻尘（亚麻、黄麻和苎麻）卫生标准。调查结果发现，亚麻、黄麻和苎麻粉尘对人体危害不尽一致。亚麻粉尘可致工人发生棉尘病，黄麻尘可引起慢性支气管炎，其患病率与接尘量之间均存在剂量－反应关系，而苎麻尘危害较亚、黄麻尘为轻。本研究提出，车间空气中含有１０％以下游离二氧化硅的亚麻、黄麻和三麻粉尘最高容许浓度分别为３ｍｇ／ｍ￣３、４ｍｇ／ｍ￣３和６ｍｇ／ｍ￣３。     

超高压静电空气离子化集尘箱治理铬酸酐粉尘的应用研究

该厂一氧化碳催化剂车间混料岗位在混料、下料时产生大量铬酸酐粉尘。为了消除粉尘危害，我们设计了超高压静电空气离子化集尘箱，使混料岗位工人操作地点呼吸带粉尘浓度由７２．６ｍｇ／ｍ＾３下降为１０．５ｍｇ／ｍ＾３，除尘率为８５．５％；下料口旁１ｍ高处粉尘浓度由１４８ｍｇ／ｍ＾３下降为９．７ｍｇ／ｍ＾３，除尘率为９３．４％；未加超高压静电时集尘箱排风口粉尘浓度为２６３．９ｍｇ／ｍ＾３，加高压后下降为１５．９     

An Emerging Role of Defective Copper Metabolism in Heart Disease

Copper is an essential trace metal element that significantly affects human physiology and pathology by regulating various important biological processes, including mitochondrial oxidative phosphorylation, iron mobilization, connective tissue crosslinking, antioxidant defense, melanin synthesis, blood clotting, and neuron peptide maturation. Increasing lines of evidence obtained from studies of cell culture, animals, and human genetics have demonstrated that dysregulation of copper metabolism causes heart disease, which is the leading cause of mortality in the US. Defects of copper homeostasis caused by perturbed regulation of copper chaperones or copper transporters or by copper deficiency resulted in various types of heart disease, including cardiac hypertrophy, heart failure, ischemic heart disease, and diabetes mellitus cardiomyopathy. This review aims to provide a timely summary of the effects of defective copper homeostasis on heart disease and discuss potential underlying molecular mechanisms.     

A UNIFIED HYPOTHESIS OF COPPER TRANSPORT AND UPTAKE

A recent paper provides evidence that albumin, ceruloplasmin, and amino acids may each function as transport agents for copper to cells.     

MENKES' DISEASE: ARE WE CLOSER TO LEARNING ITS CAUSE?

Abnormalities of metallothionein biosynthesis have been discovered in Menkes' disease, but they do not account for the entire pathophysiology of the disease.     

Effect of beta-carotene supplementation on the concentrations and distribution of carotenoids,vitamin E,vitamin A,and cholesterol in plasma lipoprotein and non-lipoprotein fractions in healthy older women.

We studied the effect of beta-carotene supplementation on the concentrations and distribution in plasma lipoprotein and non-lipoprotein fractions of carotenoids, alpha-tocopherol, retinol, and cholesterol.

Ten women ingested either 90 mg of beta-carotene or placebo daily for 3 weeks while residing in their homes and eating their usual meals. Carotenoids (beta-carotene, lycopene, lutein/zeaxanthin), retinol, alpha-tocopherol, and cholesterol were measured in plasma lipoprotein and non-lipoprotein fractions before and after treatment.

In the beta-carotene-supplemented group, total plasma beta-carotene increased 14-fold from 0.48 +/? 0.13 to 6.83 +/? 2.12 mumol/L (p = 0.04). Although the greatest increase in beta-carotene was in low-density-lipoproteins (LDL), the magnitude of increase was similar in LDL, high-density-lipoproteins (HDL), and very-low-density-lipoproteins (VLDL). Thus, the relative distribution of beta-carotene in lipoproteins was unchanged: approximately 71% was in LDL, approximately 15% in HDL and approximately 12% in VLDL, before and after beta-carotene supplementation. There were no changes in amounts and distribution in lipoproteins of the other carotenoids, alpha-tocopherol, and cholesterol. There was no change in the amount of retinol in lipoprotein-deficient plasma. There were no changes in total plasma triglycerides. Significant positive correlations were found between LDL- or VLDL-cholesterol and alpha-tocopherol in LDL or VLDL, respectively; between LDL- or VLDL-cholesterol and lutein/zeaxanthin in LDL or VLDL, respectively; and between HDL-cholesterol and beta-carotene in HDL.

beta-Carotene supplementation (90 mg/day for 3 weeks) in healthy older women results in an enrichment of all plasma lipoprotein fractions with beta-carotene, but does not alter the relative distribution of beta-carotene in lipoproteins. beta-Carotene supplementation has no effect on the amounts and relative distribution of lycopene, lutein/zeaxanthin, and alpha-tocopherol in lipoproteins, or of retinol in the non-lipoprotein fraction of plasma. Short-term beta-carotene supplementation has no effect on the concentrations of plasma total triglycerides, total cholesterol, HDL-, LDL-, and VLDL-cholesterol.     

锌、铜对大鼠血脂水平影响的研究

用雄性断乳ｗｉｓｔａｒ大鼠研究了不同水平锌、铜对大鼠血脂水平的影响。结果显示：绝对或相对铜缺乏均引起血清胆固醇、甘油三酯浓度升高；而绝对或相对锌缺乏则主要引起高密度脂蛋白胆固醇（ＨＤＬ－Ｃ）和ＨＤＬ＿２－Ｃ浓度下降。相关分析表明：血清锌与ＨＤＬ－Ｃ、ＨＤＬ＿２－Ｃ呈明显正相关；血清铜与血清胆固醇、甘油三酯呈显著负相关。病理检查显示：除对照组外，其它各组主动脉组织形态均发生不同程度的病理改变，尤以高锌低铜、高铜低锌及低锌低铜组为著。提示在保持适宜铜水平的前提下，补充适量的锌以提高血清ＨＤＬ－Ｃ水平，可预防或延缓高脂血症的发生。     

冠心病人血液微量元素锰、铬、铜、锌的分析

本实验用电感耦合等离子体发射光谱仪测定了33名正常人和63名冠心病人,(急性心肌梗塞25人,陈旧性心肌梗塞29人,慢性冠心病患者9人)血液中微量元素Mn、Cr、Cu、Zn的含量。发现1.对照组血清Mn为0.02145±0.0107ppm;Cr为0.0230±0.0167ppm;Cu为0.905±0.278ppm;Zn为0.0230±0.404ppm;Cu/Zn比值为0.973±0.395。与冠心病组血清Mn、Cr无明显差异。2.不同发作天数的急性心肌梗塞患者血清Cu、Zn和Cu/Zn比值的动态比较,结果表明,在急性心肌梗塞发作时可出现一过性的血清Cu升高,Zn降低,Cu/Zn比值高于对照组,随时间推移铜锌比值逐渐下降。3.陈旧性心肌梗塞和慢性冠心病者血清Cu、Zn和Cu/Zn比值远较对照组低,Cu/Zn比值<0.6的百分比远较对照组多(P<0.01),说明Cu/Zn比值降低可能是冠心病易患因素。4.用Feisher判别法将血清铜锌比值和其它主要易患因素作了横向比较,证明铜锌比值下降是冠心病主要易患因素,并结合国内外资料作了初步探讨。     

徐州地区78种常用食物中锌、铜、铁的含量及其意义

<正> 近年来缺锌缺铁的报告屡有发表,微营养缺乏的问题已经引起广泛的关注。调查发现徐州市少年儿童血清锌水平较低,血清铜含量较高;徐州市居民从饮水中获取的锌、铁、铜等微量元素极少。又鉴于徐州地区为铁锌性土壤,我们于1986年对徐州地区常用主要食物中锌、铜、铁的含量进行了测定和研究。     

Opioid Peptides,Adrenocorticotrophic Hormone and Dietary Copper Intake in Humans

Copper plays an important role in cardiac and brain function possibly through endocrine and neuroendocrine systems. The syndrome of copper deficiency is worsened by dietary fructose and other trace metals such as zinc. We investigated the effect of a low copper diet on plasma opioid peptides in 11 healthy young volunteers who were fed foods low in copper but adequate in all other nutrients. The study was divided into three dietary periods. Copper was added to the diet so that the diet contained 0.66 mg/day for 24 days (marginal Cu), 0.38 mg/day for 42 days (low Cu) and 2.49 mg/day for 24 days (adequate Cu). The indices of copper status, ceruloplasmin and plasma copper concentrations, declined and were significantly lower (p < 0.05) at the end of the low Cu period than at the beginning of the study and the end of the marginal Cu period. They increased significantly at the end of the adequate Cu diet to the levels of the marginal Cu diet. Plasma β-endorphin (BEN), Leu-enkephalin (LE), Met-enkephalin (ME) and Adrenocorticotropic hormone (ACTH) were measured by radioimmunoassay at the beginning of the study and at the end of each dietary period. No significant differences were observed in BEN, LE or ME during any of the periods. There were only small increases in LE and ME at the end of marginal and low copper diet periods and no significant changes were observed on copper repletion. Plasma ACTH was significantly lower at the end of low copper compared to baseline value but was not lower after marginal copper. Copper repletion had no significant effect on ACTH. The data show that plasma opioid peptides did not respond significantly to differential copper intake.     

SEX DIFFERENCES IN THE SURVIVAL OF COPPER-DEFICIENT RATS

Male rats fed fructose-based, low-copper diets show 100 percent mortality, cardiac hypertrophy, and anemia under conditions where female rats fed the same diet are unaffected.