乡镇工业职业卫生服务与初级卫生保健相结合初探

针对我国乡镇工业职业卫生面临的“高需求、低服务”。以及与农村初级卫生保健(PHC)相脱节问题。提出实施乡镇企业职业卫生与PHC相结合的必要性和迫切性。结合WHO职业卫生合作中心(上海)在华东地区的试点探索,提出两者结合的内容和方式的若干设想,强调从更新观念全面认识PHC和把职业卫生与安全作为PHC组成部分入手,深入实践,共同为卫生部领导下的全国性探索作贡献。     

现代生物力学在煤矿安全科技中的应用研究

笔者根据国内外现代生物力学的发展情况 ,结合我国煤矿安全的现状 ,探讨现代生物力学在煤矿安全方面的应用 ,并提出了现代生物力学在安全科技两个方面的应用 :①研究人体结构在冲击事故的破坏极限 ,对安全帽的防护性能做简略的生物力学分析 ;②骨力———电性质的研究对骨折愈合与康复的意义。笔者提出随着现代科学技术的迅猛发展 ,煤矿安全方面的研究能否从现代生物力学在人体安全保护、骨折治疗与康复、职业病防治机理等方面的应用去研究的新思想和新方法 ,使煤矿安全的研究达到一个新的水平。     

作业场所职业危害信息系统共享数据元标准化初探

通过对国内外数据元标准化研究现状的分析,以探索实现作业场所职业危害信息系统相关数据元标准化为前提,实现作业场所职业危害信息系统数据共享及发布为目的,指出传统基于数据集共享模式存在的统一性共享性差的问题,研究建立基于数据元和数据集相结合的标准化技术路线,并结合作业场所职业危害用人单位相关数据元采集、提取及标准化过程进行应用和示范,实现不同作业场所职业危害信息系统间相关数据共享。     

Thimerosal in childhood vaccines contributes to accumulating mercury toxicity in the kidney

Mercury (Hg) is a hazardous chemical that accumulates in many cells and tissues, thereby producing toxicity. The kidney is a key target organ for Hg accumulation and toxicity. The contributing factors to Hg accumulation in humans include: (1) elemental and inorganic Hg exposure, often occurring by inhalation of Hg vapors; (2) exposure to methyl Hg (meHg), for example, through contaminated seafood; and (3) exposure to ethyl mercury (etHg) via thimerosal-containing vaccines. Systematic investigations on the toxic effects of etHg/thimerosal on the nervous system were carried out, and etHg/thimerosal emerged as a possible risk factor for autism and other neurodevelopmental disorders. There is, however, little known about the mechanisms and molecular interactions underlying toxicity of etHg/thimerosal in the kidney, which is the focus of the current review. Susceptible populations such as infants, pregnant women, and the elderly are exposed to etHg through thimerosal-containing vaccines, and in-depth study of the potential adverse effects on the kidney is needed. In general, toxicity occurring in association with different forms of Hg is related to: intracellular thiol metabolism and oxidative stress reactions; mitochondrial function; intracellular distribution and build-up of calcium; apoptosis; expression of stress proteins; and also interaction with the cytoskeleton. Available evidence for the etHg-induced toxicity in the kidney was examined, and the main mechanisms and molecular interactions of cytotoxicity of etHg/thimerosal exposure in kidney described. Such accumulating knowledge may help to indicate molecular pathways that, if modulated, may better handle Hg-mediated toxicity.     

石英砂加工企业职业病危害防护措施与管理对策研究

通过对安徽省石英砂加工企业生产工艺流程和现场进行调查分析,得出矽尘和噪声是两种最主要的职业病危害因素,发现石英砂生产企业矽尘和噪声危害十分严重,生产作业现场未配备任何防护装备和个人防护用品,作业人员接触职业病危害的比率非常高。分析了石英砂加工企业在职业病危害防护与管理方面的欠缺与不足,提出了针对矽尘和噪声危害因素的具体工程防护措施与管理对策,从源头控制和消除职业病危害,保护劳动者的生命安全与健康。     

通用电气风险评估模式在我国中小企业干预中的应用及效果评估

为提高对职业危害的识别和控制能力,采用跨国企业风险评估模式帮助我国中小企业改善职业健康与安全管理。选用通用电气环境健康安全管理体系中的11个相关元素作为评估工具,对企业开展干预,并评估效果。结果表明,干预效果较好,工人接触有害物质的水平明显降低,个体防护用品使用率和正确使用率有较大提高,职业危害风险评估符合率有明显提高。应用风险评估模式干预的示范企业,职业卫生现状得到有效改善,为企业管理提供了借鉴。     

地表载荷对硬岩区埋地管道应力应变影响分析

为研究地表载荷对硬岩区埋地管道力学性能的影响,建立了管-土耦合三维数值模型,分析了地表载荷大小、作用面积、管道压力、管道径厚比及回填土弹性模量对管道应力分布、塑性应变、椭圆度的影响。结果表明:地表压载作用下,高应力区首先出现在管道顶部且呈椭圆形;随着地表载荷及其作用面积的增大,管道高应力区逐渐扩大,管道截面左右两侧也出现应力集中;随着回填土弹性模量、管道壁厚及内压的增加,管道顶部高应力区及最大等效应力均减小。塑性应变首先出现在管顶,且塑性区随地表载荷、载荷作用长度增加而增大,随回填土体弹性模量及管道壁厚增大而逐渐减小;当内压为0~4MPa时,管道塑性应变及塑性区随内压的增大而减小。管道椭圆度随回填土体弹性模量、管道内压、壁厚增加而逐渐减小,随地表压载增大而增大。     

前车突然切入时驾驶人应激生理特性研究

为研究前车突然切入对驾驶人生理负荷的影响,利用MP150生理监测系统对22名被试进行虚拟驾驶试验。采集记录前车突然切入时被试的生理参数。研究驾驶人心率增长率和心率变异性(HRV)指标与车速、应激距离之间的关系。结果表明:自车速度为100 km/h时,随着前车切入距离从55.6 m减小到27.8 m,被试的平均心率增长率从16.21%增大到23.27%,HRV参数低频(LF)值也呈现下降趋势。前车切入距离一定,随着自车车速从60 km/h增加到120 km/h,被试的平均心率增长率存在显著性差异,平均从13.05%上升到21.85%。差异性检验结果表明,前车切入距离和自车速度发生变化时驾驶人的生理负荷变化趋势一致,但自车速度因素对驾驶人生理负荷的影响程度高于切入距离因素。     

Involvement of mitochondrial-mediated caspase-3 activation and lysosomal labilization in acrylamide-induced liver toxicity

Acrylamide (ACR) is a chemical frequently used in both industrial and synthetic processes and may be produced during food processing. ACR at very high concentrations is postulated to exert its toxicity through the stimulation of an oxidative stress. ACR in excessive doses induces the central nervous system, reproduction, and genetic toxicity. However, ACR effects on the liver, a major organ of drug metabolism, have not been adequately explored. In addition, the role of mitochondria in an ACR-mediated hepatotoxicity is still unclear. The aim of this study was to investigate the cytotoxic mechanisms attributed to ACR using isolated rat hepatocytes. Hepatocytes were isolated by the collagenase perfusion method and incubated with an EC50_2hr concentration of ACR for 3 hr. The EC50_{2 hr} of ACR on isolated rat hepatocytes was determined to be 1 mM. Based on our results, hepatocytes cytotoxicity of ACR (1 mM) was mediated by a reactive oxygen species formation and lipid peroxidation. Incubation of hepatocytes with ACR produced rapid hepatocyte glutathione depletion which is another marker of the cellular oxidative stress. ACR cytotoxicity was also associated with mitochondrial injury as evidenced by the decline of mitochondrial membrane potential and lysosomal membrane leakiness. Our results also showed that ACR induced caspase-3 activation, the final mediator of apoptosis signaling. These findings contribute to a better understanding underlying mechanisms involved in ACR hepatotoxicity originating from the oxidative stress and ending in mitochondrial/lysosomal damage and cell death signaling.