焦炉工人血清中p21蛋白和HSPs水平的研究

目的　寻找接触焦炉逸散物的焦炉工人肺癌的早期监护指标。方法　用Ｄｏｔ ｂｌｏｔ 方法检测５６ 名焦炉作业工人及３２ 名对照组人群血清中ｒａｓ 基因产物ｐ２１ 蛋白和ＨＳＰ２７ 、ＨＳＰ７０ 的水平。结果　焦炉工人血清的ｐ２１ 蛋白明显高于对照组（ Ｐ＜ ０－０１） ,且其阳性率为３５－７ ％ ,显著高于对照组（１２－５ ％ ,Ｐ＜０－０５） ;相关分析表明,焦炉工ｐ２１ 水平与工人工龄存在极显著相关（ Ｐ＜ ０－００１） 。同时焦炉工人血清ＨＳＰ２７水平也明显高于对照组（ Ｐ＜ ０－０５） ,ＨＳＰ７０ 水平两组间无显著差异。结论　推测血清中ｐ２１ 蛋白和ＨＳＰ２７的水平的变化对于焦炉工人肺癌的早期监护具有重要意义     

焦炉作业环境对工人血抗脂过氧化活性影响的研究

采用１：１配对方法，测试了焦炉环境作业工人与对照组８５对不同人群的血超氧化歧化酶（ＳＯＤ）和谷光甘肽过氧化物酶（ＧＳＨ－ＰＸ）的活性变化。焦炉作业环境中焦炉逸散物（苯溶出物）平均浓度炼焦炉顶为３．３９ｍｇ／ｍ３，３．４苯并（ａ）芘平均浓度５４７．５～１０７．５ｕｇ／１００ｍ３。观察组与对照组ＳＯＤ和ＧＳＨ－ＰＸ的活性分别为１２４．４７±１６．６７（ＮＵ／ｍｌ）、１３１．５０±２３．３７（ＮＵ／ｍｌ）和１１７．１７±１７．２１（活力单位），７０．９９±１４．００（活力单位）。观察组的ＧＳＨ－ＰＸ活力在各组中均高于对照组，且Ｐ值均小于０．０１。揭示在焦炉环境下作业工人血抗脂过氧化活性增强，既可能是机体的防御性反应，又可能成生物监测的敏感指标     

铝熔铸作业工人神经行为功能的研究

为探讨铝对作业工人神经系统的影响，寻找对铝作业工人健康监护的早期指标，对３６名铝熔铸作业工人（车间空气中铝尘和铝浓度分别为１．６５ｍｇ／ｍ３和０．２５ｍｇ／ｍ３（ＴＷＡ））和４０名对照工人，应用ＷＨＯ－ＮＣＴＢ进行了神经行为功能测定；同时测定了尿铝、尿中高香草酸（ＨＶＡ）和香草扁桃酸（ＶＭＡ）的含量。结果发现：铝接触工人注意力、手的运动协调能力、视感知记忆力下降，反应时的标准差和最慢反应时间延长（Ｐ＝０．００２５，Ｐ＝０．００６６），提转捷度测试得分降低（Ｐ＝０．０２６），数字译码和Ｂｅｎ－ｔｏｎ视觉保留测试得分降低（Ｐ＝０．０２３，Ｐ＝０．００３）。分层分析发现：后３项分测试得分随接触时间延长而降低，铝作业工人尿ＶＭＡ和尿铝含量高于对照组。提示：铝可能对作业工人的神经系统产生影响。神经行为测试和尿ＶＭＡ测定可用于检测铝的不良效应     

焦炉作业工人血清脂质过氧化物和抗氧化酶研究

目的为了探讨焦炉逸散物对作业工人血清脂质过氧化水平的影响。方法对焦炉作业工人４５９人和对照３５６人血清ＳＯＤ、ＧＳＨＰｘ、ＭＤＡ进行了测定分析。结果焦化作业组血清ＳＯＤ活性与对照相比轻度增高,差异无显著性（Ｐ＞０．０５）;ＧＳＨＰｘ活性较对照组明显增高,有非常显著性差异（Ｐ＜０．０１）;而ＭＤＡ与对照组比较无明显变化。结论提示在一定程度上接触焦炉逸散物,可能诱导了机体的氧化适应反应,使得焦炉作业工人抗氧化功能有所增强。     

燃煤用户干预前后家庭妇女尿1－羟基芘含量

燃煤用户干预前后家庭妇女尿１－羟基芘含量陈小琳，毛惠琴，洪传洁以燃煤家庭妇女为对象，采用在燃煤厨房安装排风扇的干预措施，并分别在安装前及安装使用２年后对家庭妇女尿中１－羟基芘的含量进行测定，了解人体接触多环芳烃化合物（ＰＡＨｓ）情况，以期评价安装排风...     

苯并（a）芘代谢产物诱发BALB／3T3细胞程序外DNA合成的研究

为了解苯并（ａ）芘（ＢａＰ）代谢产物对哺乳动物细胞ＤＮＡ的损伤作用，本实验采用单标记和双标记法，分别检测４种苯并（ａ）芘代谢产物（ａｎｔｉ－ＢＰＤＥ，ｓｙｎ－ＢＰＤＥ，３－ＯＨ－ＢＰ和９－ＯＨ－ＢＰ）对ＢＡＬＢ／３Ｔ３细胞ＤＮＡ合成和程序外ＤＮＡ合成（ＵＤＳ）的影响。结果表明：ａｎｔｉ－ＢＰＤＥ、ｓｙｎ－ＢＰＤＥ、Ｅ－ＯＨ－ＢＰ和９－ＯＨ－ＢＰ均在不同程度上使ＢＡＬＢ／３Ｔ３细胞ＤＮＡ合成增加；但     

尿2－硫代噻唑烷－4－羧酸用于二硫化碳作业工人生物监测研究

本文应用高效液相色谱法对ＣＳ＿２作业工人班前、班后尿及对照组尿２－硫代噻唑烷－４－羧酸（ＴＴＣＡ）进行了测定。结果发现ＣＳ＿２作业工人班后尿ＴＴＣＡ明显高于对照组，有非常显著性差异（Ｐ＜０．０１）。ＣＳ＿２作业工人班后尿ＴＴＣＡ明显高于工作班前，亦有非常显著性差异（Ｐ＜０．０１）。高浓度接触组工人尿ＴＴＣＡ高于低浓度接触组工人尿ＴＴＣＡ，说明作业工人ＣＳ＿２的接触量与尿ＴＴＣＡ含量之间有相关性。作者认为汞ＴＴＣＡ可用于二硫化碳接触的生物监测。     

焦炉作业工人尿中1-羟基芘水平检测及其临床意义

目的 探讨焦炉作业工人尿中1-羟基芘水平及其临床意义.方法 将煤化工厂147名焦炉作业工人分为焦油组(接触焦油作业工人)60人和焦炉烟尘组(接触焦炉烟尘作业工人)87人,另选择79名非焦炉作业工人为对照组,采用高效液相色谱紫外检测方法对作业工人尿中1-羟基芘含量进行分析.结果 焦油组和焦炉烟尘组尿中1-羟基芘水平分别为(2.20±0.49)和(1.92±0.59)μg/L,明显高于对照组[(0.59±0.40)μg/L],差异有统计学意义(P＜0.01);焦油组尿中1-羟基芘水平明显高于焦炉烟尘组,差异有统计学意义(P＜0.01).焦油组与焦油烟尘组作业工人尿中1-羟基芘水平不受工龄、性别和吸烟等因素的影响.结论 焦炉作业工人尿中1-羟基芘水平明显增高,以接触者尿中1-羟基芘水平作为评价人体接触多环芳烃指标,可以较好地反映近期接触水平.     

对苯二甲酸作业人群尿液生化反应的研究

目的　探讨对苯二甲酸（ＴＰＡ） 作业人群尿酶和尿液离子水平的变化。方法　对１０７ 名工人进行个体采样并测定空气和尿中ＴＰＡ 浓度。留取１２７ 名ＴＰＡ 作业工人当日工前、工后尿样和７１ 名对照尿样,对尿样中γ谷氨酰转肽酶（γＧＧＴ） 、碱性磷酸酶（ＡＬＰ） 、乳酸脱氢酶（ＬＤＨ） 、Ｎ乙酰βＤ氨基葡糖苷酶（ＮＡＧ） 活力和尿ｐＨ 值、Ｎａ ＋ 、Ｋ＋ 、Ｃｌ－ 、Ｃａ２ ＋ 、ＮＨ４ ＋ 、ＰＯ４３ － 和ＳＯ４２ － 离子浓度进行分析。结果尿ＴＰＡ 水平与空气ＴＰＡ 浓度存在相关关系。接触组尿Ｎａ ＋ 、Ｃｌ－ 、Ｃａ２ ＋ 、ＮＨ４ ＋ 和ＳＯ４２ － 离子浓度显著高于对照组（ Ｐ＜ ０ ．０５） ;指标聚类统计分析结果显示：尿ＴＰＡ 与尿ＮＨ４ ＋ 相关系数最大（ ｒ ＝ ０ ．２１２ ５ ,Ｐ＝ ０ ．０１９ ８） ,两者之间存在剂量依赖关系;对接触组和对照组作逐步判别分析,筛选出Ｃａ２ ＋ 、ＮＨ４ ＋ 和ＮＡＧ３ 项最有价值的指标。结论　ＮＨ４ ＋ 排泄增多可引起机体负氮平衡,以尿ＮＨ４ ＋ 水平作为接触ＴＰＡ的生物学效应指标,并辅以Ｃａ２ ＋ 和ＮＡＧ 两项指标可监测ＴＰＡ 对接触人群肾功能的早期影响     

对苯二甲酸作业人群尿液离子水平的变化

探讨对苯二甲酸（ＴＰＡ）作业人群尿液离子水平的变化。方法留取２２４名ＴＰＡ作业工人和１１４名对照组工人当日工前工后尿样。对尿ｐＨ、Ｎａ＋、Ｃｌ－、Ｃａ２＋、ＮＨ４＋、ＰＯ４３－和ＳＯ４２－进行测定分析。结果接触组尿Ｎａ＋、Ｃｌ－、Ｃａ２＋和ＳＯ４２－离子浓度显著高于对照组（Ｐ＜００１）,同时ＮＨ４＋与尿ＴＰＡ负荷存在明显的剂量依赖关系;指标聚类分析表明,尿ＴＰＡ水平与尿ＮＨ４＋水平相关系数最大（ｒ＝０２４０５,Ｐ＜００１）,提示ＴＰＡ可能是导致尿ＮＨ４＋离子排泄增加的原因。结论由于ＮＨ４＋长期排泄过多,会导致机体负氮平衡,因此似可以尿ＮＨ４＋作为接触ＴＰＡ的早期生物学监测指标。     

尿中1-羟基芘作为焦炉工多环芳烃暴露监测指标研究

目的 探讨焦炉工外暴露等级与尿中1-羟基芘（1-OHPy）浓度的关系。方法 以某焦化厂120名生产工人和30名非接触者为研究对象，收集班后6h尿，并收集个人信息，用高效液相色谱法测定尿中1-羟基芘。结果 尿中1-羟基芘浓度呈炉顶〉炉侧〉炉底〉对照组的趋势。与外暴露呈显著相关性（r=0．653，P〈0．01）；同样外暴露条件下，吸烟者录中1-羟基芘水平显著高于未吸烟者（P〈0．01）。结论 焦炉工尿中1-羟基芘水平与外暴露等级存在明显的相关性，可反映多环芳烃暴露个体的内剂量水平。     

尿中1-羟基芘作为焦炉工多环芳烃暴露生物监测指标的研究

目的探讨焦炉工外暴露等级与尿中1-羟基芘(1-OHPy)浓度的关系。方法以某焦化厂120名生产工人和30名非接触者为研究对象,收集班后6h尿,并收集个人信息,用高效液相法测定尿中1-羟基芘。结果尿中1-羟基芘浓度呈炉顶>炉侧>炉底>对照组的趋势。与外暴露呈显著相关性(r=0.653,P<0.01),同样外暴露条件下,吸烟者尿中1-羟基芘显著高于未吸烟者(P<0.05)。结论焦炉工尿中1-羟基芘水平与外暴露等级存在明显的相关性,可反映多环芳烃暴露个体的内剂量水平。     

Biological monitoring of polycyclic aromatic hydrocarbon exposure in a highly polluted area of Poland.

Air pollution in Poland and particularly in Silesia is among the worst in Europe. Many coal mines and coke oven plants are located in this area, representing a major source of carcinogenic polycyclic aromatic hydrocarbons (PAHs). We quantitated the PAH exposure level in air samples using personal sampling devices, collected urine samples from the same individuals, and measured 1-hydroxypyrene with high performance liquid chromatography. Samples were collected twice, once in February and once in September. Mean PAH level of samples collected at three different coke oven plants varied from 2.3 micrograms/m3 to 12.3 micrograms/m3; the lowest mean was in September. Mean levels of 0.15 micrograms/m3 (September) and 0.44 micrograms/m3 (February) were noted for the environmentally exposed group. Mean urinary 1-hydroxypyrene varied from 2.45 to 13.48 mumol/mol creatinine at the three coke oven plants. The corresponding variation between the three different environmentally exposed groups in Silesia was 0.41-1.54 mumol/mol creatinine. In the nonindustrialized area, the mean varied from 0.20 to 0.14 mumol/mol creatinine. Seasonal variation was found both at the coke oven plants and in the environmental exposed groups in Silesia. Both PAH levels and 1-hydroxypyrene varied seasonally among coke oven workers and the environmentally exposed group. Our study shows that PAH exposure in the industrialized area of Silesia is high compared to levels in Western Europe. 1-Hydroxypyrene excretion in environmentally exposed individuals in Poland is among the highest in Europe.     

Urinary 1-hydroxypyrene levels in workers exposed to coke oven emissions at various locations in a coke oven plant

Polycyclic aromatic hydrocarbons, which are carcinogenic and mutagenic to humans, are primary compounds in coke oven emissions generated by the coking process. The authors examined the relationship between coke oven workers' urinary 1-hydroxypyrene levels and their exposure to polycyclic aromatic hydrocarbons, as determined on the basis of work category and pre- and postshift effects in a steel plant in Taiwan. Eighty-eight coke oven workers constituted the exposed group, and 61 office workers in a steel plant located 1.5 km from the coke plant constituted the control group. The benzene-soluble fraction in personal air samples, and 1-hydroxypyrene in urine samples, were measured for 3 consecutive days. The 3-day urinary 1-hydroxypyrene sampling results for topside workers (i.e., those most heavily exposed to emissions) in the coke oven group, and for the control group, as determined from postshift geometric means, were 23.8 microg/gm creatinine and 0.3 microg/gm creatinine, respectively. These values increased to 13.4 and 0.1 microg/gm creatinine, respectively, after an 8-hr work period. The major source of polycyclic aromatic hydrocarbons for the exposed group was occupational; therefore, the closer workers were to the coke oven, the greater their exposure, and, consequently, the greater their metabolite level. Urinary 1-hydroxypyrene levels of the exposed group were 80 times higher than those of the control group. Smoking had no significant effect on the excretion of urinary 1-hydroxypyrene. 1-hydroxypyrene levels in the workers' urine during an 8-day period was cumulative (half-life = 18.6 hr). The authors concluded that it would be desirable to switch highly exposed workers to a low-exposure work area, after a period of rest. In addition, urinary 1-hydroxypyrene was a confirmed, useful biological indicator for exposure to polycyclic aromatic hydrocarbons.     

Urinary 1-Hydroxypyrene Levels in Workers Exposed to Coke Oven Emissions at Various Locations in a Coke Oven Plant

Polycyclic aromatic hydrocarbons, which are carcinogenic and mutagenic to humans, are primary compounds in coke oven emissions generated by the coking process. The authors examined the relationship between coke oven workers' urinary 1-hydroxypyrene levels and their exposure to polycyclic aromatic hydrocarbons, as determined on the basis of work category and pre- and postshift effects in a steel plant in Taiwan. Eighty-eight coke oven workers constituted the exposed group, and 61 office workers in a steel plant located 1.5 km from the coke plant constituted the control group. The benzene-soluble fraction in personal air samples, and 1-hydroxypyrene in urine samples, were measured for 3 consecutive days. The 3-day urinary 1-hydroxypyrene sampling results for topside workers (i.e., those most heavily exposed to emissions) in the coke oven group, and for the control group, as determined from postshift geometric means, were 23.8 μg/gm creatinine and 0.3 μg/gm creatinine, respectively. These values increased to 13.4 and 0.1 μg/gm creatinine, respectively, after an 8-hr work period. The major source of polycyclic aromatic hydrocarbons for the exposed group was occupational; therefore, the closer workers were to the coke oven, the greater their exposure, and, consequently, the greater their metabolite level. Urinary 1 -hydroxypyrene levels of the exposed group were 80 times higher than those of the control group. Smoking had no significant effect on the excretion of urinary 1-hydroxypyrene. 1-hydroxypyrene levels in the workers' urine during an 8-day period was cumulative (half-life = 18.6 hr). The authors concluded that it would be desirable to switch highly exposed workers to a low-exposure work area, after a period of rest. In addition, urinary 1 -hydroxypyrene was a confirmed, useful biological indicator for exposure to polycyclic aromatic hydrocarbons.     

焦炉作业工人多环芳烃暴露与外周血淋巴细胞DNA损伤的关系

目的　探讨焦炉作业工人多环芳烃 (polycyclicaromatichydrocarbon ,PAHs)暴露与其外周血淋巴细胞DNA损伤的关系。方法　选取 2 35名焦炉作业工人和 30名非职业PAHs暴露者 ,使用碱性单细胞凝胶电泳技术评价外周血淋巴细胞DNA损伤 ,采用高效液相色谱法测定工作周末班后 6h尿中 1 羟基芘水平 ,收集个人职业暴露、年龄、性别、吸烟和饮酒等信息。结果　焦炉工外周血淋巴细胞的Olive尾矩高于对照组 [数值分别为 2 .4 7(0 .2 2～ 4 6 .6 8)、0 .94 (0 .4 2～ 4 .2 1) ],差异有显著性 (P <0 .0 1) ,且与尿中 1 羟基芘水平呈相关性 (Spearman偏相关系数 =0 .2 2 ,P <0 .0 1)。以非暴露者Olive尾矩的上 5分位数 1.9作为判断个体是否为DNA损伤阳性的界值 ,焦炉工发生外周血淋巴细胞DNA损伤阳性的OR =5 .38,95 %CI=2 .0 7～ 14 .0 8,且随外暴露等级或内剂量水平的增高而呈增加的趋势。结论　焦炉工PAHs暴露水平与外周血淋巴细胞DNA损伤呈良好的剂量 -效应和剂量 -反应关系。     

Benchmark guideline for urinary 1-hydroxypyrene as biomarker of occupational exposure to polycyclic aromatic hydrocarbons

Many individual polycyclic aromatic hydrocarbons (PAH) are genotoxic carcinogens. One of the parent PAH, pyrene, undergoes simple metabolism to 1-hydroxypyrene. 1-Hydroxypyrene and its glucuronide are excreted in urine. Biological monitoring of exposure to PAH has rapidly been expanded since urinary 1-hydroxypyrene was suggested as a biological index of dose of pyrene. Since pyrene is always present in PAH mixtures, the biological indicator is not only an indicator of uptake of pyrene, but also an indirect indicator of all PAH. At present, several hundreds of papers reporting on urinary concentrations of 1-hydroxypyrene in workers' urine are available. It appeared that urinary 1-hydroxypyrene is a sound biomarker and that the analytical method is robust and non-laborious. Since epidemiological studies of cancer mortality related to long-term average urinary 1-hydroxypyrene concentration are lacking, a sound health-based limit value of 1-hydroxypyrene in urine cannot be set as yet. Since PAH exposure is widespread and the dermal uptake is substantial among exposed workers, an attempt was made to propose a three-level benchmark guideline for urinary 1-hydroxypyrene. The reference value as a 95th percentile in non-occupational exposed controls is 0.24 micromol mol(-1) creatinine and 0.76 micromol mol(-1) creatinine for non-smokers and smokers, respectively. This is the first level of the benchmark guideline. A no-biological-effect-level of 1-hydroxypyrene in urine of exposed workers was found at 1.4 micromol mol(-1) creatinine. It is the lowest reported level at which no genotoxic effects were found and therefore the estimate for the second level of the benchmark guideline. In two types of industry, coke ovens and primary aluminium production, the regression of airborne PAH concentrations and urinary 1-hydroxypyrene concentrations in exposed workers has been studied. The correlation of airborne concentrations and urinary 1-hydroxypyrene in urine of workers from coke ovens and in the primary aluminium industry was used to estimate the level of urinary 1-hydroxypyrene equal to the present occupational exposure limit (OEL) of PAH. The concentration of 1-hydroxypyrene in urine equal to the OEL is 2.3 micromol mol(-1) creatinine and 4.9 micromol mol(-1) creatinine, respectively, in these two industries. These latter values present the third level of the benchmark guideline.     

焦炉作业工人神经行为功能改变的特征分析

目的 通过苯并(a)芘[B(a)P]职业接触人群调查,探讨多环芳烃所致神经行为功能改变.方法 选择某钢铁公司焦化厂健康成年男性工人200名作为接触组,以该公司的原材料处和自动化处一般情况相近的88名工人作为对照组.高效液相色谱法测定作业环境空气中B(a)P,收集调查对象的班后尿,用高效液相色谱法检测尿中1-羟基芘的水平;用WHO推荐的神经行为核心测试组合(NCTB)检测研究对象的神经行为功能.结果 作业环境空气中炉底、炉侧、炉顶的B(a)P浓度分别为0.0195、0.186、1.624 μg/m3,炉侧、炉顶的B(a)P浓度超过职业卫生标准(0.15 μg/m3)0.24倍和9.83倍.与对照组相比,焦炉工尿1-羟基芘的水平[(3.42±0.98)μmol/mol肌酐]高于对照组[(2.75±1.09)μmol/mol肌酐](t=-5.162,P=0.000),接触组与对照组在年龄、工龄、吸烟、饮酒及吃烧烤食物情况间均衡,文化水平不均衡,以文化水平为协变量进行协方差分析,焦炉工在总数字跨度、数字跨度顺序、2次打点正确数得分低于对照组,2次打点总数得分高于对照组,差异有统计学意义,按照尿1-羟基芘浓度对数值的30和70百分位数将研究对象分为3组(＜3.10 μmol/mol肌酐,3.10 μmoL/mol肌酐～,＞3.87 μmoL/mol肌酐),总数字跨度、数字跨度顺序、数字跨度倒序、习惯用手、数字译码、视觉记忆得分显示出随尿1-羟基芘浓度增高而降低的趋势;多元线性回归和偏相关分析表明,尿1-羟基芘浓度影响总数字跨度、数字跨度顺序、数字跨度倒序、数字译码和视觉记忆得分,而且与上述指标存在负相关,偏相关系数分别为-0.309、-0.284、-0.209、-0.158、-0.144.结论 多环芳烃主要引起接触人群感知、记忆功能改变.     

微粒体环氧化物水化酶基因多态性对焦炉工尿中1-羟基芘水平的影响

目的　研究外源性化学物代谢酶基因多态性与焦炉工尿中 1 羟基芘水平的关系。方法　分别选取 14 8名焦炉工和 6 9名非职业多环芳烃 (PAHs)暴露人员作为研究对象 ,使用碱水解 -高效液相色谱法测定其尿中 1 羟基芘浓度 ;分析了CYP1A1基因第 7外显子I4 6 2V位点、GSTM1、GSTT1、GSTP1基因I10 5V位点、CYP2E1基因 5’非编码区的Pst1位点和第 6内含子的Dra1位点、NQO1基因P187S位点、NAT2基因Kpn1、BamH1和Taq1位点以及mEH基因H113Y和R139H位点的多态性 ;使用调查表收集个人职业暴露史、年龄、性别、吸烟和饮酒等信息。结果　焦炉工尿中 1 羟基芘水平[(5 .6 1± 1.0 4 ) μmol molCr]高于对照组 [(0 .74± 0 .32 ) μmol molCr],差异有显著性 (P <0 .0 5 )。调整了PAHs外暴露等级和吸烟因素后 ,焦炉工中具有mEH基因 113位点变异纯合子基因型个体尿中1 羟基芘水平高于杂合子和野生型纯合子 (6 .4 1± 1.0 9>6 .2 4± 1.0 9>4 .6 2± 0 .95 μmol molCr) ,且野生型纯合子与变异型纯合子基因型个体间尿中 1 羟基芘水平的差异有显著性 (P <0 .0 5 )。在焦炉工中还发现CYP1A1和mEH基因多态性存在交互作用。结论　mEH基因 113位点的基因多态性可明显影响焦炉工尿中 1 羟基芘水平。