呼出苯和血苯作为生物接触指标的研究

对两皮鞋厂的３０名（男１１名，女１９名）苯作业工人，分别监测其呼出苯、血苯、尿酚浓度和车间空气苯以及呼出苯的毒代动力学观察。结果表明各指标间都有明显的正相关（Ｐ＜０．０１）和好的线性关系。班前呼出苯分别为０．０２６（停止接触４０ｈ）和０．１３６ｍｇ／ｍ３（停止接触１６ｈ）；血苯班前班后平均浓度分别为３．２ｌ和１０μｇ／Ｌ；班前班后血／气分配系数分别为６．６７和７．６０。１６ｈ衰减率达９９％以上。故以呼出苯和血苯作为职业性苯接触的生物监测指标，简便、灵敏、特异性好。     

尿粘康酸在苯的生物监测中的应用价值

为研究苯暴露的生物标志物，应用改进的高压液相色谱法检测了１２８名苯接触工人及４０名对照人群的尿粘康酸含量，同时测定了其尿酚含量。结果表明，当空气苯浓度为４１．４９ｍｇ／ｍ３时，接触工人的尿粘康酸含量为（５．４７±７．９４）ｍｇ／ｇＣｒ，尿酚为（３９．０９±４２．５９）ｍｇ／ｇＣｒ。对照人群的尿粘康酸含量为（０．１３±０．０９）ｍｇ／ｇＣｒ，尿酚为（１６．０１±１１．３３）ｍｇ／ｇＣｒ（均为肌酐校正值，ｘＧ±ｓ）。苯接触工人的尿粘康酸含量与所接触的空气苯浓度及尿酚含量呈良好的相关，相关系数分别为０．９１８７，０．８２０４。尿粘康酸在人群中本底值低，反映苯的内吸收情况比尿酚更特异、敏感，更适于低浓度苯暴露的生物监测。     

TNT作业工人尿中粪卟啉及δ-ALA含量的检测

采用紫外光灯观察法和原子吸收分光光度法检测了兰州某化工厂１１３名ＴＮＴ作业工人尿中粪卟啉（ＣＰ）及δ－氨基－γ－酮戊酸（δ－ＡＬＡ）含量。结果发现：接触组尿ＣＰ定性分析阳性率高达８２．３％，随着空气中ＴＮＴ浓度的增加，ＣＰ阳性率呈增加的趋势；尿δ－ＡＬＡ≥４ｍｇ／Ｌ有１７人，占１５．０％，且δ－ＡＬＡ含量的增高，在接触工龄较长（１０年以上）组表现得更为突出。７名对照尿ＣＰ定性皆为阴性，尿δ－ＡＬＡ含量都小于４．０ｍｇ／Ｌ。认为在一定条件下，尿ＣＰ检测可以作为健康监护敏感指标     

汞接触工人尿中γ-谷氨酰转移酶活力测定分析

对１２７名汞作业工人尿中γ－谷氨酰转移酶（ＧＧＴＰ）活力进行了测定,并与车间空气汞浓度、尿汞含量、汞作业工龄的关系进行相关分析。结果接汞组尿ＧＧＴＰ活力显著高于对照组（Ｐ〈０．０１）,并与车间空气汞浓度、尿汞含量呈正相关（Ｐ〈０．０５）。认为ＧＧＴＰ可作为反映工人现场汞接触的指标之一。     

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     

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     

硝基氯苯对人体健康的慢性影响调查

对１４２名长期接触硝基氯苯作业工人连续３年体检资料分析结果表明：神衰症候群、上呼吸道粘膜刺激及消化系统症状和体征检出率、ＭＨｂ定量等均高于对照组且与空气中浓度有关。均值为０．９６ｍｇ／ｍ３时，上述指标均高于对照组（Ｐ＜０．０１）；均值为０．５１ｍｇ／ｍ３，空气浓度均未超过ＭＡＣ时与对照组比较，以及接触组间比较，部分指标存在差异（Ｐ＜０．０５或Ｐ＜０．０１）。提出ＭＨｂ定量可作为接触硝基氯苯的生物监测指标，建议进一步研究其生物接触限值。     

苯的两种生物标志物现场应用价值的比较

选择了８６名苯接触工人进行现场研究。结果表明当空气苯浓度的几何均值为３１．８６ｍｇ／ｍ３时，代谢物粘康酸的几何均值为３．１５３ｍｇ／ｇ，尿酚则为３１．０２７ｍｇ／ｇ。接触的空气苯浓度分别与代谢物粘康酸和尿酚之间的相关系数为０．９０１２、０．７３０１。接触低浓度苯的人群尿酚与外接触的苯水平相关性较差；但粘康酸无论是在接触高的或低的苯浓度情况下，二者之间均有良好的相关性。粘康酸在对照组检出水平极低。提示：粘康酸可替代尿酚作为苯的生物学监测指标     

苯作业工人尿酚值与空气中苯浓度关系的探讨

对苯作业进行卫生学评价时,目前依靠作业环境空气中苯浓度的测定,但由于生产变动因素的影响,空气中苯浓度很不稳定,单测定苯浓度不易正确地反映整个接触过程的实际情况。有些作者认为,酚是苯在体内的主要代谢产物,尿酚排出量能较全面地反映作业环境苯污染的情况和机体的负荷状态。本次调查旨在通过对苯作业工人尿酚排出量与接触苯浓度关系的探讨,为以尿酚量作为接触苯的评价指标提供依据。     

甲苯的慢性危害和尿中的马尿酸作为职业性接触的生物学监测指标探讨

本文对１４０名接触以甲苯为主的有机溶剂的包漆工（平均接触工龄８．３９年）进行了横断面调查，发现头昏、头痛、失眠、乏力、腹隐痛等症状的出现率，神衰综合征和慢性咽炎的患病率明显高放对照组（Ｐ＜０．０５或Ｐ＜０．０１）。常规肝功能和血清碱性磷酸酶（Ｓ－ＡＫＰ）无明显改变（Ｐ＞０．０５）。包漆工班末尿马尿酸平均浓度显著高於班前和对照组班末的平均浓度（分别Ｐ＜０．０５，Ｐ＜０．０１）。男、女包漆工班末尿马尿酸平均浓度均高于班前（分别Ｐ＜０．０５，Ｐ＜０．０１）。空气中苯系物的浓度均在最高允许浓度范围内。结果提示，长期接触低浓度的以甲苯为主的有机溶剂，对中枢神经系统有不利影响。尿中马尿酸水平可作为反映工人接触低浓度甲苯的有用的、生物学监测指标。     

Benzene in blood and phenol in urine in monitoring benzene exposure in industry

Determinations of benzene concentration in blood and of phenol in urine were made by head-space gas chromatography techniques on samples taken near the end of the work day from two groups of workers potentially exposed to low levels of benzene in the work-place atmosphere. Preliminary results suggest that benzene in blood is more reliable than phenol tests for assessing both exposure and uptake of benzene. Normal values of phenol in urine (10 mg/liter or less) were found in nearly all those cases in which benzene was detected in the blood.     

空气苯浓度与呼出苯及尿酚的关系研究

目的对苯接触水平和接触者可能受到的有害影响进行卫生学评价。方法对１０名苯接触者和６名志愿苯接触者进行研究,用苯呼出气作为生物学监测指标。结果班前呼出苯大多为未检出,班中及班后呼出苯与空气苯时间加权平均浓度均有密切相关;班前尿酚与空气苯时间加权平均浓度无相关,班后尿酚及次晨尿酚均与空气苯ＴＷＡ浓度密切相关;班中、班后呼出苯均与班后尿酚及次晨尿酚密切相关,且以班中呼出苯与班后尿酚的相关性最高（ｒ＝０．９３５３）。呼出苯的快速排出相为脱离接触１０分钟（占班后呼出苯８２．２５％）,其排出稳定相在脱离接触后９０分钟左右。接触空气苯浓度ＴＷＡ７．９～２１７．８ｍｇ／ｍ３时,无论是呼出苯或尿酚在接触后２４小时与空气苯均无相关。结论在呼出苯的快速排出相采集终末呼出气可反映工人当时的接触浓度,采集排出稳定相终末呼出气,其浓度较稳定可反映接触者吸收入血液的浓度,并以此来估测环境浓度与接触水平。呼出苯的呼吸排出规律以及采样方便、无损伤,检出灵敏,呼出苯作为接触水平监测指标较其他指标优越。     

苯职业接触工人尿中酚和黏糠酸监测结果及意义

目的通过对苯接触工人尿中酚和反-反式黏糠酸的监测与分析,开展低苯环境下苯接触生物标志物研究,并探讨其实际应用价值。方法选取某制鞋厂员工作为研究对象,测定其尿液中酚和反-反式黏糠酸浓度,并对作业工人工作场所中苯浓度进行监测。结果接苯工人尿酚浓度与接苯浓度无显著性相关关系,尿中反-反式黏糠酸浓度与接苯浓度存在显著正相关(P0.05),接苯工人班后尿中的反-反式黏糠酸浓度显著高于班前尿(P0.05),吸烟对尿酚浓度影响较小,吸烟者尿中反-反式黏糠酸浓度显著高于非吸烟者(P0.05)。结论低浓度苯工作环境下,尿中反-反式黏糠酸可以作为一种敏感的生物标志物替代尿酚反映机体苯暴露情况。     

Excretion of 1,2,4-benzenetriol in the urine of workers exposed to benzene

Urine samples were collected from 152 workers (64 men, 88 women) who had been exposed to benzene, 53 workers (men only) exposed to a mixture of benzene and toluene, and 213 non-exposed controls (113 men, 100 women). The samples were analysed for 1,2,4-benzentriol (a minor metabolite of benzene) by high performance liquid chromatography. The time weighted average solvent exposure of each worker was monitored by diffusive sampling technique. The urinary concentration of 1,2,4-benzentriol related linearly to the intensity of exposure to benzene both in men and women among workers exposed to benzene, and was suppressed by toluene co-exposure among male workers exposed to a mixture of benzene and toluene. A cross sectional balance study in men at the end of the shift of a workday showed that only 0.47% of benzene absorbed will be excreted into urine as 1,2,4-benzenetriol, in close agreement with previous results in rabbits fed benzene. The concentration of 1,2,4-benzenetriol in urine was more closely related to the concentration of quinol than that of catechol. The fact that phenol and quinol, but not catechol, are precursors of 1,2,4-benzentriol in urine was further confirmed by the intraperitoneal injection of the three phenolic compounds to rats followed by urine analysis for 1,2,4-benzenetriol.     

Determination of catechol and quinol in the urine of workers exposed to benzene

Time weighted average concentrations of benzene in breathing zone air (measured by diffusive sampling coupled with FID gas chromatography) and concentrations of catechol and quinol in the urine (collected at about 1500 in the second half of a working week and analysed by high performance liquid chromatography) were compared in 152 workers who were exposed to benzene (64 men, 88 women). The concentration of urinary metabolites was also determined in 131 non-exposed subjects (43 men, 88 women). There was a linear relation between the benzene concentrations in the breathing zone and the urinary concentrations of catechol and quinol (with or without correction for urine density) in both sexes. Neither catechol nor quinol concentration was able to separate those exposed to benzene at 10 ppm from those without exposure. The data indicated that when workers were exposed to benzene at 100 ppm about 25% of benzene absorbed was excreted into the urine as phenolic metabolites, of which 13.2%, 1.6%, and 10.2% are phenol, catechol, and quinol, respectively.     

Occupational exposure to benzene in the shoe industry

In order to determine the possible actual exposure to benzene in the shoe industry from industrially used solvents, glues, and paints containing benzene as a nondeclared constituent, phenol in urine and benzene in blood, as indices of internal exposure to benzene, were measured in workers (N = 33). Since toluene, in contrast to benzene, is declared as a constituent in several glues, toluene in the blood of workers was also analysed. All analyses were performed using gas chromatography. Urine samples were collected on Monday morning (MI) before work and on Wednesday (WI) before and (WII) after work. Venous blood samples were taken on Wednesday only, 1/2 hour after work. There was no difference in the phenol concentrations of MI and WI, while the phenol concentration of WII was about twice as high as that in WI. In all blood samples, benzene was found, as well as toluene, which was about four times higher in comparison with benzene. A correlation (r = 0.465; p less than .01) was found between the difference in pre- and postshift phenol concentrations (WII-WI) in urine and the benzene concentrations in blood. The results presented show that a trace amount of benzene, which is often not declared as a constitutent in industrially used chemicals, could be a source of marked exposure to benzene. It can also be concluded that changes in phenol in urine (if preshift and postshift samples are taken) might be a sufficiently sensitive parameter to assess exposure to benzene even when other data concerning the presence of benzene in the working atmosphere are not available.     

Excretion of 1,2,4-benzenetriol in the urine of workers exposed to benzene.

Urine samples were collected from 152 workers (64 men, 88 women) who had been exposed to benzene, 53 workers (men only) exposed to a mixture of benzene and toluene, and 213 non-exposed controls (113 men, 100 women). The samples were analysed for 1,2,4-benzentriol (a minor metabolite of benzene) by high performance liquid chromatography. The time weighted average solvent exposure of each worker was monitored by diffusive sampling technique. The urinary concentration of 1,2,4-benzentriol related linearly to the intensity of exposure to benzene both in men and women among workers exposed to benzene, and was suppressed by toluene co-exposure among male workers exposed to a mixture of benzene and toluene. A cross sectional balance study in men at the end of the shift of a workday showed that only 0.47% of benzene absorbed will be excreted into urine as 1,2,4-benzenetriol, in close agreement with previous results in rabbits fed benzene. The concentration of 1,2,4-benzenetriol in urine was more closely related to the concentration of quinol than that of catechol. The fact that phenol and quinol, but not catechol, are precursors of 1,2,4-benzentriol in urine was further confirmed by the intraperitoneal injection of the three phenolic compounds to rats followed by urine analysis for 1,2,4-benzenetriol.     

Determination of catechol and quinol in the urine of workers exposed to benzene.

Time weighted average concentrations of benzene in breathing zone air (measured by diffusive sampling coupled with FID gas chromatography) and concentrations of catechol and quinol in the urine (collected at about 1500 in the second half of a working week and analysed by high performance liquid chromatography) were compared in 152 workers who were exposed to benzene (64 men, 88 women). The concentration of urinary metabolites was also determined in 131 non-exposed subjects (43 men, 88 women). There was a linear relation between the benzene concentrations in the breathing zone and the urinary concentrations of catechol and quinol (with or without correction for urine density) in both sexes. Neither catechol nor quinol concentration was able to separate those exposed to benzene at 10 ppm from those without exposure. The data indicated that when workers were exposed to benzene at 100 ppm about 25% of benzene absorbed was excreted into the urine as phenolic metabolites, of which 13.2%, 1.6%, and 10.2% are phenol, catechol, and quinol, respectively.     

URINARY EXCRETION OF PHENOL BY MEN EXPOSED TO VAPOUR OF BENZENE: A SCREENING TEST

The metabolism of benzene differs from that of other aromatic hydrocarbons; the excretion of phenol in the urine of workers exposed to ambient benzene bears a linear relationship to the degree of exposure. A semi-quantitative screening test using stable reagents not requiring special apparatus or laboratory facilities permits an estimation of urinary phenolic bodies, and hence the exposure to benzene. The test may be used (a) to determine whether individual workers need further investigation because of exposure to benzene, (b) as a group test to determine whether the environment is acceptable, and (c) to determine whether solvents often regarded as safe contain benzene.     

Chromosome analysis from peripheral blood lymphocytes of workers after an acute exposure to benzene.

A spillage of about 1200 gallons of benzene occurred during the loading of a ship, and 10 workers on a single shift were exposed to benzene. Shortly afterwards, an assay of the urine of these individuals showed that substantial amounts of phenol were being excreted. About three months after the incident samples of venous blood were taken from 10 individuals exposed to benzene and 11 men on a comparable shift who acted as controls. The lymphocytes were stimulated to divide in short term cultures. For each subject, 200 cells at metaphase were examined for chromosome damage using 48 h cultures, and sister chromatid exchanges (SCE) were analysed from about 30 cells in their second division, using 72 h cultures. The most frequent types of aberrations in all the individuals were chromatid gaps, with occasional breaks of chromatids and chromosomes. There were few exchanges within or between the arms of chromatids or chromosomes. More cells in the control than in the exposed group showed damage, an effect that was especially noticeable for chromatid gaps. All values, however, were considered to be within a normal range. There were slightly more SCE in some of the exposed individuals than in the controls and there was a trend towards a positive association between the frequency of SCE recorded for each individual and the maximum value for the excretion of phenol in the urine on the day after the incident. There is no evidence to indicate that benzene induced any type of lasting chromosome damage in the lymphocytes of the 10 exposed workers when cells were examined about three months after the incident.