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。     

职业性苯接触者的呼出苯生物接触限值研究

通过现场调查、临床体检和实验测定的“班前”呼出苯浓度与接触苯浓度之比和高、中、低苯浓度接触者的呼出苯的毒物动力学观察结果,结合工人体检的健康状况和其它生物学监测指标间的关系,并参照国外制订呼出苯生物阈限值的文献报道;根据我国现行苯的最高容许浓度(40mg/m~3),建议职业性苯接触者“班前”末端呼出气中苯的生物接触限值为0.40μg/L(0.12ppm)。     

苯作业者呼出苯的生物学监测

苯作业者呼出苯的生物学监测刘庆宪（上海市卢湾区卫生防疫站，上海２０００２５）利用呼出苯作为生物学监测指标，对接触水平和接触者可能受到的有害影响进行卫生学评价，为此我们对苯作业者的呼出苯排出动态及其与空气苯浓度、苯的代谢产物——尿酚的关系作了研究探讨。...     

苯接触与尿中反-反式黏糠酸和苯巯基尿酸关系研究

目的探讨职业苯接触与尿中反-反式黏糠酸(ttMA)和苯巯基尿酸(SPMA)的相关性,评定两接触标志物作为生物监测指标的适用性。方法对44名制鞋厂接苯工人进行个体苯暴露水平的作业环境监测,采集当日班前与班后尿样,分别用高效液相色谱和液质联谱测定尿中ttMA和SPMA含量。结果个体苯接触浓度为2.57~146.11 mg/m3,几何平均浓度为(27.91±3.29)mg/m3。班后尿中ttMA和SPMA含量均较班前增高,差异有统计学意义(P0.01),班后ttMA和SPMA与空气苯浓度的相关系数分别为0.905(P0.01)和0.537(P0.01),个体苯接触代谢转化为ttMA和SPMA的相对内暴露指数(RIE)随苯接触浓度的增高而下降。结论在中、高浓度的苯接触时,班后尿ttMA与空气苯浓度的相关性优于SPMA。     

职业接触苯生物监测指标的研究

苯对人体的毒作用,特别是对职业人群的血系毒性及致白血病已有大量报道。由于其毒作用的非特异性,致癌作用潜伏期长。国内外学者提出以苯机体负荷作为苯作业的监测指标。本文拟在测定职业接触苯工人呼出气中苯浓度,尿酚排出量,外周血淋巴细胞微核检出率的基础上,探讨苯接触量与呼出苯、尿酚浓度及微核检出率之间的关系,为制订我国职业性接触苯生物监测阈限值提供依据。     

醋酸纤维厂中接触丙酮工人的生物监测

为探讨两酮生物监测的最佳指标,选取醋酸纤维厂接触丙酮的男性工人110名为研究对象。平均年龄为37.6(18～56)岁,平均专业工龄为14.9(0.5～34.3)年,饮酒者占70.7%,吸烟者占74.7%于休息日后第1天工作班前收集血、尿、呼出气3种标本,8h工作班未留尿和收集呼出气。第2天班前再留尿和收集呼出气,班末最后一次采血,留尿和收集呼出气(后者均在班后5 min内完成)。如此,共采血样220份,留尿样及收集呼出气样本各440份。同时,工人配戴被动式个体采样器(呼吸带高度)以监测车间空气中丙酮浓度。上述各种样     

生产环境空气中甲苯浓度与接触者代谢产物关系的初步探讨

为探讨生产环境空气中甲苯浓度与工人尿代谢排出物的关系，寻找简便易行较为准确的环境监测和作业工人接触的生物监测指标，对木器油漆车间作业环境空气中的甲苯浓度、刷油作业工人的尿代谢产物及呼出气和外周血中甲苯进行了调查。对象及方法选择油漆车间年龄18～40岁健康作业工人31名为观察对象。正常生产1小时后分别以烘干处理好50ml注射器同步采取作业环境空气及作业工人接触0．5，1，2，4，6．5小时终未呼出的甲苯含量分析。并采集外周血变化观察。空气、呼出气中和血液苯采用SQ23V气相色谱仪分析。收集作业工人班前、班后2小时尿样，…     

尿中粘康酸HPLC方法检测在苯生物监测中的应用研究

尿粘康酸是苯代谢产物中的一个极小分支，由于其在体内极低的本底值而受到重视。本研究采用强阴离子交换树脂预处理尿样，用ＨＰＬＣ—ＵＶ检测苯作业工人班前班末尿粘康酸浓度，并与尿酚及个体苯加权平均浓度进行相关分析。研究发现，苯作业工人尿粘康酸与尿酚、苯加权平均浓度三者之间良好相关，尿粘康酸比尿酚具备更好的敏感性与特异性，并能在个体苯加权平均浓度约３．８ｍｇ／ｍ￣３水平区分个体苯接触，尿粘康酸在苯生物监测中前景广阔。     

甲苯接触者呼出气中甲苯动力学研究

对１４名职业性接触者及１８名志原受试者接触甲苯进行研究。班中呼出气中甲苯浓度波动很大。班后甲苯浓度的下降趋势符合两室动力学模型，其中快相半减期为４～５分钟，慢相半减期为２～２．５小时。引入统计矩分析与传统的室模型进行比较。因其计算方便且结果易于解释，矩分析法在动力学研究中具有潜在的意义。甲苯接触者体内平均滞留时间为１６２－２２５分钟，直观地反映出甲苯在体内的排泄。为了建立特定接触浓度的动力学方程式，我们用直线回归法估计Ｙ轴截距（Ａ、Ｂ值）。甲苯空气浓度与Ａ、Ｂ值密切相关（ｒ＝０．４３～０．９２，Ｐ＜０．０５）。从动力学方程中，推算出接触空气甲苯浓度１００ｍｇ／ｍ３（ＴＷＡ－８ｈ），脱离接触０、３０和１８０分钟以及次日晨，呼出气中甲苯职业生物接触限值分别为７０、２０、１０及０．３６ｍｇ／ｍ３。     

苯接触的生物监测指标初步评估

目的：探索可客观反映职业性苯危害的灵敏指标。方法：测定苯作业车间空气苯浓度和３３名苯作业工人及４名非苯作业工人志愿者苯接触后呼出苯浓度、血苯含量及尿酚排出量，并进行相关性分析。结果：空气苯浓度（４．５～３４８ｍｇ／ｍ３）与血苯含量呈明显正相关（Ｐ＜０．０５）；血苯含量与尿酚排出量呈非常显著正相关（Ｐ＜０．０１）。结论：在低浓度苯接触时，血苯是一个与毒性相关联的特异性敏感苯吸收指标；尿酚排出量可用作高浓度苯接触工人的生物监测指标。     

Biological monitoring of occupational exposure to tetrahydrofuran

Occupational exposure to tetrahydrofuran (THF) was studied by analysis of environmental air, blood, alveolar air, and urine from 58 workers in a video tape manufacturing plant. Head space gas chromatography (GC) with an FID detector was used for determination of THF concentration in alveolar air, urine, and blood. Environmental exposure to THF was measured by personal sampling with a carbon felt passive dosimeter. When the end of shift urinary THF concentrations were compared with environmental time weighted average (TWA) values, urinary THF concentration corrected for specific gravity correlated well with THF concentration in air (r = 0.88), and uncorrected urinary THF concentration gave a similar result (r = 0.86). Correction for creatinine in urine weakened the correlation (r = 0.56). For exposure at the TWA concentration of 200 ppm the extrapolated concentration of THF was 33 mumol/l in blood and 111.9 mumol/l (61 mumol/g creatinine) or 109 mumol/l at a specific gravity of 1.018 in urine. The correlation between exposure to THF and its concentration in exhaled breath and blood was low (r = 0.61 and 0.68 respectively). Laboratory methodological considerations together with the good correlation between urinary THF concentration and the environmental concentration suggest that THF concentration in urine is a useful biological indicator of occupational exposure to THF.     

Biological monitoring of occupational exposure to tetrahydrofuran.

Occupational exposure to tetrahydrofuran (THF) was studied by analysis of environmental air, blood, alveolar air, and urine from 58 workers in a video tape manufacturing plant. Head space gas chromatography (GC) with an FID detector was used for determination of THF concentration in alveolar air, urine, and blood. Environmental exposure to THF was measured by personal sampling with a carbon felt passive dosimeter. When the end of shift urinary THF concentrations were compared with environmental time weighted average (TWA) values, urinary THF concentration corrected for specific gravity correlated well with THF concentration in air (r = 0.88), and uncorrected urinary THF concentration gave a similar result (r = 0.86). Correction for creatinine in urine weakened the correlation (r = 0.56). For exposure at the TWA concentration of 200 ppm the extrapolated concentration of THF was 33 mumol/l in blood and 111.9 mumol/l (61 mumol/g creatinine) or 109 mumol/l at a specific gravity of 1.018 in urine. The correlation between exposure to THF and its concentration in exhaled breath and blood was low (r = 0.61 and 0.68 respectively). Laboratory methodological considerations together with the good correlation between urinary THF concentration and the environmental concentration suggest that THF concentration in urine is a useful biological indicator of occupational exposure to THF.     

Structure and validation of a pharmacokinetic model for benzene

A pharmacokinetic model for benzene has been developed and validated for the inhalation aspects of its operation. The validation shows reasonable agreement between the model outputs and human biological data for phenol in urine, benzene in alveolar air, and benzene in mixed exhaled air.     

Environmental and occupational exposure to benzene by analysis of breath and blood

Benzene exposure of chemical workers was studied, during the entire workshift, by continuous monitoring of workplace benzene concentration, and 16 hours after the end of the workshift by the measurement of alveolar and blood benzene concentrations and excretion of urinary phenol. Exposure of hospital staff was studied by measuring benzene concentrations in the alveolar and blood samples collected during the hospital workshift. Instantaneous environmental air samples were also collected, at the moment of the biological sampling, for all the subjects tested. A group of 34 chemical workers showed an eight hour exposure to benzene, as a geometric mean, of 1.12 micrograms/l which corresponded, 16 hours after the end of the workshift, to a geometric mean benzene concentration of 70 ng/l in the alveolar air and 597 ng/l in the blood. Another group of 27 chemical workers (group A) turned out to be exposed to an indeterminable eight hour exposure to benzene that corresponded, the morning after, to a geometric mean benzene concentration of 28 ng/l in the alveolar air and 256 ng/l in the blood. The group of hospital staff (group B) had a benzene concentration of 14 ng/l in the alveolar air and 269 ng/l in the blood. Instantaneous environmental samples showed that in the infirmaries the geometric mean benzene concentration was 58 ng/l during the examination of the 34 chemical workers, 36 ng/l during the examination of the 27 chemical workers (group A), and 5 ng/l during the examination of the 19 subjects of the hospital staff (group B). Statistical analysis showed that the alveolar and blood benzene concentrations in the 34 workers exposed to 1.12 microgram/l of benzene differed significantly from those in groups A and B. It was found, moreover, that the alveolar and blood benzene concentrations were higher in the smokers in groups A and B but not in the smokers in the group of 34 chemical workers. The slope of the linear correlation between the alveolar and the instantaneous environmental benzene concentrations suggested a benzene alveolar retention of about 55%. Blood and alveolar benzene concentrations showed a highly significant correlation and the blood/air partition coefficient, obtained from the slope of the regression line, was 7.4. In the group of the 34 chemical workers no correlation was found between the TWA benzene exposure and the urinary phenol excretion.     

Environmental and occupational exposure to benzene by analysis of breath and blood.

Benzene exposure of chemical workers was studied, during the entire workshift, by continuous monitoring of workplace benzene concentration, and 16 hours after the end of the workshift by the measurement of alveolar and blood benzene concentrations and excretion of urinary phenol. Exposure of hospital staff was studied by measuring benzene concentrations in the alveolar and blood samples collected during the hospital workshift. Instantaneous environmental air samples were also collected, at the moment of the biological sampling, for all the subjects tested. A group of 34 chemical workers showed an eight hour exposure to benzene, as a geometric mean, of 1.12 micrograms/l which corresponded, 16 hours after the end of the workshift, to a geometric mean benzene concentration of 70 ng/l in the alveolar air and 597 ng/l in the blood. Another group of 27 chemical workers (group A) turned out to be exposed to an indeterminable eight hour exposure to benzene that corresponded, the morning after, to a geometric mean benzene concentration of 28 ng/l in the alveolar air and 256 ng/l in the blood. The group of hospital staff (group B) had a benzene concentration of 14 ng/l in the alveolar air and 269 ng/l in the blood. Instantaneous environmental samples showed that in the infirmaries the geometric mean benzene concentration was 58 ng/l during the examination of the 34 chemical workers, 36 ng/l during the examination of the 27 chemical workers (group A), and 5 ng/l during the examination of the 19 subjects of the hospital staff (group B). Statistical analysis showed that the alveolar and blood benzene concentrations in the 34 workers exposed to 1.12 microgram/l of benzene differed significantly from those in groups A and B. It was found, moreover, that the alveolar and blood benzene concentrations were higher in the smokers in groups A and B but not in the smokers in the group of 34 chemical workers. The slope of the linear correlation between the alveolar and the instantaneous environmental benzene concentrations suggested a benzene alveolar retention of about 55%. Blood and alveolar benzene concentrations showed a highly significant correlation and the blood/air partition coefficient, obtained from the slope of the regression line, was 7.4. In the group of the 34 chemical workers no correlation was found between the TWA benzene exposure and the urinary phenol excretion.     

Evaluation of biomarkers for occupational exposure to benzene.

OBJECTIVE--To evaluate the relations between environmental benzene concentrations and various biomarkers of exposure to benzene. METHODS--Analyses were carried out on environmental air, unmetabolised benzene in urine, trans, trans-muconic acid (ttMA), and three major phenolic metabolites of benzene; catechol, hydroquinone, and phenol, in two field studies on 64 workers exposed to benzene concentrations from 0.12 to 68 ppm, the time weighted average (TWA). Forty nonexposed subjects were also investigated. RESULTS--Among the five urinary biomarkers studied, ttMA correlated best with environmental benzene concentration (correlation coefficient, r = 0.87). When urinary phenolic metabolites were compared with environmental benzene, hydroquinone correlated best with benzene in air. No correlation was found between unmetabolised benzene in urine and environmental benzene concentrations. The correlation coefficients for environmental benzene and end of shift catechol, hydroquinone, and phenol were 0.30, 0.70, and 0.66, respectively. Detailed analysis, however, suggests that urinary phenol was not a specific biomarker for exposure below 5 ppm. In contrast, ttMA and hydroquinone seemed to be specific and sensitive even at concentrations of below 1 ppm. Although unmetabolised benzene in urine showed good correlation with atmospheric benzene (r = 0.50, P < 0.05), data were insufficient to suggest that it is a useful biomarker for exposure to low concentrations of benzene. The results from the present study also showed that both ttMA and hydroquinone were able to differentiate the background level found in subjects not occupationally exposed and those exposed to less than 1 ppm of benzene. This suggests that these two biomarkers are useful indices for monitoring low concentrations of benzene. Furthermore, these two metabolites are known to be involved in bone marrow leukaemogenesis, their applications in biological monitoring could thus be important in risk assessment. CONCLUSION--The good correlations between ttMA, hydroquinone, and atmospheric benzene, even at concentrations of less than 1 ppm, suggest that they are sensitive and specific biomarkers for benzene exposure.     

Evaluation of exposure to benzene vapour during the loading of petrol

Sherwood, R. J. (1972).Brit. J. industr. Med.,29, 65-69. Evaluation of exposure to benzene vapour during loading of petrol. The exposure of three workers to benzene vapour has been determined by personal air sampling, and has been related to their intake (assessed by sampling exhaled breath), and to their metabolism of benzene (evaluated from the concentration of phenol in urine.) The results obtained agree in general with those already published in the literature and with a preliminary experimental exposure undertaken as part of the development of techniques.

The two loaders who handled the loading arms were exposed to mean concentrations of 1·6 and 2·5 p.p.m. over the 5-hour period of loading. The probability of their exposure to concentrations greater than 25 p.p.m. was about 0·1 and 1%. The weigher working between the tracks was exposed to a mean concentration of 20 p.p.m. over the same period and had a total exposure of 114 p.p.m.-hour. Samples of exhaled breath taken at the end of work showed 0·14 and 0·18 p.p.m. benzene for the loaders and 0·84 p.p.m. for the weigher. The following morning the latter showed 0·19 p.p.m. Urine samples taken from the loaders at the end of work contained 12 and 25 mg/l total phenol and for the weigher 83 mg/l. The following morning the phenol was not above natural levels in the loaders' urine, and was 38 mg/l in a sample from the weigher.

It is suggested that any or all of the methods developed for this study could be used in conjunction with appropriate clinical studies to provide a more quantitative basis for determining the hazard of occupational exposure to benzene.

     

Benzene in the blood and breath of normal people and occupationally exposed workers

Benzene was measured in blood and alveolar air of 168 men, aged 20-58 years, subdivided into four groups: blood donors, hospital staff, chemical workers occupationally exposed to benzene, and chemical workers not occupationally exposed to benzene. The group of exposed workers was employed in work places with a mean environmental exposure to benzene of 1.62 mg/M3 (8 hr TWA). Non-exposed workers were employed elsewhere in the same plant, with an environmental exposure to benzene lower than 0.1 mg/M3. Blood and alveolar air samples were collected in the morning, before the start of the work shift for the chemical workers. The group of exposed workers was found to be significantly different from the other three groups, both for blood and alveolar benzene concentrations. The mean blood benzene concentration was 789 ng/l in the exposed workers, 307 ng/l in the non-exposed workers, 332 ng/l in the hospital staff, and 196 ng/l in the blood donors. Apart from the exposed workers, blood benzene concentration was significantly higher in smokers than in non-smokers. The mean alveolar benzene concentration was 92 ng/l in the exposed workers, 42 ng/l in the non-exposed workers, 22 ng/l in the hospital staff, and 11 ng/l in the blood donors. Alveolar benzene concentration was significantly higher in smokers than in non-smokers in the groups of the hospital staff and non-exposed workers, but not in the blood donors and exposed workers. In the three groups without occupational exposure considered altogether, the alveolar benzene concentration correlated significantly with environmental benzene concentration measured at the moment of the individual examinations, both in the smokers (r = .636; p less than .001) and non-smokers (r = .628; p less than .001). In the same three groups and in the exposed workers, alveolar benzene concentration showed a significant correlation with the blood benzene concentration.     

Biological monitoring of exposure to low concentrations of styrene

A field study was conducted on 39 male workers exposed to styrene at concentrations below 40 ppm (time weighted average, TWA). Analyses were carried out on environmental air, exhaled air, blood, urine, and two major urinary metabolites of styrene: mandelic acid (MA) and phenylglycoxylic acid (PGA). Head space gas chromatography (GC) with a flame ionization detector (FID) was used for determination of styrene in blood and urine. Postexposure exhaled air was analyzed using capillary GC. Environmental styrene exposure was measured by personal sampling using carbon cloth personal samplers. Urinary metabolites of styrene were determined by high pressure liquid chromatograph (HPLC). When the end-of-shift breath, blood, and urine styrene levels were compared with environmental TWA values, blood styrene correlated best with styrene in air (r = 0.87), followed by breath styrene (r = 0.76). Poor correlation (r = 0.24) was observed between environmental styrene exposure and urine styrene. When styrene metabolites were compared with environmental styrene, the sum of urinary MA and PGA correlated better with styrene in air than MA or PGA alone. The correlations between urinary metabolites and environmental styrene improved when corrected for the specific gravity of urine. Even better correlations were observed when the urinary metabolites were corrected for creatinine. The correlation coefficients for environmental styrene and end-of-shift MA, PGA, and MA + PGA were 0.83, 0.84, and 0.86, respectively. The correlation coefficients between environmental styrene and next morning urinary metabolites fell to 0.47, 0.61, and 0.65 for MA, PGA, and MA + PGA, respectively. These results suggest that determination of the total MA and PGA in urine samples is preferred than separate measurements of MA or PGA. The good correlation between environmental exposure and styrene in the exhaled air also suggests that breath styrene level can be a useful indicator for low level styrene exposure, as the method is specific, noninvasive, and rapid. Urinary styrene seems to be a less reliable indicator for low level styrene exposure. © 1994 Wiley-Liss, Inc.