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。...     

尿苯作为苯接触指标的研究

本研究测定了职业苯接触人群的尿苯水平,观察其是否与接触苯浓度间具有线性关系,以便将尿苯作为研究苯接触的指标。选择化工厂和加油站工作的苯接触工人110名(男性90名,女性20名;吸烟者为47人;年龄20～59岁,平均42岁)作为接触组。另选40名(男性28名,女性12名;非吸烟者20名,吸烟量>20支/d的吸烟者20名作对     

无苯稀释剂可降低苯毒危害

本文采用无苯稀释剂,对金属和木质两种工件进行刷漆和喷漆现场试验。测定结果表明,苯、甲苯、二甲苯含量均已降低到国家容许浓度标准,符合国家涂装作业安全规程,这是预防苯中毒最有效的措施。     

采用无苯稀释剂降低苯毒危害

油漆和喷漆行业中,按照传统工艺,常使用香焦水作为各种油漆和喷漆的稀释剂,它含苯、甲苯和二甲苯较高,对人体健康有着严重的危害。最近,我们采用北京中国铁道科学院研制成功的一种新型“无苯稀释剂”,来代替香蕉水,这样使施工现场的苯毒污染危害大大降低,它既保护了操作工人的身体健康,又改善了作业环境的污染状况,现将使用结果报告如下。     

正己烷干扰苯检测管检测苯的特异性

目的 探讨正己烷气体对苯检测管特异性的影响,为苯检测管的选择和快速检测提供科学依据。
方法 在30~200 mg/m3的范围内,通过动态配气仪分别设定4个不同质量浓度的苯或正己烷的气体环境,同时使用国家标准方法和检气管法进行检测,通过比较检测结果,评价苯检测管检测结果的准确度,并分析正己烷气体对苯检测管特异性的影响。
结果 和国家标准方法所得检测结果相比,4种苯检测管相对误差范围为12.1%~41.1%。正己烷设定质量浓度为30 mg/m3时,2种苯检测管发生显色反应;在50 mg/m3、100 mg/m3和200 mg/m3 3个设定的质量浓度进行检测时,3种苯检测管均发生显色反应,且随着正己烷设定质量浓度的增加,苯检测管检测到的质量浓度也随之增加。
结论 使用苯检测管应注意正己烷对其检测结果的干扰作用。
     

苯与白血病

1981年国际癌症研究所(IARC)认为有证据说明苯对人有致癌效应,可损伤造血系统,引起急性髓细胞白血病,有些机构已将苯列入致癌物或可疑致癌物名单。根据美国职业安全卫生署(OSHA)1974年修订的工作场所苯浓度限值,8小时加权平均浓度为10ppm,10分钟上限浓度为25ppm,最高     

苯与白血病

苯作为有机溶剂及化工原料,其工业用途极为广泛。一个世纪以来,通过临床与动物实验观察,对苯抑制造血系统的慢性毒性已有明确认识。慢性苯中毒者常首先出现白细胞总数降低,如继续接触较高浓度的苯,进而可有血小板及红细胞减少,严重者表现为全血细胞减少,或继发性再生障碍性贫血。然而长期接触高浓度     

苯暴露尿中苯巯基尿酸的变化

目的 探讨尿苯巯基尿酸(S-phenylmercapturic acid,S-PMA)作为苯职业性暴露生物标志物的可行性.方法 动物模型研究:48只成年SPF级Wistar大鼠,随机分为对照组、低浓度组(4mg/m3)、中浓度组(6 mg/m3)和高浓度组(10 mg/m3),雌雄各半;纯苯动态染毒28 d(4个时段,每个时段染毒5 d后停止2 d).监测苯浓度,每个时段染毒后立即取5 h尿,高效液相色谱-离子阱质谱联用技术检测大鼠尿中S-PMA含量.人群研究:接触组为广州市某船厂80名接触混苯的工人,对照组为该厂40名行政管理人员,对照组除不接触混苯外,其他与接触组均衡可比;检测环境中混苯浓度,收集研究对象班后尿.尿样处理和尿S-PMA检测同鼠尿.结果 (1)动物模型研究:在不同染毒时间内,鼠尿中S-PMA浓度随着环境中苯浓度的增高而升高,低、中、高3组间尿中S-PMA含量的差异有统计学意义(P＜0.01或P＜0.05),但尿中S-PMA含量未随染毒时间延长而变化,同浓度组染毒不同时间,鼠尿中S-PMA含量的差异无统计学意义(P＞0.05).(2)人群研究:接触低浓度混苯的工人尿中S-PMA含量为(13.6±3.4)μg/L,高浓度组为(27.2±7.9)μg/L,两组比较,差异有统计学意义(P＜0.01).大鼠和人群对照组尿中S-PMA本底值均低于5 μg/L.结论 尿中S-PMA含量与环境中苯浓度有关,暴露时间长短对其没有明显影响,在低浓度暴露情况下,尿中仍能检测到S-PMA,可以认为其是反映苯职业接触水平比较敏感的生物标志物.     

苯和白血病

早在一个多世纪前已知苯是一种严重的骨髓毒物。慢性苯中毒被描述为再生障碍性贫血或再生不良性贫血。其临床特征是或呈慢性进行性再生不良性贫血,或呈多发性贫血、坏疽性咽峡炎、败血症等迅速致命的出血性白细胞缺乏症。曾经多次见到进行性再生不良性贫血,由于严重的粒细胞减少症和血小板减少症而突然恶化,最后导致出血、败血症而死亡。 1928年Delore和Borgomans描述了第一例苯白血病病例,是一位工人患急性白血病。他接触苯之严重,以致其同伴们无一能忍受二个月以上的工作而不患病者。其后不久,发表     

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。     

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.     

呼出苯样品的采集和色谱分析

The method of sampling alveolar air and gas chromatography of trace benzene is reported. The lowest detectable concentration of benzene is 7.9 x 10(-4) mg/m3 in 100 ml volume. Method parameters are r = 0.999.9, mean recovery 95.14% and mean relative deviation (CV) 4.94%. 42 non-occupational and 48 occupational workers who exposed to benzene were studied by this method. The concentrations of exhaled benzene are respectively 0.016 +/- 0.011, 0.138 +/- 0.093 (before workshift) and 10.17 +/- 4.11 mg/m3 (after the end of the workshift). The results showed that this method is a simplified method for sampling alveolar air and analysis. Besides for expiratory benzene, this method can be also applied to monitoring of atmospheric trace benzene.     

Relation between the iodine azide test and the TTCA test for exposure to carbon disulphide.

Exposure to carbon disulphide (CS2) in a viscose plant was measured by personal monitoring and by application of the iodine azide test and quantification of 2-thio-thiazolidine-4-carboxylic-acid (TTCA) in urine samples. A relation was found between the rise in urinary TTCA concentration during the workshift and the exposure index E1. The correlation (r) between the exposure index and the atmospheric concentrations of CS2 in workroom air below 100 mg CS2/m3 was 0.59 (n = 9). The correlation between the increase in TTCA concentrations during the workshift and the atmospheric CS2 concentrations was found to be higher when urine samples at the end of the workshift with creatinine concentrations below 1 mg/ml and above 3 mg/ml were disregarded (from r = 0.61; n = 20 to r = 0.84; n = 14). A high correlation was found (r = 0.86; n = 13) when the end of workshift urine samples were analysed, provided that their creatinine concentrations are not beyond the limits given above.     

人尿中酚,粘糠酸,苯巯基尿酸的生物监测

为了探索接触低浓度苯的生物监测指标，在建立了灵敏、特异的尿中反，反－粘糠酸（ｔ，ｔ－ＭＡ）的高效液相色谱（ＨＰＬＣ）、苯巯基尿酸（Ｓ－ＰＭＡ）的色谱／质谱／质谱（ＬＣ／ＭＳ／ＭＳ）测定方法的基础上，对４９位接触低浓度苯的工人及２０位非职业接触者进行了生物监测。结果表明：在苯接触浓度低于３．２ｍｇ／ｍ３（１ｐｐｍ）的情况下，作业工人的尿ｔ，ｔ－ＭＡ和Ｓ－ＰＭＡ浓度与空气中苯的ＴＷＡ浓度显著相关；尿酚与空气中苯的ＴＷＡ浓度之间的相关性很差。吸烟能增加尿ｔ，ｔ－ＭＡ和Ｓ－ＰＭＡ的浓度。     

Relation between the iodine azide test and the TTCA test for exposure to carbon disulphide

Exposure to carbon disulphide (CS2) in a viscose plant was measured by personal monitoring and by application of the iodine azide test and quantification of 2-thio-thiazolidine-4-carboxylic-acid (TTCA) in urine samples. A relation was found between the rise in urinary TTCA concentration during the workshift and the exposure index E1. The correlation (r) between the exposure index and the atmospheric concentrations of CS2 in workroom air below 100 mg CS2/m3 was 0.59 (n = 9). The correlation between the increase in TTCA concentrations during the workshift and the atmospheric CS2 concentrations was found to be higher when urine samples at the end of the workshift with creatinine concentrations below 1 mg/ml and above 3 mg/ml were disregarded (from r = 0.61; n = 20 to r = 0.84; n = 14). A high correlation was found (r = 0.86; n = 13) when the end of workshift urine samples were analysed, provided that their creatinine concentrations are not beyond the limits given above.     

Acetone excretion into urine of workers exposed to acetone in acetate fiber plants

To develop a proper protocol for biological exposure monitoring of acetone, we evaluated whether exposure to acetone on the previous day affects the biological monitoring value at the end of a work day. One hundred and ten male workers exposed to acetone in three acetate fiber manufacturing plants were monitored using a liquid passive sampler on two consecutive working days after 2 days without exposure. Urine samples were collected at the start of the workshift and the end of the shift on both days for each subject. For ten exposed workers urine samples were collected approximately every 2 h during and after the first working day until the following morning. Acetone concentrations in urine (Cu) at the start of the first working day were 1.3 ± 2.4 (range: ND-14.1) mg/l in nonexposed workers and 2.4 ± 5.6 (range: ND-40.3) mg/l in exposed workers. The urinary acetone concentration at the beginning of the second working day indicated that urinary levels of acetone do not decline to background level by the following morning when exposure concentration exceeds 300 ppm. However, linear regression analysis demonstrated that the relationship between environmental exposure level and urine level was similar on the 1st day and the 2nd day. Thus, although urine acetone levels did not return completely to baseline after high exposures, under the present exposure levels the exposure on the previous day did not significantly affect urinary acetone at the end of the workshift of the next day.     

职业性苯暴露反-反式粘糠酸生物接触限值研究

目的研究职业性苯暴露反．反式粘糠酸（t,t—MA）生物接触限值。方法实验室建立生产环境空气中苯浓度的气相色谱检测方法及作业工人尿中t,t—MA含量的高效液相色谱检测方法,并通过检测苯暴露现场工人8h苯暴露水平及班前、班后尿中t,t．MA含量,研究其相关性。结果苯暴露者班前、班后尿中t,t—MA含量与其苯暴露水平有明显的相关关系。班前y（mg／gCr）=0．924＋0．108X（me／m^3）,r=0．62,P〈0．01;班后y（mg／gCr）=2．103＋0．177X（mg／m^3）,r=0．791,P〈0．01。结论根据我国作业场所空气中苯的国家卫生标准,按回归方程推导出职业接触苯生物接触限值,推荐职业暴露苯的生物接触限值为工作班班后尿t,t．MA含量为3．0mg／gCr,下一班班前尿t,t．MA含量为1．5mg／gGr。     

Isopropanol exposure: environmental and biological monitoring in a printing works.

Occupational exposure to isopropanol was studied in 12 workers by testing environmental air, alveolar air, venous blood, and urine during their work shift. Isopropanol, which ranged in environmental air between 7 and 645 mg/m3, was detected in alveolar air, where it ranged between 4 and 437 mg/m3, but not in blood or in urine. Alveolar isopropanol concentration (Ca) was significantly correlated with environmental isopropanol concentration (Ci) at any time of exposure. The value of the arithmetical Ca/ci ratio was 0.418 (SD 0.101). Acetone, which is a metabolite of isopropanol, was found in alveolar air, blood, and urine in concentrations that were higher during exposure than before. Alveolar and blood acetone concentrations were highly correlated with alveolar isopropanol concentrations at any time during exposure. Acetone ranged between 0.76 and 15.6 mg/l in blood, between 4 and 93 micrograms/l in alveolar air, and between 0.85 and 53.7 mg/l in urine. Alveolar (Ca) and blood (Cb) acetone concentrations were highly correlated (r = 0.67), with a Cb/Ca ratio of 101. Alveolar isopropanol uptake ranged between 0.03 and 6.8 mg/min and was highly correlated with environmental isopropanol concentration (r = 0.92). During exposure, acetone eliminated by the lungs ranged between 20 and 273 mg in seven hours and in urine between 0.3 and 9.6 mg in seven hours. Acetonuria was higher the next morning than at the end of exposure.