低浓度1-溴丙烷对接触者神经系统的影响

[目的]观察低浓度1-溴丙烷(1-BP)接触对人外周神经系统和中枢神经系统功能的影响。[方法]以25名1-BP接触工人为接触组(其中男性17人)和25名非接触工人为对照组(其中男性17人),使用问卷调查收集研究对象的年龄、性别和吸烟、饮酒状况及教育程度等信息,测定1-BP接触的时间加权平均浓度(TWA),进行神经传导速度和神经行为学检查。[结果]接触组女性和暴露组女性相比,一般情况中除年龄(接触组女性年龄低于对照组,P<0．05)外,其他方面差别均无显著性;接触组男性和暴露组男性一般情况差别均无显著性。1-BP接触浓度的TWA平均值80．4(2．0-384．9)mg/m3;男性接触组与其对照组相比,运动神经传导速度减慢,末端潜伏期延长,简明情绪量表(profile of mood states,PMOS)表中紧张焦虑项得分增高,视觉记忆项得分降低,差异有显著性(P<0．05);女性接触组与其对照组各项比较差别均未见统计学意义(P>0．05)。[结论]低浓度1-BP暴露能对男性接触者外周神经传导速度和神经行为产生影响。     

Neuro-reproductive toxicities of 1-bromopropane and 2-bromopropane

2-Bromopropane was used as an alternative to chlorofluorocarbons in a Korean electronics factory and caused reproductive and hematopoietic disorders in male and female workers. This causality was revealed by animal studies, and target cells were identified in subsequent studies. After identification of 2-bromopropane toxicity, 1-bromopropane was introduced to the workplace as a new alternative to ozone-depleting solvents. 1-Bromopropane was considered less mutagenic than 2-bromopropane, but, in contrast, animal experiments revealed that 1-bromopropane is a potent neurotoxic compound compared with 2-bromopropane. It was also revealed that 1-bromopropane has reproductive toxicity, but the target cells are different from those of 2-bromopropane. Exposure to 1-bromopropane inhibits spermiation in male rats and disrupts the development of follicles in female rats, in contrast to 2-bromopropane, which targets spermatogonia and oocytes in primordial follicles. After the first animal study describing the neurotoxicity of 1-bromopropane, human cases were reported. Those cases showed decreased sensation of vibration and perception, paresthesia in the lower extremities, decreased sensation in the ventral aspects of the thighs and gluteal regions, stumbling and headache, as well as mucosal irritation, as the initial symptoms. The dose–response of bromopropanes in humans and mechanism(s) underlying the differences in the toxic effects of the two bromopropanes remain to be determined.     

An experimental study of the combined effects of n-hexane and methyl ethyl ketone.

This study was intended to determine whether or not methyl ethyl ketone (MEK) enhances the neurotoxicity of n-hexane at low concentration and after long term exposure. Separate groups of eight rats were exposed to 100 ppm n-hexane, 200 ppm MEK, 100 ppm n-hexane plus 200 ppm MEK, or fresh air in an exposure chamber for 12 hours a day for 24 weeks. The body weight, motor nerve conduction velocity (MCV), distal motor latency (DL), and mixed nerve conduction velocities (MNCVs) were measured before exposure and after four, eight, 12, 16, 20, and 24 weeks' exposure. One rat of each group was histopathologically examined after 24 weeks' exposure. Exposure of 100 ppm n-hexane did not significantly decrease the functions of the peripheral nerve throughout the experiment. Exposure to 200 ppm MEK significantly increased MCV and MNCVs and decreased DL after four weeks' exposure, but at this later stage no significant changes were found throughout the experiment by comparison with the controls. Mixed exposure to 100 ppm n-hexane plus 200 ppm MEK significantly decreased by comparison with the controls. On histopathological examination of the tail nerve, however, no changes were found in any of the exposed groups or the controls. These results suggest that MEK might enhance the neurotoxicity of n-hexane at a low concentration, and mixed exposures to n-hexane and MEK should be avoided.     

An experimental study of the combined effects of n-hexane and methyl ethyl ketone

This study was intended to determine whether or not methyl ethyl ketone (MEK) enhances the neurotoxicity of n-hexane at low concentration and after long term exposure. Separate groups of eight rats were exposed to 100 ppm n-hexane, 200 ppm MEK, 100 ppm n-hexane plus 200 ppm MEK, or fresh air in an exposure chamber for 12 hours a day for 24 weeks. The body weight, motor nerve conduction velocity (MCV), distal motor latency (DL), and mixed nerve conduction velocities (MNCVs) were measured before exposure and after four, eight, 12, 16, 20, and 24 weeks' exposure. One rat of each group was histopathologically examined after 24 weeks' exposure. Exposure of 100 ppm n-hexane did not significantly decrease the functions of the peripheral nerve throughout the experiment. Exposure to 200 ppm MEK significantly increased MCV and MNCVs and decreased DL after four weeks' exposure, but at this later stage no significant changes were found throughout the experiment by comparison with the controls. Mixed exposure to 100 ppm n-hexane plus 200 ppm MEK significantly decreased by comparison with the controls. On histopathological examination of the tail nerve, however, no changes were found in any of the exposed groups or the controls. These results suggest that MEK might enhance the neurotoxicity of n-hexane at a low concentration, and mixed exposures to n-hexane and MEK should be avoided.     

Neurotoxicity of 1-bromopropane in rats

Neurotoxicity of 1-bromopropane (1-BP) used as an alternative solvent of fluorocarbons was experimentally studied. Eight rats in the experimental group were exposed to 1-BP at 1500 ppm for six hours a day, five days a week for four weeks in an exposure chamber. Another eight rats in the control group were exposed to room air in a similar exposure chamber as those in the experimental group. During the latter half of the fourth week of exposure, all the rats in the experimental group showed a loss of body weight and ataxic gait compared with control rats. At the end of the fourth week, the rats in both groups were perfused through the ascending aorta and fixed. The cerebellum, medulla oblongata, spinal cord and peripheral nerve were processed for histopathological studies. No statistically significant difference in the frequency of axonal degeneration in both peroneal and sural nerves was found between the experimental and control groups. In the cerebellum, the frequency of degeneration of Purkinje cells in both the vermis and hemisphere was higher in the experimental group than in the control group (P < 0.05). There was no significant difference in the frequency of myelin ovoids in the fifth thoracic and in the third cervical posterior columns of the spinal cord between control and experimental groups. There was also no significant difference in the frequency of axonal swelling in the nucleus gracilis of the medulla oblongata between control and experimental groups. Ataxic gait was considered to be induced by degeneration of Purkinje cells in the cerebellum due to 1-BP exposure. However, degenerative findings of nerve fibers in the peripheral nerve, spinal posterior column and nucleus gracilis of the medulla oblongata due to 1-BP exposure were not evident. At the end of the fourth week of exposure, rats in the experimental group showed loss of body weight and markedly decreased motor activities, and it was considered that they would die if we continued the exposure into the fifth week. Therefore, we feel that our experimental schedule should be reconsidered before undertaking any further studies on the peripheral nerve toxicity of 1-BP.     

Neurologic abnormalities in workers of a 1-bromopropane factory

We reported recently that 1-bromopropane (1-BP; n-propylbromide, CAS Registry no. 106-94-5), an alternative to ozone-depleting solvents, is neurotoxic and exhibits reproductive toxicity in rats. The four most recent case reports suggested possible neurotoxicity of 1-BP in workers. The aim of the present study was to establish the neurologic effects of 1-BP in workers and examine the relationship with exposure levels. We surveyed 27 female workers in a 1-BP production factory and compared 23 of them with 23 age-matched workers in a beer factory as controls. The workers were interviewed and examined by neurologic, electrophysiologic, hematologic, biochemical, neurobehavioral, and postural sway tests. 1-BP exposure levels were estimated with passive samplers. Tests with a tuning fork showed diminished vibration sensation of the foot in 15 workers exposed to 1-BP but in none of the controls. 1-BP factory workers showed significantly longer distal latency in the tibial nerve than did the controls but no significant changes in motor nerve conduction velocity. Workers also displayed lower values in sensory nerve conduction velocity in the sural nerve, backward recalled digits, Benton visual memory test scores, pursuit aiming test scores, and five items of the Profile of Mood States (POMS) test (tension, depression, anxiety, fatigue, and confusion) compared with controls matched for age and education. Workers hired after May 1999, who were exposed to 1-BP only (workers hired before 1999 could have also been exposed to 2-BP), showed similar changes in vibration sense, distal latency, Benton test scores, and depression and fatigue in the POMS test. Time-weighted average exposure levels in the workers were 0.34-49.19 ppm. Exposure to 1-BP could adversely affect peripheral nerves or/and the central nervous system.     

Occupational health survey on workers exposed to 2-bromopropane at low concentrations

BACKGROUND: Recent case studies in Korea and animal studies revealed the reproductive and hematopoietic toxicity of 2-bromopropane introduced into workplaces as an alternative to ozone-layer depleting chlorofluorocarbons. We aimed to clarify the dose-effect relationship of 2-bromopropane in workers. METHOD: The exposure concentration of 2-bromopropane and hematological indices, hormonal levels, menstruation status, and sperm indices were examined in 25 workers (11 males, 14 females) at a 2-bromopropane factory. Regression analyses of the examined indices against time-weighted average (TWA) of exposure concentration were conducted. RESULTS: Amenorrhea or polymenorrhea was observed only in older females. Hematological indices had a significant relation with TWA of exposure concentration in females with normal menstruation. However, no other indices showed any significant relation with TWA of 2-bromopropane. CONCLUSIONS: No severe cases of reproductive or hematopoietic disorders were found at less than 10 ppm (TWA), but a possible adverse effect of 2-bromopropane on hematopoiesis could not be disproved.     

1-溴丙烷对接触工人神经毒性的剂量-效应关系

目的 探索1-溴丙烷(1-BP)对接触工人神经毒性的剂量-效应关系.方法 对国内1-BP生产工厂进行职业卫生现场调查.按1:1比例选取年龄配对的接触组和对照组女工各71人.作业环境中1-BP的浓度用直读式检气管测定,工人的8 h时间加权平均(TWA)浓度用个体采样器测定.对工人进行问卷调查、神经内科检查、神经传导速度检查、振动觉检查、血常规和血液生化检查.根据TWA值和TWA×工龄值将接触工人分为3个剂量组,进行剂量-效应关系分析.使用USEPA BMDS 2.1软件计算1-BP毒作用基准剂量(BMD)和基准剂量下限值(BMDL).结果 TWA-8 h浓度范围为0.35～535.19 mg/m3,(均值14.08 mg/m3).剂量-效应关系分析表明,1-BP接触工人在运动神经远端潜伏期(DL,线性回归系数为0.0666)、双足振动觉(线性回归系数分别为0.157 2和0.193 9)、肌酸激酶水平(线性回归系数为-1.0464)和促甲状腺激素水平(线性回归系数为0.102 4)等指标与1-BP有剂量依赖关系(P<0.05).依据DL资料计算TWA-8 h的BMD值和BMDL值分别为55.55和30.78 mg/m3.结论 1-BP对接触工人具有神经毒性,可引起胫神经DL延长、振动觉下降的剂量依赖性改变.     

1-溴丙烷对两种雄性大鼠肝脏毒性的研究

目的研究1-溴丙烷对两种雄性大鼠的肝脏毒性及谷胱甘肽S-转移酶(GST)在肝脏解毒代谢中的作用。方法将18只Fischer344大鼠和18只Wistar大鼠分别随机分为两组,一组给予新鲜空气,一组给予1000ppm1-溴丙烷,每天8h,连续暴露4周。通过血浆的生化指标和病理切片对肝脏的功能和形态进行了评价。利用化学比色法和实时定量PCR法对肝脏中的GST的活力和基因表达水平进行测量。结果1-溴丙烷暴露可引起两种大鼠体重的下降及肝脏重量的上升;病理发现肝脏中央静脉周围的肝细胞出现空泡样改变,血浆中CK、ALT和TBIL和DBIL等指标上升明显;两种大鼠肝脏细胞胞浆的GST活力增强,Fischer344大鼠微粒体GST的活力也增强;肝脏组织的GSTmRNA表达水平升高。结论1-溴丙烷暴露对两种雄性大鼠具有肝脏毒性,GST在1-溴丙烷的肝脏解毒代谢中可能起到较重要作用。     

Cerebral excitability in pup rats prenatally exposed to 1-bromopropane is suppressed by bromide accumulated in the brain

Previously, we reported that prenatal exposure to 1-bromopropane (1-BP) causes the accumulation of bromide (Br^-) in the brain of rat pups. Here, we aimed to investigate the effects of Br^- accumulation in rat pups prenatally exposed to 1-BP vapor. Dam rats were exposed to 1-BP (400 or 700 ppm; 1-BP group) by inhalation, or to NaBr (20 mM; Br^- group) in drinking water during gestation days 1–20. We also analyzed pentylenetetrazole (PTZ, 60 mg/kg, ip)-induced behavioral changes in pups prenatally exposed to 1-BP or Br^- on postnatal day (PND) 14. PTZ-induced epileptic convulsions were inhibited in both 1-BP (700 ppm) and Br^- groups. The inhibition of neuronal excitability induced by Br^- was evaluated electrophysiologically using the hippocampal slices obtained from PND14–16 pups. PTZ (2 mM) failed to induce epileptiform discharge in the presence of 1.2 mM Br^- in the slices obtained from the control group. However, it induced epileptiform discharge following the removal of Br^-, by perfusing artificial cerebrospinal fluid into the slices obtained from the Br^- group. Our results indicate that Br^- accumulates in the brain of neonatal rat pups prenatally exposed to 1-BP vapor suppressed neuronal excitability.     

1-溴丙烷暴露对大鼠认知功能的影响

目的 观察1-溴丙烷(1-bromopropane,1-BP)对大鼠学习记忆功能及对胆碱能神经系统的影响.方法 雄性Wistar大鼠40只,随机分为4组:1-BP低剂量组(200mg/kg1-BP)、中剂量组(400mg/kg1-BP)、高剂量组(800mg/kg 1-BP)和对照组,每组10只.各组动物分别经灌胃给予相应受试物7 d后,采用Morris水迷宫定位航行试验和空间探索试验检测大鼠学习和记忆功能.水迷宫试验结束后次日断头处死大鼠,迅速剥离大鼠大脑和海马,冰浴中制备匀浆,取上清液,测定乙酰胆碱酯酶(AChE)、乙酰胆碱转移酶(ChAT)的活力.结果 定位航行试验中,1-BP染毒后,与对照组相比,中、高剂基组的逃避潜伏期、游泳路程明显延长,搜索效能降低,差异均有统计学意义(P＜0.05,P＜0.01).空间探索试验中,低、中、高剂量组穿越平台次数(分别为4.30±2.6、3.78±2.0、2.50±2.1)呈降低趋势,与对照组(7.20±2.8)比较,差异均有统计学意义(P＜0.05,P＜0.01),高剂量组的平台周边时间/总时间比值(0.55±0.14)明显低于对照组(0.76±0.15)和低剂量组(0.69±0.18),差异有统计学意义(P＜0.01).中、高剂量组大鼠大脑皮层AChE活力[分别为(1.246±0.423)、(1.397±0.503)U/mgpro]明显升高,与对照组[(0.918±0.276)U/mg pro]的差异有统计学意义(P＜0.05,P＜0.01),高剂量组海马组织中AChE活力[(0.583±0.118)U/mgpro]也明显高于对照组[(0.491±0.075)U/mgpro],差异有统计学意义(P＜0.05).1-BP染毒后,大脑皮层ChAT活力有降低趋势,但与对照组相比,差异无统计学意义(P＞0.05).结论 1-BP暴露能明显损伤大鼠学习记忆能力,可能与AChE活力升高相关.     

溴丙烷两种同分异构体对雄性大鼠生殖系统的影响

目的了解溴丙烷两种同分异构体对雄性大鼠的生殖毒性和初步的毒性机制。方法将18只SPF级SD大鼠随机分为对照组、1-溴丙烷组(1g/kg)和2-溴丙烷组(1g/kg),连续腹腔注射1周。对附睾的精子数量和形态进行评价;HE和PAS染色评价睾丸的病理变化;运用TUNEL染色法和caspase-3活性的免疫组化法评价睾丸的细胞凋亡损伤;利用化学比色法对谷胱甘肽(GSH)、丙二醛(MDA)和超氧化物歧化酶(SOD)等氧化应激指标进行测量。结果溴丙烷导致睾丸重量下降、精子数量减少和精子形态异常比例增加。与对照组比较,1-溴丙烷显著增加大鼠睾丸谷胱甘肽还原酶(GR)活性(7.42±2.98vs.4.25±1.18)、附睾的MDA含量(0.49±0.20vs.0.39±0.08)和SOD活性(91.87±3.93vs.80.59±9.92)(均P0.05);2-溴丙烷显著升高睾丸和附睾的MDA含量(0.42±0.07vs.0.24±0.11;0.48±0.08vs.0.39±0.08),降低GSH含量(6.35±1.86vs.10.89±3.69),以及附睾谷胱甘肽转移酶(GST)(53.21±9.60vs.61.98±10.41)及GR活性(2.48±1.21vs.7.75±8.56)(均P0.05)。1-溴丙烷的病理切片除观察到睾丸生精小管的精子释放延迟外,未见其他病理变化,而2-溴丙烷的暴露使生精小管出现萎缩和空泡,生殖细胞发生减少、坏死。伴随着2-溴丙烷引起的睾丸病理变化,TUNEL标记结果显示每小管睾丸凋亡细胞数、凋亡百分比和凋亡指数明显高于对照组(17.72±4.59vs.5.92±1.05,P0.05;0.34±0.14vs.0.10±0.02,P0.05;6.64±3.40vs.0.59±0.20,P0.01),与1-溴丙烷组相比,凋亡百分比(0.34±0.14vs.0.12±0.03)和凋亡指数(6.64±3.40vs.0.76±0.21)明显升高(P0.05)。2-溴丙烷暴露使caspase-3活性增强,与对照组和1-溴丙烷组相比,平均每生精小管的阳性细胞数和caspase-3阳性百分比有明显的升高(均P0.01)。结论溴丙烷的两种同分异构体对雄性大鼠有一定的毒性,两种同分异构体可能具有不同的毒性机制,2-溴丙烷的毒性可能高于1-溴丙烷。     

1-溴丙烷引发雄性大鼠性腺基因表达谱的变化

目的研究1-溴丙烷(1-BP)诱发大鼠性腺基因表达谱的变化,探索1-BP雄性生殖毒性相关的mRNA改变。方法雄性F344/NSIc大鼠12只,随机分为2组,分别吸入新鲜空气或5030mg/m31-BP8h。染毒后16h处死大鼠取出睾丸,运用大鼠性腺cDNA微阵列和real-timePCR方法测定1-BP染毒后性腺相关基因表达谱的变化。结果在大鼠性腺芯片5087个cDNA微点阵中,有62个基因被1-BP显著下调,3个基因显著上调。其中包括性激素合成相关基因细胞色素P450芳香化酶(CYP19a),谷胱苷肽S-转移酶(GSTT1),肌酸激酶(Ckb),髓鞘和淋巴细胞蛋白(Mal)和S100的钙结合蛋白(S100a4)。归类分析结果显示绝大多数变化的基因与蛋白质/脂类代谢相关,其次与应激防御反应相关。实时定量PCR证实了1-BP可引起CYP19a、S100a4、GSTT1和Mal的下调。结论急性高剂量染毒1-BP可引起睾丸组织CYP19a、S100a4、GSTT1、Mal等基因的下调,提示其可能通过内分泌干扰和氧化应激效应而导致雄性生殖毒性。     

An experimental study on the combined effects of n-hexane and toluene on the peripheral nerve of the rat.

An electrophysiological study was undertaken to determine whether toluene affected the neurotoxicity of n-hexane. Separate groups of eight rats were exposed to 1000 ppm n-hexane, 1000 ppm toulene, 1000 ppm n-hexane plus 1000 ppm toluene, of fresh air in an exposure chamber for 12 hours a day for 16 weeks. The body weight, MCV, DL, MNCVs were measured before exposure, after four, eight 12, and 16 weeks exposure; and four weeks after exposure was discontinued. Exposure to 1000 ppm n-hexane considerably impaired the function of the peripheral nerve, but exposure to a mixture of 1000 ppm n-hexane plus 1000 ppm toluene resulted in only slight impairment; 1000 ppm toluene had little effect. These results strongly suggest that toluene decreases the toxic effects of n-hexane on the peripheral nerve.     

接触1-溴丙烷尿代谢指标动态变化特征分析

目的 研究员工接触1-溴丙烷(1-bromopropane,1-BP)后,尿总溴、N-乙酰-S-(正丙基) -L-半胱氨酸[N-acetyl-S-(n-propyl)-L-cysteine,AcPrCys]的动态变化特征。方法 检测一家光学玻璃制品公司清洗车间和对照车间员工一周内工作第1 d(W1)、第2 d(W2)、第4 d(W4)、第6 d(W6)班前和班后尿总溴和AcPrCys浓度,运用秩和检验方法进行统计分析,并绘制时间-浓度曲线图。结果 工作场所空气中1-BP浓度为45.6 mg/m³情况下,尿总溴检测浓度,对照组在32.8～948.1 μg/L之间,清洗组在127.6～3 937.0 μg/L之间。除W1班前,清洗组和对照组在不同时间班前和班后尿总溴浓度组间差异均有统计学意义(P＞0.05)。尿AcPrCys检测浓度,对照组在4.0～12.8 μg/L之间,清洗组在15.0～3 823.1 μg/L之间,清洗组和对照组在不同时间班前和班后尿AcPrCys浓度组间差异均有统计学意义(P＞0.05)。对照组尿总溴浓度检测范围较宽,清洗组尿总溴水平W4、W6班前浓度低,班后浓度高趋势明显,两者波幅最高达2.9倍。对照组尿AcPrCys浓度检测范围窄,清洗组波动较大,自W2开始班前班后浓度基本趋于稳定,两者波幅最高达1.6倍。结论 尿总溴、AcPrCys均可反映1-BP体内代谢情况,尿AcPrCys作为1-BP内接触生物性标志物更有特异性和敏感性。     

A survey on exposure level, health status, and biomarkers in workers exposed to 1-bromopropane

BACKGROUND: The aim of this study was to evaluate the health effects of exposure mainly to 1-bromopropane, which is an alternative to ozone-depleting solvents, and to establish biomarkers for assessing 1-bromopropane exposure. METHODS: Twenty-four female and 13 male workers of a 1-bromopropane-factory were interviewed, and their urine and blood samples were collected. Measured parameters included 1-bromopropane levels in the factory, as well as individual exposure levels, urinary 1-bromopropane levels, enzymatic activity and M subunit's concentration of serum creatine kinase (CK). RESULTS: Frequent symptoms reported by workers exposed to 1-bromopropane were nose, throat, and eyes irritation or malaise and/or headache. Urinary 1-bromopropane levels correlated significantly with individual exposure levels, but enzymatic activity or CK-M subunit did not. CONCLUSIONS: The symptoms suggested irritation of the mucous membrane and possible adverse effects on the central nervous system. There were no severe chronic symptoms suggestive of neurological damage in workers exposed to less than 170 ppm. Urinary 1-bromopropane level may be a good indicator of exposure. Am. J. Ind. Med. 45:63-75, 2004.     

Urinary 2,5-hexanedione increases with potentiation of neurotoxicity in chronic coexposure to n-hexane and methyl ethyl ketone

Objective: MEK (methyl ethyl ketone) is widely and frequently used as an ingredient of mixed solvents together with n-hexane. MEK is known to decrease urinary levels of 2,5-hexanedione dose-dependently in an acute or chronic coexposure with a constant level of n-hexane. This change in urinary 2,5-hexanedione appears to contradict the potentiation effect of MEK on n-hexane-induced neurotoxicity because it is believed that the toxicity of n-hexane is activated through n-hexane metabolism. We aimed to clarify how the urinary level of 2,5-hexanedione changes when MEK modifies the degree of n-hexane-induced neurotoxicity. Method: A total of 32 male Wistar rats were divided into 4 groups of 8 each and were then exposed to fresh air only, 2000 ppm n-hexane only, 2000 ppm n-hexane plus 200 ppm MEK, and 2000 ppm n-hexane plus 2000 ppm MEK, respectively. Inhalation exposures were performed 12 h/day, 6 days/week, for 20 weeks. Motor-nerve conduction velocity (MCV), distal latency (DL), and urinary 2,5-hexanedione were measured every 4 weeks. Results: The MCV decreased, the DL increased, and urinary levels of 2,5-hexanedione increased in the 2000-ppm n-hexane plus 2000 ppm MEK group in comparison with the 2000-ppm n-hexane only group following 4 weeks' exposure. On the 1st day of exposure, however, coexposure to MEK decreased urinary levels of 2,5-hexanedione dose-dependently. Conclusions: The present study showed that urinary concentrations of 2,5-hexanedione increased with potentiation of n-hexane neurotoxicity. Urinary 2,5-hexanedione concentration does not necessarily reflect the exposure concentration of n-hexane in coexposure to n-hexane along with MEK or other solvents, but it may be useful as a marker in the assessment of neurotoxicity in coexposure to n-hexane and other solvents. Received: 21 March 1997 / Accepted: 10 July 1997     

1-溴丙烷吸入暴露对雄性大鼠生殖系统的影响

目的研究1-溴丙烷亚急性暴露对雄性大鼠的生殖毒性.方法将48只雄性大鼠分为对照组、1-溴丙烷1 000、2000、4000 mg/m3暴露组.暴露组给予7 d,每天8 h的吸入暴露.结果1-溴丙烷高浓度暴露组大鼠的体重、前列腺和精囊质量显著下降,附睾精子运动率降低,形态异常精子增多.血浆肌酸激酶活力和肌型肌酸激酶含量降低.睾丸病理切片观察到曲细精管的精子释放延迟.结论1-溴丙烷亚急性暴露对雄性大鼠的生殖系统产生毒性影响,附睾精子运动率的下降是本次实验的最敏感指标.     

职业接触1-溴丙烷对女工神经系统和血液及生化学的影响

目的 探讨1-溴丙烷(1-BP)对职业接触女工健康的影响.方法 对4个1-BP生严工厂进行职业卫生现场调查.按1:1比例选取年龄配对的接触组和对照组女工各71人.作业环境中1-BP的监测运用直读式检气管和个体采样器测定.对工人进行问卷调查、神经行为学组表测试、胫神经和腓神经电生理检查、振动觉检查、血常规、血生化和激素水平检查.结果 作业环境中1-BP的浓度为0～402.40 mg/m3(平均32.19 mg/m3),工人时间加权平均接触浓度(TWA-8 h)为0.35～535.19 mg/m3(平均14.08 mg/m3).与对照组相比,1-BP接触工人的运动神经传导速度[(44.8±8.7)m/s]和感觉神经传导速度[(45.5±4.9)m/s]下降,远端潜伏期延长[(7.5±2.1)ms],足趾振动觉降低[双足音叉振动延迟时间分别为(6.2±4.4)和(5.7±4.4)s],神经行为学POMS量表中愤怒情绪得分增高(21.0±5.5),紧张、疲劳、迷茫情绪得分降低(7.8±5.5、5.6±4.1、6.1±3.8),差异均有统计学意义(P＜0.05).与对照组比较,接触组白细胞[(5.6±2.17)×103/μl]、红细胞[(3.9±0.4)×106/μl]、血红蛋白[(121.1±14.5)g/L]和肌酸磷酸激酶[(82.0±27.5)IU/L均明显降低,差异有统计学意义(P＜0.05),血清总蛋白[(8.0±0.5)g/dl]、乳酸脱氢酶[(335.2±356.6)IU/L]、促甲状腺激素[(3.6±2.3)μIU/ml]和尿促卵泡素水平[(18.7±24.4)mIU/ml]明显上升,差异有统计学意义(P＜0.05).结论 1-BP接触可能影响外周神经和中枢神经系统,并引起血液及生化学指标的异常.     

1-溴丙烷职业接触限值研究进展

1-溴丙烷是消耗臭氧层的化学物—氟利昂类物质的替代物,随着近年在工业上的广泛应用,不断出现职业中毒的个案报道。本文就1-溴丙烷的毒性以及国外对其职业接触限值的研究进展作一简要综述,为今后国内制定1-溴丙烷的职业接触限值提供参考。