五味子乙素对汞性大鼠急性肾损伤的影响

目的探讨五味子乙素(Sch B)对汞致大鼠急性肾损伤的影响。方法 Wistar大鼠30只,按体重随机分成5组:第1组为正常对照组,第2~4组分别为低、中、高剂量单纯染汞组,第5组为Sch B预处理组。对照组和单纯染汞组空腹以大豆油灌胃,Sch B预处理组16 mg/kg Sch B空腹灌胃,灌胃容量为5 ml/kg;2 h后,对照组皮下注射生理盐水,低、中、高剂量单纯染汞组分别皮下注射2.2μmol/kg、4.4μmol/kg、8.8μmol/kg氯化汞,Sch B预处理组皮下注射8.8μmol/kg氯化汞,注射容量为5 ml/kg。第二日重复上述操作,并将大鼠放入代谢笼,收集24 h尿液;而后将大鼠乙醚麻醉,腹主动脉采血,切取大鼠肾皮质,测定尿汞和肾皮质汞,尿β-N-乙酰氨基葡萄糖苷酶(NAG)、尿乳酸脱氢酶(LDH)及尿碱性磷酸酶(ALP)活力,尿蛋白和血尿素氮(BUN)含量,肾皮质还原型谷胱甘肽(GSH)和丙二醛(MDA)含量,超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)活力。结果与对照组比较,高剂量氯化汞组尿汞和肾皮质汞含量,尿NAG、LDH及ALP活力,尿蛋白和BUN含量,GSH和M...     

沙棘油对镉致大鼠肝损伤的拮抗作用

目的 探讨沙棘油(SBO)对急性、亚慢性染镉致大鼠肝损伤的拮抗作用.方法 急性实验时,对照组和染镉组均灌胃0.9%NaCl,SBO干预组灌胃5 ml/kg SBO(纯度为95%).2 h后,对照组皮下注射0.9%NaCl,SBO干预组和染镉组皮下注射35 μmol/kg CdCl2.亚慢性实验时,染镉组和SBO干预组皮下注射6μmol/kg CdCl2,对照组皮下注射0.9%NaCl,连续6周.然后SBO干预组灌胃5 ml/kg SBO,对照组和染镉组灌胃0.9%NaCl,共2周.腹主动脉取血并取肝脏,测定急性、亚慢性染镉大鼠血清乳酸脱氢酶(LDH)、谷丙转氨酶(GPT)活力,肝丙二醛(MDA)、谷胱甘肽(GSH)含量及超氧化物歧化酶(SOD)活力.结果 急性、亚慢性镉染毒使大鼠血清LDH、GPT活力明显升高,肝MDA、GSH含量明显升高及SOD活力明显降低.SBO干预组可使急性染镉大鼠血清LDH、GPT活力,肝MDA、GSH含量分别降至单纯染镉组的71.5%(183.77,257.02)、58.3%(15.83,27.13)和74.8%(88.49,118.27)、64.9%(6.81,10.49),差异有统计学意义(P<0.01),肝SOD活力明显升高.亚慢性染镉时,SBO处理组血清GPT活力明显低于单纯染镉组,肝MDA、GSH含量明显下降,肝SOD活力明显升高,差异有显著性(P<0.01).结论 SBO对急性、亚慢性镉染毒致大鼠肝氧化损伤有一定的拮抗作用.     

茶多酚对氯化汞染毒大鼠急性肾损伤的影响

目的探讨茶多酚(tea polyphenols,TP)对氯化汞染毒大鼠急性肾损伤的影响。方法将30只成年清洁级Wistar大鼠按体重随机分为5组,分别为对照(豆油)组,2.2、4.4、8.8μmol/kg氯化汞单独染毒组和TP(500 mg/kg)+氯化汞(8.8μmol/kg)染毒组,每组6只,雌雄各半。对照组和各氯化汞单独染毒组空腹以豆油灌胃,TP+氯化汞染毒组空腹灌胃500mg/kg TP溶液,灌胃容量为5 ml/kg,2 h后,TP+氯化汞染毒组和各氯化汞单独染毒组皮下注射染毒氯化汞,对照组注射生理盐水,染毒容量为5 ml/kg;每天染毒1次,连续染毒2 d。染毒结束后,检测尿汞、肾皮质汞含量,尿β-N-乙酰氨基葡萄糖苷酶(NAG)、尿乳酸脱氢酶(LDH)、尿碱性磷酸酶(ALP)活力,尿蛋白、血尿素氮(BUN)含量,肾皮质还原型谷胱甘肽(GSH)、丙二醛(MDA)含量,超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)活力。结果随着氯化汞染毒剂量的升高,大鼠尿汞、肾皮质汞含量,尿NAG、LDH、ALP活力,尿蛋白、血BUN含量,肾皮质GSH、MDA含量均呈上升趋势,肾皮质SOD和GSH-Px活力均呈下降趋势。与8.8μmol/kg氯化汞单独染毒组比较,TP+氯化汞染毒组大鼠尿NAG、LDH、ALP活力,尿蛋白、血BUN含量,肾皮质GSH、MDA含量均下降,肾皮质GSH、MDA含量和SOD、GSH-Px活力均上升,差异有统计学意义(P0.01);而尿汞、肾皮质汞含量间差异无统计学意义。结论 TP预处理对汞致大鼠急性肾损伤有一定的拮抗作用。     

莱菔硫烷对镉致大鼠肾脏损伤的保护作用

目的探讨亚慢性染镉对大鼠的肾脏毒性及莱菔硫烷(SFN)的保护作用。方法 Wistar大鼠32只,按体重随机分为对照组、低剂量和高剂量单纯染镉组、莱菔硫烷干预组,每组8只。对照组和低、高剂量单纯染镉组大鼠皮下注射生理盐水,SFN干预组大鼠皮下注射1 mg/kg SFN;2 h后,对照组腹腔注射生理盐水,其他三组分别腹腔注射3、6、6μmol/kg氯化镉。皮下注射隔日1次,每周3次;腹腔注射每日1次,每周5次;连续处理6周。将大鼠放入代谢笼,收集24 h尿液,测定尿蛋白含量和碱性磷酸酶(ALP)、β-N-乙酰氨基葡萄糖苷酶(NAG)和乳酸脱氢酶(LDH)活力;然后将大鼠乙醚麻醉,腹主动脉采血测定大鼠血清尿素氮(BUN)含量;切取大鼠肾皮质,测定肾皮质还原型谷胱甘肽(GSH)、丙二醛(MDA)含量和超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活力。结果与对照组比较,高剂量单纯染镉组尿蛋白和血清BUN含量及尿NAG、LDH和ALP活力明显上升(P0.01);肾皮质中GSH含量、SOD和GSH-Px活力显著降低(P0.01);MDA含量升高(P0.01)。与高剂量单纯染镉组比较,SFN干预组尿蛋白和血清BUN,尿NAG、LDH和ALP活力及肾皮质MDA含量下降;GSH-Px和SOD活力上升;差异均有统计学意义(P0.05或P0.01)。结论给大鼠亚慢性染镉可引起明显的肾脏损伤,SFN对镉致大鼠肾脏损伤有一定的保护作用。     

α-硫辛酸和牛磺酸对亚慢性镉染毒致肾损伤影响的实验研究

目的通过观察α-硫辛酸(LA)和牛磺酸(Tau)对亚慢性镉染毒致肾损伤的影响,探讨氧化损伤在镉中毒中的作用。方法实验用大鼠32只,分为4组。给3个实验组大鼠皮下注射7μmol/kg的氯化镉(CdCl2)溶液,每周5次,连续6周。对照组大鼠在相应时间皮下注射生理盐水。于第7周、第8周,两干预组大鼠分别腹腔注射35μmol/kg的LA溶液和0.8 mmol/kg的Tau溶液,对照组和单纯镉染毒组在相应时间内腹腔注射生理盐水。注射容量均为5 ml/kg,每周5次。最后1次注射后,收集大鼠12 h尿液,然后处死大鼠,切取肝、肾组织。测定尿N-乙酰-β-D氨基葡萄糖苷酶(NAG)、碱性磷酸酶(ALP)活力及尿肌酐、尿蛋白和尿镉含量,肝和肾皮质镉、丙二醛(MDA)、谷胱甘肽(GSH)含量及谷胱甘肽过氧化物酶(GSH-Px)和超氧化物歧化酶(SOD)活力。结果与对照组比较,单纯镉染毒组的肝、肾皮质和尿中镉含量显著增加,尿ALP和NAG酶活力及尿蛋白含量显著升高,肾皮质GSH和MDA含量升高到34.65μg/g蛋白和171.05 nmol/g蛋白,GSH-Px活力下降到0.23 U/mg蛋白,差异有显著性。肝GSH含量升高,SOD和GSH-Px活力均显著下降。与单纯镉染毒组比较,LA干预组的尿镉含量、尿ALP活力和尿蛋白含量显著下降,肾皮质GSH和MDA含量降低到19.72μg/g蛋白和127.47 nmol/g蛋白,GSH-Px活力升高到0.30 U/mg蛋白,肝GSH-Px和SOD活力显著升高;Tau干预组的肝膈和尿镉含量均显著降低。肾皮质GSH含量降低到26.36μg/g蛋白,GSH-Px活力升高到0.37 U/mg蛋白。结论氧化损伤是镉中毒机制的一部分,LA和Tau对镉致肾氧化损伤的恢复具有一定的促进作用。     

N-乙酰半胱氨酸和α-硫辛酸对汞急性肾功能损伤的影响

为探讨N-乙酰半胱氨酸(NAC)和α-硫辛酸(LA)对汞急性肾功能损伤的影响,将32只Wistar大鼠随机分成4组:对照组、单纯染汞组、NAC干预组、LA干预组。单纯染汞组先腹腔注射生理盐水,2 h后,皮下注射HgCl2溶液9.2μmol/kg。NAC和LA干预组先分别腹腔注射NAC溶液2 mmol/kg及LA溶液0.35 mmol/kg,2 h后,皮下注射HgCl2溶液。对照组在相应时间内注射生理盐水。染毒后12 h将鼠移至代谢笼中收集12 h尿样,染毒后48 h腹主动脉取血并切取肾脏,测定尿碱性磷酸酶(ALP)、乳酸脱氢酶(LDH)、N-乙酰-β-D-氨基葡萄糖苷酶(NAG)活性,尿蛋白、血清尿素氮(BUN)含量及尿和肾皮质中汞含量。与对照组比较,单纯染汞组尿汞、肾皮质汞含量,尿ALP、LDH、NAG活性,尿蛋白、BUN含量显著升高;NAC干预组尿汞、肾皮质汞含量及LA干预组肾皮质汞含量明显升高。与单纯染汞组比较,LA干预组尿汞含量显著降低,肾皮质汞含量明显升高;两干预组尿ALP、LDH、NAG活性及尿蛋白、BUN含量显著降低。说明NAC和LA预处理对汞急性肾功损伤有一定的保护作用,但对LA改变汞组织分布应进一步研究。     

亚硒酸钠对急性和亚慢性镉毒性的拮抗作用

目的探讨急性、亚慢性镉染毒对大鼠的肝、肾毒性以及亚硒酸钠(Na2SeO3)对镉染毒大鼠肝、肾毒性的拮抗作用。方法急性实验时,Na2SeO3干预组大鼠以10μmol/kg腹腔注射Na2SeO3溶液,对照组和镉染毒组腹腔注射0.9%氯化钠。2 h后,干预组和镉染毒组大鼠皮下注射氯化镉(CdCl2)溶液35μmol/kg,对照组皮下注射0.9%氯化钠。亚慢性实验时,大鼠皮下注射CdCl2溶液7μmol/kg,每周5 d,1次/d,连续6周。然后Na2SeO3干预组大鼠腹腔注射Na2SeO3溶液10μmol/kg,共2周,对照组在相同时间注射0.9%氯化钠。测定大鼠血清、尿液和肝、肾组织中各酶的活力。结果急性镉染毒使大鼠血清乳酸脱氢酶(LDH)、丙氨酸转氨酶(ALT)活力明显升高,肝谷胱甘肽(GSH)、丙二醛(MDA)含量明显升高,谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)活力明显下降。Na2SeO3预处理可使急性镉染毒大鼠血清ALT、LDH活力分别降低至单纯镉染毒组的63.8%(166.61,261.11)和30.1%(40.85,135.52),差异有统计学意义(P<0.01),肝GSH、MDA含量明显降低,而GSH-Px、SOD活力明显升高。亚慢性镉染毒使大鼠尿碱性磷酸酶(ALP)、N-乙酰-β-苷酶(NAG)活力和尿蛋白含量明显升高,肾皮质GSH、MDA含量明显升高,GSH-Px活力明显降低。Na2SeO3处理使亚慢性镉染毒大鼠尿ALP酶活力明显下降,肾皮质GSH、MDA含量明显降低,GSH-Px活力明显升高。结论Na2SeO3对急性镉染毒所致肝损伤具有明显的保护作用,对亚慢性镉染毒致肾损伤的恢复具有一定的促进作用。     

莱菔硫烷对汞致大鼠肾急性损伤的保护作用

目的 探讨莱菔硫烷(sulforaphane,SFN)对莱菔硫烷(sulforaphane,SFN)所致大鼠急性肾损伤的保护作用。 方法 清洁级Wistar大鼠30只按体重随机分5组,每组6只,分别为对照组,低、中、高剂量染汞组, SFN干预组。对照组及各染汞组皮下注射生理盐水,SFN干预组皮下注射2 mg/kg SFN;2 h后,对照组腹腔注射生理盐水,其他四组腹腔注射2.2、4.4、8.8、8.8 μmol/kg HgCl₂,连续3 d,染毒容量均为5 ml/kg。于最后一次染毒结束后,测定尿液中Hg及尿蛋白含量,碱性磷酸酶(ALP)、乳酸脱氢酶(LDH)和β-N-乙酰氨基葡萄糖苷酶(NAG)活力;腹主动脉采血测定血清尿素氮(BUN)含量;测定肾皮质中Hg含量和谷胱甘肽(GSH)、丙二醛(MDA)水平及超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活力。分析各组各项指标差异。 结果 与对照组比较,各剂量染汞组大鼠尿Hg、肾皮质Hg含量,尿蛋白和血清BUN 含量,尿NAG、LDH 和ALP 活力,肾皮质中GSH 和MDA含量显著升高(P<0.05或P<0.01);肾皮质SOD 和GSH-Px 活力显著降低(P<0.05或P<0.01)。与8.8 μmol/kg HgCl₂组比较,SFN 干预组尿蛋白和血清BUN 含量、尿NAG、LDH 和ALP活力、肾皮质GSH 、MDA含量均显著下降(P<0.05或P<0.01);肾皮质SOD 和GSH-Px 活力显著升高(P<0.01),而尿汞、肾皮质汞含量间差异无统计学意义(P>0.05)。 结论 莱菔硫烷对汞所致大鼠急性肾毒性有一定的保护作用。     

异搏定和氯丙嗪对镉慢性肾毒性影响的实验研究

目的:对慢性镉染毒(Cd)大鼠投予异搏定(Ver)和氯丙嗪(CPZ),探讨这两种物质对镉慢性肾损伤的影响。方法:实验用4组大鼠,单纯镉染毒组和Ver、CPZ预处理组均皮下注射含Cd 1．4mg／kg的氯化镉(CdCl2)溶液,每周3次,连续6周。Ver和CPZ预处理组在每次皮下注射CdCl2前1h,分别向腹腔注射Ver 4mg／kg和CPZ 5mg／kg,,对照组大鼠在相同时间注射生理盐水5ml／kg,,在实验开始后第2,4,6周时收集尿样,测定尿N-乙酰-B—D-氨基葡萄糖苷酶(NAG)活力和尿蛋白含量。最后一次注射后24h处死大鼠,采集血液,取肾脏,测定血清尿素氮(BUN),血、肾皮质和尿中的Cd、Ca及血、肾皮质中丙二醛(MDA)含量。结果镉染毒4周时,与单纯镉染毒组比较,Ver和CPZ预处理组的尿NAG活力和尿蛋白含量均明显降低;镉染毒6周时,Ver和CPZ预处理组的血Cd、血清BUN、尿Ca及肾皮质MDA含量均明显降低。CPZ预处理组肾皮质Cd和血MDA含量也明显降低。结论:Ver和CPZ具有防止镉所致慢性肾损伤的作用,其机制可能是减轻镉对肾脏的脂质过氧化损伤。     

2-氨基-4-(S-丁基磺酰亚氨)丁酸对汞急性毒作用影响的实验研究

目的　研究 2 -氨基 - 4 - (S -丁基磺酰亚氨 )丁酸 (BSO)对汞急性毒作用的影响 ,探讨汞的毒作用机制。方法　 32只Wistar大鼠随机分成 4组 :对照组 ,皮下注射生理盐水 ;汞染毒 1组和 2组 ,分别皮下注射HgCl2 溶液 (0 75 ,1 5mg/kg) ;BSO预处理组 ,腹腔注射BSO (0 5mmol/kg) ,4h后皮下注射HgCl2 溶液 (0 75mg/kg)。测定肝、肾皮质和尿中汞含量 ,尿N -乙酰 - β -D氨基葡萄糖苷酶 (NAG)、碱性磷酸酶 (ALP)、乳酸脱氢酶 (LDH)活力和蛋白含量 ,肝和肾皮质谷胱甘肽 (GSH)和丙二醛 (MDA)含量。结果　对照组、汞染毒 1组和 2组尿NAG活力分别为 4 3 6 5 ,6 1 0 6 ,89 2 7U/ gCr ,尿ALP活力分别为2 4 5 2 ,6 2 98,93 0 5U/ gCr,尿LDH活力分别为 0 85 ,6 5 0 ,18 17U/ gCr,尿蛋白含量分别为 0 77,1 2 1,2 2 9mg/ gCr,肾皮质GSH含量分别为 9 0 0 ,12 96 ,16 0 2 μmol/ g蛋白 ,肾皮质MDA含量分别为10 2 2 2 ,12 5 99,2 0 6 34nmol/ g蛋白。BSO预处理组尿NAG、ALP、LDH活力和蛋白含量明显高于对照组和汞染毒 1组 (P <0 0 5 ) ,肝、肾皮质GSH含量明显低于汞染毒 1组 (P <0 0 5 ) ,肝脏MDA含量高于对照组 (P <0 0 5 )和汞染毒 1组 ,肾皮质MDA含量明显高于对照组和汞染毒 1组 (P <0 0 5 )。结论　BS     

Self-reported health problems among Swedish miners one year after unemployment

Unemployment is considered to be a public health concern sincedeterioration in the health of the unemployed is often anticipated.However, for some groups, such as miners, unemployment mightimprove health due to a cessation of potentially harmful occupationalexposures. This study evaluates the health of 79 miners in oneSwedish iron-ore mine, and 226 age-matched controls from thegeneral population, during one year after the closure of themine. The participants received a questionnaire regarding medicalhistory and subjective symptoms at the beginning of the studyperiod, and after one year. Statistically significant negativeeffects on self-reported health attributable to unemploymentwere not found, although neuropsychiatric symptoms were morecommon among the unemployed miners. The miners reported a statisticallysignificant improvement in grip force (p=0.031). They had asignificantly higher prevalence of symptoms associated withmining related exposures when compared with the population controls;pain in the upper extremities [relative risk (RR)=2.27, 95%confidence interval (Cl)=1.44–3.59), back pain (RR=1.84;Cl=1.237–2.75), vasospastic disease of the fingers (RR=2.05;Cl=1.18–3.57) and obstructive respiratory symptoms (attacksof dyspnea and wheezing: RR=3.67; Cl=1.167–11.6).     

Excès de cas humains et animaux de tularémie en France au cours de l’hiver 2007–2008 : émergence ou phénomène isolé ?

Context

Tularemia is a zoonosis affecting humans and hares in France. We describe the results of surveillance in both species, in 2007 and 2008.

Methods

Human tularemia cases are mandatorily notifiable in France since 2003. In hares, surveillance relies on volunteer hunter associations in all districts of the country. Data from mandatory reports and volunteer surveillance in 2007/2008 were analyzed and compared with previous results.

Results

In 2007/2008, 144 cases were reported in humans and 117 cases in hares. This was a 100% increase compared to previous years. Human cases differed from those of previous years only by the frequency of contact with breeding animals. Human cases without any documented risk exposure were also more frequent.

Conclusion

An increase of tularemia cases occurred in 2007/2008 in both species. Complementary studies are needed to identify the species reservoir in France to understand the causes of this peak of cases.     

Occupational health hazards in mining: an overview

This review article outlines the physical, chemical, biological, ergonomic and psychosocial occupational health hazards of mining and associated metallurgical processes. Mining remains an important industrial sector in many parts of the world and although substantial progress has been made in the control of occupational health hazards, there remains room for further risk reduction. This applies particularly to traumatic injury hazards, ergonomic hazards and noise. Vigilance is also required to ensure exposures to coal dust and crystalline silica remain effectively controlled.     

Manufacture and use of nanomaterials: current status in the UK and global trends

This paper provides an overview of the production and use of nanomaterials (NMs), particularly in the UK. Currently, relatively few companies in the UK are identifiable as NM manufacturers, the main emphasis being the bulk markets in metals and metal oxides, and some niche markets such as carbon nanotubes and quantum dots. NM manufacturing in the UK does not reflect the global emphasis on fullerenes, nanotubes and fibres. Some assumptions have been made about the types of NM that are likely to be imported into the UK, which currently include fullerenes, modified fullerenes and other carbon-based NMs including nanotubes. Many university departments, spin-offs and private companies have developed processes for the manufacture of NMs but may only be producing small quantities for research and development (R&D) purposes. However, some have the potential to scale up to produce large quantities. The nanotechnology industry in the UK has strong R&D backup from universities and related institutions. This review has covered R&D trends at such institutions, and appropriate information has been added to a searchable database. While several companies are including NMs in their products, only a few (e.g. manufacturers of paints, coatings, cosmetics, catalysts, polymer composites) are using nanoparticles (NPs) in any significant quantities. However, this situation is likely to change rapidly. There is a need to collect more information about exposure to NPs in both manufacturing and user scenarios. As the market grows, and as manufacturers switch from the micro- to the nanoscale, the potential for exposure will increase. More research is required to quantify any risks to workers and consumers.     

Investigating clusters in the workplace and beyond

Clusters of disease are common and occur in the workplace and in the general community. They often arouse considerable concern among the population. Investigations have sometimes lead to exciting new knowledge, but in general the investigation of clusters is difficult and often unrewarding, especially for community clusters. In the workplace, investigations are more likely to find associations and even new causes, but still many clusters remain enigmatic. Despite this, there are many reasons for investigating clusters, including allaying community concern and identifying uncontrolled exposures. A structure for investigating clusters in the workplace is suggested.     

Assessing occupational and environmental exposure

Exposure assessment is a poorly understood component of the science of epidemiology. The relationship between exposure to chemicals and ill-health outcomes is often calculated using crude exposure measures such as ever/never exposed or duration. When investigating subtle effects, exposures need to be characterized much more fully in terms of intensity, frequency, duration and route. While occupational exposures tend to be much greater than those experienced from the wider environment there is a need to remember that, for many chemicals, exposure can occur occupationally, environmentally and through consumer use of products containing the material of interest. Inhalation exposure has generally been the traditional focus for most epidemiological investigations but there is now growing awareness of the importance of the dermal and ingested routes of contact and internalization. Quantification of the exposure also needs to be related to a biological mechanism of action and exposure metrics need to be selected accordingly. Occupational exposures can generally be measured using simple well-validated techniques. Environmental exposures require much more sensitive instruments and are more difficult to assess. Exposure modelling, particularly for the environmental fate of chemicals has undergone many recent developments and Monte Carlo techniques can be used to characterize model uncertainty and variability. This approach to exposure assessment can now be used in the setting of the wider environment and will enable a far better understanding of the relationship between exposure and disease.     

Mercury toxicity due to the smelting of placer gold recovered by mercury amalgam

A 19-year-old man developed tremor in both hands and fatigue after starting work at a placer gold mine where he was exposed to mercury-gold amalgam. Examination revealed an intention tremor, dysdiadochokinesis and mild rigidity. The 24-h urinary mercury concentration reached a peak of 715 nmol/l (143 ug/l) shortly before the clinical examination, after which he was removed from working in the gold room [Mercury No. Adverse Effect Level: 250 nmol/l (50 ug/l)]. On review 7 weeks later his tremor had almost resolved and the dysdiadochokinesis and rigidity had gone. The 24-h urinary mercury concentration had fallen to 160 nmol/l (32 ug/l). The principal exposure to mercury was considered to be the smelting of retorted gold with previously unrecognized residual mercury in it. The peak air concentration of mercury vapour during gold smelting was 0.533 mg/m3 (Mercury Vapour ACGIH TLV: 0.05 mg/m3 TWA). Several engineering and procedural controls were instituted. This episode occurred at another mine site, unrelated to Mount Isa Mines Limited.     

How Adults with Acquired Brain Damage Perceive Computer Training as a Rehabilitation Tool: A Focus-group Study

The aim of this study was to explore and describe how adult outpatients with acquired brain damage and referred to occupational therapy perceive computer training with the RehaCom programs, in order to evaluate the method of treatment as a tool in the rehabilitation of persons with cognitive disorders. By using focus-group discussions as a qualitative method of research when analysing the result, five themes with corresponding categories emerged, describing a development of understanding and learning about capacities. Themes describing how the participants could apply strategies to overcome shortcomings in daily occupations and the therapeutic role of the occupational therapist were identified as well. The result shows that a computer training program such as RehaCom can be used as an educational tool, for example, to guide a person who is trying to adopt compensatory strategies to avoid overload by taking pauses. It was found that anything the participants learned was also applicable to occupational performance in daily life.