职业性肌肉骨骼损伤疾患的生物标志物

职业性肌肉骨骼损伤（OccupationalMusculoskeletalInjury）是一类与工作有关的疾患，它包括肌肉骨骼系统各个部位损伤与症状。近几十年来，与职业有关的慢性肌肉骨骼损伤疾患问题日趋突出。据前西德统计，因此类疾患造成的缺勤占整个工业缺勤天数的15％～22％“‘。加拿大每年因肌肉骨骼损伤疾患而导致的直接和间接经济损失高达996亿美元D‘。国内研究报道我国机械工人的职业性慢性肌肉骨防损伤患病率达到了64％［’j。利用生物标志物（Biomarker）来检测亚临床肌肉骨骼损伤，监测个体和群体肌肉骨骼损伤状况的可能性正越来越受到各国职…     

职业性肌肉骨骼损伤疾患研究

因工作引起的肌肉骨骼损伤性疾患骼,是一种常见的职业性多发病.目前在一些国家已成为主要的职业健康问题,欧美等国将其列入职业病范畴.由于各作业性质、劳动方式、劳动强度、劳动条件等的不同,肌肉骨骼损伤的好发部位各国报道不一,主要以腰背部、肩颈、手臂为主.可分为下背痛、腕管综合症及颈肩腕综合症等3大类.这类疾病在工业发达国家职业病发生中占第2位,并且是影响工作年龄组人员劳动能力的主要原因,并且已引起特别的关注.     

缝纫工职业性慢性肌肉骨骼损伤调查

对从事流水作业缝纫工２０７人和对照组１２７人进行了健康调查。对其作业体位，人－机测量，劳动强度和工作环境有关因素监测，应用计算机ＳＡＳ语言进行统计分析。结果表明：从事流水作业的缝纫工慢性肌肉骨骼损伤的症状以下背疼痛，双上肢和双肩疼痛最为明显。参考两组人－机测量所得的数据，建议坐位工作人员工作台与工作椅高度之差除以身高值，宜在０．２０ｃｍ左右，座椅高度除以高身值，宜在０．２６ｃｍ左右。     

243 职业性肌肉骨骼损伤与生物力学研究

职业性肌肉骨骼损伤是当今最常见的职业相关疾患之一，国内外均有大量研究。本文对肌肉骨骼损伤的流行病学状况及可能的危险因素，生物力学在肌肉骨骼损伤研究和预防中的应用等做了简要综述。     

管道焊接工职业性肌肉骨骼损伤的调查

大口径管道运输为石油、天然气的主要设施.在管道铺设过程中,焊接工多采取强迫体位作业,其中以俯、蹲、仰位为主,其职业性慢性肌肉骨骼损伤（CMI）患病率较高.我们对正在建设中的长距离天然气输送工程“陕京二线”焊接工职业性CMI的发生情况进行了横断面调查.     

缝纫工职业性慢性肌肉骨骼损伤调查

对从事流水作业缝纫工207人和对照组127人进行了健康调查。对其作业体位、人-机测量、劳动强度和工作环境有关因素监测,应用计算机SAS语言进行统计分析。结果表明:从事流水作业的缝纫工慢性肌肉骨骼损伤的症状以下背疼痛、双上肢和双肩疼痛最为明显。参考两组人-机测量所得的数据,建议坐位工作人员工作台与工作椅高度之差除以身高值,宜在0.20cm左右,座椅高度除以身高值,宜在0.26cm左右。     

南昌市三级医院护理人员职业性肌肉骨骼损伤现状调查

目的了解南昌市三级医院护士职业性肌肉骨骼损伤的现状并分析其影响因素,为进一步制定针对性干预措施提供参考依据。方法采用方便抽样法,于2019年2—3月采用一般资料问卷、护士职业性肌肉骨骼损伤症状自评问卷对南昌市4所三级医院1 284名临床护士进行调查,并对数据进行分析。结果南昌市三级医院护理人员职业性肌肉骨骼损伤患病人数为1 037例,患病率为80.76%,≥2个部位患病人数为948例,患病率为73.83%。年龄、低头工作时间、工作弯腰时间、日均搬运患者频次、工作强度、工作环境舒适度及防护措施是护理人员职业性肌肉骨骼损伤的主要影响因素(均P<0.05)。结论南昌市三级医院护士职业性肌肉骨骼损伤发病率高,护理管理者应根据影响因素采取针对性干预措施,降低职业性肌肉骨骼损伤患病率,提升护理人员身心健康,促进护理队伍健康发展。     

职业性慢性肌肉骨骼损伤早期诊断手段探讨

职业性慢性肌肉骨骼损伤早期诊断手段探讨北京医科大学劳动卫生教研室（１０００８３）牛云彤（综述）王生（审校）随着工作和生产自动化、专一化程度的提高，与职业有关的慢性肌肉骨骼损伤问题日趋突出，引起许多国家重视。世界劳工组织已认可肩颈痛为职业病；美国确认职...     

Occupational liver injury

Summary Epidemiological studies have mapped the occurrence of hepatitis B among health personnel with the use of specific serologic markers and thereby made rational preventive precautions possible. Follow-up studies have demonstrated the effect of this prevention, and the newly developed hepatitis B vaccine has further improved the possibilities for effective prophylaxis against occupational hepatitis B. On the other hand, there is the chemically induced occupational liver damage. Only a few of the thousands of industrially used chemicals have been sufficiently investigated for hepatotoxicity and the list of suspected and confirmed hepatotoxic agents is still growing. The worrisome example of vinylchloride-induced serious liver disease among PVC-workers, revealed after 42 years of industrial use by alert clinicians, calls for intensified activities in the field of occupational hepatotoxicity. However, the clinical, biochemical, and morphological features of liver disease are often vague and unspecific. A non-invasive, convenient quantitative liver function test is needed. Circumstantial evidence and a few epidemiological studies suggest that part of the so-called cryptogenic liver diseases, such as liver cirrhosis, may be caused by occupational exposure to chemicals. This should be further studied. Animal experiments have shown that one chemical agent may potentiate the hepatotoxic effect of another chemical agent. This should be the subject of investigations in the work environment, where exposure to various chemicals is the rule rather than the exception. Alcohol consumption may also interfere with the hepatotoxicity of occupationally used chemicals.     

Occupational chronic exposure to metals

Summary Stainless steel welders (n = 103) were examined. To estimate external exposure, personal air sampling was used. Internal exposure was quantified by the determination of nickel levels in erythrocytes, plasma and urine. Men and women (n = 123) were examined for control purposes. In the plasma and erythrocytes of the controls the nickel concentration was below the level of detection (< 1.81 μg/l). The element concentrations in urine were between < 0.1 and 13.3 μg/l. Of the controls 95% showed nickel levels in urine below 2.2 μg/l (reference value). The average concentration of nickel in the air was 93 ± 81 μg/m³. The average concentration of nickel in the plasma samples was 4.9 ± 4.0 μg/l (95th percentile 12.8 μg/L). In erythrocytes nickel could not be detected. The nickel concentrations in the urine of the welders were 18.5 ± 28.5 μg/l on average (95th percentile 52.5 μg/l). Only a weak correlation between the nickel levels of plasma and urine could be detected (C_urine = 2.07 + 8.45 C_plasma; r = 0.294; p < 0.01). Based on our results and on the reported literature a future limit value for the nickel concentration in urine should lay between 30 and 50 μg/l. This value corresponds to an external exposure of 500 μg nickel per cubic metre.     

Occupational chronic exposure to metals

Summary External and internal chromate exposure of 103 stainless steel welders who were using manual metal arc welding (MMA), metal inert gas welding (MIG) and both methods, were measured by ambient and biological monitoring. At the working places the maximum chromium trioxide concentrations were 80 g/m³. The median values were 4 g/m³ (MMA) and 10 g/m³ (MIG). The median chromium concentrations in erythrocytes, plasma and urine of all welders were < 0.60, 9.00 and 32.50 g/l. For biological monitoring purposes, chromium levels in erythrocytes and simultaneously in plasma seem to be suitable parameters. According to our results, chromium levels in plasma and urine in the order of 10 and 40 g/l seem to correspond to an external exposure of 100 g chromium trioxide per cubic metre, the technical guiding concentration (TRK-value). Chromium concentrations in erythrocytes greater than 0.60 g/l indicate an external chromate exposure greater than the TRK-value.     

Occupational chronic exposure to metals

Stainless steel welders (n = 103) were examined. To estimate external exposure, personal air sampling was used. Internal exposure was quantified by the determination of nickel levels in erythrocytes, plasma and urine. Men and women (n = 123) were examined for control purposes. In the plasma and erythrocytes of the controls the nickel concentration was below the level of detection (less than 1.8 micrograms/l). The element concentrations in urine were between less than 0.1 and 13.3 micrograms/l. Of the controls 95% showed nickel levels in urine below 2.2 micrograms/l (reference value). The average concentration of nickel in the air was 93 +/- 81 micrograms/m3. The average concentration of nickel in the plasma samples was 4.9 +/- 4.0 micrograms/l (95th percentile 12.8 micrograms/l). In erythrocytes nickel could not be detected. The nickel concentrations in the urine of the welders were 18.5 +/- 28.5 micrograms/l on average (95th percentile 52.5 micrograms/l). Only a weak correlation between the nickel levels of plasma and urine could be detected (Curine = 2.07 + 8.45 Cplasma; r = 0.294; p less than 0.01). Based on our results and on the reported literature a future limit value for the nickel concentration in urine should lay between 30 and 50 micrograms/l. This value corresponds to an external exposure of 500 micrograms nickel per cubic metre.