Lucchini R, Placidi D, Toffoletto F, Alessio L
Institute of Occupational Health, University of Brescia, Italy.
Int Arch Occup Environ Health. 1996;68(3):188-92. doi: 10.1007/BF00381630.
Occupational exposure to high concentrations of anesthetic gases (more than 500 ppm of nitrous oxide and more than 15 ppm of halothane and enflurane) can cause neurobehavioral effects in operating room personnel. Factors such as stress and work organization play an additional role in reducing performance capacities. It is still unclear whether these conditions may become the predominant factor in behavioral impairment when exposure to anesthetic gases is reduced; in addition, we wished to ascertain the extent of neurobehavioral and neuroendocrine effects at relatively low levels of exposure to such gases. Therefore the same group of 30 operating room personnel was examined with neurobehavioral tests during gaseous and nongaseous anesthesia. In this way, the neuropsychological performance was examined under the same stress conditions, but with different exposure levels to anesthetic gases. Serum cortisol was measured as an additional "biological stress indicator." Prolactin secretion was examined to study possible interference of anesthetic gases with the dopaminergic system. The results were compared with those in a control group of 20 hospital workers from other departments, with similar characteristics in respect of age, sex, and education. During work with gaseous anesthesia, average airborne concentrations (geometric mean) of nitrous oxide were 50.9 ppm (SD 20.8) on the first day of the working week, and 54.2 ppm (SD 22.1) on the last day of the working week, whereas average urinary nitrous oxide (geometric mean) were 21.54 micrograms/l on the first day of the working week and 25.67 micrograms/l on the last day of the working week. The operating room workers showed slower reaction times at the end of the week with gaseous anesthesia, compared with workers using nongaseous anesthesia and the control group. At the same time they also showed increased secretion of prolactin, whereas cortisol remained unchanged. Therefore, it can be concluded that lower levels of exposure to anesthetic gases (and not only high exposure levels) cause an impairment of neurobehavioral performance, with the action of stress being less relevant. The mechanism of anesthetics' neurotoxic action seems to be related to interference with the dopaminergic system.
职业性接触高浓度麻醉气体（氧化亚氮超过500 ppm，氟烷和恩氟烷超过15 ppm）可导致手术室工作人员出现神经行为效应。压力和工作组织等因素在降低工作能力方面起额外作用。当麻醉气体接触量减少时，这些状况是否会成为行为损害的主要因素仍不清楚；此外，我们希望确定在相对低水平接触此类气体时神经行为和神经内分泌效应的程度。因此，对同一组30名手术室工作人员在气体麻醉和非气体麻醉期间进行了神经行为测试。通过这种方式，在相同压力条件下，但对麻醉气体的接触水平不同，对神经心理表现进行了检查。测量血清皮质醇作为额外的“生物应激指标”。检查催乳素分泌以研究麻醉气体对多巴胺能系统可能的干扰。将结果与来自其他科室的20名医院工作人员组成的对照组进行比较，对照组在年龄、性别和教育方面具有相似特征。在进行气体麻醉工作期间，工作周第一天氧化亚氮的平均空气传播浓度（几何均值）为50.9 ppm（标准差20.8），工作周最后一天为54.2 ppm（标准差22.1），而工作周第一天尿中氧化亚氮的平均浓度（几何均值）为21.54微克/升，工作周最后一天为25.67微克/升。与使用非气体麻醉的工作人员和对照组相比，手术室工作人员在气体麻醉工作周结束时反应时间较慢。同时，他们还表现出催乳素分泌增加，而皮质醇保持不变。因此，可以得出结论，较低水平的麻醉气体接触（不仅是高接触水平）会导致神经行为表现受损，压力的作用相对较小。麻醉剂神经毒性作用的机制似乎与对多巴胺能系统的干扰有关。
