Zendehdel Rezvan, Fazli Zohreh, Mazinani Mohammad
Safety Promotion and Injury Preventation Research Centre, Beheshti University of Medical Sciences, Tehran, Iran.
Department of Occupational Hygiene, School of Public Health, Shahid Beheshti University, Tehran, Iran.
Environ Monit Assess. 2016 Nov;188(11):648. doi: 10.1007/s10661-016-5662-z. Epub 2016 Oct 31.
Over the years, neurotoxicity and cognitive dysfunction have separately been associated with endogenous formaldehyde and reduction of acetylcholine signals. However, a limited number of studies have shown a relationship between cholinergic neurotransmitter and formaldehyde exposure. Therefore, the aim of this study was to assess the neurological effect on workers from melamine-dish preparation workshop, who were exposed to formaldehyde. A total of 35 formaldehyde-exposed workers were compared with 32 control employees from the food industry. Occupational exposure to formaldehyde was conducted using the National Institute of Occupational Safety and Health 3500 methods. Using the Ellman method, acetylcholinesterase (AChE) as a biomarker for neurotoxicity was analyzed in blood erythrocyte. The effects of alcohol dehydrogenase III (ADH3) and Mn-superoxide dismutase (Mn-SOD) polymorphism were used to survey the level of AChE activity. In this study, it was found that exposure to airborne formaldehyde increased from 0.024 to 0.74 ppm and the median personnel exposure was 0.057. Induction of AChE activity was observed in formaldehyde-exposed workers as compared with the control group (p < 0.01), while AChE activity increased in 64 % of the exposed subjects. Spearman's correlation (p < 0.02) was used to evaluate the association between AChE activity and occupational exposure to formaldehyde. Exposed subjects containing ADH3 genotype had higher AChE than others. The findings of this study suggest that the neurotoxic effect of formaldehyde depends on the AChE activity, which is affected by metabolism. It can be concluded that cholinergic signal reduction in cases of cognitive dysfunction could be associated with endogenous formaldehyde.
多年来，神经毒性和认知功能障碍分别与内源性甲醛及乙酰胆碱信号减少有关。然而，仅有少数研究表明胆碱能神经递质与甲醛暴露之间存在关联。因此，本研究旨在评估来自三聚氰胺餐具制备车间且接触甲醛的工人的神经学影响。总共35名接触甲醛的工人与32名来自食品行业的对照员工进行了比较。采用美国国家职业安全与健康研究所3500方法进行职业性甲醛暴露检测。使用埃尔曼法，分析血红细胞中作为神经毒性生物标志物的乙酰胆碱酯酶（AChE）。利用酒精脱氢酶III（ADH3）和锰超氧化物歧化酶（Mn-SOD）多态性来检测AChE活性水平。在本研究中，发现空气中甲醛暴露量从0.024 ppm增加到0.74 ppm，人员暴露中位数为0.057 ppm。与对照组相比，在接触甲醛的工人中观察到AChE活性升高（p < 0.01），同时64%的暴露受试者AChE活性增加。采用斯皮尔曼相关性分析（p < 0.02）评估AChE活性与职业性甲醛暴露之间的关联。含有ADH3基因型的暴露受试者AChE水平高于其他受试者。本研究结果表明，甲醛的神经毒性作用取决于受代谢影响的AChE活性。可以得出结论，认知功能障碍病例中的胆碱能信号减少可能与内源性甲醛有关。
