李文静, 袁春满, 高婷, 赵小燕, 牛侨, 路小婷, 王林平, 宋静. 血糖升高在职业铝暴露致工人认知障碍中的中介作用[J]. 环境与职业医学, 2021, 38(3): 217-222. DOI: 10.13213/j.cnki.jeom.2021.20454
引用本文: 李文静, 袁春满, 高婷, 赵小燕, 牛侨, 路小婷, 王林平, 宋静. 血糖升高在职业铝暴露致工人认知障碍中的中介作用[J]. 环境与职业医学, 2021, 38(3): 217-222. DOI: 10.13213/j.cnki.jeom.2021.20454
LI Wenjing, YUAN Chunman, GAO Ting, ZHAO Xiaoyan, NIU Qiao, LU Xiaoting, WANG Linping, SONG Jing. Mediation effect of elevated fasting blood glucose on cognitive impairment induced by occupational aluminum exposure among workers[J]. Journal of Environmental and Occupational Medicine, 2021, 38(3): 217-222. DOI: 10.13213/j.cnki.jeom.2021.20454
Citation: LI Wenjing, YUAN Chunman, GAO Ting, ZHAO Xiaoyan, NIU Qiao, LU Xiaoting, WANG Linping, SONG Jing. Mediation effect of elevated fasting blood glucose on cognitive impairment induced by occupational aluminum exposure among workers[J]. Journal of Environmental and Occupational Medicine, 2021, 38(3): 217-222. DOI: 10.13213/j.cnki.jeom.2021.20454

血糖升高在职业铝暴露致工人认知障碍中的中介作用

Mediation effect of elevated fasting blood glucose on cognitive impairment induced by occupational aluminum exposure among workers

  • 摘要: 背景

    长期职业铝暴露不仅会导致工人的认知障碍,还会引起血糖升高以及增大患糖尿病的风险。尽管糖尿病与认知功能障碍的关联已得到证实,但血糖升高在职业铝暴露致工人认知障碍中是否发挥作用尚未明确。

    目的

    探究血糖升高在职业铝暴露致工人认知障碍中的作用。

    方法

    于2019年采用整群抽样的方法选取山西某大型铝厂电解铝车间、氧化铝车间及热电车间的男性铝作业在岗工人(共184人),采用问卷调查工人基本信息,并采集其血液。采用电感耦合等离子体质谱法测定血浆铝浓度。以血铝质量浓度(后称浓度)P25P75为界,将工人分为Q1、Q2、Q3组。采用葡萄糖氧化酶法测定空腹血糖(FBG)浓度,以其P25P75为界进行分组。采用蒙特利尔认知评估量表(MocA量表)评价工人认知功能,MocA量表总分为30分,评分 < 26提示发生认知障碍。采用多元logistic回归分析铝暴露、FBG和MocA量表总分之间的关系,采用中介效应分析流程探讨FBG在铝暴露与MocA量表总分关系中的作用。

    结果

    工人血铝浓度中位数(P25P75)为40.14(30.71,49.78)μg·L-1,FBG浓度中位数(P25P75)为5.02(4.77,5.22)mmol·L-1,MocA总分中位数(P25P75)为23(22,26)。logistic回归结果表明,校正了工种、年龄、吸烟、饮酒、锻炼、体重指数和教育水平后,血铝水平与FBG水平呈正相关,调整OR值为1.046(1.019~1.074);在不同血铝浓度的分组中,Q2和Q3组工人发生认知障碍的风险分别是Q1组的2.096(2.022~6.045)倍、2.831(1.091~7.351)倍。在不同FBG浓度分组中,高水平组(>P75)和中水平组(P25~P75)工人发生认知损伤的风险分别是低水平组(< P25)的2.464(1.897~8.169)倍、1.889(1.783~4.558)倍。中介分析结果表明,中介效应占总效应的25.1%。

    结论

    铝暴露、FBG水平分别和认知障碍呈剂量反应关系,并且铝暴露导致的认知障碍有部分可能是由血糖升高引起的。

     

    Abstract: Background

    Long-term occupational aluminum exposure can not only cause cognitive impairment, but also boost the blood glucose and increase the risk of diabetes in workers. Although the association between diabetes and cognitive impairment has been confirmed, the role of blood glucose increasing in cognitive impairment induced by occupational aluminum exposure has not been identified.

    Objective

    This study aims to identify the role of blood glucose increasing in cognitive impairment induced by occupational aluminum exposure in workers.

    Methods

    A total of 184 male workers were selected from the electrolytic aluminum workshop, alumina workshop, and thermoelectric workshop of a large aluminum plant in Shanxi Province by cluster sampling method in 2019. These workers were asked to complete a questionnaire survey on general information and their blood samples were collected. They were divided into Q1, Q2 and Q3 groups according to plasma aluminum level (< P25, P25-P75, and >P75) determined by inductively coupled plasma mass spectrometry (ICP-MS); fasting blood glucose (FBG) was measured by glucose oxidase method and categorized into three levels (<P25, P25-P75, and >P75). The Montreal Cognitive Assessment Scale (MocA Scale) was used to evaluate the cognitive function of workers; the total possible score of the scale is 30 points, and a score of < 26 indicated cognitive impairment. Multiple logistic regression was used to analyze the relationship between aluminum exposure, FBG, and MocA score, and mediation effect analysis was used to analyze the role of FBG in the correlation between aluminum exposure and MocA score.

    Results

    These workers' medians (P25, P75) of plasma aluminum concentration, FBG concentration, and MocA score were 40.14 (30.71, 49.78) μg·L-1, 5.02 (4.77, 5.22) mmol·L-1, and 23 (22, 26), respectively. The multiple logistic regression analysis results showed that plasma aluminum level was positively correlated with FBG level (adjusted OR=1.046, 95% CI: 1.019-1.074), and the risks of cognitive impairment of workers in the Q2 and the Q3 groups were 2.096 (2.022-6.045) times and 2.831 (1.091-7.351) times higher than that of the Q1 group, after adjusting for type of work, age, smoking, drinking, exercise, body mass index, and education. Moreover, the risks of cognitive impairment of workers with high-level (>P75) and intermediate-level (P25-P75) FBG were 2.464 (1.897-8.169) times and 1.889 (1.783-4.558) times higher than that of the low-level FBG group (< P25). The results of mediation effect analysis showed that the mediation effect accounted for 25.1% of the total effect.

    Conclusion

    There are dose-response relationships of aluminum exposure with FBG level and cognitive impairment, and the cognitive impairment induced by aluminum exposure may partially arise from elevated blood glucose.

     

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