远洋航行船员睡眠质量及其影响因素

孙占颖, 甘雪洋, 苏清清, 陈静茹, 高远

孙占颖, 甘雪洋, 苏清清, 陈静茹, 高远. 远洋航行船员睡眠质量及其影响因素[J]. 环境与职业医学, 2024, 41(8): 892-897. DOI: 10.11836/JEOM24099
引用本文: 孙占颖, 甘雪洋, 苏清清, 陈静茹, 高远. 远洋航行船员睡眠质量及其影响因素[J]. 环境与职业医学, 2024, 41(8): 892-897. DOI: 10.11836/JEOM24099
SUN Zhanying, GAN Xueyang, SU Qingqing, CHEN Jingru, GAO Yuan. Sleep quality and influencing factors of mariners during ocean voyages[J]. Journal of Environmental and Occupational Medicine, 2024, 41(8): 892-897. DOI: 10.11836/JEOM24099
Citation: SUN Zhanying, GAN Xueyang, SU Qingqing, CHEN Jingru, GAO Yuan. Sleep quality and influencing factors of mariners during ocean voyages[J]. Journal of Environmental and Occupational Medicine, 2024, 41(8): 892-897. DOI: 10.11836/JEOM24099

远洋航行船员睡眠质量及其影响因素

基金项目: 军队护理创新与培育专项项目(2021HL070);军事理论自研项目(LB2023A06-C025)
详细信息
    作者简介:

    孙占颖(1994—),女,硕士生;E-mail:1206224470@qq.com

    通讯作者:

    高远,E-mail:gaoyuanzd@163.com

  • 中图分类号: R135

Sleep quality and influencing factors of mariners during ocean voyages

Funds: This study was funded.
More Information
  • 摘要:
    背景

    远洋航行船员睡眠质量明显低于普通人群且睡眠障碍发生率较高。睡眠障碍容易导致船员疲劳和认知功能下降,增加差错率和事故率,是船舶航行的重大安全隐患。目前,我国针对远洋航行船员睡眠质量影响因素研究不够全面且有待深入。

    目的

    调查远洋航行船员睡眠质量并分析其影响因素,以期为远洋航行船员构建睡眠干预方案,改善睡眠障碍提供参考。

    方法

    采取整体便利抽样法,选取某船队2024年3月21日返航的408名船员作为调查对象。运用一般资料调查表、《匹兹堡睡眠质量指数》(PSQI)、《焦虑自评量表》(SAS)进行问卷调查,使用SPSS 26.0软件进行数据分析。

    结果

    回收有效问卷399份,有效回收率97.8%。远洋航行船员PSQI总分为(6.41±2.44)分,其中存在睡眠障碍的占总人数的33.6%(134/399)。不同家庭结构(t=2.235,P=0.031)、劳动类型(F=3.789,P=0.023)、噪声暴露(F=53.218,P<0.001)、饮食规律(F=63.311,P<0.001)、运动习惯(F=16.416,P<0.001)和焦虑状态(t=5.963,P<0.001)的船员PSQI总分存在差异。多重线性回归分析显示,原生家庭结构为单亲(β=0.102,P=0.010)、噪声暴露(β=0.323,P<0.001)和焦虑状态(β=0.117,P=0.006)均正向影响PSQI总分,饮食规律(β=−0.331,P<0.001)和运动习惯(β=−0.147,P<0.001)负向影响PSQI总分,5个变量可共同解释远洋航行船员PSQI总分总变异的38.9%(F=37.159,P<0.01)。

    结论

    远洋航行船员睡眠质量较低且睡眠障碍发生率较高,受到家庭结构、噪声暴露、饮食规律、运动习惯和焦虑状态等因素共同影响。

     

    Abstract:
    Background

    The average sleep quality of mariners during ocean voyages is notably worse than that of the general populace, and the incidence of sleep disorders among them is higher. Sleep disorders closely associate with fatigue and cognitive decline, increasing error and accident rates, and are a major safety hazard in marine navigation. At present, research on factors influencing the sleep quality of mariners during ocean voyages in China is limited and needs further investigation.

    Objective

    To investigate the sleep quality of mariners during ocean voyages and analyze its influencing factors, in order to provide reference for constructing sleep intervention plans and mitigating their sleep disorders.

    Methods

    Using convenience cluster sampling, a questionnaire survey was carried out in 408 crew members of a fleet who returned from a voyage on March 21, 2024. The questionnaires included a general information questionnaire, Pittsburgh Sleep Quality Index (PSQI) , and Self Rating Anxiety Scale (SAS), and the data were analyzed by SPSS 26.0 software.

    Results

    A total of 399 valid questionnaires were collected, with an effective recovery rate of 97.8%. The mean score of PSQI for the mariners during ocean voyages was (6.41±2.44), with 33.6% (134/399) of the mariners reporting sleep disorders. The PSQI scores varied by family structures (t=2.235, P=0.031), labor types (F=3.789, P=0.023), noise exposure (F=53.218, P<0.001), dietary patterns (F=63.311, P<0.001), exercise habits (F=16.416, P<0.001), and anxiety states (t=5.963,P<0.001). The results of linear regression showed that incomplete family structure (β=0.102, P=0.010), noise exposure (β=0.323, P<0.001), and anxiety (β=0.117, P=0.006) positively associated with the total score of PSQI, while dietary patterns (β=-0.331, P<0.001) and exercise habits (β=-0.147, P<0.001) negatively associated with the total PSQI score, and the 5 variables jointly explained 38.9% of the total variation in the PSQI score (F=37.159, P<0.01).

    Conclusion

    The sleep quality of mariners during ocean voyages is relatively low and the incidence of sleep disorders is relatively high, which is jointly influenced by factors such as family structure, noise exposure, dietary habits, exercise habits, and anxiety.

     

  • 温石棉是自然界中储量丰富的矿物纤维材料,具有耐腐蚀、耐高温、绝缘性好等特点,广泛应用于纺织、建材、化工、机械和国防等领域。中国的温石棉矿产丰富,全国超百万人被职业暴露,且近年来温石棉暴露所致疾病的发病率呈上升趋势[1]。温石棉通过呼吸过程进入人体,穿透呼吸道防御屏障,沉积于肺部,对肺和胸膜的损害较大,可导致肺纤维化、石棉肺、肺癌和胸膜间皮瘤等疾病,且长期接触温石棉会使肺癌风险增加6倍,肺纤维化风险增加3倍[2]。上皮间质转化(epithelial mesenchymal transition, EMT)是上皮细胞失去上皮特征获得间充质细胞迁移性的过程,具有促进肺纤维化,增强肺肿瘤细胞迁移和侵袭的特征[3]。研究显示,温石棉长期暴露诱导EMT主要与炎症因子水平变化和丝裂原活化蛋白激酶(mitogen-activated protein kinase, MAPK)/细胞外调节蛋白激酶(extracellular regulated protein kinase, ERK)通路的激活等有关[4-6]。因此,为深入研究温石棉如何促进肺纤维化和肺癌等疾病的发生,本文总结了温石棉暴露诱导EMT的机制研究现状。

    在炎症微环境中,多种炎症因子在参与炎症的同时,也参与对EMT的调控。炎症因子是细胞经刺激而合成、分泌的小分子可溶性蛋白质,通过不同的通路调节机体的炎症反应。研究表明,温石棉暴露可改变转化生长因子-β(transforming growth factor-β, TGF-β)、高迁移率族蛋白B1(high mobility group box1, HMGB1)、肿瘤坏死因子-α(tumor necrosis factor-α, TNF-α)和白介素(interleukin, IL)-1β等炎症因子的表达水平[7-8]。因此,研究炎症因子的表达水平有助于探讨温石棉诱导EMT的机制。

    TGF-β作为多功能蛋白,其关键作用是调节炎症相关反应,同时也可通过多种正、负反馈调节机制调控细胞生长、分化以及细胞外基质的产生[9]。TGF-β被认为是诱导EMT的主要诱导剂之一,主要经SMAD(small mothers against decapentaplegic)蛋白途径和SMAD非依赖途径介导。SMAD途径中,TGF-β信号通过与I型和II型TGF-β受体(TGF-β receptor, TGF-βR),即TGF-βRI、TGF-βRII结合,使磷酸化的SMAD2/3与SMAD4结合形成复合物发挥正反馈作用介导EMT[10];SMAD6和SMAD7通过负反馈调节抑制SMAD受体的激活,阻断信号的传导[11]。SMAD非依赖途径通过活化的蛋白激酶B(protein kinases B, Akt)或磷脂酰肌醇3-激酶(phosphatidylinositol 3-kinase, PI3K)等进行转录调控介导EMT[12]

    研究表明,温石棉暴露可通过诱导肺上皮细胞过度表达TGF-β促进EMT,参与肺纤维化等病理过程[13]。Gulino等[14]发现长期暴露于温石棉的人肺上皮细胞系BEAS-2B细胞分泌TGF-β,并通过SMAD非依赖性途径Akt / 糖原合成酶激酶-3β(glycogen synthase kinase-3β, GSK-3β) / Snail家族转录抑制因子1(Snail-1)诱导发生EMT。Turini等[4]通过比较暴露于温石棉或TGF-β的MeT-5A细胞中SMAD2及EMT标志物的表达水平,发现温石棉可通过TGF-β介导的SMAD途径诱导EMT。可见,TGF-β介导的SMAD途径和SMAD非依赖途径为探讨温石棉诱导EMT的机制提供了可靠依据。

    HMGB1是一种核蛋白,不仅能参与细胞分化过程,还可作为促炎因子诱导炎症因子的产生。大量研究表明,HMGB1作为上游因子调控TGF-β1、IL-6、TNF-α等炎症因子的表达与EMT的发生密切相关[15-16]。HMGB1既能促进TGF-β1的表达,还可通过抑制SMAD2/3[17]和SMAD1[18]通路的信号传导来逆转TGF-β1诱导的EMT。Hao等[19]证实,抑制HMGB1的表达会导致IL-6、IL-8和TNF-α等炎症因子表达水平降低,从而抑制EMT的发生。此外,HMGB1也可在部分非编码RNA的调控下介导EMT,如长链非编码RNA(long non-coding RNA, lncRNA)牛磺酸上调基因1 (taurine upregulated gene 1, TUG1)海绵吸附于miR-181b上调HMGB1的表达,从而促进鼠气道组织EMT[20]。以上说明HMGB1作为重要介质可通过多种调控途径介导EMT。

    现有学者提出HMGB1可作为温石棉相关疾病的潜在生物标志物[8]。温石棉暴露使HMGB1的表达水平发生改变,且HMGB1可上调TGF-β等炎症因子的表达,从而促进EMT的发生[21]。HMGB1还能诱导产生活性氧(reactive oxygen species, ROS)和细胞自噬,并通过ROS和细胞自噬促进细胞EMT[22]。由此可见,HMGB1能通过自噬反应、炎症反应和氧化应激等多种机制促进温石棉暴露诱导的EMT,具有重要的调控作用。

    TNF-α是由巨噬细胞和单核细胞产生的多向性先导感染炎症因子,在许多病理状态下表达水平均会增加,如恶性肿瘤和慢性炎性疾病[23]。研究发现,长期暴露于温石棉环境或石棉肺患者体内的TNF-α含量明显高于健康人群[7]。其原因是温石棉长期暴露会诱导TNF-α过度表达,并且TNF-α可通过核转录因子(nuclear factor kappa-B, NF-κB)进一步促进温石棉与肺上皮细胞结合,使肺上皮细胞发生转化[24]。Qi等[25]发现,温石棉暴露分泌的TNF-α会使E-钙粘蛋白和β-连环蛋白表达减少,波形蛋白和α-平滑肌肌动蛋白(alpha-smooth muscle actin, α-SMA)表达增加,但此变化与温石棉暴露时长有关。说明TNF-α参与了温石棉诱发EMT的过程,并且EMT标志物在温石棉短期暴露时表达变化的持续性较短,需长期暴露才能为探讨EMT机制提供可靠依据。

    IL作为主要的炎症因子,在激活与调节免疫细胞及炎症反应中起重要作用。目前较多的研究者认为IL参与EMT过程,如IL-1β通过激活ZEB1基因、Snail-1蛋白等信号促进EMT,并且其促进分泌的IL-6也可诱导EMT[26]。此外,研究发现,温石棉暴露会促进IL-1β和IL-6等炎症因子表达。其中,温石棉通过自身激活、裂解炎症小体释放IL-1β,使体外正常的细胞发生EMT[27]。温石棉暴露也可通过分泌IL-6介导E盒结合锌指蛋白1(zinc finger E-box binding homeobox 1, ZEB1)、Snail-1等信号传导[4, 28]。ZEB1、Snail-1现已被证明参与EMT的发生发展,因此,IL可通过介导ZEB1、Snail-1的传导参与温石棉诱导的EMT。目前被发现参与温石棉诱导EMT过程的IL较少,以此为研究方向将为深入研究温石棉诱发与EMT相关的肺纤维化、癌症等疾病的作用机制提供新思路。

    MAPK是一组丝氨酸-苏氨酸蛋白激酶,经MAPK激酶和MAPK激酶激酶发生三级信号传递,共同调控细胞增殖、分化和肿瘤的侵袭、转移等生理活动[29]。在MAPK介导EMT的各种通路中,研究较广泛的是ERK通路。Papa等[30]研究显示,温石棉暴露会激活ERK,而ERK可经MAPK通路参与细胞的生长与分化。Tamminen等[31]发现,温石棉暴露可通过MAPK/ERK通路使A549细胞E-钙黏蛋白表达降低,α-SMA表达升高,使细胞间的连接减弱。这些说明温石棉可通过MAPK/ERK信号通路诱导细胞发生EMT。

    此外,成纤维细胞生长因子(fibroblast growth factor, FGF)也可参与肺上皮细胞发生EMT的过程[32]。FGF与FGF受体(FGF receptor, FGFR)结合后形成二聚体并通过激酶结构域的磷酸化作用募集衔接蛋白激活下游信号传导,从而调节EMT的发生[33]。表皮生长因子(epidermal growth factor, EGF)与FGF作用相似,通过与受体结合激活信号传导,来促进细胞发生EMT[34]。研究显示,长期暴露于温石棉环境中,EGF、FGF及其受体的表达水平会发生变化并影响EMT过程[35-36]。通过蛋白质印迹法检测温石棉暴露后EGF受体(EGF receptor, EGFR)、磷酸化ERK1/2的表达水平,发现EGFR可使ERK磷酸化,从而激活MAPK/ERK通路[37]。说明FGF和EGF可通过MAPK/ERK通路介导温石棉暴露诱发EMT。

    氧化应激与EMT密切相关。氧化应激是生物体受到刺激后,产生高水平、高活性物质,使机体氧化还原失衡并倾向于氧化的一种状态。氧化应激可通过调节细胞因子的表达及相关信号通路来影响EMT的进程[38-39]。其中,ROS作为氧化应激产生的高活性物质在此过程中发挥着重要作用。研究表明,温石棉暴露会使ROS积累,导致组织氧化损伤,并且机体氧化应激程度随温石棉暴露时间的延长而持续加深,从而促进EMT[40-41]。Sullivan等[42]发现,TNF-α和TGF-β1在温石棉诱导EMT过程中表达上调,并且TGF-β1可由ROS促进表达。由此说明,ROS不仅自身能促进温石棉诱导EMT,还可通过促进TGF-β1等转录因子的表达参与其中;并且温石棉经氧化应激发生EMT的程度与温石棉暴露时长有关。

    发生EMT的其中一个标志是上皮细胞间的黏附被逐渐降解,而基质金属蛋白酶(matrix metalloproteinases, MMPs)进行蛋白水解正是此降解的主要因素。研究显示,温石棉暴露会诱导MMP-2[4]和MMP-7[43]等蛋白酶过度表达,其中作为EMT标志物的MMP-2被认为与TGF-β的相互调控是发生EMT的可能机制,并且MMP-7可促进MMP-2分泌。说明MMPs在温石棉暴露所致的EMT过程中发挥着一定作用。

    温石棉作为生活中广泛应用的矿物材料,与肺纤维化、肺癌和间皮瘤等疾病有着密切联系。研究者们通过研究炎症反应、MAPK途径和氧化应激等不同通路,发现了温石棉诱导EMT的新机制。然而,温石棉暴露引起EMT的机制研究仍有很多方面需要进一步探讨:(1)TNF-α和IL等炎症因子参与温石棉诱导EMT的结论主要集中在炎症因子会影响EMT标志物的表达水平,其具体调控机制尚未有研究说明,有待进一步研究;(2)现已知多种信号分子可通过不同的通路参与EMT过程,但目前针对温石棉诱导EMT仅TGF-β和MAPK/ERK相关通路被具体说明,其他通路的具体调控机制还有待探讨;(3)目前针对温石棉中ROS的研究,主要集中在其通过氧化应激诱导细胞凋亡,少见有研究关注ROS在温石棉诱导EMT中的具体机制;(4)温石棉由多种金属元素及二氧化硅组成,但目前对温石棉诱导EMT的研究均是从温石棉纤维整体出发,尚未有人从温石棉的组成成分来解释温石棉诱导EMT的机制,这有望成为一个新的研究点。综上所述,进一步研究温石棉诱导细胞发生EMT的具体机制,有望为温石棉致肺纤维化和肺癌等疾病的研究提供依据和参考。

  • 表  1   不同人口信息学特征远洋航行船员PSQI总分比较(n=399)

    Table  1   Comparison of PSQI scores of mariners during ocean voyages by demographic characteristics (n=399)

    特征人数(构成比/%)分值,$\overline \chi \pm {\text{s}} $F/tP
    性别0.0400.968
     男383(96.0)6.41±2.44
     女16(4.0)6.44±2.58
    年龄/岁0.0930.991
     20~25147(36.8)6.36±2.50
     26~30158(39.6)6.41±2.34
     31~4894(23.6)6.50±2.54
    婚姻状况0.8200.935
     未婚220(55.1)6.40±2.48
     已婚179(44.9)6.42±2.40
    原生家庭结构2.2350.031
     双亲家庭360(90.2)6.31±2.35
     单亲家庭39(9.8)7.41±2.99
    是否独生子女0.8450.398
     是190(47.6)6.31±2.51
     否209(52.4)6.51±2.37
    工龄/年0.6340.531
     0~5141(35.3)6.50±2.45
     6~10127(31.8)6.21±2.35
     >10131(32.8)6.52±2.52
    岗位职责0.8150.444
     指挥管理71(17.8)6.39±2.45
     系统操作195(48.9)6.27±2.29
     后勤保障133(33.3)6.63±2.64
    劳动类型3.7890.023
     轻体力劳动211(52.9)6.10±2.31
     脑力劳动87(21.8)6.72±2.54
     重体力劳动101(25.3)6.80±2.54
    每日工作时长/h2.4640.086
     0~8150(37.6)6.08±2.32
     >8~12162(40.6)6.54±2.43
     >1287(21.8)6.75±2.61
    噪声暴露53.218<0.001
     不会163(40.9)5.36±2.11
     偶尔139(34.8)6.39±2.28
     经常97(24.3)8.23±2.11
    BMI分级/(kg·m−2)1.1310.336
     低体重(0~<18.5)7(1.8)7.29±2.22
     正常(18.5~<24)235(58.9)6.26±2.45
     超重(24~<28)140(35.1)6.66±2.45
     肥胖(≥28)17(4.3)6.18±2.16
    吸烟0.1150.909
     否206(51.6)6.43±2.31
     是193(48.4)6.40±2.57
    饮酒5.0710.183
     否297(74.4)6.31±2.37
     是102(25.6)6.71±2.62
    饮咖啡2.0330.132
     从不142(35.6)6.57±2.47
     偶尔212(53.1)6.20±2.41
     经常45(11.3)6.91±2.39
    饮茶0.8290.437
     从不52(13.0)6.46±2.13
     偶尔251(62.9)6.30±2.45
     经常96(24.1)6.68±2.58
    饮食规律63.311<0.001
     经常错过51(12.8)9.06±2.30
     偶尔错过250(62.7)6.46±2.83
     按时就餐98(24.6)4.93±1.65
    运动习惯16.416<0.001
     不太运动29(7.3)8.51±1.98
     偶尔运动194(48.6)6.68±2.44
     经常运动176(44.1)5.51±2.30
    焦虑状态5.963<0.001
     否298(72.4)5.98±2.33
     是110(27.6)8.51±2.37
    下载: 导出CSV

    表  2   远洋航行船员PSQI总分影响因素的多重线性回归分析

    Table  2   Multiple linear regression of the influencing factors on the PSQI score of mariners during ocean voyages

    自变量bβtP
    年龄−0.168−0.053−1.3310.184
    原生家庭结构0.8380.1022.5900.010
    劳动类型−0.175−0.060−1.5100.132
    噪声暴露0.9960.3237.826<0.001
    饮食规律−1.345−0.331−7.775<0.001
    运动习惯−0.584−0.147−3.627<0.001
    焦虑状态0.6360.1172.7900.006
    [注] b:回归系数;β:标准化回归系数;自变量赋值方式:原生家庭结构(双亲家庭=1;单亲家庭=2)、劳动类型(轻体力劳动=1;脑力劳动=2;重体力劳动=3)、噪声暴露(不会=1;偶尔=2;经常=3)、饮食规律(经常错过=1;偶尔错过=2;按时就餐=3)、运动习惯(不太运动=1;偶尔运动=2;经常运动=3)、焦虑状态(否=1;是=2)。
    下载: 导出CSV
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