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Article(id=1241034448586723700, tenantId=1146029695717560320, journalId=1227665162245664772, issueId=1241034441380917539, articleNumber=null, orderNo=null, doi=10.20043/j.cnki.MPM.202502264, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1739808000000, receivedDateStr=2025-02-18, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1773815269848, onlineDateStr=2026-03-18, pubDate=1749484800000, pubDateStr=2025-06-10, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1773815269848, onlineIssueDateStr=2026-03-18, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1773815269848, creator=13701087609, updateTime=1773815269848, updator=13701087609, issue=Issue{id=1241034441380917539, tenantId=1146029695717560320, journalId=1227665162245664772, year='2025', volume='52', issue='11', pageStart='1921', pageEnd='2112', issueExtLink='null', onlineDate='null', pubDate='null', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1773815268130, creator=13701087609, updateTime=1773815340947, updator=13701087609, preIssue=null, nextIssue=null, ext={EN=IssueExt(id=1241034746873049765, tenantId=1146029695717560320, journalId=1227665162245664772, issueId=1241034441380917539, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1241034746873049766, tenantId=1146029695717560320, journalId=1227665162245664772, issueId=1241034441380917539, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null}, startPage=2101, endPage=2106, ext={EN=ArticleExt(id=1241034449001959830, articleId=1241034448586723700, tenantId=1146029695717560320, journalId=1227665162245664772, language=EN, title=The mediating role of prefrontal cortex volume in the association between long-term exposure to air pollution and the incidence of type 2 diabetes, columnId=1228016569138213037, journalTitle=Modern Preventive Medicine, columnName=Clinical Medicine and Prevention, runingTitle=null, highlight=null, articleAbstract=
Objective

To investigate the mediating effect of prefrontal cortex volume in the association between long-term exposure to air pollution and the incidence of Type 2 Diabetes (T2DM), providing a basis for alleviating the burden and understanding the etiology of T2DM.

Methods

Utilizing data from the UK Biobank cohort, we analyzed the relationships among four air pollutants, eight prefrontal cortex volumes, and T2DM using multiple linear regression and logistic regression models. A multiple mediation analysis was conducted to estimate the overall mediating effect of the eight prefrontal cortex volumes.

Results

A total of 26 624 participants were included in the study, with a T2DM incidence rate of approximately 2.0%. There was an overall negative correlation between air pollutant concentrations and prefrontal cortex volume. Increased concentrations of air pollutants were associated with a higher risk of T2DM; specifically, for every 1 standard deviation increase in PM2.5 concentration, the odds ratio (OR) (95% confidence interval [CI]) was 1.062 (1.003-1.159). Decreased volumes of the right medial prefrontal cortex, left superior frontal gyrus, bilateral orbital frontal cortex, and right frontal pole were associated with increased T2DM risk, with OR (95%CI) values of 0.869 (0.755-0.949), 0.808(0.745-0.925), 0.897 (0.815-0.988), 0.823 (0.738-0.917), and 0.881 (0.796-0.974), respectively. The volume of the prefrontal cortex mediated the association between the four air pollutants and T2DM risk.

Conclusion

The study indicates that increased air pollutant concentrations elevate the risk of T2DM, and prefrontal cortex volume may serve as a significant mediating factor in the relationship between air pollution and T2DM. Reducing exposure to air pollutants and targeted interventions addressing factors affecting brain vitality, such as sleep and exercise, may effectively prevent the occurrence and progression of T2DM.

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目的

本研究旨在探讨前额叶皮质体积在大气污染长期暴露和2型糖尿病（type 2 diabetes mellitus，T2DM）发病关联中的中介效应，为减轻T2DM的负担和病因学提供依据。

方法

基于英国生物银行队列数据，使用多因素线性回归和logistic回归模型分析四种大气污染物、八个前额叶皮质体积、2型糖尿病三者之间的关联。使用多中介分析估计八个前额叶皮质体积整体的中介作用。

结果

研究最终纳入26 624人，T2DM发病率约为2.0%。大气污染物浓度与前额叶皮质体积总体上呈负相关关系。大气污染物浓度升高会增加T2DM的发病风险，其中，PM2.5浓度每增加1个SD，其OR (95%CI)为1.062(1.003～1.159)；右部内侧前额叶皮质体积、左侧额盖皮质体积、左右两侧眶额皮质体积内侧、右侧额极体积减小会增加T2DM的风险，其OR(95%CI)分别为0.869(0.755～0.949)、0.808(0.745～0.925)、0.897(0.815～0.988)、0.823(0.738～0.917)、0.881(0.796～0.974)。前额叶皮质体积介导了四种大气污染物与T2DM发病风险的关联。

结论

研究表明，大气污染物浓度的增加会提高T2DM的发生风险，前额叶皮质体积可能是大气污染物与T2DM的关联中重要的中介因子。通过减少大气污染物暴露，以及针对性地干预睡眠、运动等影响大脑活力的因素，能够有针对性地预防T2DM的发生与发展。

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张菊英，E-mail:
, copyrightStatement=本刊刊出的所有文章不代表中华预防医学会和本刊编委会的观点，除非特别声明。, copyrightOwner=中华预防医学会和四川大学华西公共卫生学院, extLink=null, articleAbsUrl=null, sourceXml=3Zqjb5k2sGKZyqxVf9j+eA==, magXml=g+Znp/p9qqgYqVmKu0Ot8w==, pdfUrl=null, pdf=gYSDQuI9Tmzv7i5rrpjprg==, pdfFileSize=644188, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=l0omnwvV2QciIAO4j+JEIQ==, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=zkmVgjUGMhu6Wnd28yUSOQ==, mapNumber=null, authorCompany=null, fund=null, authors=

宋婷（1998—），女，硕士在读，研究方向：流行病与卫生统计

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注：NDE和NIE分别表示自然直接和间接效应OR（95%CI）；*表示P<0.05。

, figureFileSmall=GSMrAN4q38BWWcbu94oEoQ==, figureFileBig=EXHZ+BiuE70qf9Ytkr32Yw==, tableContent=null), ArticleFig(id=1241050840245531610, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1241034448586723700, language=EN, label=Table 1, caption=

Basic characteristics of the study subjects ［n=26 624，（），n（%）］

, figureFileSmall=null, figureFileBig=null, tableContent=
特征总人群(n=26 624)非T2DM (n=26 078)T2DM(n=546)P值
年龄（岁）55.08 ±7.4655.03±7.4657.46±7.22<0.001
性别
女性13 549 (50.9)13 355 (51.2)194 (35.5)<0.001
男性13 075 (49.1)12 723 (48.8)352 (64.5)
评估中心
英格兰26 517 (99.6)25 973 (99.6)544 (99.6)0.831
苏格兰17 (0.1)17 (0.1)0 (0.0)
威尔士90 (0.3)88 (0.3)2 (0.4)
教育水平
大学及以上12 615 (47.4)12 448 (47.7)167 (30.6)<0.001
高中及以下13 965 (52.5)13 589 (52.1)376 (68.9)
不清楚44 (0.2)41 (0.2)3 (0.5)
家庭年收入（英镑）
< 31 0008 067 (30.3)7 830 (30.0)237 (43.4)<0.001
≥31 00016 651 (62.5)16 384 (62.8)267 (48.9)
不清楚1 906 (7.2)1 864 (7.1)42 (7.7)
就业情况
主动就业19 165 (72.0)18 824 (72.2)341 (62.5)<0.001
被动就业7 318 (27.5)7 118 (27.3)200 (36.6)
不清楚141 (0.5)136 (0.5)5 (0.9)
饮酒状况
在饮25 549 (96.0)25 037 (96.0)512 (93.8)0.001
从未饮酒584 (2.2)563 (2.2)21 (3.8)
戒酒486 (1.8)474 (1.8)12 (2.2)
不清楚5 (0.0)4 (0.0)1 (0.2)
吸烟状况
在吸1 594 (6.0)1 546 (5.9)48 (8.8)<0.001
从未吸烟16 273 (61.1)15 994 (61.3)279 (51.1)
戒烟8 723 (32.8)8 505 (32.6)218 (39.9)
不清楚34 (0.1)33 (0.1)1 (0.2)
BMI(kg/m2)26.41± 4.0426.32±3.9730.48 ±5.04<0.001
体力活动强度
高10 704 (40.2)10 498 (40.3)206 (37.7)0.013
中11 191 (42.0)10 974 (42.1)217 (39.7)
低4 729 (17.8)4 606 (17.7)123 (22.5)
PM2.5(μg/m3)9.91±1.059.91±1.0510.01±1.050.038
PM10(μg/m3)16.00±1.8716.00±1.8616.26±2.040.001
NO2(μg/m3)25.77±7.3425.76±7.3426.33±7.490.072
NOX(μg/m3)42.62±14.7642.59±14.7344.03±16.010.024
内侧前额叶皮质体积（左，mm3）2 413.21±400.322 414.77±400.472 338.77±386.35<0.001
内侧前额叶皮质体积（右，mm3）2 420.00±407.212 421.54±407.282 346.51±397.66<0.001
额盖皮质体积（左，mm3）1 931.77±317.371 933.31±317.481 857.90±303.74<0.001
额盖皮质体积（右，mm3）1 715.77±300.271 716.59±299.811 676.59±319.640.002
眶额皮质体积（左，mm3）8 482.78±917.058 487.82±916.398 241.94±916.82<0.001
眶额皮质体积（右，mm3）7 726.68±850.157 730.90±850.247 524.77±821.72<0.001
额极体积（左，mm3）29 723.99±2 785.8329 739.25±2 782.4228 995.29±2 853.19<0.001
额极体积（右，mm3）33 688.31±3 060.6333 707.67±3 061.4632 763.53±2 875.18<0.001
), ArticleFig(id=1241050840404915169, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1241034448586723700, language=CN, label=表1, caption=

研究对象基本情况［n=26 624，（），n（%）］

, figureFileSmall=null, figureFileBig=null, tableContent=
特征总人群(n=26 624)非T2DM (n=26 078)T2DM(n=546)P值
年龄（岁）55.08 ±7.4655.03±7.4657.46±7.22<0.001
性别
女性13 549 (50.9)13 355 (51.2)194 (35.5)<0.001
男性13 075 (49.1)12 723 (48.8)352 (64.5)
评估中心
英格兰26 517 (99.6)25 973 (99.6)544 (99.6)0.831
苏格兰17 (0.1)17 (0.1)0 (0.0)
威尔士90 (0.3)88 (0.3)2 (0.4)
教育水平
大学及以上12 615 (47.4)12 448 (47.7)167 (30.6)<0.001
高中及以下13 965 (52.5)13 589 (52.1)376 (68.9)
不清楚44 (0.2)41 (0.2)3 (0.5)
家庭年收入（英镑）
< 31 0008 067 (30.3)7 830 (30.0)237 (43.4)<0.001
≥31 00016 651 (62.5)16 384 (62.8)267 (48.9)
不清楚1 906 (7.2)1 864 (7.1)42 (7.7)
就业情况
主动就业19 165 (72.0)18 824 (72.2)341 (62.5)<0.001
被动就业7 318 (27.5)7 118 (27.3)200 (36.6)
不清楚141 (0.5)136 (0.5)5 (0.9)
饮酒状况
在饮25 549 (96.0)25 037 (96.0)512 (93.8)0.001
从未饮酒584 (2.2)563 (2.2)21 (3.8)
戒酒486 (1.8)474 (1.8)12 (2.2)
不清楚5 (0.0)4 (0.0)1 (0.2)
吸烟状况
在吸1 594 (6.0)1 546 (5.9)48 (8.8)<0.001
从未吸烟16 273 (61.1)15 994 (61.3)279 (51.1)
戒烟8 723 (32.8)8 505 (32.6)218 (39.9)
不清楚34 (0.1)33 (0.1)1 (0.2)
BMI(kg/m2)26.41± 4.0426.32±3.9730.48 ±5.04<0.001
体力活动强度
高10 704 (40.2)10 498 (40.3)206 (37.7)0.013
中11 191 (42.0)10 974 (42.1)217 (39.7)
低4 729 (17.8)4 606 (17.7)123 (22.5)
PM2.5(μg/m3)9.91±1.059.91±1.0510.01±1.050.038
PM10(μg/m3)16.00±1.8716.00±1.8616.26±2.040.001
NO2(μg/m3)25.77±7.3425.76±7.3426.33±7.490.072
NOX(μg/m3)42.62±14.7642.59±14.7344.03±16.010.024
内侧前额叶皮质体积（左，mm3）2 413.21±400.322 414.77±400.472 338.77±386.35<0.001
内侧前额叶皮质体积（右，mm3）2 420.00±407.212 421.54±407.282 346.51±397.66<0.001
额盖皮质体积（左，mm3）1 931.77±317.371 933.31±317.481 857.90±303.74<0.001
额盖皮质体积（右，mm3）1 715.77±300.271 716.59±299.811 676.59±319.640.002
眶额皮质体积（左，mm3）8 482.78±917.058 487.82±916.398 241.94±916.82<0.001
眶额皮质体积（右，mm3）7 726.68±850.157 730.90±850.247 524.77±821.72<0.001
额极体积（左，mm3）29 723.99±2 785.8329 739.25±2 782.4228 995.29±2 853.19<0.001
额极体积（右，mm3）33 688.31±3 060.6333 707.67±3 061.4632 763.53±2 875.18<0.001
), ArticleFig(id=1241050840513967082, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1241034448586723700, language=EN, label=Table 2, caption=

Associations between air pollutants and prefrontal cortex

, figureFileSmall=null, figureFileBig=null, tableContent=
前额叶皮质体积大气污染物浓度每增加1个SD所对应的 β 值
PM2.5PM10NO2NOX
内侧前额叶皮质体积（左）-4.505*-3.141**-3.617*-4.590*
内侧前额叶皮质体积（右）-6.321**-3.277**-5.352*-7.273***
额盖皮质体积（左）-2.707**-4.802**-3.822*-4.426***
额盖皮质体积（右）0.5071.8830.066-1.010**
眶额皮质体积（左）-7.655*-9.768*-13.569**-14.795**
眶额皮质体积（右）-12.442*-10.113*-12.148*-12.769**
额极体积（左）-58.686**-38.553*-63.911***-59.723***
额极体积（右）-45.177**-37.049*-61.054***-63.003***
), ArticleFig(id=1241050840765625332, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1241034448586723700, language=CN, label=表2, caption=

大气污染物与前额叶皮质体积的关联

, figureFileSmall=null, figureFileBig=null, tableContent=
前额叶皮质体积大气污染物浓度每增加1个SD所对应的 β 值
PM2.5PM10NO2NOX
内侧前额叶皮质体积（左）-4.505*-3.141**-3.617*-4.590*
内侧前额叶皮质体积（右）-6.321**-3.277**-5.352*-7.273***
额盖皮质体积（左）-2.707**-4.802**-3.822*-4.426***
额盖皮质体积（右）0.5071.8830.066-1.010**
眶额皮质体积（左）-7.655*-9.768*-13.569**-14.795**
眶额皮质体积（右）-12.442*-10.113*-12.148*-12.769**
额极体积（左）-58.686**-38.553*-63.911***-59.723***
额极体积（右）-45.177**-37.049*-61.054***-63.003***
), ArticleFig(id=1241050840916620284, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1241034448586723700, language=EN, label=Table 3, caption=

Associations among air pollutants, prefrontal cortex and T2DM

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变量OR值(95%CI）P值
暴露
PM2.51.062(1.003～1.159)0.044
PM101.116(1.026～1.214)0.010
NO21.083(1.004～1.184)0.022
NOX1.091(1.002～1.189)0.040
中介
内侧前额叶皮质体积（左）0.944(0.860～1.037)0.213
内侧前额叶皮质体积（右）0.869(0.755～0.949)0.042
额盖皮质体积（左）0.808(0.745～0.925)0.020
额盖皮质体积（右）0.924(0.851～1.113)0.168
眶额皮质体积（左）0.897(0.815～0.988)0.011
眶额皮质体积（右）0.823(0.738～0.917)0.020
额极体积（左）0.909(0.824～1.003)0.057
额极体积（右）0.881(0.796～0.974)0.013
), ArticleFig(id=1241050841113751554, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1241034448586723700, language=CN, label=表3, caption=

大气污染物、前额叶皮质体积和T2DM的关联

, figureFileSmall=null, figureFileBig=null, tableContent=
变量OR值(95%CI）P值
暴露
PM2.51.062(1.003～1.159)0.044
PM101.116(1.026～1.214)0.010
NO21.083(1.004～1.184)0.022
NOX1.091(1.002～1.189)0.040
中介
内侧前额叶皮质体积（左）0.944(0.860～1.037)0.213
内侧前额叶皮质体积（右）0.869(0.755～0.949)0.042
额盖皮质体积（左）0.808(0.745～0.925)0.020
额盖皮质体积（右）0.924(0.851～1.113)0.168
眶额皮质体积（左）0.897(0.815～0.988)0.011
眶额皮质体积（右）0.823(0.738～0.917)0.020
额极体积（左）0.909(0.824～1.003)0.057
额极体积（右）0.881(0.796～0.974)0.013
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宋婷 , 许欢 , 唐雪薇 , 郭冰 , 赵星 , 张菊英
现代预防医学 | 临床与预防 2025,52(11): 2101-2106
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现代预防医学 | 临床与预防 2025, 52(11): 2101-2106
前额叶皮质体积在大气污染长期暴露与2型糖尿病发病中的中介作用
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宋婷, 许欢, 唐雪薇, 郭冰, 赵星, 张菊英
作者信息
  • 四川大学华西公共卫生学院/华西第四医院流行病与卫生统计学系，四川 成都 610041

    • 宋婷（1998—），女，硕士在读，研究方向：流行病与卫生统计

通讯作者:

张菊英，E-mail:
The mediating role of prefrontal cortex volume in the association between long-term exposure to air pollution and the incidence of type 2 diabetes
Ting SONG, Huan XU, Xue-wei TANG, Bing GUO, Xing ZHAO, Ju-ying ZHANG
Affiliations
  • Department of Epidemiology and Health Statistics, West China School of Public Health/West China Fourth Hospital, Sichuan University, Chengdu, Sichuan 610041, China
出版时间: 2025-06-10 doi: 10.20043/j.cnki.MPM.202502264
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摘要
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目的

本研究旨在探讨前额叶皮质体积在大气污染长期暴露和2型糖尿病（type 2 diabetes mellitus，T2DM）发病关联中的中介效应，为减轻T2DM的负担和病因学提供依据。

方法

基于英国生物银行队列数据，使用多因素线性回归和logistic回归模型分析四种大气污染物、八个前额叶皮质体积、2型糖尿病三者之间的关联。使用多中介分析估计八个前额叶皮质体积整体的中介作用。

结果

研究最终纳入26 624人，T2DM发病率约为2.0%。大气污染物浓度与前额叶皮质体积总体上呈负相关关系。大气污染物浓度升高会增加T2DM的发病风险，其中，PM2.5浓度每增加1个SD，其OR (95%CI)为1.062(1.003～1.159)；右部内侧前额叶皮质体积、左侧额盖皮质体积、左右两侧眶额皮质体积内侧、右侧额极体积减小会增加T2DM的风险，其OR(95%CI)分别为0.869(0.755～0.949)、0.808(0.745～0.925)、0.897(0.815～0.988)、0.823(0.738～0.917)、0.881(0.796～0.974)。前额叶皮质体积介导了四种大气污染物与T2DM发病风险的关联。

结论

研究表明，大气污染物浓度的增加会提高T2DM的发生风险，前额叶皮质体积可能是大气污染物与T2DM的关联中重要的中介因子。通过减少大气污染物暴露，以及针对性地干预睡眠、运动等影响大脑活力的因素，能够有针对性地预防T2DM的发生与发展。

大气污染  /  2型糖尿病  /  前额叶皮质体积  /  中介分析
Objective

To investigate the mediating effect of prefrontal cortex volume in the association between long-term exposure to air pollution and the incidence of Type 2 Diabetes (T2DM), providing a basis for alleviating the burden and understanding the etiology of T2DM.

Methods

Utilizing data from the UK Biobank cohort, we analyzed the relationships among four air pollutants, eight prefrontal cortex volumes, and T2DM using multiple linear regression and logistic regression models. A multiple mediation analysis was conducted to estimate the overall mediating effect of the eight prefrontal cortex volumes.

Results

A total of 26 624 participants were included in the study, with a T2DM incidence rate of approximately 2.0%. There was an overall negative correlation between air pollutant concentrations and prefrontal cortex volume. Increased concentrations of air pollutants were associated with a higher risk of T2DM; specifically, for every 1 standard deviation increase in PM2.5 concentration, the odds ratio (OR) (95% confidence interval [CI]) was 1.062 (1.003-1.159). Decreased volumes of the right medial prefrontal cortex, left superior frontal gyrus, bilateral orbital frontal cortex, and right frontal pole were associated with increased T2DM risk, with OR (95%CI) values of 0.869 (0.755-0.949), 0.808(0.745-0.925), 0.897 (0.815-0.988), 0.823 (0.738-0.917), and 0.881 (0.796-0.974), respectively. The volume of the prefrontal cortex mediated the association between the four air pollutants and T2DM risk.

Conclusion

The study indicates that increased air pollutant concentrations elevate the risk of T2DM, and prefrontal cortex volume may serve as a significant mediating factor in the relationship between air pollution and T2DM. Reducing exposure to air pollutants and targeted interventions addressing factors affecting brain vitality, such as sleep and exercise, may effectively prevent the occurrence and progression of T2DM.

Air pollution  /  Type 2 diabetes  /  Prefrontal cortex volume  /  Mediation analysis
宋婷, 许欢, 唐雪薇, 郭冰, 赵星, 张菊英. 前额叶皮质体积在大气污染长期暴露与2型糖尿病发病中的中介作用. 现代预防医学, 2025 , 52 (11) : 2101 -2106 . DOI: 10.20043/j.cnki.MPM.202502264
Ting SONG, Huan XU, Xue-wei TANG, Bing GUO, Xing ZHAO, Ju-ying ZHANG. The mediating role of prefrontal cortex volume in the association between long-term exposure to air pollution and the incidence of type 2 diabetes[J]. Modern Preventive Medicine, 2025 , 52 (11) : 2101 -2106 . DOI: 10.20043/j.cnki.MPM.202502264
正文
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2型糖尿病（type 2 diabetes mellitus，T2DM）是一种以胰岛素抵抗和高血糖为特征的代谢紊乱的疾病[1]。据估计，到2040年全球T2DM患者将达到6.42亿[2]。肥胖、吸烟、不合理饮食以及缺乏身体活动等代谢和行为风险因素，被公认是导致T2DM发病与疾病负担加剧的主要原因[3]。与此同时，越来越多的研究指出，大气污染暴露也是不可忽视的重要致病因素，它作为一种较强效的促炎因子，极大影响着人体健康[4]。一项包括五项横断面研究和五项前瞻性队列研究的meta分析表明，暴露于大气颗粒物或二氧化氮（NO2）会增加患T2DM的风险[5]。许多流行病学研究提示，大气污染物不仅通过诱发全身性炎症与氧化应激直接损害胰岛β细胞功能并加剧胰岛素抵抗[6]，还可能通过损伤中枢神经系统干扰代谢调控，从而增加T2DM风险。前额叶皮质作为高级认知与自主神经调控的核心脑区，通过下丘脑-垂体-肾上腺轴（HPA轴）和自主神经系统参与糖脂代谢调节[7]，提示前额叶损伤可能是连接环境污染与T2DM的关键神经枢纽。然而，前额叶皮质体积在大气污染与T2DM关联中的中介作用尚未被人群研究证实，其潜在通路亟待阐明。
本研究基于英国生物银行（UK Biobank）队列，通过多中介模型来探索前额叶皮质体积在大气污染暴露和T2MD发病中的中介作用，为阐明大气污染暴露致T2DM的神经机制及制定靶向干预策略提供证据支持。
1　对象与方法
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1.1　对象
本研究的参与者来自英国生物银行队列，该队列基于人口登记系统，在2006—2010年抽样选取了大约50万名年龄在40～69岁的参与者。参与者通过问卷调查和体格检查提供了人口统计学、健康状况及社会经济等方面的信息，这些参与者均通过触摸屏问卷的方式签署了知情同意书。
本研究纳入的个体在2014年之后接受了首次影像学检查，共46 393例，参与者提供了相应的脑成像数据。研究排除了以下调查对象：（1）第一次影像学检查之前发生T2DM的686名患者；（2）暴露、中介、协变量数据不完整的11 618例个体；（3）被诊断患有神经系统感染、头部或神经损伤或外伤、中风等神经系统疾病的7 465例个体。最终纳入26 624名参与者。本研究获得了英国生物银行队列的批准，申请号为117185。
1.2　方法
1.2.1　暴露测量
本研究采用欧洲空气污染效应队列研究开发的土地利用回归模型（land use regression,LUR）对大气污染物浓度进行评估。该模型通过关联研究对象基线访视时提供的居住地址信息，对PM2.5、PM10、NO2、氮氧化物（NOX）指标进行浓度估算。由于数据可及性的限制，我们采用了2010年的大气污染物年平均浓度数据来代表个体长期污染物暴露水平。同时研究表明，大气污染物浓度在英国生物银行队列调查期间保持稳定。
1.2.2　脑影像标志物测量
脑成像数据是通过西门子Skyra 3T扫描仪和32通道射频接收头线圈采集的。T1加权MPRAGE序列的具体参数如下：分辨率为1 mm×1 mm×1 mm，视野矩阵为208×256×256，扫描时长为5 min。成像过程和质量控制由英国生物银行团队完成[8]。研究纳入了左右内侧前额叶皮质体积、左右额盖皮质体积、左右眶额皮质体积、左右额极体积八个前额叶皮质体积。这些数据均已根据头围大小进行了标准化。一般来讲，更小的前额叶皮质体积与更严重的脑萎缩有关[9]。
1.2.3　协变量
根据既往文献回顾，我们在模型中控制了年龄、性别、评估中心、文化程度、家庭收入、吸烟、饮酒、自我报告健康状况、运动情况、BMI、膳食情况、父母是否患糖尿病。所有协变量均在基线调查中收集。若被调查者回答“不知道”或者“不愿意回答”，则定义为“不清楚”。将巴茨、伯明翰、利物浦等23个评估中心按归属位置分为英格兰、苏格兰、威尔士。将教育变量分为三类：低于大学水平、大学或更高水平和不清楚。家庭平均年收入被分为以下几类：低于3.1万英镑、3.1万及以上英镑和不清楚。吸烟状态变量将参与者分为从不吸烟者、戒烟者、在吸者和不清楚。同样，饮酒状态变量将参与者分为从不饮酒者、戒酒者、在饮者和不清楚。采用国际身体活动问卷（IPAQ）对身体活动强度进行评估，并将其分为低、中、高水平。健康饮食指数基于美国心脏协会指南，通过以下指标评估膳食健康程度：蔬菜（≥4勺/天）、水果（≥3份/天）、鱼类（≥2次/周）、未加工红肉（≤2次/周）及加工肉类（≤2次/周）。每项达标计1分，总分0～5分，分值越高表明饮食模式越接近健康标准。若父母中至少一人患病（包括父亲、母亲或双亲）定义为存在家族史，若父母均未患病定义为不存在家族史。
1.3　统计分析
采用R 4.3.3版本进行一般描述性分析，连续性变量用（均数±标准差）表示，分类变量用频数（构成比）表示，运用t检验或χ2检验进行单因素分析，多因素线性回归和logistic回归模型分析四种大气污染物、八个前额叶皮质体积、T2DM三者之间的关联。使用“CMAverse”包进行多中介分析来估计了大气污染物和T2DM的直接、间接和总效应以及八个前额叶皮质体积总体的介导比例。检验水准α=0.05。
2　结果
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2.1　一般情况
研究最终纳入26 624人，T2DM新发546人，发病率约为2.0%，中位随访时间为13.8年（四分位数间距：13.1～14.5年）。相比于T2DM患者，未患T2DM的研究对象有较低的年龄、较高的教育程度和家庭收入、更低的BMI和较高的体力活动、更低浓度的PM2.5、PM10及NOX污染物暴露、更大的前额叶皮质体积情况。见表1。
2.2　大气污染物与前额叶皮质体积的关联
表2显示大气污染物浓度与前额叶皮质体积呈负相关关系，PM2.5、PM10及NO2每增加1个SD，除右侧额盖皮质以外的各前额叶皮质体积减小（脑萎缩）的风险增加；NOX浓度每增加1个SD，各前额叶皮质体积减小（脑萎缩）的风险增加。
2.3　大气污染物、前额叶皮质体积和T2DM中的关联
表3显示大气污染物浓度、前额叶皮质体积和T2DM之间的关联。大气污染物浓度升高会增加T2DM的发病风险，其中，PM2.5浓度每增加1个SD，其OR(95%CI)为1.062(1.003～1.159)；右部内侧前额叶皮质体积、左侧额盖皮质体积、左右两侧眶额皮质体积、右侧额极体积减小会增加T2DM的风险，其OR(95%CI)分别为0.869(0.755～0.949)、0.808(0.745～0.925)、0.897(0.815～0.988)、0.823(0.738～0.917)、0.881(0.796～0.974)。
2.4　大气污染物-前额叶皮质体积-T2DM的中介效应
图1显示前额叶皮质体积介导了四种大气污染物与T2DM发病风险的关联。该中介因子在PM2.5-前额叶皮质体积-T2DM、PM10-前额叶皮质体积-T2DM、NO2-前额叶皮质体积-T2DM及NOx-前额叶皮质体积-T2DM通路中分别解释了6.7%、4.5%、5.0%、5.4%的效应。
3　讨论
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本研究基于英国生物银行队列，首次探讨了大气污染长期暴露与T2DM关联的中间途径，发现大气污染物长期暴露与右部内侧前额叶皮质体积、左右两侧眶额皮质体积内侧等前额叶皮质体积减小有关。污染物浓度增加、部分前额叶皮质体积减小可使T2DM发病风险升高。此外，前额叶皮质体积部分介导了PM2.5、PM10、NO2、NOx与T2DM之间的关系，且这种介导关系因污染物的种类而不同，其中PM2.5的中介作用占比最大。
T2DM是一类以血糖调节受损为主要特征的代谢性疾病，通常与肥胖症高度相关[10-11]。PM2.5等污染物可通过激活交感神经系统引发下丘脑炎症，同时长期暴露于PM10、NO2等污染物会加剧系统性低度炎症及氧化应激[12]，这为T2DM发生奠定病理基础。除了经典的炎症途径外，大气污染物介导的自主神经平衡改变可能会通过交感神经系统的过度活跃进一步加剧全身胰岛素抵抗[13]。此外一些研究表明暴露于环境细颗粒物与胰岛素抵抗有关[14-15]。
本研究结果提示前额叶皮质体积改变可能部分介导了大气污染物与T2DM关联。四种大气污染物与八个前额叶皮质体积呈负相关关系，其中，PM2.5和NOx与八个前额叶皮质体积均呈负相关且关联有统计学意义。一项墨西哥城的大气污染与儿童前额叶白质损伤的研究同样显示大气污染与前额叶体积之间呈负相关[16]。另一项采用不同神经影像学技术测量脑体积的研究也发现，在平均年龄为70.5岁的1 365名女性样本中，PM2.5与背外侧和内侧前额叶区域的灰质体积减少有关[17]。一项动物研究还表明大气污染暴露可能会通过诱导氧化应激和炎症因子释放，破坏血脑屏障的完整性，致使毒性物质渗入脑实质，进而引发神经炎症、神经元凋亡及灰质密度降低，造成神经生物学损伤[18]。由此可见，大气污染物暴露可能是影响前额叶皮质体积的重要因素。不仅如此，本研究发现前额叶皮质体积减小与T2DM的高风险有关。前额叶皮质中的瘦素受体基因网络不仅通过影响瘦素水平影响葡萄糖代谢，还能通过D2受体介导的前额叶皮质中多巴胺能系统影响进食行为和调节食欲，从而增加肥胖风险和内分泌紊乱发展的风险[19-20] 。因此，前额叶皮质功能障碍可以解释大气污染物与T2DM之间的潜在影响机制。总的来说，这一新发现提示了大气污染物通过影响前额叶皮质功能进而影响T2DM风险的潜在机制，为精确干预提供了有价值的信息，提示我们可以通过减少大气污染物接触和控制影响中介因子的变量来预防T2DM的发生。
大气污染物对T2DM发病风险的总体影响仅有部分能够通过前额叶皮质体积的改变解释。大气污染物影响糖尿病的潜在途径是多样的。后续研究需要将其他潜在的中介因素纳入考量，以进一步探索大气污染物诱导T2DM的机制。本研究存在一定的局限性：第一，由于并不是所有参与者都接受了脑成像检查，研究可能会受到选择偏倚的影响。其次，我们的研究是横断面设计，限制了我们建立因果关系的能力。然而，本研究也具有许多优势：第一，本研究首次探讨了大气污染物与T2DM关联的中间途径，发现前额叶皮质体积在其中的中介作用，这一发现有助于后续研究中更有针对性地探索大气污染物诱导T2DM的机制；第二，本研究以社区为基础选取样本，全面纳入了涉及健康和社会人口指标等多个混杂变量；第三，该研究排除了患有神经系统疾病的个体，因为这些个体的大脑可能会发生一些难以预测的改变，从而影响我们的结果。
综上所述，大气污染物的增加可使T2DM发生风险升高，前额叶皮质体积部分介导了大气污染物和T2DM之间的关系，以PM2.5最为明显。这些发现可以为前额叶皮质体积的中介作用提供证据，对制定公共政策意义重大。通过干预睡眠、运动等影响大脑活力的因素，有望预防T2DM的发生发展。
基金
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  • 国家自然科学基金(82103943)
  • 国家自然科学基金(82073667)
  • 四川省科技厅(2025ZNSFSC1784)
文献
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doi: 10.20043/j.cnki.MPM.202502264
  • 接收时间：2025-02-18
  • 首发时间：2026-03-18
  • 出版时间：2025-06-10
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  • 收稿日期：2025-02-18
基金
国家自然科学基金(82103943)
国家自然科学基金(82073667)
四川省科技厅(2025ZNSFSC1784)
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    四川大学华西公共卫生学院/华西第四医院流行病与卫生统计学系，四川 成都 610041

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2种不同金属材料的力学参数
科
Family		 属数
Number of
genus		 种数
Number of
species		 占总种数比例
Percentage of
total species (%)		 属
Genus		 种数
Number of
species		 占总种数比例
Percentage of total
species (%)
鹅膏菌科Amanitaceae 2 11 5.26 鹅膏菌属 Amanita 10 4.78
小菇科 Mycenaceae 2 12 5.74 丝盖伞属 Inocybe 5 2.39
多孔菌科 Polyporaceae 8 14 6.70 蜡蘑属 Laccaria 5 2.39
红菇科 Russulaceae 3 23 11.00 小皮伞属 Marasmius 6 2.87
小菇属 Mycena 11 5.26
光柄菇属 Pluteus 5 2.39
红菇属 Russula 17 8.13
栓菌属 Trametes 5 2.39
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