Fine particulate matter

细颗粒物
  • 文章类型: Journal Article
    背景:关于细颗粒物(PM2.5)结合的重金属与肺功能之间的关联的报道很少。
    目的:评估单一和混合PM2.5重金属与肺功能的关系。
    方法:本研究包括武汉-珠海队列中224名中国成年人在两个研究期间的316个观察结果,并测量参与者的个人PM2.5结合重金属和肺功能。三种线性混合模型,包括单成分模型,PM2.5调整成分模型,和成分残差模型用于评估单一金属与肺功能之间的关联。混合暴露模型包括贝叶斯核机回归(BKMR)模型,加权分位数和(WQS)模型,和可解释的机器学习模型用于评估PM2.5结合的重金属混合物与肺功能之间的关系。
    结果:在单次暴露分析中,PM2.5结合铅的显著负相关,锑,观察到峰值呼气流量(PEF)的镉。在混合暴露分析中,1s用力呼气量(FEV1)/用力肺活量(FVC)显著下降,最大呼气中流量(MMF),75%的肺容积(FEF75)的用力呼气流量与PM2.5结合的重金属混合物增加有关。BKMR模型表明PM2.5结合的铅和锑与肺功能呈负相关。此外,PM2.5结合铜与FEV1/FVC呈正相关,MMF,FEF75可解释的机器学习模型表明,FEV1/FVC,MMF,FEF75随着PM2.5结合铅的升高而降低,锰,和钒,并随着PM2.5结合铜的升高而增加。
    结论:在PM2.5结合的重金属混合物与FEV1/FVC之间检测到负相关,MMF,以及FEF75。在PM2.5结合的重金属混合物中,PM2.5结合铅,锑,锰,钒与FEV1/FVC呈负相关,MMF,和FEF75,而PM2.5结合铜与FEV1/FVC呈正相关,MMF,FEF75
    BACKGROUND: There are a few reports on the associations between fine particulate matter (PM2.5)-bound heavy metals and lung function.
    OBJECTIVE: To evaluate the associations of single and mixed PM2.5-bound heavy metals with lung function.
    METHODS: This study included 316 observations of 224 Chinese adults from the Wuhan-Zhuhai cohort over two study periods, and measured participants\' personal PM2.5-bound heavy metals and lung function. Three linear mixed models, including the single constituent model, the PM2.5-adjusted constituent model, and the constituent residual model were used to evaluate the association between single metal and lung function. Mixed exposure models including Bayesian kernel machine regression (BKMR) model, weighted quantile sum (WQS) model, and Explainable Machine Learning model were used to assess the relationship between PM2.5-bound heavy metal mixtures and lung function.
    RESULTS: In the single exposure analyses, significant negative associations of PM2.5-bound lead, antimony, and cadmium with peak expiratory flow (PEF) were observed. In the mixed exposure analyses, significant decreases in forced expiratory volume in 1 s (FEV1)/forced vital capacity (FVC), maximal mid-expiratory flow (MMF), and forced expiratory flow at 75% of the pulmonary volume (FEF75) were associated with the increased PM2.5-bound heavy metal mixture. The BKMR models suggested negative associations of PM2.5-bound lead and antimony with lung function. In addition, PM2.5-bound copper was positively associated with FEV1/FVC, MMF, and FEF75. The Explainable Machine Learning models suggested that FEV1/FVC, MMF, and FEF75 decreased with the elevated PM2.5-bound lead, manganese, and vanadium, and increased with the elevated PM2.5-bound copper.
    CONCLUSIONS: The negative relationships were detected between PM2.5-bound heavy metal mixture and FEV1/FVC, MMF, as well as FEF75. Among the PM2.5-bound heavy metal mixture, PM2.5-bound lead, antimony, manganese, and vanadium were negatively associated with FEV1/FVC, MMF, and FEF75, while PM2.5-bound copper was positively associated with FEV1/FVC, MMF, and FEF75.
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  • 文章类型: Journal Article
    背景:短期暴露于颗粒物空气污染与COPD的恶化有关,但其与COPD死亡率的关系尚未完全阐明.我们旨在使用个体水平数据评估中国短期颗粒物暴露与COPD死亡风险之间的关系。
    方法:我们从2013年至2019年中国大陆的国家死亡登记数据库中得出了226万例COPD死亡。通过1×1km分辨率的基于卫星的模型评估了细颗粒物(PM2.5)和粗颗粒物(PM2.5-10)的暴露情况,并根据居住地址分配给每个人。使用时间分层病例交叉设计和分布滞后模型的条件逻辑回归检查PM2.5和PM2.5-10与COPD死亡率的关系。我们进一步按年龄进行了分层分析,性别,教育水平,和季节。
    结果:短期暴露于PM2.5和PM2.5-10与COPD死亡风险增加相关。这些关联在并发的一天出现并达到顶峰,在5或7天后减弱并变得无意义,分别。暴露-反应曲线是近似线性的,没有可辨别的阈值。PM2.5和PM2.5-10浓度的四分位数间距增加与4.23%(95%CI:3.75%,4.72%)和2.67%(95%CI:2.18%,3.16%)滞后0-7d,COPD死亡率风险更高,分别。PM2.5和PM2.5-10的相关性略有减弱,但在相互调节模型中仍然显着。在温暖的季节观察到PM2.5-10的关联更大。
    结论:这个个体层面,全国范围内,病例交叉研究表明,PM2.5和PM2.5-10的短期暴露可能是COPD死亡的环境危险因素之一.
    背景:本研究得到了国家重点研究发展计划(2023YFC3708304和2022YFC3702701)的支持,国家自然科学基金(82304090和82030103),《上海市加强公共卫生体系建设三年行动计划》(GWVI-11.2-YQ31),上海市科学技术委员会(21TQ015)。
    BACKGROUND: Short-term exposure to particulate matter air pollution has been associated with the exacerbations of COPD, but its association with COPD mortality was not fully elucidated. We aimed to assess the association between short-term particulate matter exposure and the risk of COPD mortality in China using individual-level data.
    METHODS: We derived 2.26 million COPD deaths from a national death registry database in Chinese mainland between 2013 and 2019. Exposures to fine particulate matter (PM2.5) and coarse particulate matter (PM2.5-10) were assessed by satellite-based models of a 1 × 1 km resolution and assigned to each individual based on residential address. The associations of PM2.5 and PM2.5-10 with COPD mortality were examined using a time-stratified case-crossover design and conditional logistic regressions with distributed lag models. We further conducted stratified analyses by age, sex, education level, and season.
    RESULTS: Short-term exposures to both PM2.5 and PM2.5-10 were associated with increased risks of COPD mortality. These associations appeared and peaked on the concurrent day, attenuated and became nonsignificant after 5 or 7 days, respectively. The exposure-response curves were approximately linear without discernible thresholds. An interquartile range increase in PM2.5 and PM2.5-10 concentrations was associated with 4.23% (95% CI: 3.75%, 4.72%) and 2.67% (95% CI: 2.18%, 3.16%) higher risks of COPD mortality over lag 0-7 d, respectively. The associations of PM2.5 and PM2.5-10 attenuated slightly but were still significant in the mutual-adjustment models. A larger association of PM2.5-10 was observed in the warm season.
    CONCLUSIONS: This individual-level, nationwide, case-crossover study suggests that short-term exposure to PM2.5 and PM2.5-10 might act as one of the environmental risk factors for COPD mortality.
    BACKGROUND: This study is supported by the National Key Research and Development Program of China (2023YFC3708304 and 2022YFC3702701), the National Natural Science Foundation of China (82304090 and 82030103), the 3-year Action Plan for Strengthening the Construction of the Public Health System in Shanghai (GWVI-11.2-YQ31), and the Science and Technology Commission of Shanghai Municipality (21TQ015).
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  • 文章类型: Journal Article
    为了追求碳中和,中国2060年的目标主要是减少温室气体排放,较少强调空气质量和公共卫生的相应好处。这项研究转向了这一关键关系,探索中国的碳中和与世界卫生组织关于细颗粒物(PM2.5)暴露的空气质量指南(WHOAQG)的一致性。耦合技术丰富的综合评估模型,排放浓度响应面模型,以及暴露和健康评估,我们发现脱碳降低了二氧化硫(SO2),氮氧化物(NOx),和PM2.5排放量超过90%;减少非甲烷挥发性有机化合物(NMVOCs)超过50%;同时减少各地区的差异。严重的,我们的分析表明,进一步有针对性地减少空气污染物,特别是NH3和非能源相关的NMVOCs,可能使大多数中国城市比完全专注于碳中和的途径早5至10年达到世卫组织PM2.5的AQG。因此,将空气污染控制措施纳入碳中和战略将为中国实现健康和环境平等提供重大机遇。
    In the pursuit of carbon neutrality, China\'s 2060 targets have been largely anchored in reducing greenhouse gas emissions, with less emphasis on the consequential benefits for air quality and public health. This study pivots to this critical nexus, exploring how China\'s carbon neutrality aligns with the World Health Organization\'s air quality guidelines (WHO AQG) regarding fine particulate matter (PM2.5) exposure. Coupling a technology-rich integrated assessment model, an emission-concentration response surface model, and exposure and health assessment, we find that decarbonization reduces sulfur dioxide (SO2), nitrogen oxides (NOx), and PM2.5 emissions by more than 90%; reduces nonmethane volatile organic compounds (NMVOCs) by more than 50%; and simultaneously reduces the disparities across regions. Critically, our analysis reveals that further targeted reductions in air pollutants, notably NH3 and non-energy-related NMVOCs, could bring most Chinese cities into attainment of WHO AQG for PM2.5 5 to 10 years earlier than the pathway focused solely on carbon neutrality. Thus, the integration of air pollution control measures into carbon neutrality strategies will present a significant opportunity for China to attain health and environmental equality.
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  • 文章类型: Journal Article
    背景:增强心血管健康(CVH)与降低死亡风险有关,而长期暴露于细颗粒物(PM2.5),提升了这些风险。长期暴露于PM2.5是否会抵消高CVH的健康益处尚不清楚。该研究旨在评估生命必需8(LE8)评估的CVH与死亡的关联在不同PM2.5暴露的参与者之间是否一致。
    方法:我们纳入了2013年8月至2014年6月中国慢性病及危险因素监测现场调查的134,727名参与者。参与者的死亡是通过与国家死亡率监测系统(2013-2018)链接获得的。通过卫星反演获得环境数据。使用LE8方法计算参与者的CVH评分。使用Cox回归模型计算死亡率的危险比(HR)和95%置信区间(95CI)。
    结果:共记录了2936例全因死亡和1158例心血管疾病(CVD)死亡。与低CVH相比,高CVH显示全因死亡率的风险降低,与PM2.5暴露水平无关(P<0.05,所有交互作用P>0.05)。此外,与那些低CVH和最高PM2.5暴露的人相比,高CVH和低PM2.5暴露的成年人在全因死亡率方面的HR为0.18(95CI,0.12-0.25),在CVD死亡率方面的HR为0.13(95CI,0.08-0.22).
    结论:高CVH与全因死亡风险降低相关,无论PM2.5暴露水平如何。对于中国成年人来说,维持高CVH是可取的,不管他们居住的地方。
    BACKGROUND: Enhanced cardiovascular health (CVH) is linked to reduced mortality risks, whereas long-term exposure to fine particulate matter (PM2.5), elevates these risks. Whether long-term exposure to PM2.5 counteracts the health benefits of high CVH is unknown. The study aims to evaluate whether the association of CVH assessed by Life\'s Essential 8 (LE8) with death was consistent between participants with different PM2.5 exposures.
    METHODS: We included 134,727 participants in the field survey of China Chronic Disease and Risk Factor Surveillance which was conducted from August 2013 to June 2014. The deaths of participants were obtained by linking to the National Mortality Surveillance System (2013-2018). The environmental data is obtained by satellite inversion. The participants\' CVH scores were calculated using the LE8 method. Hazard ratio (HR) and 95% confidence intervals (95%CI) for mortality were calculated using Cox regression models.
    RESULTS: A total of 2,936 all-cause deaths and 1,158 cardiovascular disease (CVD) deaths were recorded. Compared to those with low CVH, adults with high CVH demonstrated a reduced risk of all-cause mortality, irrespective of their PM2.5 exposure levels (P < 0.05, all P for interaction >0.05). Furthermore, in comparison to those with low CVH and highest PM2.5 exposure, adults with high CVH and lowest PM2.5 exposure exhibited HR of 0.18 (95%CI, 0.12-0.25) for all-cause mortality and 0.13 (95%CI, 0.08-0.22) for CVD mortality.
    CONCLUSIONS: High CVH is associated with reduced all-cause mortality risk, regardless of PM2.5 exposure levels. For Chinese adults, sustaining high CVH is advisable, irrespective of their residential location.
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  • 文章类型: Journal Article
    细颗粒物(PM2.5)可破坏气道上皮屏障。阴离子转运系统在气道上皮屏障中起着至关重要的作用。然而,PM2.5对阴离子转运系统的有害作用和机制尚不清楚。在这项研究中,使用气道上皮细胞和卵清蛋白(OVA)诱导的哮喘小鼠。在Transwell模型中,暴露于PM2.5后,三磷酸腺苷(ATP)诱导的跨上皮阴离子短路电流(Isc)和气道表面液(ASL)显着降低。此外,PM2.5暴露降低了P2Y2R的表达水平,CFTR和细胞质游离钙,但是ATP可以增加这些蛋白质的表达。PM2.5暴露导致支气管肺泡灌洗液Th2相关细胞因子水平升高,肺部炎症,胶原沉积和杯状细胞增生。有趣的是,给予ATP对PM2.5诱导的肺部炎症有抑制作用。一起,我们的研究表明,PM2.5通过下调P2Y2R/CFTR途径损害ATP诱导的跨上皮阴离子Isc,该过程可能参与加重气道高反应性和气道炎症。这些发现可能为PM2.5介导的气道上皮损伤提供重要见解。
    Fine particulate matter (PM2.5) can damage airway epithelial barriers. The anion transport system plays a crucial role in airway epithelial barriers. However, the detrimental effect and mechanism of PM2.5 on the anion transport system are still unclear. In this study, airway epithelial cells and ovalbumin (OVA)-induced asthmatic mice were used. In transwell model, the adenosine triphosphate (ATP)-induced transepithelial anion short-circuit current (Isc) and airway surface liquid (ASL) significantly decreased after PM2.5 exposure. In addition, PM2.5 exposure decreased the expression levels of P2Y2R, CFTR and cytoplasmic free-calcium, but ATP can increase the expressions of these proteins. PM2.5 exposure increased the levels of Th2-related cytokines of bronchoalveolar lavage fluid, lung inflammation, collagen deposition and hyperplasisa of goblet cells. Interestingly, the administration of ATP showed an inhibitory effect on lung inflammation induced by PM2.5. Together, our study reveals that PM2.5 impairs the ATP-induced transepithelial anion Isc through downregulating P2Y2R/CFTR pathway, and this process may participate in aggravating airway hyperresponsiveness and airway inflammation. These findings may provide important insights on PM2.5-mediated airway epithelial injury.
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  • 文章类型: Journal Article
    苦瓜(MC),通常被称为GAC水果,是一种富含抗氧化剂和生物活性化合物的热带水果。本研究旨在阐明MC对表皮角质形成细胞HaCaT细胞中直径小于10μm( Momordica cochinchinensis (MC), commonly known as gac fruit, is a tropical fruit rich in antioxidants and bioactive compounds. This research aimed to elucidate the effect of MC on apoptosis induced by fine particulate matter with a diameter of less than 10 μm (< PM10) in epidermal keratinocyte HaCaT cells. We found that PM10 significantly diminish the viability of HaCaT cells through cytotoxic mechanisms. However, the treatment with MC at a concentration of 10 μg/mL notably restored the cellular viability decreased by PM10. MC reduced the activation of extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase (MAPK) by mainly preventing the generation of reactive oxygen species (ROS) in HaCaT cells subjected to PM10. Furthermore, MC exhibited a regulatory effect on the expression of genes associated with apoptosis, including B-Cell Lymphoma 2 (Bcl-2), Bcl-2 associated X protein (Bax), and cleaved caspase-3 by inhibiting the activation of the transcription factor nuclear factor-kappa B (NF-κB). These findings demonstrate that MC aids in neutralizing the apoptotic signaling pathway of free radicals produced by environmental pollutants such as PM10, which have the potential to damage skin cells and accelerate the aging process.
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  • 文章类型: Journal Article
    青藏高原,被称为“第三极”由于其独特的高海拔环境,容易受到地面臭氧(O3)和细颗粒物(PM2.5)的污染。本研究利用地面测量数据和气象卫星的多源数据构建了随机森林回归模型,预测了青藏高原7个主要城市两年来地面O3和PM2.5浓度的变化及其影响因素。这些模型成功地再现了O3和PM2.5的水平,R平方值分别为0.71和0.73。结果表明,与燃烧相关的一氧化碳(CO)和二氧化氮(NO2)对O3和PM2.5浓度的影响最大。太阳辐射,地理因素,气象变量在驱动污染物变化中也起着至关重要的作用。相反,与运输相关的因素和人类活动因素表现出相对较低的显著性。高O3和PM2.5污染发生在季风前和季风后/冬季,受太阳辐射和排放的驱动,分别。虽然CO一直在城市和季节做出贡献,关键影响因素局部不同。这项研究揭示了控制整个青藏高原空气污染物变化的关键驱动力,在这个独特的高海拔地区,照亮了复杂的大气过程。
    The Tibetan Plateau, known as the \"Third Pole\", is susceptible to ground-level ozone (O3) and fine particulate matter (PM2.5) pollution due to its unique high-altitude environment. This study constructed random forest regression models using multi-source data from ground measurements and meteorological satellites to predict variations in ground-level O3 and PM2.5 concentrations and their influencing factors across seven major cities in the Tibetan Plateau over two-year periods. The models successfully reproduced O3 and PM2.5 levels with satisfactory R-squared values of 0.71 and 0.73, respectively. Results reveal combustion-related carbon monoxide (CO) and nitrogen dioxide (NO2) as the most substantial influences on O3 and PM2.5 concentrations. Solar radiation, geographical factors, and meteorological variables also played crucial roles in driving pollutant variations. Conversely, transport-related and human activity factors exhibited relatively lower significance. High O3 and PM2.5 pollution occurred during pre-monsoon and post-monsoon/winter seasons, driven by solar radiation and emissions, respectively. While CO consistently contributed across cities and seasons, key influencing factors varied locally. This study unveils the key driving forces governing air pollutant variations across the Tibetan Plateau, shedding light on complex atmospheric processes in this unique high-altitude region.
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  • 文章类型: Journal Article
    背景:以前的研究主要集中在普通人群中的细颗粒物(PM2.5)与骨骼健康之间的联系,而不是PM2.5成分和特定人群。我们旨在调查中老年女性PM2.5成分与骨骼健康之间的关系。
    方法:从湖北省32个街道/村随机抽取748名中老年妇女。从中国追踪空气污染(TAP)数据集中提取了各个居民区的环境PM2.5及其成分的浓度。骨矿物质密度测量是从研究参与者的双能X射线吸收测量扫描中获得的。采用多变量逻辑和线性模型评估PM2.5及其成分与骨丢失之间的关系。
    结果:硝酸盐(NO3-)和铵(NH4+)浓度的每四分位数间距(IQR)增加与1.65[95%置信区间(CI):1.13,2.30]和1.77(95%CI:1.26,2.49)增加骨质疏松症的几率相关,分别。长期接触硫酸盐(SO42-),NO3-,NH4+与L1-L4腰椎的T评分和骨密度呈负相关。此外,老年人,14岁后有初潮的女性和绝经后的女性更容易受到PM2.5水溶性无机盐的影响。
    结论:该研究强调需要针对空气质量的全面政策,特别关注中老年妇女等弱势群体。旨在降低环境PM2.5浓度和尽量减少其有害成分暴露的公共卫生干预措施对于减轻对骨骼健康的不利影响和改善社区的整体福祉至关重要。
    BACKGROUND: Previous studies have primarily focused on the links between fine particulate matter (PM2.5) and bone health among the general population instead of PM2.5 components and the specific population. We aimed to investigate the associations between PM2.5 components and bone health among middle-aged and elderly women.
    METHODS: A total of 748 middle-aged and elderly women were randomly sampled from 32 streets/villages in Hubei Province. The concentrations of ambient PM2.5 and its components were extracted across various residential areas from the Tracking Air Pollution in China (TAP) dataset. Bone mineral density measurements were obtained from dual-energy X-ray absorptiometry scans of study participants. Multivariable logistic and linear models were employed to assess the relationship between PM2.5 and its components and bone loss.
    RESULTS: Per interquartile range (IQR) increase in nitrate (NO3-) and ammonium (NH4+) concentrations were associated with 1.65 [95% confidence intervals (CI): 1.13, 2.30] and 1.77 (95% CI: 1.26, 2.49) times higher odds of osteoporosis, respectively. Long-term exposure to sulfate (SO42-), NO3-, and NH4+ was negatively associated with T-scores and bone mineral density in L1-L4 lumbar vertebrae. In addition, the elderly, women who have experienced menarche after the age of 14, and postmenopausal women were more susceptible to the water-soluble inorganic salts of PM2.5.
    CONCLUSIONS: The study emphasizes the need for comprehensive policies addressing air quality, with a specific focus on vulnerable populations such as middle-aged and elderly women. Public health interventions aimed at reducing ambient PM2.5 concentrations and minimizing exposure to its harmful components are crucial in mitigating the adverse impact on skeletal health and improving the overall well-being of communities.
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  • 文章类型: Journal Article
    产前暴露于细颗粒物(PM2.5)与神经发育障碍增加有关。然而,PM2.5中最有害的成分和最脆弱的暴露时间窗口仍未确定,尤其是在PM2.5水平较高的地区。在一项涉及4494个母子双子的前瞻性队列研究中,我们检查了产前暴露于PM2.5及其四个主要成分与儿童神经发育和行为问题(NBPs)的关系,分别在三个怀孕三个月。使用泊松回归和广义加性模型来描述线性和非线性关联,分别。应用加权分位数和贝叶斯核机回归模型来检查暴露于混合成分和单个成分的影响。结果表明,在三个三个月中暴露于PM2.5及其成分会增加儿童NBPs的风险(妊娠早期的PM2.5风险比:1.16,95%置信区间1.14-1.18/μg/m3;妊娠中期为1.15,1.12-1.17;妊娠中期为1.06,1.04-1.08),随着妊娠进展,相关性逐渐减弱(趋势的P值<0.05)。在PM2.5的四个主要成分中,暴露于SO42-对儿童NBPs构成最高风险,而有机物对PM2.5暴露的总体影响所占比例最大。这些结果强调了减少孕妇PM2.5暴露对降低后代神经发育障碍风险的重要性。我们的研究结果将为PM2.5暴露的风险评估提供信息,并有助于制定针对高暴露水平的类似地区PM2.5特定成分的精确预防策略。
    Prenatal exposure to fine particulate matter (PM2.5) has been linked with increased neurodevelopmental disorders. However, the most detrimental component of PM2.5 and the most vulnerable exposure time windows remain undetermined, especially in areas with high PM2.5 levels. In a prospective cohort study involving 4494 mother-child dyads, we examined the associations of prenatal exposure to PM2.5 and its four main components with children\'s neurodevelopmental and behavioral problems (NBPs), separately in three pregnancy trimesters. Poisson regression and generalized additive models were used to depict the linear and nonlinear associations, respectively. Weighted quantile sum and Bayesian kernel machine regression models were applied to examine the effects of exposure to both mixed and individual components. Results showed that exposure to PM2.5 and its components throughout the three trimesters increased the risk of children\'s NBPs (Risk ratio for PM2.5: 1.16, 95 % confidence interval 1.14-1.18 per μg/m3 in the first trimester; 1.15, 1.12-1.17 in the second trimester; 1.06, 1.04-1.08 in the third trimester), with associations gradually diminishing as pregnancy progressed (P values for trends < 0.05). Among the four main components of PM2.5, exposure to SO42- posed the highest risks on children\'s NBPs, while organic matter contributed the largest proportion to the overall impacts of PM2.5 exposure. These results underscore the significance of mitigating PM2.5 exposure in pregnant women to reduce the risk of neurodevelopmental disorders in offspring. Our findings would inform risk assessment of PM2.5 exposure and facilitate the development of precision preventive strategies targeting specific components of PM2.5 in similar areas with high levels of exposure.
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  • 文章类型: Journal Article
    尽管环境细颗粒物(PM2.5)对2型糖尿病的不利影响以及体育锻炼(PA)的有益作用,PM2.5对PA与2型糖尿病关系的影响尚不清楚.
    在这项有71,689名参与者的前瞻性研究中,PA通过问卷进行评估,并将其分为体积四分位数和强度分为三组。长期PM2.5暴露是使用1公里分辨率的基于卫星的PM2.5估计值计算的。通过队列分层Cox比例风险模型评估PM2.5暴露和PA对2型糖尿病的影响,单独和组合。
    在488,166人年的随访中,观察到5487例2型糖尿病事件。PM2.5改变了PA与2型糖尿病之间的关系。与PA体积的最低四分位数相比,最高四分位数与低PM2.5分层(≤65.02µg/m3)的2型糖尿病风险降低相关,而不是高PM2.5分层(>65.02µg/m3),风险比(HR)为0.75(95%置信区间[CI]:0.66-0.85)和1.10(95%CI:0.99-1.22),分别。对于PA强度观察到类似的结果。高PM2.5暴露与最高PA水平增加2型糖尿病的风险最大(对于PA体积,HR=1.79,95%CI:1.59-2.01;对于PA强度,HR=1.82,95%CI:1.64-2.02)。
    PA可以降低低污染地区的2型糖尿病风险,但是高PM2.5暴露可能会削弱甚至逆转PA的保护作用。对于长期受污染的居民,应全面评估PA的安全和健康益处。
    UNASSIGNED: Despite the adverse effects of ambient fine particulate matter (PM2.5) on type 2 diabetes and the beneficial role of physical activity (PA), the influence of PM2.5 on the relationship between PA and type 2 diabetes remains unclear.
    UNASSIGNED: In this prospective study with 71,689 participants, PA was assessed by a questionnaire and was categorized into quartiles for volume and three groups for intensity. Long-term PM2.5 exposure was calculated using 1-km resolution satellite-based PM2.5 estimates. PM2.5 exposure and PA\'s effect on type 2 diabetes were assessed by cohort-stratified Cox proportional hazards models, individually and in combination.
    UNASSIGNED: In 488,166 person-years of follow-up, 5487 incident type 2 diabetes cases were observed. The association between PA and type 2 diabetes was modified by PM2.5. Compared with the lowest quartile of PA volume, the highest quartile was associated with reduced type 2 diabetes risk in low PM2.5 stratification (≤65.02 µg/m3) other than in high PM2.5 stratification (>65.02 µg/m3), with the hazard ratio (HR) of 0.75 (95% confidence interval [CI]: 0.66-0.85) and 1.10 (95% CI: 0.99-1.22), respectively. Similar results were observed for PA intensity. High PM2.5 exposure combined with the highest PA levels increased the risk of type 2 diabetes the most (HR = 1.79, 95% CI: 1.59-2.01 for PA volume; HR = 1.82, 95% CI: 1.64-2.02 for PA intensity).
    UNASSIGNED: PA could reduce type 2 diabetes risk in low-pollution areas, but high PM2.5 exposure may weaken or even reverse the protective effects of PA. Safety and health benefits of PA should be thoroughly assessed for long-term polluted residents.
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