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Residential Outdoor Air Pollution and Brain Morphology in the Adult Health and Behavior (AHAB Ⅱ) Cohort and Pittsburgh

机译:成年人和健康行为(AHABⅡ)队列和匹兹堡的居民室外空气污染和脑形态

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Background: Air pollution exposure is associated with increased inflammatory risk, and may adversely impact brain morphology through systemic inflammation, disruption of the blood-brain barrier, or translocation via olfactory mucosa. Currently, little is known about the relationship between air pollutants (particulate matter (PM_(2.5)), black carbon (BC), trace metal constituents) and brain morphology. The AHAB-Ⅱ cohort is a community-based registry to identify neural and biobehavioral predictors of physical and mental health in midlife. We combine individual brain morphology indicators with fine-scale air pollution exposure estimates to explore their associations. Aims: Geographic information system (GIS) was used to geocode participant addresses and assign individual air pollution exposure estimates. We developed models to examine associations between outdoor air pollution and brain morphology. Methods: Air pollution data were obtained from a monitoring campaign with 36 sites across the Pittsburgh region. Land use regression (LUR) models were developed for PM2.5, BC, and lead. We assigned mean pollutant concentrations within a 300 m buffer of each participant's residential location (n=306; mean age = 43 yrs; 45% men). Structural neuroimaging methods were used to determine indicators of brain morphology. Results: Preliminary results suggest that a 1 μg/m3 increase in summer PM_(2.5) exposure is associated with a -0.019 mm (p ≤ .05) decrease in cortical thickness after controlling for intracranial volume and age. Future analyses will examine other outcomes, and potentially mediating factors related to inflammation. Conclusions: This is among the first studies to examine associations between residence-specific air pollution exposures and brain morphology. Observed associations may have implications for pollution effects on brain-based functional outcomes (e.g., early cognitive declines).
机译:背景:暴露于空气污染会增加炎症风险,并可能通过全身性炎症,破坏血脑屏障或通过嗅觉粘膜移位而对大脑形态产生不利影响。目前,关于空气污染物(颗粒物(PM_(2.5)),黑碳(BC),痕量金属成分)与大脑形态之间关系的知识鲜为人知。 AHAB-Ⅱ队列是一个基于社区的注册表,用于识别中年人身心健康的神经和生物行为预测因子。我们将个体的大脑形态学指标与精细的空气污染暴露估算值结合起来,以探索它们的关联。目的:使用地理信息系统(GIS)对参加者的地址进行地理编码,并分配单个的空气污染暴露估算值。我们开发了模型来检查室外空气污染与大脑形态之间的关联。方法:空气污染数据来自匹兹堡地区36个地点的监测活动。针对PM2.5,BC和铅开发了土地利用回归(LUR)模型。我们在每个参与者居住地的300 m缓冲区内指定了平均污染物浓度(n = 306;平均年龄= 43岁; 45%的男性)。结构神经影像学方法被用来确定大脑形态的指标。结果:初步结果表明,控制颅内体积和年龄后,夏季PM_(2.5)暴露量增加1μg/ m3与皮质厚度减少-0.019 mm(p≤.05)有关。未来的分析将检查其他结果,以及与炎症相关的潜在中介因素。结论:这是检查居住场所特定的空气污染暴露与脑形态之间关系的第一批研究之一。观察到的联想可能会对污染对基于大脑的功能结果(例如早期认知能力下降)的影响产生影响。

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