Department of Psychology, Yale University, New Haven, CT, United States of America.
NYU Langone Health Department of Population Health, New York, NY, United States of America; Nathan Kline Institute for Psychiatric Research, Orangeburg, NY, United States of America.
Schizophr Res. 2020 Apr;218:63-69. doi: 10.1016/j.schres.2020.03.001. Epub 2020 Mar 10.
Air pollution has recently been linked to central nervous system (CNS) diseases, possibly mediated by inflammation and oxidative stress. Hippocampal atrophy in individuals with first episode schizophrenia (FES) has also been associated with biomarkers of inflammation and oxidative stress, whereas hippocampal atrophy was not observed in matched healthy controls with similar biomarker levels of inflammation and oxidative stress. Fine particulate matter (PM2.5), one component of air pollution, is most strongly implicated in CNS disease. The present study examined the association between PM2.5 and hippocampal volume in individuals with FES who participated in a 52-week placebo-controlled clinical trial of citalopram added to clinician-determined antipsychotic treatment at four sites in the US and China. Left hippocampal volumetric integrity (LHVI; inversely related to atrophy) was measured at baseline and week 52 using an automated highly-reliable algorithm. Mean annual PM2.5 concentrations were obtained from records compiled by the World Health Organization. The relationships between baseline LHVI and PM2.5 and change in LHVI and PM2.5 were evaluated using regression analyses. 89 participants completed imaging at baseline and 46 participants completed imaging at week 52. Mean annual PM2.5 was significantly associated with both baseline LHVI and change in LHVI after controlling for age, sex, baseline LHVI, duration of untreated psychosis and baseline antipsychotic medication dose. Air pollution may contribute to the progression of hippocampal atrophy after a first episode of illness, but these findings should be considered preliminary since other unmeasured factors may have differed between cities and contributed to the observed effect.
空气污染最近与中枢神经系统 (CNS) 疾病有关,可能通过炎症和氧化应激介导。首次发作精神分裂症 (FES) 患者的海马萎缩也与炎症和氧化应激的生物标志物有关,而在炎症和氧化应激标志物水平相似的匹配健康对照中未观察到海马萎缩。细颗粒物 (PM2.5) 是空气污染的一个组成部分,与 CNS 疾病的关系最为密切。本研究在美国和中国的四个地点参与了为期 52 周的安慰剂对照西酞普兰临床试验,对接受临床医生确定的抗精神病药物治疗的 FES 患者进行了 PM2.5 与海马体积之间的关联研究。在基线和第 52 周使用自动化高可靠性算法测量左海马容积完整性 (LHVI; 与萎缩呈负相关)。平均年 PM2.5 浓度从世界卫生组织汇编的记录中获得。使用回归分析评估基线 LHVI 与 PM2.5 之间以及 LHVI 和 PM2.5 变化之间的关系。89 名参与者在基线完成了成像,46 名参与者在第 52 周完成了成像。在控制年龄、性别、基线 LHVI、未治疗精神病的持续时间和基线抗精神病药物剂量后,平均年 PM2.5 与基线 LHVI 和 LHVI 变化均显著相关。空气污染可能导致首次发病后海马萎缩的进展,但这些发现应被认为是初步的,因为其他未测量的因素可能因城市而异,并导致观察到的影响。