Grande Giulia, Wu Bolin, Wu Jing, Kalpouzos Grégoria, Laukka Erika J, Bellander Tom, Rizzuto Debora
Aging Research Center, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet and Stockholm University, Sweden (G.G., B.W., G.K., E.J.L., T.B., D.R.).
Stockholm Gerontology Research Centre, Sweden (G.G., E.J.L., D.R.).
Stroke. 2025 Jul;56(7):1816-1822. doi: 10.1161/STROKEAHA.124.048096. Epub 2025 May 12.
Accumulating evidence links air pollution exposure to late-life cognitive deterioration. Whether air pollution alters brain structure remains poorly understood. Thus, we aimed to quantify the association between long-term exposure to particulate matter ≤2.5 µm and ≤10 µm (PM and PM, respectively) and late-life brain structural changes.
In the Swedish National Study on Aging and Care in Kungsholmen, Stockholm, 555 participants free from dementia underwent brain magnetic resonance imaging (MRI) scans at baseline and after 6 years (cohorts <78 years) or after 3 and 6 years (cohorts aged ≥78 years). After the exclusion of participants with neurological conditions (including previous stroke) and suboptimal MRI quality, we had 457 participants with available repeated MRI examinations, where total brain tissue volume, ventricles, hippocampus, and white matter hyperintensities volumes were assessed. PM and PM have been assessed since 1990 using dispersion models at residential addresses. Brain volumes have been standardized using baseline mean and SD. Long-term exposure to PM and PM in relation to the baseline and longitudinal brain MRI volumes were tested through multiadjusted (age, sex, educational level, smoking, socioeconomic status, and neighborhood household mean income) linear regression models.
At study entry, the mean (SD) age of the participants was 70 (SD, 8.9) years and 41% were males. Individuals who before baseline had been exposed to levels of PM or PM above the median (8.5 and 14.9 μg/m, respectively) had smaller total brain tissue volume (β, -0.20 [95% CI, -0.33 to -0.06] and β, -0.14 [95% CI, -0.28 to -0.01], respectively) at baseline than those with lower PM and PM levels. Participants exposed during the follow-up to PM>8.7 μg/m had on average an annual shrinkage of total brain tissue volume of 0.22 (95% CI, -0.43 to -0.01) and an annual increase of 0.25 (95% CI, 0.07-0.43) of the white matter hyperintensities as compared with participants exposed to PM<8.7 μg/m. No association was detected between PM and an annual rate of change in brain MRI volumes.
Long-term exposure to comparatively low levels of PM was associated with a greater load of structural brain changes, encompassing brain atrophy and vascular pathology. These findings, in a dementia- and cerebrovascular disease-free sample, underscore the importance of addressing air pollution as a modifiable risk factor for late-life cognitive decline, and highlight the need for targeted interventions to prevent its detrimental effects on brain integrity.
越来越多的证据表明，接触空气污染与晚年认知能力下降有关。空气污染是否会改变大脑结构仍知之甚少。因此，我们旨在量化长期接触粒径≤2.5微米和≤10微米的颗粒物（分别为PM₂.₅和PM₁₀）与晚年大脑结构变化之间的关联。
在瑞典斯德哥尔摩国王岛的老龄化与护理全国性研究中，555名无痴呆症的参与者在基线时以及6年后（年龄<78岁的队列）或3年和6年后（年龄≥78岁的队列）接受了脑磁共振成像（MRI）扫描。在排除患有神经系统疾病（包括既往中风）和MRI质量欠佳的参与者后，我们有457名参与者可进行重复的MRI检查，评估了全脑组织体积、脑室、海马体和白质高信号体积。自1990年起，使用扩散模型在居住地址评估PM₂.₅和PM₁₀。脑体积已使用基线均值和标准差进行标准化。通过多因素调整（年龄、性别、教育水平、吸烟、社会经济地位和邻里家庭平均收入）的线性回归模型，测试了长期接触PM₂.₅和PM₁₀与基线和纵向脑MRI体积之间的关系。
在研究开始时，参与者的平均（标准差）年龄为70（标准差，8.9）岁，41%为男性。在基线前接触PM₂.₅或PM₁₀水平高于中位数（分别为8.5和14.9微克/立方米）的个体，其基线时的全脑组织体积比PM₂.₅和PM₁₀水平较低的个体更小（β分别为-0.20[95%置信区间，-0.33至-0.06]和β为-0.14[95%置信区间，-0.28至-0.01]）。与接触PM₂.₅<8.7微克/立方米的参与者相比，随访期间接触PM₂.₅>8.7微克/立方米的参与者全脑组织体积平均每年萎缩0.22（95%置信区间，-0.43至-0.01），白质高信号每年增加0.25（95%置信区间，0.07 - 0.43）。未检测到PM₁₀与脑MRI体积年变化率之间的关联。
长期接触相对低水平的PM₂.₅与更大的脑结构变化负担相关，包括脑萎缩和血管病变。在无痴呆症和脑血管疾病的样本中的这些发现，强调了将空气污染作为晚年认知能力下降的一个可改变风险因素加以应对的重要性，并突出了需要有针对性的干预措施来预防其对脑完整性的有害影响。
