Mental Health and Neuroscience Research Institute (MHeNs), Maastricht University, Maastricht, the Netherlands; Alzheimer Centrum Limburg, Department of Psychiatry and Neuropsychology, Maastricht University, Maastricht, the Netherlands.
Mental Health and Neuroscience Research Institute (MHeNs), Maastricht University, Maastricht, the Netherlands; Alzheimer Centrum Limburg, Department of Psychiatry and Neuropsychology, Maastricht University, Maastricht, the Netherlands.
Environ Int. 2024 Oct;192:109048. doi: 10.1016/j.envint.2024.109048. Epub 2024 Oct 3.
Given the absence of curative interventions and the rising global incidence of dementia, research is increasingly focusing on lifestyle factors for prevention. However, identifying shared environmental risk for dementia, next to individual factors, is crucial for optimal risk reduction strategies. Therefore, in the present study we investigated the association between air pollution, cognitive functioning, and markers of structural brain damage.
We used cross-sectional data from 4,002 participants of The Maastricht Study on volumetric markers of brain integrity (white and grey matter volume, cerebrospinal fluid volume, white matter hyperintensities volume, presence of cerebral small vessel disease) and cognitive functioning (memory, executive functioning and attention, processing speed, overall cognition). Individuals were matched by postal code of residence to nationwide data on air pollution exposure (particulate matter < 2.5 μm (PM), particulate matter <10 μm (PM), nitrogen dioxide (NO), soot). Potentia linear and non-linear associations were investigated with linear, logistic, and restricted cubic splines regression. All analyses were adjusted for demographic characteristics and a compound score of modifiable dementia risk and protective factors.
Exposure to air pollutants was not related to cognitive functioning and most brain markers. We found curvilinear relationships between high PM exposures and grey matter and cerebrospinal fluid volume. Participants in the low and high range of exposure had lower grey matter volume. Higher cerebrospinal fluid volumes were only associated with high range of exposure, independent of demographic and individual modifiable dementia risk factors. After additional post hoc analyses, controlling for urbanicity, the associations for grey matter volume became non-significant. In men only, higher exposure to all air pollutants was associated with lower white matter volumes. No significant associations with white matter hyperintensities volume or cerebral small vessel disease were observed.
Our findings suggest that higher PM exposure is associated with more brain atrophy.
鉴于目前尚无治愈干预措施，且痴呆症在全球的发病率不断上升，因此越来越多的研究将重点放在预防的生活方式因素上。然而，除了个体因素外，确定痴呆症的共同环境风险对于最佳的风险降低策略至关重要。因此，在本研究中，我们调查了空气污染、认知功能与结构脑损伤标志物之间的关联。
我们使用了来自 4002 名马斯特里赫特大脑完整性体积标记物研究（白质和灰质体积、脑脊液体积、白质高信号体积、脑小血管疾病的存在）和认知功能（记忆力、执行功能和注意力、处理速度、整体认知）的横断面数据。个体通过居住的邮政编码与全国性空气污染暴露数据（<2.5μm 颗粒物（PM）、<10μm 颗粒物（PM）、二氧化氮（NO）、煤烟）相匹配。使用线性、逻辑和限制性立方样条回归来研究潜在的线性和非线性关联。所有分析均根据人口统计学特征和可改变的痴呆风险和保护因素的综合评分进行调整。
暴露于空气污染物与认知功能和大多数脑标志物无关。我们发现 PM 高暴露与灰质和脑脊液体积之间存在曲线关系。低暴露和高暴露组的灰质体积较低。只有高暴露范围与脑脊液体积较高相关，且独立于人口统计学和个体可改变的痴呆风险因素。在进一步的事后分析中，控制城市化因素后，灰质体积的相关性变得不显著。仅在男性中，所有空气污染物的高暴露与较低的白质体积相关。未观察到与白质高信号体积或脑小血管疾病的显著关联。
我们的研究结果表明，较高的 PM 暴露与更多的脑萎缩有关。
