Jang Heeseon, Sohn Jungwoo, Kim Hee Jin, Seo Sang Won, Noh Young, Koh Sang-Baek, Cho Jaelim, Kim Changsoo
Department of Preventive Medicine, Yonsei University College of Medicine, Seoul, Republic of Korea.
Department of Preventive Medicine, Jeonbuk National University Medical School, Jeonju, Republic of Korea.
Heliyon. 2024 Aug 2;10(15):e35614. doi: 10.1016/j.heliyon.2024.e35614. eCollection 2024 Aug 15.
There is an emerging body of evidence concerning the neurological effect of air pollutants on cognitive function and increased risk of neurodegeneration. Although previous studies have suggested that polycyclic aromatic hydrocarbons (PAHs) are neurotoxic, the effect of PAHs exposure on neurodegeneration remains unclear. This study aimed to investigate the association between PAH exposure and the risk of developing amnestic mild cognitive impairment (aMCI) and Alzheimer's disease (AD). For this matched case-control cross-sectional study, we recruited patients aged ≥50 years diagnosed with aMCI and AD from the Samsung Medical Center, Seoul, Korea, between 2014 and 2019. For each patient, we randomly selected four cognitively healthy controls through frequency matching based on sex, age group, and education level. Urinary levels of four PAH metabolites, 1-hydroxypyrene (1-OHP), 1-hydroxyphenanthrene (1-OHPhe), 2-hydroxyfluorene (2-OHFlu), and 2-naphthol (2-NAP), were measured. A conditional logistic regression model was used to evaluate the association, adjusting for potential confounders. A total of 212 patients with aMCI with 848 matched controls, and 267 patients with AD with 1068 matched controls were included in the analyses to estimate the risk of PAH exposure. We found that elevated urinary levels of PAH metabolites (specifically, 1-OHP and 2-NAP) were significantly associated with an increased risk of aMCI and AD. An increase of one unit in log-transformed level of urinary 1-OHP was associated with a 1.15- and 1.16-times higher risk of aMCI and AD, respectively. An increase of one unit in log-transformed level of urinary 2-NAP was associated with a 1.11- and 1.13-times higher risk of aMCI and AD, respectively. These findings indicate that PAH exposure may increase the risk of aMCI and AD, especially for the elderly population. Considering the widespread distribution of PAHs in the environment, reducing PAH exposure may be an effective strategy for the prevention of neurodegenerative diseases.
关于空气污染物对认知功能的神经学影响以及神经退行性变风险增加，有越来越多的证据。尽管先前的研究表明多环芳烃（PAHs）具有神经毒性，但PAHs暴露对神经退行性变的影响仍不清楚。本研究旨在调查PAHs暴露与发生遗忘型轻度认知障碍（aMCI）和阿尔茨海默病（AD）风险之间的关联。对于这项匹配病例对照横断面研究，我们在2014年至2019年期间从韩国首尔三星医疗中心招募了年龄≥50岁、被诊断为aMCI和AD的患者。对于每位患者，我们根据性别、年龄组和教育水平通过频率匹配随机选择了四名认知健康的对照。测量了四种PAH代谢物1-羟基芘（1-OHP）、1-羟基菲（1-OHPhe）、2-羟基芴（2-OHFlu）和2-萘酚（2-NAP）的尿水平。使用条件逻辑回归模型评估关联，并对潜在混杂因素进行调整。共有212例aMCI患者及848例匹配对照，以及267例AD患者及1068例匹配对照纳入分析，以估计PAHs暴露风险。我们发现，PAH代谢物尿水平升高（特别是1-OHP和2-NAP）与aMCI和AD风险增加显著相关。尿1-OHP对数转换水平每增加一个单位，分别与aMCI和AD风险高1.15倍和1.16倍相关。尿2-NAP对数转换水平每增加一个单位，分别与aMCI和AD风险高1.11倍和1.13倍相关。这些发现表明，PAHs暴露可能会增加aMCI和AD的风险，尤其是对老年人群。考虑到PAHs在环境中的广泛分布，减少PAHs暴露可能是预防神经退行性疾病的有效策略。
