潮汐中的神经毒性:呼吁对海洋微塑料和大脑健康采取行动

IF 4.5 2区 医学 Q1 CLINICAL NEUROLOGY
Raffaele Marfella, Ulf Kallweit
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引用次数: 0

摘要

长期以来,海洋中无处不在的塑料垃圾一直鲜明地提醒着我们人类对环境的影响和对自然的不反思。但是一个更阴险的威胁正在浮出水面。微塑料(MPs)曾经被认为主要是海洋生态问题,现在越来越多地与人类健康问题联系在一起,更确切地说,与大脑健康有关。Makwana等人最近发表在本期《欧洲神经病学杂志》上的研究结果标志着一个关键的转折点:海洋微塑料暴露与神经和功能残疾之间存在人群层面的关联。在对美国218个沿海县的分析中,作者发现了一个惊人的模式。暴露于非常高水平海洋微塑料的社区,即使在调整了年龄、社会经济脆弱性、合并症和获得医疗保健的可能性之后,认知、活动、自我护理和独立生活障碍的患病率也显著升高。他们还考虑了其他因素,比如空气污染。虽然不能从这些横断面数据中建立因果关系,但关联的一致性和生物学上的合理性使研究结果难以忽视。微塑料——定义为小于5毫米的塑料颗粒——不是无害的环境残留物。实验研究表明,它们可以穿过肠道屏障,进入血液,并穿透血脑屏障(BBB)[2,3]。一旦进入神经组织,微塑料就会引发氧化应激,破坏神经递质系统,并激活促炎级联反应。最令人担忧的是,它们似乎促进了α-突触核蛋白和淀粉样蛋白-β等错误折叠蛋白的聚集,这两种蛋白分别是帕金森病和阿尔茨海默病的标志性病理[5,6]。这对神经学的影响是深远的。几十年来,人们一直认为细微颗粒物(PM2.5)等环境风险因素与中风、认知能力下降和神经发育障碍有关。空气污染和微塑料暴露在机制上的相似之处——两者都涉及全身炎症、血脑屏障(BBB)破坏和蛋白质病变——表明我们可能正在目睹一种新的环境神经毒素的出现[4,7]。最近的证据强调了这一问题的紧迫性。《新英格兰医学杂志》(New England Journal of Medicine) 2024年的一项研究发现,在动脉粥样硬化斑块中发现了微塑料和纳米塑料,它们与包括中风在内的心血管事件增加有关——进一步将塑料暴露与神经血管损伤联系起来。更令人信服的是,Nihart和Campen等人在2025年发表在《自然医学》(Nature Medicine)上的一项研究表明,人类死后脑组织中存在微塑料积累,在被诊断为痴呆症的个体中,微塑料的浓度明显更高。这些人类研究结果证实了动物研究,并提出了MPs可能在人群水平上导致神经退行性疾病的可能性。参见表S1。然而,与PM2.5不同的是,微塑料在临床环境中没有受到监测,它们的暴露途径往往是不可见的。沿海人口可能受到不成比例的影响,因为他们对海产品的依赖程度更高,而且海水入侵可能造成地下水污染[1,10]。然而,微塑料现已在人体血液、胎盘、肺和脑组织中被检测到[3,9]。这不是一个沿海地区的问题,而是一个全球性的问题。当然,目前的研究有很大的局限性。生态设计排除了个人水平暴露的测量。不能完全排除迁徙、饮食变化和未测量的混杂因素。此外,认知和运动障碍都是自我报告的。尽管如此,这些关联的规模和一致性值得关注。神经系统残疾,特别是老龄人口中的神经系统残疾,是日益加重的公共卫生负担。确定可改变的环境因素既紧迫又必要。作为神经科医生,我们接受的训练是发现模式,询问原因,并倡导预防。正如我们现在认识到血管危险因素和空气污染是导致神经退化的因素一样,我们必须开始考虑塑料污染对神经系统的影响。这需要神经科学家、环境卫生专家、流行病学家和政策制定者之间的跨学科合作。我们还需要从根本上扩展我们对大脑健康的概念,并将环境因素更多地纳入其中。Makwana等人的工作是对行动的呼吁。它提醒我们,大脑并不是孤立于我们周围的世界而存在的。我们的环境塑造了它——有时在分子水平上,有时在社会规模上。海洋微塑料,曾经是忽视环境的象征,现在正成为神经系统危害的潜在因素。是时候认真对待这种威胁了。 Raffaele Marfella:概念化,写作-审查和编辑,写作-原稿。Ulf Kallweit:构思,写作-原稿,写作-审查和编辑。作者声明无利益冲突。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Neurotoxicity at the Tides: A Call to Action on Marine Microplastics and Brain Health

The ubiquity of plastic waste in our oceans has long served as a stark reminder of human impact on the environment and the unreflective approach to nature. But a more insidious threat is now surfacing—literally. Microplastics (MPs), once considered primarily a marine ecological issue, are now increasingly linked to human health concerns, more precisely to brain health. Recent findings by Makwana et al. published in this issue of the European Journal of Neurology, mark a critical turning point: the demonstration of a population-level association between exposure to marine microplastics and neurological and functional disabilities [1]. In their analysis of 218 coastal counties in the United States, the authors observed a striking pattern. Communities exposed to very high levels of marine microplastics showed a significantly elevated prevalence of cognitive, mobility, self-care, and independent living disabilities—even after adjusting for age, socioeconomic vulnerability, comorbidities, and access to healthcare. They also accounted for other exposures, such as air pollution. While causation cannot be established from this cross-sectional data, the consistency of associations and biological plausibility make the findings difficult to ignore [1]. Microplastics—defined as plastic particles smaller than 5 mm—are not benign environmental remnants. Experimental studies have shown that they can cross the intestinal barrier, enter the bloodstream, and penetrate the blood–brain barrier (BBB) [2, 3]. Once in neural tissue, microplastics can trigger oxidative stress, disrupt neurotransmitter systems, and activate pro-inflammatory cascades [4]. Most concerning, they appear to promote the aggregation of misfolded proteins such as α-synuclein and amyloid-β, which are hallmark pathologies in Parkinson's and Alzheimer's diseases, respectively [5, 6]. The implications for neurology are profound. For decades, environmental risk factors such as delicate particulate matter (PM2.5) have been linked to stroke, cognitive decline, and neurodevelopmental disorders. The mechanistic parallels between air pollution and microplastic exposure—both of which involve systemic inflammation, blood–brain barrier (BBB) disruption, and proteinopathy—suggest that we may be witnessing the emergence of a new environmental neurotoxin [4, 7]. Recent evidence underscores the urgency of this issue. In a 2024 New England Journal of Medicine study, micro- and nanoplastics were identified in atherosclerotic plaques and were associated with increased cardiovascular events, including stroke—further linking plastic exposure to neurovascular injury [8]. Even more compelling, a 2025 study in Nature Medicine by Nihart and Campen et al. demonstrated microplastic accumulation in human post-mortem brain tissue, with significantly higher concentrations in individuals diagnosed with dementia [9]. These human findings corroborate animal studies and raise the possibility that MPs may be contributing to neurodegenerative disease at the population level. See also Table S1. Yet, unlike PM2.5, microplastics are not monitored in clinical settings, and their exposure pathways are often invisible. Coastal populations may be disproportionately affected due to their greater reliance on seafood and potential groundwater contamination resulting from seawater intrusion [1, 10]. However, microplastics are now being detected in human blood, placenta, lungs, and brain tissue [3, 9]. This is not a coastal problem—it is a global one. There are, of course, significant limitations to the current study. The ecological design precludes the measurement of individual-level exposure. Migration, dietary variation, and unmeasured confounders cannot be entirely ruled out. Also, cognitive and motor disabilities were only self-reported. Still, the magnitude and consistency of the associations warrant attention. Neurological disability, especially in aging populations, represents a growing public health burden. Identifying modifiable environmental contributors is both urgent and essential. As neurologists, we are trained to detect patterns, interrogate causes, and advocate for prevention. Just as we now recognize vascular risk factors and air pollution as contributors to neurodegeneration, we must begin to reckon with the neurological impact of plastic pollution. This will require interdisciplinary collaboration among neuroscientists, environmental health experts, epidemiologists, and policymakers. We also need to fundamentally expand our concept of brain health and include environmental factors much more [11]. Makwana et al.'s work is a call to action. It reminds us that the brain does not exist in isolation from the world around us. Our environment shapes it—sometimes at the molecular level, sometimes on a societal scale. Marine microplastics, once a symbol of environmental neglect, are now emerging as potential agents of neurological harm. It is time to take the threat seriously.

Raffaele Marfella: conceptualization, writing – review and editing, writing – original draft. Ulf Kallweit: conceptualization, writing – original draft, writing – review and editing.

The authors declare no conflicts of interest.

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来源期刊
European Journal of Neurology
European Journal of Neurology 医学-临床神经学
CiteScore
9.70
自引率
2.00%
发文量
418
审稿时长
1 months
期刊介绍: The European Journal of Neurology is the official journal of the European Academy of Neurology and covers all areas of clinical and basic research in neurology, including pre-clinical research of immediate translational value for new potential treatments. Emphasis is placed on major diseases of large clinical and socio-economic importance (dementia, stroke, epilepsy, headache, multiple sclerosis, movement disorders, and infectious diseases).
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