Plastic Accumulation in Residual Brain Tissues From Hemorrhagic Events: Neurological Outcomes and Pathogenetic Evidence (PARTENOPE Study)

Spontaneous intracerebral hemorrhage is a severe and life-threatening neurological condition representing approximately 10-15% of all strokes worldwide and is associated with high early mortality and substantial long-term disability. Despite significant advances in neuroimaging, neurosurgical techniques, and neurocritical care, clinical outcomes remain poor, and the biological mechanisms underlying hemorrhage initiation, expansion, and secondary brain injury are still incompletely understood.

The pathophysiology of intracerebral hemorrhage is characterized by a complex interplay of vascular, inflammatory, and neurotoxic processes. Structural vascular alterations, endothelial dysfunction, and disruption of the blood-brain barrier contribute to vessel rupture and hematoma formation. Following the initial bleeding event, secondary brain injury is driven by hematoma-induced mechanical damage, oxidative stress, activation of resident and infiltrating immune cells, and release of pro-inflammatory mediators. Microglial activation, macrophage infiltration, and inflammasome-related pathways are recognized as important contributors to neuronal injury and neurological deterioration.

While traditional risk factors such as hypertension and small vessel disease are well established, the contribution of environmental exposures to cerebrovascular vulnerability has been largely overlooked. In recent decades, environmental exposure to micro- and nanoplastics has emerged as a global health concern. The exponential increase in plastic production has resulted in widespread distribution of plastic-derived particles across ecosystems, leading to chronic human exposure through ingestion, inhalation, and dermal contact.

Microplastics and nanoplastics have been detected in multiple biological matrices, including blood, lung tissue, placenta, and cardiovascular structures. Experimental and translational studies suggest that these particles may interact with biological systems by promoting oxidative stress, immune activation, endothelial dysfunction, and tissue inflammation. Microplastics and nanoplastics have also been described in vascular tissues, supporting the rationale for investigating their potential association with cerebrovascular disease.

The central nervous system is particularly susceptible to vascular and inflammatory insults, and preservation of blood-brain barrier integrity plays a critical role in maintaining neural homeostasis. Emerging evidence indicates that nanoscale particles may cross biological barriers and potentially contribute to neuroinflammation, microglial activation, and neuronal dysfunction. However, the presence, distribution, and potential biological impact of microplastics and nanoplastics in cerebrovascular diseases, particularly intracerebral hemorrhage, have not been systematically investigated.