Narrative review: neutrophil activation and NETosis in carbon nanotube-induced lung injury reveal mechanistic insights and biomarker based risk assessment.

OBJECTIVE

Carbon nanotubes (CNTs) are increasingly applied in industrial and biomedical fields, yet their fiber-like geometry and structural durability raise concerns about inhalation risks in occupational settings. This review synthesizes current evidence on neutrophil recruitment, activation, and extracellular trap (NET) formation in CNT-induced lung injury, with emphasis on biomarker discovery, therapeutic strategies, and worker protection.

METHODS

A narrative synthesis integrating mechanistic, experimental, and translational studies on CNT-induced neutrophil activation and NETosis was conducted.

RESULTS AND DISCUSSION: Experimental data show that CNT deposition in distal airways rapidly recruits and activates neutrophil, initiating the release of reactive oxygen species (ROS), proteolytic enzymes, and chromatin-based NETs. While these responses contribute to host defense, sustained activation promotes epithelial injury and fibrotic remodeling. Translational studies in exposed workers reveal elevated myeloperoxidase (MPO), neutrophil elastase, neutrophil gelatinase-associated lipocalin (NGAL), and circulating DNA, supporting their value as early biomarkers of pulmonary injury. Remaining challenges include the absence of long-term human cohort data, heterogeneity in CNT physicochemical features, and technical limitations in detecting biologically meaningful exposure endpoints.

CONCLUSIONS

Neutrophil activation and NETosis represent important contributing pathways in CNT-induced inflammation and fibrosis, although current evidence does not establish NETosis as a central or predictive mechanism. Future strategies should focus on safer CNT design, strengthened occupational controls, biomarker-based surveillance, and mechanism-targeted interventions to minimize health risks while advancing sustainable nanotechnology.