Abstract Evidence that inhaled particulate matter reaches the central nervous system has increased over the past two decades, alongside the growing use of nanoparticles (NPs). We examined the effects of silica NPs (SiO₂) on a lung triculture model to assess lung-blood barrier integrity, and on the neurobehavior of C. elegans wild-type (N2) and neurodegenerative disease models—GMC101 (Alzheimer’s) and NL5901 (Parkinson’s). Characterization of SiO₂ (DLS, XRD, XPS) showed a hydrodynamic diameter of 135.6 ± 2.1 nm, PDI = 0.136 ± 0.036, amorphous structure, and an O/Si ratio of 1.94. Preliminary results using the lung model (10 to 100 µg/cm²/72 h) under submerged and quasi-ALI conditions did not alter TEER values. In contrast, continuous exposure of C. elegans (0.005 to 50 µg/mL SiO₂) caused developmental delays and reduced reproductive capacity, with significant toxicity from 5 µg/mL. Growth rate declined from 3.01 ± 0.71 µm²/h (control) to 2.22 ± 0.82 µm²/h, and progeny accumulation decreased from 4.41 ± 1.44 to 3.25 ± 1.45 progeny/h. Neurobehavioral assays revealed impaired locomotion—reduced body bending frequency and velocity—in all strains (N2, GMC101, NL5901) after 11 days of exposure to 5 µg/mL SiO₂. Survival rates were unaffected, indicating that neurotoxicity occurred independent of lethality. The mechanism of translocation from the lung under our experimental conditions seems to be independent of the tight junction integrity. Regarding our in vivo model, these results show that SiO₂ NPs cause developmental and neurobehavioral toxicity in C. elegans, suggesting a general mechanism of neurotoxicity not limited to neurodegenerative disease models.
Alfaro‐Moreno et al. (Thu,) studied this question.