J Neurotrauma. 2026 Apr 20:8977151261442215. doi: 10.1177/08977151261442215. Online ahead of print.

ABSTRACT

Repetitive low-level blast overpressure exposure is an increasingly recognized occupational hazard for military, law enforcement, and specialist breaching personnel. Unlike high-level blast exposures that commonly result in overt traumatic brain injury, acute low-level blast events have not been demonstrated to produce clinically detectable concussion or neurological injury in isolation. Nevertheless, growing concern has emerged that repeated low-level blast exposure may impart cumulative biomechanical stress, capable of producing biologically and clinically meaningful adverse brain effects over time. This narrative review synthesizes human epidemiological, clinical, neuroimaging, and biomarker evidence published between 2010 and 2025, regarding the neurological impact of repetitive low-level blast exposure. We review exposure contexts and operational epidemiology, blast physics, and candidate mechanistic pathways, including axonal and glial stress, cerebrospinal fluid-tissue interface effects, and blast-related vascular perturbation with blood-brain barrier dysfunction, that are supported by converging human translational findings. Clinical manifestations are examined across cognitive, vestibular, oculomotor, auditory, headache, and psychological domains, highlighting the subtle, cumulative, and often subclinical nature of observed effects. We further evaluate emerging fluid biomarkers and advanced neuroimaging modalities that provide evidence of astroglia activation, axonal stress, neurovascular perturbation, and network-level dysfunction in occupationally exposed cohorts. Importantly, current evidence does not demonstrate that repetitive low-level blast exposure alone is sufficient to cause neurodegenerative disease. Rather, findings support a model in which cumulative low-level blast may act as a modifier of neural vulnerability, particularly in individuals with mixed exposure histories or additional risk factors. We conclude by identifying critical gaps in exposure quantification, longitudinal data, and dose-response modeling, and discuss implications for future research and occupational brain-health surveillance.

PMID:42010363 | DOI:10.1177/08977151261442215