Impact of Blast Exposures

Blast exposure has been associated with a wide range of negative outcomes, including alterations in brain structure and function, poorer cognitive functioning, and increased severity of psychiatric and health symptoms. Long-term effects also include chronic secondary downstream effects, such as neuroinflammation, neurotoxicity, cellular senescence, and neurodegeneration.

Now, a recent US Department of Veterans Affairs (VA) study of 114 post-9/11 combat veterans suggests that lifetime blast exposure severity is independently associated with accelerated epigenetic aging, even after accounting for PTSD and TBI. The field of epigenetics refers to how environment influences genes by changing the chemicals attached to them. 

This cross-sectional study analyzed participants enrolled in 2 coordinated VA research protocols: the Chronic Effects of Neurotrauma Consortium Study 34 and the Post-Deployment Mental Health Study. Researchers measured biological aging using DunedinPACE, an epigenetic biomarker derived from whole-blood DNA methylation data.

Greater blast exposure severity was significantly associated with faster DunedinPACE. Mild TBI history was also independently associated with faster aging, whereas PTSD diagnosis was not. No significant interaction effects were observed. Exploratory analyses suggested that higher-intensity and more frequent blast exposures contributed to more accelerated aging. 

The researchers said their findings suggest that accelerated biological aging may represent a pathway linking blast exposure to increased vulnerability for age-related disease and could inform early identification of at-risk veterans. 

Preclinical work has “undeniably demonstrated that primary blast forces can directly induce neurotrauma with associated, ongoing symptoms,” according to the authors of a 2024 study. “[H]owever, these findings have not translated into clinical work.” Most human studies of blast exposure use data obtained from assessments of TBI. That approach is limited, they said, because blast exposure does not always result in symptoms of concussion or TBI, and clinical symptoms of TBI are not necessary for blast-induced neurotrauma to occur. 

Moreover, understanding how and why blast exposure often results in negative consequences is still lagging, and interventions and treatments have lagged comparatively, the researchers noted. In large part, they added, this is because there is no broadly endorsed definition of blast exposure. They illustrated their point with examples of terms used in earlier research: blast TBI, primary blast TBI, pressure severity, distance from the blast, and frequency of exposure. The lack of standardized language, they suggested, “prevents synthesis of existing literature into a cohesive understanding of the field.”

Those researchers called for concerted and collaborative efforts to advance the study of blast exposure, including developing a standardized definition of blast exposure and curating an empirical literature base allowing clear comparisons of results across studies. They also urged raising awareness about blast-related negative outcomes with education at all levels: continuing education opportunities, round tables at annual conference meetings, grand rounds in hospital or academic medical center settings, and journal clubs.