Given the frequent use of improvised explosive devices (IEDs) around the world, the study of traumatic blast injuries is ofincreasing interest. The ear is the most common organ affected by blast injury because it is the bodyﾒs most sensitivepressure transducer. We fabricated a blast chamber to re-create blast profiles similar to that of IEDs and used it to develop areproducible mouse model to study blast-induced hearing loss. The tympanic membrane was perforated in all mice afterblast exposure and found to heal spontaneously. Micro-computed tomography demonstrated no evidence for middle ear orotic capsule injuries; however, the healed tympanic membrane was thickened. Auditory brainstem response and distortionproduct otoacoustic emission threshold shifts were found to be correlated with blast intensity. As well, these thresholdshifts were larger than those found in control mice that underwent surgical perforation of their tympanic membranes,indicating cochlear trauma. Histological studies one week and three months after the blast demonstrated no disruption ordamage to the intra-cochlear membranes. However, there was loss of outer hair cells (OHCs) within the basal turn of thecochlea and decreased spiral ganglion neurons (SGNs) and afferent nerve synapses. Using our mouse model thatrecapitulates human IED exposure, our results identify that the mechanisms underlying blast-induced hearing loss does notinclude gross membranous rupture as is commonly believed. Instead, there is both OHC and SGN loss that produce auditorydysfunction.
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