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Accidental burst of hydrogen pipeline can generate highly destructive blast wave, highlighting the importance of predicting the blast wave intensity for industrial safety and protection. However, current methods for predicting overpressure fail to consider the coupling effect between the blast wave and dynamic rupture. Therefore, a fluid-structure-rupture coupling model is constructed to address this limitation. The accuracy of the model is verified through a comparison of fracture morphology, crack propagation, and internal pressure decay between the simulation and experimental results. On this basis, the effects of dynamic rupture on blast wave formation and propagation, overpressure decay histories, and peak overpressure are investigated. Results indicate that the traditional CFD method tends to overestimate the peak overpressure in the near field while underestimating it in the middle and far fields. Furthermore, it is discovered that the blast waves from bursts of hydrogen pipelines with different diameters exhibit a consistent decay law under the same burst pressure by defining dimensionless distance and peak overpressure. Accordingly, the dimensionless blast curve is proposed for predicting overpressure from hydrogen pipeline burst with diameters ranging from 250 mm to 1000 mm and burst pressures ranging from 4 MPa to 12 MPa. The results can serve as a reference for the accurate and fast evaluation of blast wave intensity from hydrogen pipeline burst. • The proposed model effectively couples the dynamic rupture and blast wave. • Propagation of blast wave from hydrogen pipeline burst is quantitatively depicted. • Previous methods underestimate the peak overpressure in the middle and far fields. • Blast curve is developed to improve the prediction accuracy of peak overpressure. [ABSTRACT FROM AUTHOR]

Evidence suggests that low-level blast (LLB) overpressure exposure from military heavy weapons training is associated with subclinical adverse brain health and performance (H &P) outcomes. Existing DOD safety policies related to blast overpressure exposure are not specific to LLB-related brain health effects. This study sought to synthesize the available literature and analyze the relevancy of a specific blast metric to LLB exposures and the manifestation of adverse brain H &P outcomes. A literature search yielded 311 unique articles, from which 220 were identified as human studies on LLB published from 2010 to 2021. After more exhaustive exclusion criteria were applied, 14 articles met the criteria for inclusion. Findings on brain H &P changes were examined in relation to quantified LLB measurements (e.g., peak overpressure) to identify trends. Overall, the included studies suggested that alterations of reaction time, a metric for neurocognitive performance, as well as symptom reporting can occur following cumulative LLB exposures above 4 psi (27.6 kPa). Biomarkers and neurosensory changes have not demonstrated consistent associations with LLB exposures. These findings suggest that cumulative blast overpressure exposures above 4 psi (27.6 kPa) based on current measurement methodologies for body-worn sensors may be associated with adverse brain H &P outcomes. Current research efforts seek to better quantify LLB exposure, the relationships between LLB (e.g., intensity, duration, dose) and brain health, as well as to assess brain H &P domains more comprehensively. These efforts will serve to promote a better understanding of the interaction between LLB exposures and adverse brain H &P outcomes. [ABSTRACT FROM AUTHOR]

United States (US) Special Operations Forces (SOF) are frequently exposed to explosive blasts in training and combat, but the effects of repeated blast exposure (RBE) on SOF brain health are incompletely understood. Furthermore, there is no diagnostic test to detect brain injury from RBE. As a result, SOF personnel may experience cognitive, physical, and psychological symptoms for which the cause is never identified, and they may return to training or combat during a period of brain vulnerability. In 30 active-duty US SOF, we assessed the relationship between cumulative blast exposure and cognitive performance, psychological health, physical symptoms, blood proteomics, and neuroimaging measures (Connectome structural and diffusion MRI, 7 Tesla functional MRI, [11C]PBR28 translocator protein [TSPO] positron emission tomography [PET]-MRI, and [18F]MK6240 tau PET-MRI), adjusting for age, combat exposure, and blunt head trauma. Higher blast exposure was associated with increased cortical thickness in the left rostral anterior cingulate cortex (rACC), a finding that remained significant after multiple comparison correction. In uncorrected analyses, higher blast exposure was associated with worse health-related quality of life, decreased functional connectivity in the executive control network, decreased TSPO signal in the right rACC, and increased cortical thickness in the right rACC, right insula, and right medial orbitofrontal cortex--nodes of the executive control, salience, and default mode networks. These observations suggest that the rACC may be susceptible to blast overpressure and that a multimodal, network-based diagnostic approach has the potential to detect brain injury associated with RBE in active-duty SOF. [ABSTRACT FROM AUTHOR]

Low-level blast (LLB) exposure can lead to alterations in neurological health, cerebral vasculature, and cerebral blood flow (CBF). The development of cognitive issues and behavioral abnormalities after LLB, or subconcussive blast exposure, is insidious due to the lack of acute symptoms. One major hallmark of LLB exposure is the initiation of neurovascular damage followed by the development of neurovascular dysfunction. Preclinical studies of LLB exposure demonstrate impairment to cerebral vasculature and the blood–brain barrier (BBB) at both early and long-term stages following LLB. Neuroimaging techniques, such as arterial spin labeling (ASL) using magnetic resonance imaging (MRI), have been utilized in clinical investigations to understand brain perfusion and CBF changes in response to cumulative LLB exposure. In this review, we summarize neuroimaging techniques that can further our understanding of the underlying mechanisms of blast-related neurotrauma, specifically after LLB. Neuroimaging related to cerebrovascular function can contribute to improved diagnostic and therapeutic strategies for LLB. As these same imaging modalities can capture the effects of LLB exposure in animal models, neuroimaging can serve as a gap-bridging diagnostic tool that permits a more extensive exploration of potential relationships between blast-induced changes in CBF and neurovascular health. Future research directions are suggested, including investigating chronic LLB effects on cerebral perfusion, exploring mechanisms of dysautoregulation after LLB, and measuring cerebrovascular reactivity (CVR) in preclinical LLB models. [ABSTRACT FROM AUTHOR]

To improve the efficiency and protection level of combustible gas explosion relief in urban underground pipeline corridors, we built a 150 × 150 × 2000 mm³ transparent pipeline experimental platform to simulate underground pipeline corridors and studied the effect of different positions and diameters of explosion relief conduits on the side of the pipeline on the characteristics of the explosion of methane in the pipeline. The results show that the flame is twisted and deformed at the bend, increasing the contact area between the fuel and oxygen, thus causing flame acceleration. Wall conduit relief bend in the flame has a certain hysteresis, in the front end of the bend, and the back end of the pipe wall conduit were installed, the flame propagation time of 254 ms, and 200 ms, respectively, increased by 71 ms, and 17 ms, the delay ratio of 38.80%, 9.29%, respectively. When the front part of the pipe wall conduit pipe diameter of 60 mm, 80 mm, and 100 mm, the flame propagation time was delayed 71 ms, 82 ms, and 105 ms, the delay ratio of 38.80%, 44.81%, 57.38%, and the position of the front of the pipe wall conduit pipe diameter is larger, the lower the peak explosion pressure. [ABSTRACT FROM AUTHOR]

Background and Objectives: Epidemiological data indicate that blast exposure is the most common morbidity responsible for mild TBI among Service Members (SMs) during recent military operations. Blast-induced tinnitus is a comorbidity frequently reported by veterans, and despite its wide prevalence, it is also one of the least understood. Tinnitus arising from blast exposure is usually associated with direct structural damage that results in a conductive and sensorineural impairment in the auditory system. Tinnitus is also believed to be initiated by abnormal neuronal activities and temporal changes in neuroplasticity. Clinically, it is observed that tinnitus is frequently accompanied by sleep disruption as well as increased anxiety. In this study, we elucidated some of the mechanistic aspects of sensorineural injury caused by exposure to both shock waves and impulsive noise. The isolated conductive auditory damage hypothesis was minimized by employing an animal model wherein both ears were protected. Materials and Methods: After the exposure, the animals' hearing circuitry status was evaluated via acoustic startle response (ASR) to distinguish between hearing loss and tinnitus. We also compared the blast-induced tinnitus against the well-established sodium salicylate-induced tinnitus model as the positive control. The state of the sensorineural auditory system was evaluated by auditory brainstem response (ABR), and this test helped examine the neuronal circuits between the cochlea and inferior colliculus. We then further evaluated the role of the excitatory and inhibitory neurotransmitter receptors and neuronal synapses in the auditory cortex (AC) injury after blast exposure. Results: We observed sustained elevated ABR thresholds in animals exposed to blast shock waves, while only transient ABR threshold shifts were observed in the impulsive noise group solely at the acute time point. These changes were in concert with the increased expression of ribbon synapses, which is suggestive of neuroinflammation and cellular energy metabolic disorder. It was also found that the onset of tinnitus was accompanied by anxiety, depression-like symptoms, and altered sleep patterns. By comparing the effects of shock wave exposure and impulsive noise exposure, we unveiled that the shock wave exerted more significant effects on tinnitus induction and sensorineural impairments when compared to impulsive noise. Conclusions: In this study, we systematically studied the auditory system structural and functional changes after blast injury, providing more significant insights into the pathophysiology of blast-induced tinnitus. [ABSTRACT FROM AUTHOR]

The biomechanics and efficacy of personal protective equipment in mitigating injuries from blast overpressure remain unclear. The objectives of this study were to define intrathoracic pressures in response to blast wave (BW) exposure and biomechanically evaluate a soft-armor vest (SA) at diminishing these perturbations. Male Sprague–Dawley rats were instrumented with pressure sensors in the thorax and were exposed laterally to multiple exposures ranging from 33 to 108 kPa BW with SA and without SA. There were significant increases in rise time, peak negative pressure, and negative impulse in the thoracic cavity compared to the BW. Esophageal measurements were increased to a greater extent when compared to the carotid and the BW for all parameters (except positive impulse, which decreased). SA minimally altered the pressure parameters and energy content. This study establishes the relationship of external blast flow conditions and intra-body biomechanical responses in the thoracic cavity of rodents with and without SA. [ABSTRACT FROM AUTHOR]

Abstract Background Adverse pathophysiological and behavioral outcomes related to mild traumatic brain injury (mTBI), posttraumatic stress disorder (PTSD), and chronic pain are common following blast exposure and contribute to decreased quality of life, but underlying mechanisms and prophylactic/treatment options remain limited. The dynorphin/kappa opioid receptor (KOR) system helps regulate behavioral and inflammatory responses to stress and injury; however, it has yet to be investigated as a potential mechanism in either humans or animals exposed to blast. We hypothesized that blast-induced KOR activation mediates adverse outcomes related to inflammation and affective behavioral response. Methods C57Bl/6 adult male mice were singly or repeatedly exposed to either sham (anesthesia only) or blast delivered by a pneumatic shock tube. The selective KOR antagonist norBNI or vehicle (saline) was administered 72 h prior to repetitive blast or sham exposure. Serum and brain were collected 10 min or 4 h post-exposure for dynorphin A-like immunoreactivity and cytokine measurements, respectively. At 1-month post-exposure, mice were tested in a series of behavioral assays related to adverse outcomes reported by humans with blast trauma. Results Repetitive but not single blast exposure resulted in increased brain dynorphin A-like immunoreactivity. norBNI pretreatment blocked or significantly reduced blast-induced increase in serum and brain cytokines, including IL-6, at 4 h post exposure and aversive/anxiety-like behavioral dysfunction at 1-month post-exposure. Conclusions Our findings demonstrate a previously unreported role for the dynorphin/KOR system as a mediator of biochemical and behavioral dysfunction following repetitive blast exposure and highlight this system as a potential prophylactic/therapeutic treatment target.

CONQUER is a pilot blast monitoring program that monitors, quantifies, and reports to military units the training-related blast overpressure exposure of their service members. Overpressure exposure data are collected using the BlackBox Biometrics (B3) Blast Gauge System (BGS, generation 7) sensors mounted on the body during training. To date, the CONQUER program has recorded 450,000 gauge triggers on monitored service members. The subset of data presented here has been collected from 202 service members undergoing training with explosive breaching charges, shoulder-fired weapons, artillery, mortars, and 0.50 caliber guns. Over 12,000 waveforms were recorded by the sensors worn by these subjects. A maximum peak overpressure of 90.3 kPa (13.1 psi) was recorded during shoulder-fired weapon training. The largest overpressure impulse (a measure of blast energy) was 82.0 kPa-ms (11.9 psi-ms) and it was recorded during explosive breaching with a large wall charge. Operators of 0.50 caliber machine guns have the lowest peak overpressure impulse (as low as 0.62 kPa-ms or 0.09 psi-ms) of the blast sources considered. The data provides information on the accumulation of blast overpressure on service members over an extended period of time. The cumulative peak overpressure, peak overpressure impulse, or timing between exposures is all available in the exposure data. [ABSTRACT FROM AUTHOR]

• Male and female mice differ in blast-induced loss of righting time but not acute weight loss. • Disparate patterns of blast-induced cytokine and gut microbiome changes in male and female mice. • Blast exposure increases blood brain barrier permeability in both male and female mice. • Only male mice show behavioral deficits one-month post blast exposure. Repetitive blast-related mild traumatic brain injury (mTBI) caused by exposure to high explosives is increasingly common among warfighters as well as civilians. While women have been serving in military positions with increased risk of blast exposure since 2016, there are few published reports examining sex as a biological variable in models of blast mTBI, greatly limiting diagnosis and treatment capabilities. As such, here we examined outcomes of repetitive blast trauma in female and male mice in relation to potential behavioral, inflammatory, microbiome, and vascular dysfunction at multiple timepoints. In this study we utilized a well-established blast overpressure model to induce repetitive (3x) blast-mTBI in both female and male mice. Acutely following repetitive exposure, we measured serum and brain cytokine levels, blood–brain barrier (BBB) disruption, fecal microbial abundance, and locomotion and anxiety-like behavior in the open field assay. At the one-month timepoint, in female and male mice we assessed behavioral correlates of mTBI and PTSD-related symptoms commonly reported by Veterans with a history of blast-mTBI using the elevated zero maze, acoustic startle, and conditioned odorant aversion paradigms. Repetitive blast exposure resulted in both similar (e.g., increased IL-6), and disparate (e.g., IL-10 increase only in females) patterns of acute serum and brain cytokine as well as gut microbiome changes in female and male mice. Acute BBB disruption following repetitive blast exposure was apparent in both sexes. While female and male blast mice both exhibited acute locomotor and anxiety-like deficits in the open field assay, only male mice exhibited adverse behavioral outcomes that lasted at least one-month. Representing a novel survey of potential sex differences following repetitive blast trauma, our results demonstrate unique similar yet divergent patterns of blast-induced dysfunction in female vs. male mice and highlight novel targets for future diagnosis and therapeutic development. [ABSTRACT FROM AUTHOR]

Blast-induced auditory trauma is a common injury in military service members and veterans that leads to hearing loss. While the inner ear response to blast exposure is difficult to characterize experimentally, computational models have advanced to predict blast wave transmission from the ear canal to the cochlea; however, published models have either straight or spiral cochlea with fluid-filled two chambers. In this paper, we report the recently developed 3D finite element (FE) model of the human ear mimicking the anatomical structure of the 3-chambered cochlea. The model consists of the ear canal, middle ear, and two and a half turns of the cochlea with three chambers separated by the Reissner's membrane (RM) and the basilar membrane (BM). The blast overpressure measured from human temporal bone experiments was applied at the ear canal entrance and the Fluent/Mechanical coupled fluid–structure interaction analysis was conducted in ANSYS software. The FE model-derived results include the pressure in the canal near the tympanic membrane (TM) and the intracochlear pressure at scala vestibuli, the TM displacement, and the stapes footplate (SFP) displacement, which were compared with experimentally measured data in human temporal bones. The validated model was used to predict the biomechanical response of the ear to blast overpressure: distributions of the maximum strain and stress within the TM, the BM displacement variation from the base to apex, and the energy flux or total energy entering the cochlea. The comparison of intracochlear pressure and BM displacement with those from the FE model of 2-chambered cochlea indicated that the 3-chamber cochlea model with the RM and scala media chamber improved our understanding of cochlea mechanics. This most comprehensive FE model of the human ear has shown its capability to predict the middle ear and cochlea responses to blast overpressure which will advance our understanding of auditory blast injury. [ABSTRACT FROM AUTHOR]

CONQUER is a pilot blast monitoring program that monitors, quantifies, and reports to military units the training-related blast overpressure exposure of their service members. Overpressure exposure data are collected using the BlackBox Biometrics (B3) Blast Gauge System (BGS, generation 7) sensors mounted on the body during training. To date, the CONQUER program has recorded 450,000 gauge triggers on monitored service members. The subset of data presented here has been collected from 202 service members undergoing training with explosive breaching charges, shoulder-fired weapons, artillery, mortars, and 0.50 caliber guns. Over 12,000 waveforms were recorded by the sensors worn by these subjects. A maximum peak overpressure of 90.3 kPa (13.1 psi) was recorded during shoulder-fired weapon training. The largest overpressure impulse (a measure of blast energy) was 82.0 kPa-ms (11.9 psi-ms) and it was recorded during explosive breaching with a large wall charge. Operators of 0.50 caliber machine guns have the lowest peak overpressure impulse (as low as 0.62 kPa-ms or 0.09 psi-ms) of the blast sources considered. The data provides information on the accumulation of blast overpressure on service members over an extended period of time. The cumulative peak overpressure, peak overpressure impulse, or timing between exposures is all available in the exposure data.

Background: Adverse pathophysiological and behavioral outcomes related to mild traumatic brain injury (mTBI), posttraumatic stress disorder (PTSD), and chronic pain are common following blast exposure and contribute to decreased quality of life, but underlying mechanisms and prophylactic/treatment options remain limited. The dynorphin/kappa opioid receptor (KOR) system helps regulate behavioral and inflammatory responses to stress and injury; however, it has yet to be investigated as a potential mechanism in either humans or animals exposed to blast. We hypothesized that blast-induced KOR activation mediates adverse outcomes related to inflammation and affective behavioral response.Methods: C57Bl/6 adult male mice were singly or repeatedly exposed to either sham (anesthesia only) or blast delivered by a pneumatic shock tube. The selective KOR antagonist norBNI or vehicle (saline) was administered 72 h prior to repetitive blast or sham exposure. Serum and brain were collected 10 min or 4 h post-exposure for dynorphin A-like immunoreactivity and cytokine measurements, respectively. At 1-month post-exposure, mice were tested in a series of behavioral assays related to adverse outcomes reported by humans with blast trauma.Results: Repetitive but not single blast exposure resulted in increased brain dynorphin A-like immunoreactivity. norBNI pretreatment blocked or significantly reduced blast-induced increase in serum and brain cytokines, including IL-6, at 4 h post exposure and aversive/anxiety-like behavioral dysfunction at 1-month post-exposure.Conclusions: Our findings demonstrate a previously unreported role for the dynorphin/KOR system as a mediator of biochemical and behavioral dysfunction following repetitive blast exposure and highlight this system as a potential prophylactic/therapeutic treatment target. [ABSTRACT FROM AUTHOR]

Background and Objectives: Epidemiological data indicate that blast exposure is the most common morbidity responsible for mild TBI among Service Members (SMs) during recent military operations. Blast-induced tinnitus is a comorbidity frequently reported by veterans, and despite its wide prevalence, it is also one of the least understood. Tinnitus arising from blast exposure is usually associated with direct structural damage that results in a conductive and sensorineural impairment in the auditory system. Tinnitus is also believed to be initiated by abnormal neuronal activities and temporal changes in neuroplasticity. Clinically, it is observed that tinnitus is frequently accompanied by sleep disruption as well as increased anxiety. In this study, we elucidated some of the mechanistic aspects of sensorineural injury caused by exposure to both shock waves and impulsive noise. The isolated conductive auditory damage hypothesis was minimized by employing an animal model wherein both ears were protected. Materials and Methods: After the exposure, the animals’ hearing circuitry status was evaluated via acoustic startle response (ASR) to distinguish between hearing loss and tinnitus. We also compared the blast-induced tinnitus against the well-established sodium salicylate-induced tinnitus model as the positive control. The state of the sensorineural auditory system was evaluated by auditory brainstem response (ABR), and this test helped examine the neuronal circuits between the cochlea and inferior colliculus. We then further evaluated the role of the excitatory and inhibitory neurotransmitter receptors and neuronal synapses in the auditory cortex (AC) injury after blast exposure. Results: We observed sustained elevated ABR thresholds in animals exposed to blast shock waves, while only transient ABR threshold shifts were observed in the impulsive noise group solely at the acute time point. These changes were in concert with the increased expression of ribbon synapses, which is suggestive of neuroinflammation and cellular energy metabolic disorder. It was also found that the onset of tinnitus was accompanied by anxiety, depression-like symptoms, and altered sleep patterns. By comparing the effects of shock wave exposure and impulsive noise exposure, we unveiled that the shock wave exerted more significant effects on tinnitus induction and sensorineural impairments when compared to impulsive noise. Conclusions: In this study, we systematically studied the auditory system structural and functional changes after blast injury, providing more significant insights into the pathophysiology of blast-induced tinnitus.

Multiple finite-element (FE) models to predict the biomechanical responses in the human brain resulting from the interaction with blast waves have established the importance of including the brain-surface convolutions, the major cerebral veins, and using non-linear brain-tissue properties to improve model accuracy. We hypothesize that inclusion of a more detailed network of cerebral veins and arteries can further enhance the model-predicted biomechanical responses and help identify correlates of blast-induced brain injury. To more comprehensively capture the biomechanical responses of human brain tissues to blast-wave exposure, we coupled a three-dimensional (3-D) detailed-vasculature human-head FE model, previously validated for blunt impact, with a 3-D shock-tube FE model. Using the coupled model, we computed the biomechanical responses of a human head facing an incoming blast wave for blast overpressures (BOPs) equivalent to 68, 83, and 104 kPa. We validated our FE model, which includes the detailed network of cerebral veins and arteries, the gyri and the sulci, and hyper-viscoelastic brain-tissue properties, by comparing the model-predicted intracranial pressure (ICP) values with previously collected data from shock-tube experiments performed on cadaver heads. In addition, to quantify the influence of including a more comprehensive network of brain vessels, we compared the biomechanical responses of our detailed-vasculature model with those of a reduced-vasculature model and a no-vasculature model for the same blast-loading conditions. For the three BOPs, the predicted ICP values matched well with the experimental results in the frontal lobe, with peak-pressure differences of 4–11% and phase-shift differences of 9–13%. As expected, incorporating the detailed cerebral vasculature did not influence the ICP, however, it redistributed the peak brain-tissue strains by as much as 30% and yielded peak strain differences of up to 7%. When compared to existing reduced-vasculature FE models that only include the major cerebral veins, our high-fidelity model redistributed the brain-tissue strains in most of the brain, highlighting the importance of including a detailed cerebral vessel network in human-head FE models to more comprehensively account for the biomechanical responses induced by blast exposure.

As an organ that is sensitive to pressure changes, the ear is often damaged when a person is subjected to blast exposures resulting in hearing loss due to tissue damage in the middle ear and cochlea. While observation of middle ear damage is non-invasive, examining the damage to the cochlea is difficult to quantify. Previous works have modeled the cochlear response often when subjected to an acoustic pressure input, but the inner ear mechanics have rarely been studied when the ear is exposed to a blast wave. In this study we aim to develop a finite element (FE) model of the entire ear, particularly the cochlea, for predicting the blast wave transmission from the ear canal to cochlea. We utilized a FE model of the ear, which includes the ear canal, middle ear, and uncoiled two-chambered cochlea, to simulate the cochlear response to blast overpressure (BOP) at the entrance of the ear canal with ANSYS Mechanical and Fluent in a fluid–structure interface coupled analysis in the time domain. This model was developed based on previous middle and inner ear models, and the cochlea was remeshed to improve BOP simulation performance. The FE model was validated using experimentally measured blast pressure transduction from the ear canal to the middle ear and cochlea in human cadaveric temporal bones. Results from the FE model showed significant displacements of the tympanic membrane, middle ear ossicles, and basilar membrane (BM). The stapes footplate displacement was observed to be as high as 60 µm, far exceeding the displacement during normal acoustic stimulation, when the 30 kPa (4.35 psi, 183 dB (SPL), Sound Pressure Level) of BOP was applied at the ear canal entrance. The large stapes movement caused pressures in the cochlea to exceed the physiological pressure level [< 10 Pa, 120 dB (SPL)] at a peak of 49.9 kPa, and the BM displacement was on the order of microns with a maximum displacement of 26.4 µm. The FE model of the entire human ear developed in this study provides a computational tool for prediction of blast wave transmission from the ear canal to cochlea and the future applications for assisting the prevention, diagnosis, and treatment of blast-induced hearing loss. [ABSTRACT FROM AUTHOR]

We performed a characterization of the shock wave loading on the response of the specimen representing a simplified head model. A polycarbonate cylinder (2-in. outer diameter, wall thickness: 0.06 or 0.12 in.) was filled with two fluids: pure de-ionized water and 40% glycerol in water, which differ only slightly in their constitutive material properties. These two fluids were selected to represent the cerebrospinal fluid and cerebral blood, using their high strain rate viscosity as a primary selection criterion. The model specimen was exposed to a single shock wave with two nominal intensities: 70 and 130?kPa overpressure. The response of the model was measured using three strain gauges and three pressure sensors, one mounted on the front face of the cylinder and two embedded in the cylinder to measure the pressure inside of the fluid. We noted several discriminant characteristics in the collected data, which indicate that the type of fluid is strongly influencing the response. The vibrations of the cylinder walls are strongly correlated with the fluid kind. The similarity analysis via the Pearson coefficient indicated that the pressure waveforms in the fluid are only moderately correlated, and these results were further corroborated by Euclidean distance analysis. Continuous wavelet transform of pressure waveforms revealed that the frequency response is strongly correlated with the properties of the fluid. The observed differences in strain and pressure modalities stem from relatively small differences in the properties of the fluids used in this study. [ABSTRACT FROM AUTHOR]

Background: Blast exposure is a potential hazard in modern military operations and training, especially for some military occupations. Helmets, peripheral armor, hearing protection, and eye protection worn by military personnel provide some acute protection from blast effects but may not fully protect personnel against cumulative effects of repeated blast overpressure waves experienced over a career. The current study aimed to characterize the long-term outcomes of repeated exposure to primary blast overpressure in experienced career operators with an emphasis on the assessment of hearing and vestibular outcomes.Methods: Participants included experienced “breachers” (military and law enforcement explosives professionals who gain entry into structures through controlled detonation of charges) and similarly aged and experienced “non-breachers” (non-breaching military and law enforcement personnel). Responses to a clinical interview and performance on audiological and vestibular testing were compared.Results: Hearing loss, ringing in the ears, irritability, and sensitivity to light or noise were more common among breachers than non-breachers. Breachers reported more combat exposure than non-breachers, and subsequently, memory loss and difficulty concentrating were associated with both breaching and combat exposure. Vestibular and ocular motor outcomes were not different between breachers and non-breachers.Conclusion: Hearing-related, irritability, and sensitivity outcomes are associated with a career in breaching. Future studies examining long-term effects of blast exposure should take measures to control for combat exposure.

The interaction of explosion-induced blast waves with the torso is suspected to contribute to brain injury. In this indirect mechanism, the wave-torso interaction is assumed to generate a blood surge, which ultimately reaches and damages the brain. However, this hypothesis has not been comprehensively and systematically investigated, and the potential role, if any, of the indirect mechanism in causing brain injury remains unclear. In this interdisciplinary study, we performed experiments and developed mathematical models to address this knowledge gap. First, we conducted blast-wave exposures of Sprague-Dawley rats in a shock tube at incident overpressures of 70 and 130 kPa, where we measured carotid-artery and brain pressures while limiting exposure to the torso. Then, we developed three-dimensional (3-D) fluid-structure interaction (FSI) models of the neck and cerebral vasculature and, using the measured carotid-artery pressures, performed simulations to predict mass flow rates and wall shear stresses in the cerebral vasculature. Finally, we developed a 3-D finite element (FE) model of the brain and used the FSI-computed vasculature pressures to drive the FE model to quantify the blast-exposure effects in the brain tissue. The measurements from the torso-only exposure experiments revealed marginal increases in the peak carotid-artery overpressures (from 13.1 to 28.9 kPa). Yet, relative to the blast-free, normotensive condition, the FSI simulations for the blast exposures predicted increases in the peak mass flow rate of up to 255% at the base of the brain and increases in the wall shear stress of up to 289% on the cerebral vasculature. In contrast, our simulations suggest that the effect of the indirect mechanism on the brain-tissue-strain response is negligible (

Background: Blast exposure is a potential hazard in modern military operations and training, especially for some military occupations. Helmets, peripheral armor, hearing protection, and eye protection worn by military personnel provide some acute protection from blast effects but may not fully protect personnel against cumulative effects of repeated blast overpressure waves experienced over a career. The current study aimed to characterize the long-term outcomes of repeated exposure to primary blast overpressure in experienced career operators with an emphasis on the assessment of hearing and vestibular outcomes. Methods: Participants included experienced "breachers" (military and law enforcement explosives professionals who gain entry into structures through controlled detonation of charges) and similarly aged and experienced "non-breachers" (non-breaching military and law enforcement personnel). Responses to a clinical interview and performance on audiological and vestibular testing were compared. Results: Hearing loss, ringing in the ears, irritability, and sensitivity to light or noise were more common among breachers than non-breachers. Breachers reported more combat exposure than non-breachers, and subsequently, memory loss and difficulty concentrating were associated with both breaching and combat exposure. Vestibular and ocular motor outcomes were not different between breachers and non-breachers. Conclusion: Hearing-related, irritability, and sensitivity outcomes are associated with a career in breaching. Future studies examining long-term effects of blast exposure should take measures to control for combat exposure. [ABSTRACT FROM AUTHOR]

This study demonstrates the orientation and the "shape factor" have pronounced effects on the development of the localized pressure fields inside of the helmet. We used anatomically accurate headform to evaluate four modern combat helmets under blast loading conditions in the shock tube. The Advanced Combat Helmet (ACH) is used to capture the effect of the orientation on pressure under the helmet. The three modern combat helmets: Enhanced Combat Helmet (ECH), Ops-Core, and Airframe, were tested in frontal orientation to determine the effect of helmet geometry. Using the unhelmeted headform data as a reference, we characterized pressure distribution inside each helmet and identified pressure focal points. The nature of these localized "hot spots" is different than the elevated pressure in the parietal region of the headform under the helmet widely recognized as the under-wash effect also observed in our tests. It is the first experimental study which indicates that the helmet presence increased the pressure experienced by the eyes and the forehead (glabella). Pressure fingerprinting using an array of sensors combined with the application of principle component analysis (PCA) helped elucidate the subtle differences between helmets. [ABSTRACT FROM AUTHOR]

Injuries from exposure to explosions rose dramatically during the Iraq and Afghanistan wars, which motivated investigations of blast-related neurotrauma and operational breaching. In this study, military "breachers" were exposed to controlled, low-level blast during a 10-day explosive breaching course. Using an omics approach, we assessed epigenetic, transcriptional, and inflammatory profile changes in blood from operational breaching trainees, with varying levels of lifetime blast exposure, along with daily self-reported symptoms (with tinnitus, headaches, and sleep disturbances as the most frequently reported). Although acute exposure to blast did not confer epigenetic changes, specifically in DNA methylation, differentially methylated regions (DMRs) with coordinated gene expression changes associated with lifetime cumulative blast exposures were identified. The accumulative effect of blast showed increased methylation of PAX8 antisense transcript with coordinated repression of gene expression, which has been associated with sleep disturbance. DNA methylation analyses conducted in conjunction with reported symptoms of tinnitus in the low versus high blast incidents groups identified DMRS in KCNE1 and CYP2E1 genes. KCNE1 and CYP2E1 showed the expected inverse correlation between DNA methylation and gene expression, which have been previously implicated in noise-related hearing loss. Although no significant transcriptional changes were observed in samples obtained at the onset of the training course relative to chronic cumulative blast, we identified a large number of transcriptional perturbations acutely pre- versus post-blast exposure. Acutely, 67 robustly differentially expressed genes (fold change ≥1.5), including UFC1 and YOD1 ubiquitin-related proteins, were identified. Inflammatory analyses of cytokines and chemokines revealed dysregulation of MCP-1, GCSF, HGF, MCSF, and RANTES acutely after blast exposure. These data show the importance of an omics approach, revealing that transcriptional and inflammatory biomarkers capture acute low-level blast overpressure exposure, whereas DNA methylation marks encapsulate chronic long-term symptoms. [ABSTRACT FROM AUTHOR]

The problems of assessing the consequences of fuel-air mixtures and their prevention are topical and of practical interest. Such the explosions pose a real danger during processing, transportation and storage of fuels at various industrial and civil facilities. Forecast of possible consequences of explosions of fuel-air mixtures is a key element in development of protective measures. Today, various calculation methods have been developed and approved by different departments and organizations. The authors of the article have previously verified methods of Gosatomnadzor (RB G-05-039-96), Rostechnadzor (RD 03-409-01, PB 09-540-03, Method for assessment of consequences of accidental explosions of fuel-air mixtures, General explosion safety rules for explosive chemicals, petrochemicals and refineries), EMERCOM of Russia (GOST R 12.3.047-98, GOST R 12.3.047-2012, SP 12.13130.2009), Netherlands Organisation for Applied Scientific Research, Dorofeev, Baker-Strehlow and Baker-Strehlow-Tang for prediction of consequences of air-fuel mixture explosions at the example of real explosions. It is established that the detonation regime is best described by the Dorofeev's method and multi-energy method of Netherlands Organisation for Applied Scientific Research (ME-TNO) for deflagration regime. Thus, it is promising to create a synthesis method that could combine approaches of the methods. Detonation mode was picked out using the ME-TNO method and replaced by Dorofeev's method. Such a technique allowed proposing a new equation for predicting explosion pressure of fuel-air mixtures. As a result of the research, a new equation is proposed. An equation allows calculating the overpressure of explosion, which more accurately predicts the consequences of fuel-air explosions at petroleum and gas, petrochemical and chemical industries.

Exposure to blast overpressure may result in cerebrovascular impairment, including cerebral vasospasm. The mechanisms contributing to this vascular response are unclear. The aim of this study was to evaluate the relationship between blast and functional alterations of the cerebral microcirculation and to investigate potential underlying changes in vascular microstructure. Cerebrovascular responses were assessed in sham- and blast-exposed male rats at multiple time points from 2 h through 28 days after a single 130-kPa (18.9-psi) exposure. Pial microcirculation was assessed through a cranial window created in the parietal bone of anesthetized rats. Pial arteriolar reactivity was evaluated in vivo using hypercapnia, barium chloride, and serotonin. We found that exposure to blast leads to impairment of arteriolar reactivity >24 h after blast exposure, suggesting delayed injury mechanisms that are not simply attributed to direct mechanical deformation. Observed vascular impairment included a reduction in hypercapnia-induced vasodilation, increase in barium-induced constriction, and reversal of the serotonin effect from constriction to dilation. A reduction in vascular smooth muscle contractile proteins consistent with vascular wall proliferation was observed, as well as delayed reduction in nitric oxide synthase and increase in endothelin-1 B receptors, mainly in astrocytes. Collectively, the data show that exposure to blast results in delayed and prolonged alterations in cerebrovascular reactivity that are associated with changes in the microarchitecture of the vessel wall and astrocytes. These changes may contribute to long-term pathologies involving dysfunction of the neurovascular unit, including cerebral vasospasm. [ABSTRACT FROM AUTHOR]

Exposure to blast waves is suspected to cause primary traumatic brain injury. However, existing finite-element (FE) models of the rat head lack the necessary fidelity to characterize the biomechanical responses in the brain due to blast exposure. They neglect to represent the cerebral vasculature, which increases brain stiffness, and lack the appropriate brain material properties characteristic of high strain rates observed in blast exposures. To address these limitations, we developed a high-fidelity three-dimensional FE model of a rat head. We explicitly represented the rat's cerebral vasculature and used high-strain-rate material properties of the rat brain. For a range of blast overpressures (100 to 230 kPa) the brain-pressure predictions matched experimental results and largely overlapped with and tracked the incident pressure–time profile. Incorporating the vasculature decreased the average peak strain in the cerebrum, cerebellum, and brainstem by 17, 33, and 18%, respectively. When compared with our model based on rat-brain properties, the use of human-brain properties in the FE model led to a three-fold reduction in the strain predictions. For simulations of blast exposure in rats, our findings suggest that representing cerebral vasculature and species-specific brain properties has a considerable influence in the resulting brain strain but not the pressure predictions. [ABSTRACT FROM AUTHOR]

This study demonstrates the orientation and the "shape factor" have pronounced effects on the development of the localized pressure fields inside of the helmet. We used anatomically accurate headform to evaluate four modern combat helmets under blast loading conditions in the shock tube. The Advanced Combat Helmet (ACH) is used to capture the effect of the orientation on pressure under the helmet. The three modern combat helmets: Enhanced Combat Helmet (ECH), Ops-Core, and Airframe, were tested in frontal orientation to determine the effect of helmet geometry. Using the unhelmeted headform data as a reference, we characterized pressure distribution inside each helmet and identified pressure focal points. The nature of these localized “hot spots” is different than the elevated pressure in the parietal region of the headform under the helmet widely recognized as the under-wash effect also observed in our tests. It is the first experimental study which indicates that the helmet presence increased the pressure experienced by the eyes and the forehead (glabella). Pressure fingerprinting using an array of sensors combined with the application of principle component analysis (PCA) helped elucidate the subtle differences between helmets.

United States Special Operations Forces (SOF) personnel are frequently exposed to explosive blasts in training and combat. However, the effects of repeated blast exposure on the human brain are incompletely understood. Moreover, there is currently no diagnostic test to detect repeated blast brain injury (rBBI). In this "Human Performance Optimization" article, we discuss how the development and implementation of a reliable diagnostic test for rBBI has the potential to promote SOF brain health, combat readiness, and quality of life., (2023.)

Exposure to high intensity (blast) sounds can result in both conductive and sensorineural damage to hearing. This includes rupture of the tympanic membrane and dislocation of the middle ear ossicles, as well as damage to the inner and outer hair cells in the cochlea. A clearer understanding of how the hearing system responds to blast could help us better prevent auditory trauma, and support those who have been exposed to such sounds. Chinchillas are often used in studies of hearing due to the similarity between the chinchilla and human audiograms. The suitability of their use in research on auditory trauma from blast noise will depend on the extent to which cochlear pressures generated in chinchillas compare to those in humans. In order to gain a more detailed understanding of the response of the ear to high intensity sounds, a custom built sound concentrating horn was used to expose chinchilla cadaveric ears to a series of single frequency tones between 10 and 1280 Hz, with varying intensities from 90 to 194 dB SPL while intracochlear pressures were measured simultaneously in the scala vestibuli and scala tympani. These results were then compared to similar, previously published data from human cadavers. In both human and chinchillas, intracochlear pressures increased with applied sound pressure up to about 120 dB SPL, but began to saturate at higher intensities. The exact saturation point and the saturation pressures showed a strong frequency dependence. Intracochlear pressure magnitudes in chinchillas show some similarities with those measured in humans, but also significant differences, particularly at very high intensity levels such as those found in a blast. These differences should be taken into account when conducting blast studies in chinchillas. [ABSTRACT FROM AUTHOR]

Introduction Injuries to the peripheral auditory system are among the most common results of high intensity impulsive acoustic exposure. Prior studies of high intensity sound transmission by the ossicular chain have relied upon measurements in animal models, measurements at more moderate sound levels (i.e. < 130 dB SPL), and/or measured responses to steady-state noise. Here, we directly measure intracochlear pressure in human cadaveric temporal bones, with fiber optic pressure sensors placed in scala vestibuli (SV) and tympani (ST), during exposure to shock waves with peak positive pressures between ∼7 and 83 kPa. Methods Eight full-cephalic human cadaver heads were exposed, face-on, to acoustic shock waves in a 45 cm diameter shock tube. Specimens were exposed to impulses with nominal peak overpressures of 7, 28, 55, & 83 kPa (171, 183, 189, & 192 dB pSPL), measured in the free field adjacent to the forehead. Specimens were prepared bilaterally by mastoidectomy and extended facial recess to expose the ossicular chain. Ear canal (EAC), middle ear, and intracochlear sound pressure levels were measured with fiber-optic pressure sensors. Surface-mounted sensors measured SPL and skull strain near the opening of each EAC and at the forehead. Results Measurements on the forehead showed incident peak pressures approximately twice that measured by adjacent free-field and EAC entrance sensors, as expected based on the sensor orientation (normal vs tangential to the shock wave propagation). At 7 kPa, EAC pressure showed gain, calculated from the frequency spectra, consistent with the ear canal resonance, and gain in the intracochlear pressures (normalized to the EAC pressure) were consistent with (though somewhat lower than) previously reported middle ear transfer functions. Responses to higher intensity impulses tended to show lower intracochlear gain relative to EAC, suggesting sound transmission efficiency along the ossicular chain is reduced at high intensities. Tympanic membrane (TM) rupture was observed following nearly every exposure 55 kPa or higher. Conclusions Intracochlear pressures reveal lower middle-ear transfer function magnitudes (i.e. reduced gain relative to the ear canal) for high sound pressure levels, thus revealing lower than expected cochlear exposure based on extrapolation from cochlear pressures measured at more moderate sound levels. These results are consistent with lowered transmissivity of the ossicular chain at high intensities, and are consistent with our prior report measuring middle ear transfer functions in human cadaveric temporal bones with high intensity tone pips. [ABSTRACT FROM AUTHOR]

This study employed the Suite for the Assessment of Flammable, Explosive, and Toxic Impacts to synergize the environmental data, risk frequency, and physical and chemical properties of chemical‐induced fires and explosions at accident sites and thereby establish an integrated assessment model. In addition, the suite was used to visualize fires and explosions resulting from domino effects caused by thermal radiation and blast overpressure in initial accidents at chemical plants. The simulation results were successfully utilized to respond to a chemical plant fire, assist the fire command officer to determine the range of domino effects during rescue, and extinguish the ignition source. In addition, the model provided safety distances for rescue to enable the proper deployment of rescuers and vehicles and to prevent their exposure to deadly hazards. The simulation results also provided the integrated safety distances including acceptable safety distances for rescuers with the appropriate protective equipment and the range of domino effect during the first accident and the second accident. © 2017 American Institute of Chemical Engineers Process Saf Prog 37: 186–193, 2018 [ABSTRACT FROM AUTHOR]

This paper presents the results of a small scale experimental study of BLEVE overpressure effects. Testing consisted of a sealed aluminum tube (0.6 L) filled with either water or propane, being heated by a flame until the internal pressure led to catastrophic failure and explosion. Three parameters were controlled during the experiments: the failing pressure, the weakened length on the tube and the fill level. BLEVEs were obtained with tests involving water and propane. Blast gages and optical techniques were used to characterize the shock wave escaping from the failing tube. The results obtained suggest that the lead shock was primarily generated by the vapor space. Overpressure results obtained were compared with the predictions of existing models and found to be in reasonable agreement except for overpressures measured vertically above the cylinder where the overpressures were highest. A prediction model based on only vapor space characteristics was developed. Images show that the shock was fully formed at some distance away from the vessel opening and this was due to the non-ideal opening of the vessel. The model developed was based on the characteristics of the shock when fully formed away from the tube. These characteristics were defined using a combination of imaging, pressure measurements, and predictions from shock tube theory. [ABSTRACT FROM AUTHOR]

Blast-induced traumatic brain injury is associated with acute and possibly chronic elevation of intracranial pressure (ICP). The outcome after TBI is dependent on the progression of complex processes which are mediated by oxidative stress. So far, no effective pharmacological protection against TBI exists. In this study, rats were exposed to a single or repetitive blast overpressure (BOP) at moderate intensities of 72 or 110 kPa in a compressed air-driven shock tube. The degree and duration of the increase in ICP were proportional to the intensity and frequency of the blast exposure(s). In most cases, a single dose of antioxidant N-acetylcysteine amide (NACA) (500 mg/kg) administered intravenously 2 h after exposure to BOP significantly attenuated blast-induced increase in ICP. A single dose of NACA was not effective in improving the outcome in the group of animals that were subjected to repetitive blast exposures at 110 kPa on the same day. In this group, two treatments with NACA at 2 and 4 h post-BOP exposure resulted in significant attenuation of elevated ICP. Treatment with NACA prior to BOP exposure completely prevented the elevation of ICP. The findings indicate that oxidative stress plays an important role in blast-induced elevated ICP as treatment with NACA-ameliorated ICP increase, which is frequently related to poor functional recovery after TBI.

The intent of this paper will be to review the methods utilized at the Eastman Kingsport site in determining magnitude of consequences of toxic, thermal, and blast overpressure scenarios. This will include discussion on dispersion modeling, dose-response methods for toxic, and thermal probits as well as assessing occupant vulnerability through the use of BakerRisk's Explosion Risk Cooperative tools. © 2017 American Institute of Chemical Engineers Process Saf Prog 36: 338-352, 2017 [ABSTRACT FROM AUTHOR]

Upon impingement of blast waves on the head, stress waves generated at the interface of the skull are transferred into the cranium and the brain tissue and may cause mild to severe blast traumatic brain injury. The intensity of the shock front, defined by the blast overpressure (BoP), that is, the blast-induced peak static overpressure, significantly affects head kinematics as well as the tissue responses of the brain. While evaluation of global linear and rotational accelerations may be feasible, an experimental determination of dynamic responses of the brain in terms of intracranial pressure (ICP), maximum shear stress (MSS), and maximum principal strain (MPS) is almost impossible. The main objective of this study is to investigate possible correlations between head accelerations and the brain's ICP, MSS, and MPS. To this end, three different blasts were simulated by modeling the detonation of 70, 200, and 500 g of TNT at a fixed distance from the head, corresponding to peak BoPs of 0.52, 1.2, and 2 MPa, respectively. A nonlinear multi-material finite element algorithm was implemented in the LS-DYNA explicit solver. Fluid-solid interaction between the blast waves and head was modeled using a penalty-based method. Strong correlations were found between the brain's dynamic responses and both global linear and rotational accelerations at different blast intensities ( $$R^{2 }\ge $$ 98%), implying that global kinematic parameters of the head might be strong predictors of brain tissue biomechanical parameters. [ABSTRACT FROM AUTHOR]

The rupture of tympanic membrane (TM) has long been viewed as an indicator of blast injury, especially for hearing loss. However, little is known about damage to the TM caused by blast with pressure lower than the rupture threshold. In this paper, we present our study on the effect of blast overpressure on the static mechanical properties of TM. Chinchilla was used as the animal model and exposed to multiple blasts with pressures lower than the rupture threshold of the TM. Using a micro-fringe projection method, we observed the alteration of the static mechanical properties of post-blast chinchilla's TMs as compared to those of control TMs. Specifically, after exposing to multiple blasts, the Young's modulus of chinchilla TM decreased by ∼53% while the ultimate failure pressure decreased by ∼33%. Scanning Electron Microscope (SEM) images show the damage formation in the post-blast TM as compared with its control counterpart. [ABSTRACT FROM AUTHOR]

Several methodologies, based on different thermodynamic assumptions and requiring substance properties and thermodynamic data, have been proposed in the literature for the prediction of the mechanical energy released by a Boiling Liquid Expanding Vapour Explosion (BLEVE) and the associated overpressure. A new method, simple and easy to use, is presented which only requires the vessel filling degree and the temperature at failure as input variables to estimate this energy. The polynomial approach has been used to obtain the equation corresponding to the diverse substances most commonly involved in these explosions. The comparison of the predicted values with experimental data shows a good agreement. [ABSTRACT FROM AUTHOR]

Blast overpressure causes dynamic damage to middle ear components, and tympanic membrane (TM) rupture is the most frequent middle ear injury. However, it is unclear how the blast waves change mechanical properties of the TM and affect sound transmission through the ear. This paper reports the current study on dynamic properties of the TM after exposure to blast waves by using acoustic loading and laser Doppler vibrometry (LDV). The TM specimens were prepared from human temporal bones following exposures to blast overpressure. Vibration of the TM specimen induced by acoustic loading was measured by LDV over a frequency range of 200-8000 Hz. An inverse-problem solving method with finite element modeling was used to determine the complex modulus of the TM specimen. The post-blast storage modulus ranged from 23.1 to 26.9 MPa, and loss modulus ranged from 0.09 to 3.78 MPa as frequency increased from 200 to 8000 Hz. Compared to the complex modulus of normal TM reported in the literature, the post-blast storage and loss modulus decreased significantly across the frequency range. The scanning electron microscopy (SEM) images of the post-blast TM samples showed microstructural changes of the tissue, which explained the alteration of mechanical properties of the TM samples. [ABSTRACT FROM AUTHOR]

Bio-shock tubes (BSTs) can approximately simulate the typical blast waves produced by nuclear or chemical charge explosions for use in biological damage studies. The profile of an ideal blast wave in air is characterized by the overpressure, the negative pressure, and the positive pressure duration, which are determined by the geometric configurations of BSTs. Numerical experiments are carried out using the Eulerian equations by the dispersion-controlled dissipative scheme to investigate the effect of different structural components on ideal blast waveforms. The results show that cylindrical and conical frustum driver sections with an appropriate length can produce typical blast wave profiles, but a flattened peak pressure may appear when using a tube of a longer length. Neither a double-expansion tube nor a shrinkage tube set in BSTs is practical for the production of an ideal blast waveform. In addition, negative pressure recovery will occur, exceeding the ambient pressure with an increase in pressure in the vacuum section. [ABSTRACT FROM AUTHOR]

Blast-induced traumatic brain injury is associated with acute and possibly chronic elevation of intracranial pressure (ICP). The outcome after TBI is dependent on the progression of complex processes which are mediated by oxidative stress. So far, no effective pharmacological protection against TBI exists. In this study, rats were exposed to a single or repetitive blast overpressure (BOP) at moderate intensities of 72 or 110 kPa in a compressed air-driven shock tube. The degree and duration of the increase in ICP were proportional to the intensity and frequency of the blast exposure(s). In most cases, a single dose of antioxidant N-acetylcysteine amide (NACA) (500 mg/kg) administered intravenously 2 h after exposure to BOP significantly attenuated blast-induced increase in ICP. A single dose of NACA was not effective in improving the outcome in the group of animals that were subjected to repetitive blast exposures at 110 kPa on the same day. In this group, two treatments with NACA at 2 and 4 h post-BOP exposure resulted in significant attenuation of elevated ICP. Treatment with NACA prior to BOP exposure completely prevented the elevation of ICP. The findings indicate that oxidative stress plays an important role in blast-induced elevated ICP as treatment with NACA-ameliorated ICP increase, which is frequently related to poor functional recovery after TBI. [ABSTRACT FROM AUTHOR]

The mechanical effects of a BLEVE are overpressure and ejection of fragments. Although fragments reach much longer distances, peak overpressure can be very strong over a certain area. Diverse authors have proposed methodologies for the estimation of the explosion energy and peak overpressure from these type of explosions, based on different thermodynamic and physical assumptions. Here these methodologies are commented and compared. Their predictions, which show an important scattering, are checked by comparison with two sets of experimental data taken from the literature. The results obtained indicate that none of the models take into account Reid's theory. The models based on ideal gas behaviour and constant volume energy addition, isentropic expansion and isothermal expansion give quite conservative (i.e., high) values of both energy released and overpressure, while those assuming real gas behaviour and adiabatic irreversible expansion give lower values, much closer to the real/experimental ones. The diverse uncertainty factors affecting the prediction of peak overpressure are also commented. [ABSTRACT FROM AUTHOR]

• A novel experimental platform was developed. • Stapes footplate movement and cochlear pressure were measured simultaneously. • New methodology for quantitatively measuring energy flux into the cochlea during blast. • Peak experimental values are consistent with published results and modeling data. Blast-induced auditory injury is primarily caused by exposure to an overwhelming amount of energy transmitted into the external auditory canal, the middle ear, and then the cochlea. Quantification of this energy requires real-time measurement of stapes footplate (SFP) motion and intracochlear pressure in the scala vestibuli (Psv). To date, SFP and Psv have not been measured simultaneously during blast exposure, but a dual-laser experimental approach for detecting the movement of the SFP was reported by Jiang et al. (2021). In this study, we have incorporated the measurement of Psv with SFP motion and developed a novel approach to quantitatively measure the energy flux entering the cochlea during blast exposure. Five fresh human cadaveric temporal bones (TBs) were used in this study. A mastoidectomy and facial recess approach were performed to identify the SFP, followed by a cochleostomy into the scala vestibuli (SV). The TB was mounted to the "head block", a fixture to simulate a real human skull, with two pressure sensors – one inserted into the SV (Psv) and another in the ear canal near the tympanic membrane (P1). The TB was exposed to the blast overpressure (P0) around 4 psi or 28 kPa. Two laser Doppler vibrometers (LDVs) were used to measure the movements of the SFP and TB (as a reference). The LDVs, P1, and Psv signals were triggered by P0 and recorded simultaneously. The results include peak values for Psv of 100.8 ± 51.6 kPa (mean ± SD) and for SFP displacement of 72.6 ± 56.4 μm, which are consistent with published experimental results and finite element modeling data. Most of the P0 input energy flux into the cochlea occurred within 2 ms and resulted in 10–70 μJ total energy entering the cochlea. Although the middle ear pressure gain was close to that measured under acoustic stimulus conditions, the nonlinear behavior of the middle ear was observed from the elevated cochlear input impedance. For the first time, SFP movement and intracochlear pressure Psv have been successfully measured simultaneously during blast exposure. This study provides a new methodology and experimental data for determining the energy flux entering the cochlea during a blast, which serves as an injury index for quantifying blast-induced auditory damage. [ABSTRACT FROM AUTHOR]

• Ear canal and intracochlear pressures are described during shock wave exposure. • Hearing protective devices reduce ear canal and cochlear exposures. • Measures of hearing protection insertion loss differ in ear canal and cochlea. • Repeating and averaging measurements improves signal to noise. Injuries to the peripheral auditory system are among the most common results of high intensity impulsive noise exposure. Hearing protection can mitigate this injury, but careful assessment of the insertion loss they provide is necessary. Insertion loss is typically measured using microphone-based acoustic manikins to measure the decrease in sound pressure level transmitted into the ear canal, which precisely measure the change in air conducted sound, but neglect alternate pathways to the inner ear such as bone conduction. In a previous study we reported intracochlear pressures in cadaveric human specimens to acoustic shock waves, which revealed a substantial bone conducted component (Greene, et al., 2018). Here we evaluate insertion loss to several hearing protection devices (HPDs) in those same specimens using intracochlear pressure measurements. Human cadaver heads were exposed to impulsive acoustic pressure waves with peak overpressures of 7 and 28 kPa (171 & 183 dB SPL). Ear canal (EAC), middle ear, and intracochlear sound pressure levels were measured bilaterally with fiber-optic pressure sensors. Surface-mounted sensors measured SPL and skull strain near the opening of each EAC and at the forehead. Responses were measured with specimen ears unoccluded, as reported previously, as well as fitted with four types of HPDs. Impulse peak insertion loss (IPIL) and impulse spectrum insertion loss (ISIL) were calculated for each HPD. For all HPDs, IPIL generally increases with exposure level, though ISIL tended to be more consistent, and the spectral characteristics across frequency appear to be highly dependent on exposure level. ISIL measured in the ear canal tended to overestimate insertion loss measured in the cochlea, particularly at frequencies > 1 kHz; however, low signal-to-noise in intracochlear pressures limited comparisons. As a proof of concept, 36 low-level unoccluded exposures, were averaged together, and the resulting signal-to-noise ratio was improved by up to 15 dB. Insertion loss measured in the cochlea was lower than in the ear canal, suggesting substantial contributions from transmission pathways in parallel with air conduction (e.g., bone conduction) were present, which will require novel strategies to mitigate. However, high variance was observed, and noise reduction strategies should be utilized in future studies to facilitate more precise insertion loss estimates. [ABSTRACT FROM AUTHOR]