Tools
Acute Acoustic Trauma
Introduction
The human ear functions as a biological pressure transducer. Noise exposure is a significant global health issue, with approximately 5% of hearing loss in the worldwide population attributed to noise-induced hearing loss (NIHL).[1] Perception of loudness varies based on individual sensitivity to noise and is influenced by the below-mentioned 3 key aspects of sound.
- Sound pressure level (acoustic pressure level): This logarithmic measure quantifies the effective pressure of sound relative to a reference level, expressed in decibels (dB). Examples are provided below.[2]
- Party balloon rupture or jet engine: 150 dB.
- Loudest human voice: 135 dB.
- Typical pain threshold: 120 dB.
- Hearing damage from long-term exposure (not necessarily continuous): 85 dB.
- Frequency content.
- Duration of sound.[3]
Most individuals with normal hearing are particularly sensitive to sounds in the 2 to 4 kHz range, which corresponds to high-intensity impulse noises such as blasts. Human voices have fundamental frequencies, which represent the lowest frequency of a periodic waveform or the pitch in music, ranging from 90 to 155 Hz for males and 165 to 255 Hz for females. The sensitivity of the human ear varies based on perceived loudness at different frequencies.
A lesser-known subtype of NIHL is acute acoustic trauma (AAT), defined by sudden sensorineural hearing loss resulting from exposure to intense impulse noise, such as blasts or gunshots. This occurs when noise levels exceed the elastic limits of the auditory system, typically exceeding 140 dB for less than 0.2 seconds. In contrast, NIHL generally develops after prolonged exposure—lasting several minutes to hours—to intense sounds in the 100 to 120 dBA range, commonly found in workplaces or combat zones.[4] AAT and NIHL often occur concurrently.
AAT often results from mechanical and metabolic injuries to the auditory system, causing symptoms such as hearing loss, tinnitus, otalgia, ear fluttering, pain, vertigo, and hyperacusis. Characteristic audiometric findings can be observed following AAT, and prompt recognition and referral to otolaryngology may help prevent permanent hearing impairment.[5][6] Despite its distinct history and audiometric profile, AAT has not garnered as much research attention in the literature as NIHL. Additionally, patient awareness and urgency in seeking treatment for AAT are often low. Many individuals underreport AAT or continue to expose themselves to further trauma due to their responsibilities and circumstances, particularly in military settings. A retrospective study revealed that relatively few patients report symptoms immediately after the trauma, with most incidents occurring in military environments.[7]
AAT may damage both the middle and inner ear, leading to issues such as tympanic membrane perforation, disruption of the ossicular chain, and direct injuries to the cochlear or vestibular apparatus from blunt force or ballistic trauma. The resulting hearing loss can be conductive, mixed, or sensorineural, though it is most commonly sensorineural. Accompanying symptoms may include vertigo, tinnitus, and pain. The extent of hearing impairment depends on factors such as noise intensity, duration of exposure, the adequacy of hearing protection used, and the individual’s genetic susceptibility.
Sensorineural hearing loss may be accompanied by a diminished sensitivity to specific frequencies, subtle difficulties in hearing in noisy environments, and bothersome sensations of ear ringing or fluttering. A classic presentation following AAT might involve a patient with an intact tympanic membrane but decreased hearing thresholds above 3 kHz after a blast, as intense weapon noise typically falls within the 2 to 5 kHz range.[8] The sensory cells of the cochlea are particularly susceptible following AAT, with the initial structural change often being damage to the stereocilia bundle.[9]
Sensorineural hearing loss can be either temporary or permanent. Individuals with this condition may no longer hear low-level sounds, while high-level sounds might still be perceived as equally loud by those with normal hearing. This phenomenon can be explained by the following 2 theories.
- Loudness recruitment: An abnormally rapid increase in loudness.[10]
- Softness imperception: Soft sounds perceived by individuals with sensorineural hearing loss are louder than the faintest sounds heard by those with normal hearing.[11]
Many insights regarding AAT can be drawn from similar clinical scenarios, such as sudden-onset sensorineural hearing loss and ototoxicity from chemotherapeutic agents. Both conditions share common mechanisms involving the development of reactive oxygen and nitrogen species, free radicals, and oxidative stress.[12]
The most effective initial step in preserving hearing for patients exposed to AAT is hearing protection. Hearing protection devices (HPDs) can significantly reduce noise levels at these frequencies. HPDs can be classified as either passive or active. Both military and civilian leaders and clinicians strongly recommend using HPDs to prevent temporary threshold shifts and permanent hearing loss.[13]
Passive Hearing Protection Devices
Passive HPDs rely on physical barriers without embedded electronics and function in 2 ways, as mentioned below.
- Noise level–dependent HPDs:
- These HPDs, such as solid earplugs, provide attenuation that varies with noise intensity.
- Noise level–independent HPDs:
- Provide consistent noise reduction across different frequencies and intensities.
- Feature a narrow inner channel along the earplug’s length, causing acoustic impedance to increase nonlinearly with external sound.
- Nonlinear HPDs reduce harmful impulse noise while allowing speech and softer sounds to remain audible for communication and safety.
Active Hearing Protection Devices
Active HPDs work differently, using noise reduction algorithms within electronic devices to cancel noise actively. These devices optimize the signal-to-noise ratio to enhance the desired result, such as speech and communication amid noisy environments. These devices combine passive components, such as physical barriers, with active elements, such as preamplifiers and microphones. Some models also feature external signal processors, operating switches, and volume controls for added functionality.
Active HPDs feature directional microphones that enhance communication and hearing protection. However, they can impair sound localization, particularly from behind—referred to as a soldier’s “6” in combat. The impact of blast-type noises varies based on proximity, device type, and whether the environment is open or enclosed. Diagnosing hearing loss from AAT requires audiological evaluation and access to high-quality equipment. Advances in technology, such as smartphone screening apps and audiometric headsets, may enhance future diagnostic capabilities.
Patients with suspected AAT presenting with symptoms such as acute tinnitus, muffled hearing, or ear fullness should undergo a comprehensive head and neck examination, including a detailed otologic evaluation, ideally with otomicroscopy. Audiometric testing is the primary diagnostic tool and should be performed if hearing loss persists beyond 72 hours. Cortical evoked response audiometry may be indicated for patients suspected of exaggerating their hearing loss.[14]
Further noise exposure should be avoided, especially if vertigo accompanies the hearing loss, to prevent risks during activities like driving or operating heavy machinery. Absolute indications for otolaryngology referral include suspected temporal bone fracture, tympanic membrane perforation, persistent clear or discolored ear drainage that does not resolve within a few days, facial nerve paralysis, and hearing loss in a patient with a single functional ear.
The most significant challenges in AAT include the following:
- Accurate diagnosis
- Delays in seeking medical care (underreporting)
- Repeat acoustic trauma
- Blast-type noise
- Concomitant prolonged noise exposure
Management of AAT should be personalized and initiated promptly. Treatment outcomes and prognosis vary, and patients should be informed that hearing recovery remains unpredictable, regardless of intervention.
Etiology
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Etiology
Noise from loud explosions can damage the inner ear by overstimulating the auditory nerve fibers that relay sound information to the brain. The sound blasts may be associated with high pressures or blast overpressure, which can harm the outer ear, ear canal, tympanic membrane, and middle ear ossicles. These explosions may also generate strong blast winds or pressure gradients. Additionally, penetrating ballistic injuries can occur alongside the sound blast, causing blunt trauma. Lastly, explosions can expose individuals to toxic substances from gases, fuels, or metals, potentially resulting in burns to otologic structures.
AAT can occur in occupational settings, such as the military, or environmental contexts, such as exposure to gunfire or work-related blasts.[15] Depending on the intensity and characteristics of AAT, hearing loss may be permanent despite treatment. Genetic factors contribute to individual susceptibility to NIHL and AAT, including the Ahl gene, CDH23 (which encodes cadherin 23), myosin 14, and other related genes.[16][17][18][19][20][21][22]
Epidemiology
A 2019 study by the OSHA Information System revealed that from 1972 to 2019, there were 119,305 violations of OSHA noise standards related to occupational noise exposure in general industry.[23] More males than females are reported to have NIHL, with no significant age differences noted. Many individuals with occupational hearing loss also experience depression and sleep disorders.[24]
Recreational firearm use in the United States is more prevalent than in any other country in the world. Many individuals may be unaware of the associated hazards, as nearly all firearms produce peak impulse noise levels exceeding 140 dB. According to the Aural Blast Injury/Acoustic Trauma and Hearing Loss guidelines, AAT contributes to veteran disability at an annual rate of 13% to 18% in the United States.[25]
A retrospective study of French military personnel assessed the prevalence of long-term hearing loss in individuals exposed to AAT. Audiograms taken an average of 448 days after AAT indicated a long-term hearing loss prevalence exceeding 20%.[26] Another study examined hearing loss following a single episode of AAT, estimating a 1% incidence of hearing loss over a 20-year follow-up period.[27]
Pathophysiology
Prolonged exposure to loud noise can result in hearing loss, whether acute or chronic. Overstimulation of hair cells may cause mechanical damage to the cochlea, reduce blood flow due to the formation of vasoactive lipid products, and trigger inflammation, oxidative stress, and excitotoxicity. Acoustic overstimulation leads to excessive release of the neurotransmitter glutamate, which interferes with the functioning of the cochlea. This disruption can cause swelling of the stria vascularis and depolymerization of actin filaments in the stereocilia, leading to a temporary threshold shift. If left untreated, this process may progress to apoptosis and necrosis of hair cells and the organ of Corti due to free radical release, ultimately resulting in permanent sensorineural hearing loss.[28][29]
AAT induces cochlear inflammation.[30] The pathophysiology of AAT involves the formation of reactive oxygen and nitrogen species in the inner ear. These substances can directly damage DNA and cell membranes while signaling the upregulation of genes associated with apoptotic cell death. Research indicates that these substances spread from the basal to the apical cochlea over a period of 7 to 10 days. Following AAT, studies on guinea pig cochleas revealed progressive hair cell loss, which correlated with the delayed formation of reactive species, stabilizing after 2 weeks.[31]
The inner cochlear hair cells convert sound into nerve signals, while the outer hair cells amplify sound sensitivity. In cases of AAT, the outer hair cells are typically the first to be affected, leading to hearing loss ranging from 40 to 60 dB. Continued damage can further harm the inner hair cells, exacerbating hearing loss. Temporary threshold shifts correspond anatomically to decreased stiffness of the stereocilia in the outer hair cells.[32] The stereocilia become disarrayed and nonfunctional. In instances of severe noise exposure, complete hearing loss may occur if the entire organ of Corti is damaged. Hearing loss is often more pronounced at frequencies higher than 4 kHz.[33]
Histopathologically, the primary damage site is the rootlets connecting the stereocilia to the top of the hair cell. Apoptosis of the sensory cells results in progressive Wallerian degeneration and, ultimately, loss of primary auditory nerve fibers. High-intensity noise can damage hair cells and spiral ganglion neurons, as well as cause middle ear injuries, including tympanic membrane perforation, ossicular chain dislocation, and oval or round window rupture, which may lead to a perilymphatic fistula.[34]
In addition to causing inner ear damage, AAT disrupts middle ear function by interfering with the muscles involved in hearing, specifically the stapedius and tensor tympani muscles.
Stapedius muscle: This is the smallest skeletal muscle in the human body, measuring approximately 1 mm in length, that protects the cochlea by contracting in response to loud noises, which produces a dampening effect.
Tensor tympani muscle: This muscle inserts between the cartilage of the Eustachian tube and the neck of the malleus. The tensor tympani muscle shares a tendon with the tensor veli palatini muscle and is innervated by the mandibular branch of the trigeminal nerve.[35] AAT causes hypercontraction of the tensor tympani muscle, likely leading to muscle strain, fatigue, or overload.[36]
Some authors have compared tensor tympani hypercontraction to a myofascial trigger point or a "micro-cramp."[37] Tensor tympani hypercontraction may be severe and could explain the fluttering sensation experienced in AAT.[38] Prolonged contraction, or muscle overload, can result in injury to the tensor tympani, with the following proposed consequences:[39]
- Compression of blood vessels reduces oxygen supply.
- Production of adenosine triphosphate (ATP) decreases.
- The body shifts to anaerobic glycolysis, leading to lactic acid production and decreased pH.[40]
- Mastocyte migration occurs, resulting in the release of histamine and platelet-activating factors, which triggers serotonin release from platelets and the release of neuropeptides such as substance P and calcitonin gene–related peptide.[41]
- The prolonged, intense inflammatory response in the middle ear mucosa may extend across the round window, leading to inner ear damage.[42]
Referred pain from AAT may arise from tensor tympani injury, chronic inflammation, and neural hyperactivity in the trigeminal pathways.[38] Otalgia related to AAT is likely due to motor and autonomic reflexes.[43] The origin of tinnitus associated with AAT remains unclear.[38] In addition to its direct effects on the auditory system, noise can induce psychological and physiological stress. The sensitivity of the auditory system can be modulated by the hypothalamus-pituitary-adrenal axis, which may be activated by acoustic stress.[44]
History and Physical
Critical information in the medical history of a patient with suspected AAT includes the type, intensity, duration, and characteristics of exposure to brief, intense noise, as well as the severity and duration of the resulting sudden hearing loss. Accompanying symptoms, such as tinnitus and dizziness, should also be documented. In some cases, a condition known as acoustic shock may occur, characterized by symptoms like pain in and around the ear, tinnitus, hyperacusis, ear fullness and tension, and dizziness.[39]
The physical examination for patients with AAT may be more crucial than for those with NIHL, as patients with prolonged noise exposure may show no physical findings. Detailed otomicroscopy is essential in AAT cases to assess any trauma to the ear canal, tympanic membrane, or ossicles. If the AAT resulted from a blast injury, any debris should be removed from the ear canal, and topical fluoroquinolone and steroid-containing ear drops should be prescribed. Topical drops containing aminoglycosides, such as neomycin, should be avoided to prevent ototoxicity. Patients should follow dry ear precautions. A thorough neurological examination must include an assessment of the cranial nerves, especially the facial nerve.
If the AAT is part of a more extensive trauma, a comprehensive full-body trauma examination is essential.
Evaluation
Currently, no specific professional guidelines exist for managing AAT. However, clinicians can reference the American Academy of Otolaryngology–Head and Neck Surgery (AAOHNS) guidelines for sudden hearing loss, the American College of Occupational and Environmental Medicine guidance on occupational noise-induced hearing loss, and the Joint Trauma System (JTS) Clinical Practice Guidelines on Aural Blast Injury/Acoustic Trauma and Hearing Loss.[45][46][25]
The diagnosis of AAT requires a comprehensive evaluation, considering other potential causes of acute sudden hearing loss. Following a detailed history and physical examination, a battery of audiological tests is typically the next step.
According to the JTS Practice Guidelines, all patients with subjective hearing loss after AAT should undergo the following tests.
- Screening audiometry: This should be conducted as soon as possible after the initial trauma unless more urgent treatment or altered mental status prohibits evaluation.
- Audiological evaluation: This test should follow the presentation of signs of concussion.[25]
- Comprehensive audiogram: This includes tympanometry, bone-conducted thresholds, speech discrimination, and acoustic reflexes if hearing loss lasts for more than 72 hours.
Patients with a temporary threshold shift greater than 25 dB should be considered for steroid treatment, either orally or via transtympanic injection. Follow-up audiometry is essential to monitor progress.
Pure-Tone Audiometry
Pure-tone audiometry assesses the function of the outer ear, middle ear, cochlea, cranial nerve VIII (CNVIII), and central auditory system. Studies examining audiometric configurations in military patients with AAT consistently show high-frequency hearing loss, typically presenting with a notch between 2 and 6 kHz and recovery at 8 kHz.
Conversely, some authors reported normal hearing thresholds within the conversational range, with deterioration at higher frequencies.[47][48] They concluded that limiting hearing tests to the standard frequency range of 0.5 to 8 kHz may result in missed cases of AAT. A high-frequency hearing test covering up to 16 kHz is recommended to ensure accurate assessment.[47]
Audiometry results in AAT can resemble those of presbycusis. However, presbycusis typically presents with greater hearing loss at 8 kHz than at 3, 4, or 6 kHz. In contrast, AAT often shows more significant loss at 6 kHz than 8 kHz, with similar thresholds at 4 and 8 kHz, and peak loss sometimes occurring at 3 kHz.[49][50]
A study of 24 young military personnel conducted follow-up audiometry at 24 hours, 72 hours, and 15 days after AAT caused by firearm discharge, confirming that mid-to-high frequency loss is characteristic of AAT. Notches at 3 and 4 kHz were present in 71% of patients, with losses ranging from 10 to 70 dB. Hearing improved over time, with an average loss of 24 ± 16 dB at 24 hours, 14 ± 13 dB at 72 hours, and 12 ± 14 dB by day 15.[51]
Pure-tone audiometry was performed on 361 Finnish conscripts who experienced AAT during military service. Over 75% of affected ears showed hearing loss in the high-frequency range (above 2 kHz), while the speech frequency range was impacted in the remaining 25%.[52] Perez et al evaluated 143 patients exposed to explosions, finding that 46% of audiograms exhibited a downsloping pattern above 2 kHz, 41% showed a mid-frequency notch, and 12% had a flat configuration.[53]
Pure-tone audiometry is subjective; obtaining acoustic reflex thresholds is essential to identify potential malingering in patients.
Otoacoustic Emissions
Otoacoustic emissions (OAEs) are a valuable tool for hearing screening after AAT, especially in cases where a patient may be feigning hearing loss. OAEs assess the peripheral auditory system, including the outer and middle ears, and the cochlea. OAEs are reliable and reproducible, providing important clinical insights, particularly when patients do not respond truthfully during pure-tone audiometry following a blast explosion.
OAEs are sounds generated by the movement of outer hair cells in a properly functioning cochlea when stimulated by external sounds. This objective, sensitive, and user-friendly test involves an aural probe with a speaker that delivers an acoustic stimulus while a microphone detects the resulting emissions. Distortion product OAEs can identify early NIHL with 82% sensitivity and 92.5% specificity, even when pure-tone audiometry results are normal.[54] However, there is a risk of false positives associated with this test.[55]
OAEs can assess auditory function following AAT. The connection between noise exposure and OAEs is well-documented, emphasizing their utility as sensitive indicators of hearing loss, particularly after AAT. Numerous studies have shown a reduction in OAE amplitude following exposure to loud noise, even when audiometric thresholds remain unaffected. This highlights the superior sensitivity of OAEs in detecting changes in hearing.[56][57][58][59][60]
Auditory Brainstem Response Audiometry
Auditory brainstem response audiometry serves as a critical tool for detecting patient malingering during pure-tone audiometry. Typically, auditory brainstem response is particularly beneficial for identifying retrocochlear pathology and assessing symptoms related to eighth nerve disorders. The application of this test is most valuable when comparing auditory brainstem response results to magnetic resonance imaging (MRI) or computed tomography (CT) in patients who have experienced significant auditory trauma.
Treatment / Management
Despite promising outcomes, conflicting evidence exists regarding a definitive treatment protocol for patients with AAT. The JTS Practice Guidelines prioritize primary prevention over treatment, recommending that individuals at risk be educated on the importance of using ear protection and minimizing noise exposure. Emphasis is also placed on educating individuals to recognize AAT symptoms and the importance of self-reporting for evaluation.[25]
The treatment of patients with AAT can vary based on several factors, and it is essential for each patient to understand that no treatment guarantees complete restoration of hearing. If there is visible trauma from a blast injury to the outer ear, ear canal, tympanic membrane, or middle ear, addressing these issues should be the priority. In such instances, the management approach may involve staged healing and potential surgical repair as needed, with the acknowledgment that some degree of hearing loss may still occur.
If the hearing loss is purely sensorineural and no other otologic or brain trauma is evident, several treatment strategies are available, as described below.
Corticosteroids: These may be effective whether administered intravenously, orally, or intratympanically.[61][62][63][64][65] (A1)
- Intravenous corticosteroids: These regimens may include methylprednisolone at 125 mg on the first day of treatment, 80 mg on the second day, and 40 mg on the final day.[64]
- Oral prednisone: This drug may be administered at a dosage of 1 mg/kg, up to a maximum of 60 mg daily, for 1 to 2 weeks. Longer courses often yield better outcomes in patients who can tolerate high-dose steroids for more than 1 week.[65][61]
- Steroid injections: The JTS guideline recommends high-dose oral or transtympanic steroid injections, when not contraindicated, for patients with threshold shifts of more than 25 dB in 3 consecutive frequencies. The injection regimen typically includes transtympanic dexamethasone at a concentration of 24 mg/mL. Patients should undergo weekly audiometric evaluations, regardless of the treatment approach. If follow-up audiograms indicate some recovery, additional injections are recommended, up to a total of 3.[25]
Antioxidants and neurotrophins: These may provide benefits in the acute treatment of NIHL.[66] Although the evidence supporting the use of antioxidants and neurotrophins is limited, they are generally well-tolerated.(B3)
Hyperbaric oxygen therapy: This therapy may be beneficial for AAT, particularly if corticosteroid therapy is ineffective. Treatment typically involves 120-minute dives to pressures ranging from 200 to 280 kPa daily for 10 days.[64][67][68][49][50] The AAOHNS guidelines on sudden sensorineural hearing loss indicate that if there is no response to initial therapy, hyperbaric oxygen therapy combined with corticosteroids can serve as salvage therapy within 1 month of onset.[45] Temporary placement of ear ventilation tubes may also be necessary.(A1)
In summary, key management factors include the prior use of HPDs, whether in a linear or nonlinear manner, and the initiation of early steroid treatment following an AAT injury, preferably within 24 to 72 hours.[64] Hearing recovery may vary based on age and comorbidities, necessitating individualized clinical treatment. Despite guideline recommendations, oral steroid treatment may be more favorable than transtympanic steroid injections and hyperbaric oxygen therapy in clinical practice.
Differential Diagnosis
Differential diagnoses for AAT include:
- Sudden sensorineural hearing loss
- Head trauma causing inner ear, cochleovestibular nerve injury, or brainstem pathology
- Stroke - posterior circulation cerebrovascular accident, typically characterized by sudden onset of hearing loss and frequently associated with other neurological deficits [69]
- Viral infections (primarily)
- Autoimmune diseases
- Chemotherapy for cancer or infections
- Neurological disorders, such as multiple sclerosis
- Ménière disease
Prognosis
The time interval from AAT to triage, initial audiometry, and treatment by an otolaryngologist is crucial for improving prognosis, especially if steroid therapy is initiated. In a study involving 263 healthy participants, half received steroids, whereas the other half did not receive any treatment following AAT. Those treated within 24 hours with high-dose steroids for at least 7 days demonstrated significantly better hearing outcomes compared to the untreated group.
The steroid-treated group experienced an average improvement of 13 to 14 dB in bone conduction thresholds at 3 and 4 kHz (P = .001) and an additional 7 to 8 dB improvement in air conduction thresholds at 6 and 8 kHz compared to the untreated group (P < .0001).[61] Patients exhibiting a threshold shift greater than 60 dB across three consecutive frequencies for 10 or more days after noise exposure are unlikely to resolve spontaneously and are at a higher risk of permanent hearing loss.[25]
Complications
The effects of loud noise exposure are pathological, psychological, and sociological. Hearing loss can impact interpersonal communication, leading to diminished self-esteem and strained relationships. This may also reduce attention and cognitive function, increasing the risk of dementia. While noise can affect work performance, the extent of this impact often depends on individual predisposition. Additionally, the financial burden of hearing loss and compensation costs for employers can be significant.
Deterrence and Patient Education
The World Health Organization (WHO) reports that hearing loss is among the 20 leading causes of disease burden and the most common disability globally. NIHL is the most preventable cause of hearing loss. However, AAT may be less predictable and preventable in occupational or military settings.
A critical component of prevention efforts is education at all levels. Individuals at risk, such as military personnel, must understand that hearing can only be protected through efforts to reduce exposure to hazardous noise. The importance of wearing HPDs and referring individuals to specialists after AAT—regardless of the level of hearing loss—should be emphasized in hearing conservation programs.
Pearls and Other Issues
AAT presents various challenges and considerations in prevention, diagnosis, and treatment. Critical facts to keep in mind regarding AAT include:
- AAT can be prevented with the use of hearing protection.
- Hearing loss resulting from blast injuries may recover spontaneously in some cases.
- The underlying pathophysiology likely involves changes to the middle ear muscles and cochlea.
- AAT may also be underreported and undertreated, highlighting the need for increased awareness.
- Evaluation begins with a thorough otomicroscopy and audiometry assessment.
- Treatment should be individualized, with realistic expectations communicated to each patient, as permanent hearing loss remains a possibility.
Enhancing Healthcare Team Outcomes
Addressing the impact of noise on human health requires a collaborative approach involving a team of medical professionals and policymakers, including primary care providers, otolaryngologists, audiologists, occupational health nurses, and government administrators. Support from concerned employers, regulatory agencies, and the mass media is essential to raise public awareness and facilitate the screening and treatment of AAT. Additionally, further research is necessary to gather more data, which may help develop holistic and integrated healthcare solutions for individuals affected by AAT.
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