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Natarajan, N., Batts, S., & Stankovic, K. M. (2023). Noise-Induced Hearing Loss. Journal of Clinical Medicine, 12(6), 2347. https://doi.org/10.3390/jcm12062347

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Noise damages sensory cells of inner ear through direct mechanical stress of intense sound pressure and by activation of stress-induced molecular pathways, including generation of reactive oxygen species and calcium overload.

"The mechanisms by which loud noise induces hearing loss include mechanical damage of cochlear structures, reduction in blood flow, sterile inflammation, and oxidative stress and excitotoxicity due to overstimulation of hair cells and nerves".

Loss of hair cells (stereocillia via apoptosis/programmed cell death)

Exposures include:

Workplaces - factories, occupations

Lifestyle - if you go clubbing and like to party

One time exposures to significant sounds - such as an explosion, shooting firearms

There are also risk factors:

Genetic

Health conditions

Lifestyle factors - smoking

This can affect:

Activities and participation

E.g. ability enjoy playing sports, enjoy music, social communication (more difficult)

Occupation - might lose your job

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Exposure to noise, ototoxic drugs, degenerative effects of aging on the cochlea

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Description

Chronic Disorder

Affects balance and hearing that causes severe dizziness, ringing in the ears, and hearing loss

Disorder or the inner ear

Hearing Test Results

PTA - Flat audiometric pattern

PTA are gold-standard for Meniere's Disease testing as it useful to show fluctuations, progressions - but detailed case history is need

Speech audiometry testing is to measure patient's ability to identify speech stimuli and confirm results of PTA and rule of presence of non-organic hearing loss

Sensorineural hearing loss

Decreased sensorineural hearing at lower and higher frequencies

Trouble hearing low frequencies and combined high/low frequencies

Impacts on communication and intervention

Speech Perception

Speech may be slurred or garbled

Speech Pathology Intervention

Hearing Loss Management: SLPs can work with individuals who experience hearing loss due to Ménière's disease. They provide strategies for improving communication, such as lip reading, and using assistive listening devices

Auditory Training: This involves exercises that help improve the brain’s ability to process sound, especially in cases where hearing aids or cochlear implants are used

Tinnitus Management - Education and Counseling: SLPs can educate patients on how to manage tinnitus (ringing in the ears), which is a common symptom of Ménière's disease. This might include relaxation techniques, sound therapy, and strategies to reduce the impact of tinnitus on daily life

Compensatory Strategies: For those with fluctuating hearing loss, SLPs can teach communication strategies to help patients maintain effective communication. This might include environmental modifications (e.g., reducing background noise) or using non-verbal communication cues

Family Training: Involving family members in therapy to ensure they understand the challenges and can support the patient effectively

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impacts: Aboriginal and Torres Strait Islander Peoples experience excessive rates of ear and hearing problems which can have profound impacts on overall health and quality of life. These problems may limit opportunities for education, work, personal relationships and wider community engagement. Importantly, ear and hearing problems affect the passing of Indigenous cultural knowledge and immersion in culture. (https://www.aihw.gov.au/reports/indigenous-australians/ear-and-hearing-health-of-aboriginal-torres-strait/summary)

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Australian Institute of Health and Welfare

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This is the inaugural Australian Institute of Health and Welfare (AIHW) national report on the ear and hearing health of Aboriginal and Torres Strait Islander children and adults.

Indigenous Australians experience excessive rates of ear and hearing problems which can have profound impacts on overall health and quality of life. These problems may limit opportunities for education, work, personal relationships and wider community engagement. Problems affecting children can have ongoing impacts, affecting speech, language, cognitive and behavioural development. Importantly, ear and hearing problems affect the passing of Indigenous cultural knowledge and immersion in culture. Much ear disease and hearing loss affecting Indigenous Australians, particularly children and younger adults, is preventable.

This report brings together information on the prevalence of ear and hearing problems among Indigenous Australians along with insights on key protective and risk factors. It presents information on accessibility and use of ear and hearing health-care services by Indigenous Australians, from screening to treatment to rehabilitation and includes on-the-ground experiences of Indigenous specific primary health-care service providers. The report identifies key data gaps and potential areas for data development.

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Ear and hearing health of Aboriginal and Torres Strait Islander people 2021, Summary

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This is the inaugural national report on the ear and hearing health of Aboriginal and Torres Strait Islander children and adults. Indigenous Australians experience excessive rates of ear and...

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Adults: likely to experience sensorineural hearing loss, particularly at older ages. Risk factors: ageing, exposure to loud noise, genetic causes, infectious and chronic diseases, use of ototoxic medicines, and injuries and accidents. Indigenous adults can also experience ongoing ear and hearing problems because of otitis media in childhood. (https://www.aihw.gov.au/getmedia/557cc818-3c84-4138-b8a5-daf1b35f28ba/aihw-ihw-262.pdf?v=20230605181821&inline=true)

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o   Chronic otitis media: middle ear infection highly prevalent in Aboriginal and Torres Straight Islander Peoples - if left untreated it ca lead to significant hearing loss.

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Otitis media is caused by bacteria and viruses that colonise the back of the nasal passages and ‘access the middle ear space via the Eustachian tube.’ The build-up of fluid in the middle ear prevents the eardrum vibrating and conducting sound to the brain

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Group 6: Impacts on communication and intervention

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Group 6: Impacts on communication and intervention

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Educational and social impacts:

Learning difficulties: untreated hearing loss can lead to challenges in communication, literacy and educational attainment

Social isolation: Impact intergration in communities, as well as personal and social relationships

Economic impact:

Employment: hearing loss can effect employment opportunties, if not managed effectively

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Pathology: Sudden hearing loss, also known as sudden sensorineural hearing loss (SSHL), is an unexplained rapid loss of hearing that can happen all at once or over a few days. It frequently affects only one ear.

Damage to the inner hair cells in the cochlear leading the cell death (could be due to acoustic trauma or exposure to ototokins

Can be caused by damage to the sensitive hair cells inside the inner ear, earwax buildup, ear infection, and ruptured eardrums.

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1. Audiology Assessment

Initial Evaluation: An audiologist will perform a thorough hearing assessment, including pure-tone audiometry, speech audiometry, and tympanometry, to determine the degree and type of hearing loss.

Differential Diagnosis: Audiologists help differentiate between conductive and sensorineural hearing loss and identify the underlying causes, which may include viral infections, vascular issues, or autoimmune disorders.

2. Medical Management

Referral to ENT Specialist: Immediate referral to an otolaryngologist (ENT specialist) is essential for medical evaluation and potential treatments like corticosteroids, either orally or via intratympanic injection, which are commonly used in the early stages.

3. Speech-Language Pathology

Aural Rehabilitation: Speech-language pathologists (SLPs) provide aural rehabilitation to help patients adapt to hearing changes. This may include auditory training, speech-reading (lip-reading), and communication strategies.

4. Psychological Support

Mental Health Screening: Sudden hearing loss can be distressing and may lead to anxiety, depression, or social withdrawal. Psychologists or counselors can offer support and mental health interventions as needed.

5. Occupational Therapy

Adaptation Strategies: Occupational therapists (OTs) may assist patients in adapting their daily routines and environments to accommodate hearing loss, ensuring they maintain independence.

Assistive Devices: OTs might recommend and train patients in using assistive listening devices (e.g., FM systems, alerting devices) to improve communication in various settings.

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Hearing test results for sudden hearing loss:

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Hearing test results for sudden hearing loss:

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It would be within normal limits for 16 to 25 dB HL, but for children this is slight hearing loss.

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Not as bad for acquired compared to congenital due to still learning through the developmental stage.

If it is unilateral, speaker can have trouble understanding/hearing speaker on the affected ear.

Speech disruption in perception - making it difficult to understand speech clearly, especially in noisy environments.

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Pathology (Cause): Presbycusis is sensorineural hearing loss due to aging, characterized by degeneration of cochlear hair cells, auditory nerve fibers, reduced blood supply, and oxidative stress. It primarily affects high-frequency hearing.

Hearing Test Results:

Pure-Tone Audiometry (PTA):

High-frequency hearing loss with a downward-sloping audiogram.

Speech Audiometry:

Elevated speech recognition thresholds and reduced word recognition, especially in noise.

Tympanometry:

Typically normal (Type A), as middle ear function is unaffected.

Impacts on Communication:

Difficulty understanding speech, especially in noisy environments.

Social isolation and increased cognitive effort to follow conversations.

Intervention Options:

Medical:

Managing underlying conditions and overall health.

Audiological:

Hearing aids, cochlear implants, and assistive listening devices.

Allied Health Management:

Speech Therapy: Auditory training and communication strategies.

Psychology: Addressing emotional impact.

Occupational Therapy: Communication tools for daily activities.

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Common conditions include changes in the inner ear that affect hearing, changes along the neural pathway that can affect hearing, and long-term exposure to loud noises. Based on new research, these conditions can be hereditary.

The gradual loss can be unrecognisable for self-aware individuals. Significant symptoms can include trouble comprehension and an inability to understand in a loud, noisy environment. It's important to note that hearing loss affects both ears equally, highlighting the need for comprehensive care.

The medical term of the condition is known as presbycusis.

there are two types of presbycusis1) sensory2) neural

Management is using a hearing aid, it can't restore hearing and can always be progressive.

Prevention: Wear ear plugs,

turn down the volume,

move away from loud noises,

and take care of your health.

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Otosclerosis is a term derived from oto, meaning “of the ear,” and sclerosis, meaning “abnormal hardening of body tissue.” The condition is caused by abnormal bone remodeling in the middle ear. Bone remodeling is a lifelong process in which bone tissue renews itself by replacing old tissue with new. In otosclerosis, abnormal remodeling disrupts the ability of sound to travel from the middle ear to the inner ear.

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Otosclerosis is a term derived from oto, meaning "of the ear," and sclerosis, meaning "abnormal hardening of body tissue." The condition is caused by abnormal bone remodeling in the middle ear. Bone remodeling is a lifelong process in which bone tissue renews itself by replacing old tissue with new.

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Indigenous Hearing Loss in  Children : Otitis 

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Summary

Hearing loss among Aboriginal and Torres Strait Islander children in Australia is notably high and primarily attributed to otitis media, which is a treatable and preventable condition. Disparities in hearing health are further complicated by socioeconomic and environmental factors, leading to significant impacts on cognitive and social development. Although progress has been made through various government interventions aimed at reducing ear disease prevalence, systemic barriers remain that hinder effective treatment and management of hearing issues within Indigenous communities.

Key Points

Ear disease and hearing loss are particularly prevalent among Aboriginal and Torres Strait Islander children, often due to conditions like otitis media.

Otitis media is prevalent among Indigenous children, especially during early developmental years, and can lead to long-term hearing loss if untreated.

The incidence of otitis media and related hearing loss occurs at a significantly higher rate for Indigenous children compared to their non-Indigenous counterparts.

Environmental factors such as household overcrowding and exposure to smoke from tobacco or wood significantly increase the risk of ear infections.

Socioeconomic disadvantages, including inadequate access to healthcare and nutritional deficiencies, are closely linked to higher rates of ear disease in Indigenous communities.

Barriers to healthcare access often result in delayed diagnoses and treatments, prolonging periods of hearing loss and impairments.

Various government programs aimed at improving Indigenous children's ear health have shown success, but substantial gaps in healthcare access and preventive efforts continue to exist.

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Ear Disease Indigenous Australian (closing the gap) 

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Pathological Causes of Noise Induced Hearing Loss

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Pathological Causes of Noise Induced Hearing Loss

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Noise-induced hearing loss is primarily caused by damage to the sensory hair cells in the cochlea due to exposure to high levels of noise.

Key pathological causes:

Mechanical Stress: Loud noises exert intense sound pressure, causing direct mechanical damage to the cochlear hair cells, which are crucial for converting sound vibrations into neural signals.

Molecular Pathways Activation: Noise exposure triggers stress-induced molecular pathways, including the generation of reactive oxygen species (ROS) and calcium overload, leading to cellular damage and death of hair cells.

Threshold Shifts:

Temporary Threshold Shift (TTS): A temporary decrease in hearing that resolves after noise exposure.

Permanent Threshold Shift (PTS): Prolonged or repeated exposure results in irreversible hearing loss due to hair cell death.

Synaptic Damage: Even noise levels causing TTS can lead to permanent cochlear damage, specifically the loss of hair-cell ribbon synapses, affecting neurotransmitter release and potentially leading to "hidden hearing loss." This synaptic damage may not be immediately apparent but can impact hearing function over time.

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Noise-induced hearing loss (NIHL) is a consequence of multifactorial damage to auditory structures following exposure to occupational, environmental, or recreational sources of loud sound. Noise has been recognized as a factor contributing to hearing loss long before rigorous data collection, sophisticated analyses, and careful experimental design became the norm. Although earplugs were patented in 1864, hearing protection devices are mentioned in ancient Greek mythology [ 1]. NIHL was formally acknowledged as a medical condition in the United States (US) during the Industrial Revolution, first named 'boilermaker's disease' as a reference to the hearing loss suffered by workers building engines that powered transportation and production [ 2]. Historical data on US women who worked in the factories during World War I and II reveal devastating health effects, including hearing loss, although disorders caused by exposure to chemicals received more attention than those attributable to noise [ 3]. Noted physician and Nobel Prize winner Robert Koch predicted in 1910 that "one day man will have to fight noise as fiercely as cholera and pest" [ 4]. Despite this prediction and the long-standing knowledge of the adverse effects of noise on hearing and extensive research in the modern era, hearing loss continues to rank among the most common work-related illnesses both in the US and the world [ 5].

NIHL may be unilateral (affecting one ear) or bilateral (affecting both ears), and the hearing deficits may be transient or permanent [ 6]. The duration and severity of NIHL depends on the extent and location of cellular damage, which correlates with intensity and duration of the sound stimulus. Because the mammalian auditory sensory epithelium-the organ of Corti-does not spontaneously regenerate when sensory cells are lost, noise-induced hair cell or neural degeneration can result in permanent hearing loss particularly in the setting of repeated exposure [ 6, 7]. Furthermore, NIHL is frequently irreversible and can have a profoundly negative impact on an individual's quality of life and on the economy and society at large. However, NIHL is largely a preventable condition when appropriate precautions, such as the use of hearing protection, can be taken. Therefore, implementing measures to detect and attenuate causative factors, raising awareness of the condition and implementing protective strategies, and developing therapies that protect against or mitigate damage from noise exposure can aid in the prevention of this common condition. In this review, we describe the epidemiology, anatomy, pathophysiology, diagnosis, and prevention strategies of NIHL and protective pharmacological agents which have demonstrated some efficacy in humans, and we close with an outlook on emerging therapies.

The most recent Global Burden of Disease report (2019) estimated that 1.57 billion people, or 20.3% of the world population, are affected by any kind of hearing loss, with 62% over the age of 50 years [ 8]. As NIHL is the second most common cause of hearing loss after presbycusis (age-related hearing loss) [ 9, 10], it imposes an enormous burden on individuals and health systems. Globally, NIHL is estimated to affect approximately 5% of the population and is generally more common among adult men [ 11, 12]. However, this may be an underestimate as the prevalence of NIHL varies widely across populations and age groups. For example, greater exposure to occupational and urban noise in developing nations increases the risk of NIHL, and limited access to healthcare and screening tests may leave much of the burden undetected [ 13, 14, 15]. Further, developing nations may lack governmental guidance or legislation to limit noise exposure or lack public education measures to encourage the use of hearing protection. This can be observed in data on the prevalence of occupational NIHL across nations within the same geographic region. Approximately 16% of disabling hearing loss in adults globally is attributed to occupational noise, ranging from 7 to 21% across various geographic regions [ 16]. Both the highest and lowest rates are in the West Pacific region (as defined by the World Health Organization (WHO)): rates are lowest among developed nations including Australia, Japan, New Zealand, and Singapore, and the highest in the region include Cambodia, Laos, Malaysia, Philippines, and Vietnam [ 16].

Due to lack of public records and funding for research on NIHL, the true burden of NIHL in the developing world is unknown, although several studies in India and Africa have highlighted it [ 17, 18]. For example, a survey of the effects of urban noise on traffic police in Hyderabad, India, reported that 76% had NIHL, and high rates of NIHL were observed in workers in textile, mining, and heavy engineering industries [ 17]. Similarly, a cross-sectional study reported that the prevalence of NIHL among Tanzanian iron/steel workers was significantly higher than among schoolteachers (48% vs. 31%) but was high in both groups [ 19].

NIHL is also common among developed nations. In the US, interviews and hearing tests conducted by the Centers for Disease Control and Prevention (CDC) National Health and Nutrition Examination Survey (NHANES) led to estimates that at least 6% and up to 24% of adults have hearing loss in one or both ears due to noise exposure, with higher rates among males [ 20, 21]. An estimated 17% of US youths (aged 12-19 years) have hearing tests indicative of NIHL, with higher rates among females, primarily attributable to unsafe recreational noise levels [ 22]. In the European Union, noise is a main cause of disabling hearing loss, affecting over 34.4 million people in 2019 and contributing to over 185 billion euros in annual costs related to reduced quality of life and lost productivity [ 23]. NIHL is also reported to be more prevalent in eastern and central Europe compared to western Europe [ 24]. In the United Kingdom (UK), approximately 180,000 people aged 35-64 years were estimated to have severe hearing difficulties attributable to noise at work in 2002 [ 25]. NIHL and occupational deafness have been declining in the UK but are still estimated to impact over 11,000 workers annually [ 26].

3.1. Harmful Noise Levels

Sound frequency is measured in Hertz (Hz), and intensity (loudness) is measured by sound pressure level on a logarithmic decibel (dB) scale, which ranges from safe to unsafe exposure levels ( Figure 1). Normal human sound discrimination typically begins at 0 dB within the frequency ranges of 20 Hz to 20,000 kHz [ 27]. In comparison, a normal conversation is approximately 60 dB, traffic is 80 dB, very loud music at a rock concert or nightclub is 120 dB, and a jet engine is 140 dB. Broad categories of noise exposure include continuous noise, which is sustained over time, and impulsive noise, which occurs rapidly (i.e., a gunshot or explosion) and is generally at a higher sound pressure level [ 28]. A sound pressure level above 110 dB is considered discomfort threshold, and above 130 dB is the pain threshold [ 3]. Sustained noise above 70 dB can result in cumulative hearing loss while noise above 120 dB can cause immediate hearing loss [ 29].

3.2. Auditory Structures and Functions Impacted by Noise

3.2.1. Sound Transmission from the Outer to the Middle and Inner Ear

The damage associated with NIHL begins when harmful sound is channeled to auditory structures from the outer ear via the auditory canal ( Figure 2a). The unique shape of the auditory canal, where it is closed at one end by the tympanic membrane and open at the lateral end, serves as a quarter-wave resonator tube funneling sound to the middle ear [ 32]. Sound waves vibrate the tympanic membrane which transmits information about the frequency and amplitude of sound through the air-filled middle ear cavity via the tiny ossicles (malleus, incus, and finally to the stapes) [ 33]. Amplification of sound pressure is a key feature of the transmission of sound from the middle to inner ear, allowing the stapes push against the higher resistance fluid in the inner ear behind the oval window [ 34, 35, 36]. As a result of the larger surface area of the tympanic membrane compared to the cochlea's oval window (a ratio of 20:1), the sound pressure ultimately received by the oval window is approximately 20 times greater than the original sound stimulus [ 37]. Resonance in the ear canal produces amplification of acoustic frequencies whose wavelengths are approximately four times the length of the canal, which, in humans, results in enhancement of frequencies around 4 kHz [ 38].

The mammalian cochlea is a spiral-shaped structure divided into three fluid-filled chambers-the scala tympani, the scala vestibuli, and the scala media (i.e., the cochlear duct) ( Figure 2b). In humans, the cochlea has a conical central canal (modiolus) around which the cochlear duct makes two- and three-quarter turns. The footplate of the stapes rests on the cochlea's oval window and moves in a piston-like manner to transmit sound vibrations to the cochlear duct commensurate with the loudness and intensity of the sound stimulus. Accordingly, vibrations from displacement of the oval window spiral up the cochlea to cause physical movement of fluids and of the flexible basilar membrane. The basilar membrane does not vibrate as a whole; rather, specific areas vibrate in response to different sound frequencies. This is achieved by variations in stiffness and width along its length: it is thin and stiff at the base and broader and more flexible toward the apex. Therefore, lower frequencies vibrate the basilar membrane closer to the apex of the cochlea while higher frequencies produce vibrations closer to the base, near the oval window. This arrangement is known as a tonotopic organization [ 39, 40]. Thus, our ability to differentiate sounds of varying loudness and pitch depends on the ability of the cochlea to respond appropriately to transmitted sound amplitudes and frequencies.

3.2.2. Auditory Transduction in the Organ of Corti

The cochlea's scala media contains the organ of Corti, the cellular apparatus for transduction of sound vibration into neural signals that can be interpreted by the brain. The organ of Corti is a mosaic of sensory hair cells and non-sensory supporting cells which, in mammals, does not have the capacity to replace lost cells once damaged ( Figure 2c). There are two types of sensory hair cells: a single row of inner hair cells (IHC; ~3500 in humans) and three to five rows of outer hair cells (OHC; ~12,000) [ 41]. Both types of hair cells have 3-4 rows of actin-rich "hairs" called stereocilia, which increase in height along the basilar membrane from base to apex. The roles of the supporting cells are to generally provide structural, metabolic, and immune support to the organ of Corti and are essential for hair cell survival. These include pillar cells, separating IHC and OHC to form the tunnel of Corti, as well as Deiters', Hensen's, and Claudius cells [ 42].

While the scala vestibuli communicates with the scala tympani at the apex of the cochlea (helicotrema), the scala media is separated from both chambers by Reissner's membrane and the basilar membrane, respectively. This separation is crucial for the maintenance of the unique ionic composition of the extracellular fluids in these chambers, generating the endocochlear potential which is essential for auditory transduction. Specifically, the scala vestibuli and scala tympani contain perilymph which is K+-poor and Na+-rich. Conversely, the scala media is filled with K+-rich and Na+-poor endolymph which is secreted by a specialized epithelium called the stria vascularis. The tips of the hair cells' stereocilia are embedded in the flexible tectorial membrane and move in response to sound vibrations. The stereocilia bundles are also connected to each other (within the same hair cell) via extracellular tip links formed in part by cadherin 23 (CDH23) and protocadherin 15 (PCDH15) proteins [ 43]. These links allow the stereocilia to move together and cause non-selective mechanically gated ion channels to open, conducting inward currents of cations (K⁺ and Ca ²⁺) from endolymph [ 44].

While the endocochlear potential of endolymph in the scala media is +80 mV compared to perilymph [ 45], hair cells have a potential of −55 mV to up to −150 to mV [ 46]. Thus, the influx of cations depolarizes the hair cell, resulting in different effects in OHCs and IHCs. OHCs physically elongate and contract, activating the "cochlear amplifier" to narrow the area of excitation and give the traveling sound waves more sensitivity [ 47, 48]. This aids in frequency discrimination and in the detection of quiet sounds. Meanwhile, IHCs release the neurotransmitter glutamate to synaptic boutons of type I (myelinated) spiral ganglion neurites (SGNs) which form the auditory nerve. Glutamate activates the AMPA glutamate receptors in the afferent nerve fibers which in turn transmit the neural signal to the cochlear nucleus and higher auditory processing regions. A single IHC synapses with approximately 10 boutons from 10 different spiral ganglion cells, but the number varies tonotopically (can be up to 20 boutons in the most sensitive frequency regions). IHCs have synaptic ribbons which sustain high rates of glutamate release and maintain synchronous auditory signaling [ 49, 50, 51, 52]. The temporal change in neuronal firing is rapid in the ear, to the effect of 2 to 5 kHz, and distinctions between these various frequencies facilitates sound discrimination [ 51, 53].

3.3. Mechanisms of Damage in NIHL

The mechanisms by which loud noise induces hearing loss include mechanical damage of cochlear structures, reduction in blood flow, sterile inflammation, and oxidative stress and excitotoxicity due to overstimulation of hair cells and nerves ( Figure 3). The loss of hair cells via apoptosis is ultimately the most severe injury and contributes to permanent hearing loss [ 54, 55]. Noise at specific frequencies can cause discrete areas of hair cell damage which manifest as frequency-specific hearing deficits [ 56, 57].

3.3.1. Mechanical Damage

Because the hair cells sit atop the basilar membrane and because their stereocilia are embedded in the tectorial membrane, they are subject to mechanical shearing forces in response to sound vibrations. This continuous mechanical stress causes damage over time and is a feature of typical age-related hearing loss. However, in the context of intense or persistent noise, the shearing forces can cause stereocilia core breakage, destruction of tip links, and ultimately premature hair cell death [ 61]. At low frequencies of 2 kHz and below, the middle ear muscle reflexes may contract on exposure to noise and provide a degree of protection against mechanical shearing forces [ 62]. Non-linearities in these frequencies, auditory responses, and the mechanical response differences in the basilar membrane explain the finding that low-frequency hearing thresholds are less vulnerable to the loss of apical OHCs [ 63, 64].

Loss of stereocilia tip links due to excessive force, uncoupling the mechanoelectrical transduction (MET) channel, precludes mechanotransduction by the hair cell [ 65]. However, the tip links have some capacity to repair via replacement of PCDH15 and CDH23 proteins. In mammals, tip links broken in vitro have been observed to repair within 24 h, followed by restoration of mechanotransduction, although the MET current remains impaired for 36 h [ 66, 67]. This phenomenon is suggested to underlie TTS after noise exposure, although PTS may occur if the tip links are damaged too extensively to repair. Furthermore, noise may damage the F-actin core of the stereocilia itself. Mechanical overstimulation can decrease the stiffness of the core, leaving stereocilia with a "floppy" appearance resulting from actin depolymerization, loss of actin cross-links, or fusion with other stereocilia [ 68]. As the stereocilia have some capacity to repair actin, this can result in TTS or PTS depending on the extent of the damage to the stereocilia core [ 61, 68].

3.3.2. Oxidative Stress and Reduced Blood Flow

Apart from their function in the Krebs cycle, the mitochondria play an essential role in apoptosis and oxidative stress. Following infection, trauma, and in this context, noise-induced trauma, cellular damage or degradation of cell connections may lead to the activation of apoptotic pathways by hair cells [ 73]. Reactive oxygen species (ROS, e.g., superoxide, hydroxyl ion, hydrogen peroxide) may acquire an unstable number of electrons which also triggers pro-apoptotic pathways [ 73, 74]. On receiving apoptotic signals, the balance between pro-apoptotic proteins, such as BAX or BAD, and anti-apoptotic proteins, such as those in the BCL family, is tilted [ 75]. Outer mitochondrial membrane permeability increases, leading to the transport of cytochrome c from the inner mitochondrial membrane to the cytoplasm [ 76]. Caspase enzymes in the cytoplasm are activated, resulting in cell degradation [ 76]. Yamane et al. demonstrated the stagnation of blood flow and the disturbance of strial circulation following acoustic trauma [ 77] and the appearance of free radicals such as the superoxide ion in the luminal surface of the stria vascularis marginal cells [ 78]. Stress and ischemia activate MAP3 kinases which in turn activate the JNK pathway, and phosphorylated JNK enters the nucleus and activates pro-apoptotic pathways such as c-Jun and Fos [ 79]. The downstream products lead to the expression of transcription factors and cellular effectors of apoptosis [ 76].

Peroxynitrite (ONOO-), a highly reactive nitrogen species (RNS) derived from NO and superoxide, is one of the most harmful free radicals to hair cells [ 80]. Noise-induced generation of RNS and ROS continues as an active biochemical process, not just in the immediate aftermath of exposure, but progresses over more than ten days post-exposure and can cause subsequent damage to cochlear structures [ 81]. Antioxidant enzymes such as superoxide dismutase play an important role in countering free radicals by catalyzing the dismutation of superoxide to hydrogen peroxide [ 82]. Other enzymes such as glutathione, glutathione peroxide, and catalase then balance with Sod1 to provide cellular defense, and the loss of Sod1 in knockout mice increased the susceptibility to noise-induced PTS [ 83].

Additionally, free radical formation in response to high-intensity noise can lead to vasoconstriction and reperfusion of cochlear cells, with subsequent cell death [ 81, 89, 90]. The calcium-magnesium ratio plays a vital role in controlling membrane permeability, voltage-dependent calcium and potassium channels, and polarization. Magnesium is also a potent vasodilator, co-operatively binds with potassium, and has a calcium channel blocker mimetic effect. A decrease in magnesium results in increased membrane permeability, an influx of calcium and sodium into the hair cell, and an efflux of potassium via passive diffusion [ 91]. In animal models, magnesium deficiency has been reported to exacerbate cochlear trauma in response to noise [ 92]. A sustained rise in intracellular calcium can deplete cell energy and can also lead to eventual cell death [ 93, 94, 95]. Additionally, low magnesium states have been associated with increased catecholamines and prostaglandins inducing vasoconstriction [ 93, 96, 97, 98, 99]. Thus, a decrease in magnesium and an increase in calcium-magnesium ratio can increase blood viscosity, reduce cochlear blood flow, and exacerbate the vasoconstrictor effects of acoustic trauma.

3.3.3. Inflammation

Neuroinflammation, a critical component of maintaining homeostasis in the central and peripheral nervous system, has been implicated in a wide range of pathological processes, including NIHL. There is extensive evidence showing that pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α), interleukins, and chemokines (i.e., CCL2) are induced in the mammalian cochlea after noise trauma [ 100, 101, 102, 103, 104]. Additionally, noise exposure results in the recruitment of inflammatory cells such as macrophages to the cochlea [ 105, 106, 107, 108]. It is currently unclear whether these inflammatory processes cause or exacerbate the threshold shifts associated with NIHL, although some of these molecules have demonstrated ototoxicity. For example, perfusion of TNF-α into the cochlea of guinea pigs resulted in synaptic degeneration and reduced auditory nerve compound action potentials, which could be protected against by blocking TNF-α [ 109].

3.3.4. Excitotoxicity and Synaptopathy

Louder sounds cause more hair cells to depolarize, causing greater release of glutamate by IHC ribbon synapses and increased motility of OHC. Noise exposure causes a rapid reduction in the number of IHC ribbon synapses, which is irreversible after neuropathic noise exposure [ 34, 110, 111]. Furthermore, excessive release of glutamate leads to glutamate excitotoxicity, characterized by an increased influx of ions in the postsynaptic cochlear nerve terminals leading to swelling of the postsynaptic cell bodies and dendrites [ 112]. This overstimulation can cause the loss of spiral ganglion cells, even after a delay of several months, and the damage can progress over years [ 113]. The long-term consequences of primary neuronal loss are progressive and present despite the recovery of threshold sensitivity [ 34]. Indeed, long-term noise exposure, even beneath the levels to induce cochlea trauma, can result in increased spontaneous firing rates and reorganization of cortical tonotopic maps in mammals [ 114, 115, 116, 117]. The most common cause of cochlear damage leading to deafferentation is environmental noise overexposure [ 118, 119, 120].

Ribbon synapses and the peripheral dendrites of afferent neurons can be damaged by noise levels that are not as high as those required to effectuate threshold shifts [ 34, 121, 122]. This deafferentation of the IHC (no contact between them and the dendrites) is termed "synaptopathy" and may not result in detectable threshold shifts. However, as fewer neurons connect to the hair cells, the amplitude growth of neural excitation is reduced, and hearing may be impacted. This phenomenon occurs at noise levels previously thought not to be very harmful. The injury is permanent and not typically detected on an audiogram, hence the term "hidden hearing loss" [ 34, 121, 122]. IHCs have two orientation axes: pillar-modiolar and the habenular cuticular. The auditory neurons have high spontaneous rates and lower thresholds on the pillar face, while the modiolar facing neurons have low spontaneous rates and higher thresholds [ 123, 124]. Neurons on the modiolar side of hair cells have smaller receptor patches and more synapses that are more sensitive to noise-induced degeneration compared to the pillar side [ 125]. In addition, these neurons show a reversible downregulation of protective glutamate receptor expression in peripheral terminals [ 122]. This spatial distribution of loss of high threshold neurons compared to low threshold neurons might explain the absence of threshold shifts even in the presence of synaptopathy [ 122].

3.4. Additional Negative Effects of Noise on the Inner Ear

3.4.1. Tinnitus

Tinnitus is the conscious perception of sound without an external auditory stimulus, often experienced as ringing or buzzing [ 126]. Tinnitus is typically self-reported and is primarily subjective [ 126]. Nevertheless, chronic tinnitus with or without hearing loss has been associated with low-level DPOAEs [ 127] and low-level transiently evoked otoacoustic emissions [ 128] compared with people without tinnitus and the same hearing level. Exposure to loud occupational, leisure-time, and firearm noise has been associated with higher prevalence of tinnitus and more frequent symptoms [ 118, 120, 129]. Although the precise mechanism of tinnitus remains an area of active research, cochlear deafferentation is thought to play a role. The most common cause of cochlear damage leading to deafferentation is environmental noise overexposure [ 118, 119, 120]. Similar to NIHL, neuroinflammation in the auditory cortex may also contribute to tinnitus, with elevated pro-inflammatory cytokines and microglial activation demonstrated in murine models [ 130, 131].

Hearing loss is present in approximately 60% of people with tinnitus [ 132, 133], suggestive of similar pathological processes after harmful noise exposure. The variability between tinnitus and hearing loss in noise-exposed subjects can be due to the differential vulnerability of cochlear and central components to the duration and intensity of noise exposure. A retrospective study of 531 patients with chronic tinnitus found that 83% had a high-frequency hearing loss corresponding to NIHL, and the degree of hearing loss was positively correlated with tinnitus loudness [ 7]. Similarly, several studies have reported that high proportions (i.e., up to 80%) of military personnel with NIHL also have tinnitus [ 7, 134]. Additionally, the degree of hearing loss positively correlated with the two subscales ("intrusiveness" and "auditory perceptional difficulties") of the Tinnitus Questionnaire [ 7]. A study of acute acoustic trauma in the Finnish armed forces found that 47% of personnel reported hearing impairment, and 94% reported tinnitus immediately following acute acoustic trauma, which persisted until discharge in 45% of cases [ 135]. In addition, otoacoustic emissions were better predictors of tinnitus persistence in a cohort of French military personnel than hearing thresholds alone as early as 24 h after an acute acoustic trauma [ 136].

3.4.2. Vestibular Dysfunction

The vestibular system consists of the utricle and saccule, which detect gravitational forces and horizontal and vertical plane movements, respectively, as well as three perpendicular semicircular canals [ 137]. The primary function of the vestibular system is the maintenance of gaze and postural stability, informing head position and spatial orientation, which are crucial to balance [ 137]. Movement of the endolymph in the semicircular canals during head rotation corresponds to the plane of rotation. Endolymph flows into the ampulla, an expansion of the semicircular canal containing mechanotransducing hair cells, causing deflection of the stereocilia and the release of neurotransmitters that send information about the plane of movement to the brain.

The vestibular labyrinth Is in proximity to and interconnected with the auditory system, and the fluids in the vestibular system have a degree of patency with the cochlea [ 138]. The cochlea and vestibular hair cells have similar ultrastructure; the balance and auditory receptors share the membranous labyrinth and a common arterial blood supply. These factors increase the likelihood of vestibular trauma in concurrence with NIHL [ 138]. Similar to the cochlea, vestibular end organ damage by noise can occur via direct mechanical destruction, metabolic decompensation with sensory degeneration, excitotoxicity, and free radical damage [ 28, 139]. Indeed, neurophysiological studies have shown that, similar to the cochlea, the vestibular organs, particularly the saccule and utricle, are vulnerable to noise [ 140, 141, 142]. Accordingly, multiple studies have reported associations between NIHL and vestibular dysfunction or balance disorders such as vertigo, oscillopsia, postural instability, and/or motion intolerance [ 138, 143, 144, 145, 146, 147].

Neurophysiological studies have measured the effects of noise on the vestibular system via vestibular evoked myogenic potentials (VEMPs) [ 28, 148, 149]. Vestibular afferents give rise to VEMPs, which are short-latency myogenic potentials in response to air-conducted sound or bone-conducted vibration. Cervical VEMPs are a measure of the sacculocollic pathway, and ocular VEMPs are a measure of utricular/superior vestibular nerve function [ 28, 148, 149]. A cross-sectional observational study of 43 military personnel with bilateral asymmetric hearing loss found that the severity of NIHL was associated with cervical VEMP, suggesting that the sacculocollic pathway is susceptible to noise damage [ 150]. Indeed, there are saccular neurons responsive to sound [ 151]. Another measure of vestibular function, particularly of otolith function, is the vestibular short-latency evoked potential [ 149]. Jerk amplitudes are used to elicit far-field potential responses generated by irregular primary vestibular afferent discharges [ 152, 153]. Studies have shown that vestibular damage can occur due to brief exposure to elevated sound levels and sustained exposure to low-frequency continuous sound at more moderate levels [ 154, 155, 156, 157]. A study of 258 military personnel found that vestibular damage from intense noise exposure was corelated with asymmetric NIHL [ 138]. Additionally, symptoms of vestibular dysfunction were observed in 11.2% of individuals in the study with symmetrical hearing loss compared to 21% with asymmetrical hearing loss, which could be attributed to compensation by the vestibular system to symmetrical progressive injury [ 138]. Additionally, individuals with higher levels of hearing loss (pure tone audiometry [PTA] >40 dB) had more abnormal vestibular test results and worse dual-task performance than those without NIHL [ 158]. However, participants' reports of imbalance intensity via the Visual Analog Scale were similar, highlighting the need for vestibular evaluation in patients with hearing loss [ 158].

4.1. Screening

Screening of NIHL is typically performed via taking a patient's history of noise exposure and performing audiograms, and clinicians will distinguish sensorineural from conductive hearing loss. However, it is often difficult to precisely quantify the noise exposure of individuals, and the type of exposure may vary (i.e., intense blast noise, cumulative noise, single tones, or wide-spectrum noise), leading to different patterns of damage. Thus, other tests may include the measurement of distortion product otoacoustic emissions (DPOAE), speech-in-noise testing, and auditory brainstem response (ABR), as detailed below. Each of these methods have notable strengths and limitations. Clinical assessments of signs of tinnitus and vestibular dysfunction may also be included if appropriate.

4.1.1. Audiograms

PTA, which measures the lowest intensity at which sound can still be heard across a range of audible frequencies (hearing threshold), is performed as a baseline evaluation test for hearing loss [ 159]. Air and bone conduction tests are typically performed over a range of frequencies from 125 to 8000 Hz [ 160]. NIHL produces characteristics audiometric signatures, where hearing is normal from low to mid frequencies, and there is a sudden drop past 3000 Hz, most pronounced at 4000 Hz, and a slight recovery in higher frequencies ( Figure 4) [ 161]. Multiple factors contribute to this characteristic pattern, including the length and volume of the outer ear canal and the outer ear resonant frequency [ 60, 161, 162]. As the duration of noise exposure increases, the notch deepens to involve both higher and lower frequencies.

4.1.2. Speech-in-Noise Testing

While PTA testing helps identify hearing loss, it does not account for the ability to discriminate sound in the presence of background noise, a primary presenting complaint of patients with NIHL [ 167]. PTA is limited in its ability to effectively predict speech perception because it indicates the patient's access to sound rather than their functional hearing ability [ 168]. The speech-in-noise test simulates real-world situations by adding background noise or a competing signal in an isolated sound chamber and better represents the processing of speech [ 169]. This test measures a patient's speech recognition threshold and responses to suprathreshold speech (i.e., stimuli presented above the detection threshold) [ 170]. Signal-to-noise ratio (SNR) loss refers to the increase in SNR required by a listener to repeat words, sentences, or words in sentences with 50% accuracy compared to typical performance [ 171]. Commonly performed tests are Hearing in Noise Tests, Speech Perception in Noise Test-Revised (SPIN-R), the Bamford-Kowal-Bench Speech-In-Noise (BKB-SIN) test, and QuickSIN [ 172, 173]. In the rapid (~2 min) QuickSIN, test sentences are played at a high SNR of +25 dB to a low SNR of 0 dB, and the patient repeats the sentences back to the audiologist [ 171]. The number of words that are repeated inaccurately is subtracted from the accurate number.

Speech-in-noise testing gives a useful baseline estimation of hearing impairment, helps to infer the degree of benefit from different assistive hearing devices, and allows the quantification of improvement [ 174]. Speech-in-noise testing can be used to determine the potential utility of hearing aids for a patient because hearing aids are very effective at improving the ability to understand speech in quiet settings but are less effective in noisy settings [ 175]. This can result in better alignment with patient treatment priorities, and a 2021 systematic review found that patients who underwent speech-in-noise testing had higher measures of hearing aid satisfaction [ 176]. Further, this test can potentially detect hearing impairments that may not be evident in PTA testing. For example, when comparing ten noise-exposed Royal Air Force aircrew pilots with ten age/sex-matched unexposed administrators, the groups had comparable audiograms, but the exposed group had relatively elevated SIN thresholds, potentially reflecting abnormal retrocochlear processing [ 177].

4.1.3. Distortion Product Otoacoustic Emissions (DPOAE) Measurement

The OHCs amplify the intensity and sharpen the peak of the traveling sound wave in the cochlea via prestin-mediated elongation and contraction [ 178]. The resulting nonlinear electromechanical distortion of the sound wave by OHC motility can be measured via the DPAOE testing [ 179, 180]. In addition to the distortion mechanism, otoacoustic emissions are also attributed to the reflection caused by the random scatter of the incoming traveling wave [ 180, 181]. Therefore, the presence of DPOAEs is a marker of normal cochlear function and, specifically, of OHC health [ 182].

DPOAEs are evoked via a probe placed into the ear canal which emits two sounds at designated intensity levels (L1 and L2) and frequencies (f1 and f2), while a microphone detects the otoacoustic emission [ 182]. Cochlear stimulation with two pure tones, f1 and f2, results in a family of distortion products mathematically related to the input tones. Of these, the cubic distortion product 2f1-f2 is most commonly used in clinical and research settings [ 182]. The test is easy to implement and provides quick results [ 183].

4.1.4. ABR Measurement

ABR, or auditory brainstem evoked potentials, are electrical signals produced by the nervous system within the first 10-15 ms following a transient acoustic stimulus [ 188]. A typical ABR consists of a sequence of five vertex positive waves with negative throughs [ 189]. Regarding the origins of component ABR waves, there are slight differences between humans and rodent models. In humans, wave I and II are believed to originate from the distal and proximal auditory nerve fibers, respectively; wave III is generated by the cochlear nucleus; IV reflects activity in the superior olivary complex; and wave V is associated with the lateral lemniscus [ 190]. In mice, wave II is believed to be generated by the posterior ventral cochlear nucleus; wave III is believed to be generated by the anterior ventral cochlear nuclear and trapezoid body; wave IV is believed to be generated by the superior olivary complex; and wave V is believed to be generated by the lateral lemniscus and inferior colliculus [ 191, 192, 193]. There is also some variation between mammalian models, as reported for rats [ 192, 194, 195], guinea pigs [ 196], and cats [ 197]. The sound intensity is directly proportional to the waves' amplitude and inversely proportional to latency.

ABR is not routinely used in clinical screening of NIHL but does have expanded applications for neurodiagnostic testing, intraoperative monitoring, hearing screening/audiometry, and neurophysiological research [ 193]. In animal models, noise-induced synaptopathy results in a permanent decrease in the supra-threshold growth of ABR wave I amplitude despite full recovery of otoacoustic emission amplitudes and ABR thresholds [ 110]. A similar pattern of reduced suprathreshold ABR wave I amplitude has been observed in humans exposed to noise, although synaptopathy has not yet been confirmed [ 198] and is termed "hidden hearing loss" because these functional deficits are hidden by otherwise normal ABR thresholds [ 63, 110]. However, some studies have shown a lack of sensitivity of ABR to noise exposure, which makes wave 1 amplitude a less ideal measure of cochlear synaptopathy for individuals with NIHL [ 56, 170]. These findings underscore the importance of incorporating suprathreshold audiological testing when screening for NIHL to accurately understand a patient's functional hearing ability.

4.2. Diagnosis

5.1. Prevention

Environmental noise level is conventionally measured via a sound level meter. However, they are expensive for small businesses and require maintenance and calibration, thereby limiting their widespread implementation. However, smartphone applications for this purpose are now available and provide inexpensive alternatives to specialist calibrated sound meters. An evaluation of the reliability of nine applications found the NIOShH Sound Level Meter to be the most accurate [ 209]. A free, accessible, and reliable app may help increase compliance with legislation and easy monitoring of environmental noise levels [ 210]. Additionally, in 2009, the European Commission mandated that output levels in new personal audio devices should be set to a standard of 85 dB, allowing users to increase the volume to a maximum of 100 dB. When users raise the volume to maximum level, a message was required to pop up that warns of the potential for hearing loss.

Hearing protective devices (HPDs) such as earmuffs and earplugs play an important role in protection against noise exposure. Plugs need to be inserted to ensure coverage of the entire ear canal's circumference to provide protection and minimize irritation. Noise Reduction Ratings (NRRs) are calibrations to assess the protection range of HPDs in a single attenuation value (in dB). Because NRRs are derived via laboratory-based testing, they may overestimate the actual protection provided in non-experimental environments. Therefore, the NRR is derated by 50% on a dB scale before estimating exposure protection [ 211]. A Cochrane systematic review (2017) of interventions to prevent occupational NIHL found evidence that training on the proper insertion of ear plugs significantly reduced short-term noise exposure but called for more studies on the effectiveness of stricter legislation or better use of hearing protection devices [ 212]. Additionally, a randomized controlled trial showed that effective training of earplug usage led to significant improvement in the efficacy of HPDs in comparison to the usage of a device with higher NRR [ 213]. HPD fit-testing systems provide a customized fit for increased attenuation; however, they often require special facilities for testing such as a quiet room or audiometric booth or specialized equipment. Compliance in wearing HPDs is a barrier, especially in the military, as they are thought to decrease auditory situational awareness (e.g., sound detection, sound localization, and speech perception) [ 211, 214]. However, novel fit test techniques (i.e., via a smartphone application) may enable better training and monitoring compliance [ 211].

Finally, clinicians can actively counsel patients at risk of NIHL on hearing protection strategies and the hazards of noise exposure in the workplace or recreationally (i.e., concerts, sports events, gun ranges, etc.). Simple strategies outlined by the US Centers for Disease Control and Prevention include avoiding exposure to excessive noise, turning down the volume on music, moving away from sources of noise, and using HPDs to reduce exposure to safe levels [ 215].

5.2. Clinical Management

There is no cure for NIHL and, to date, no approved pharmacological treatment indicated for its treatment. Although there are currently no clinical practice guidelines specifically for NIHL management, such guidelines exist for sensorineural hearing loss in adults (i.e., from the American Academy of Otolaryngology-Head and Neck Surgery (AAOHNS) [ 216], American Academy of Audiology [ 217], and the UK National Institute for Health and Care Excellence [ 218]) and are applicable. Relevant recommendations include exclusion of conductive hearing loss, audiometric confirmation of sensorineural hearing loss (SNHL) characteristic of noise trauma, and exclusion of retrocochlear pathology in case of asymmetric SNHL based on contrast-enhanced brain MRI or ABR testing. NIHL is clinically managed with hearing aids and/or use of hearing protection during exposure, although if hearing loss worsens, patients may be eligible for cochlear implants [ 56]. In some cases of acute noise-induced TTS, clinicians may consider the use of intratympanic steroids such as dexamethasone [ 219, 220], although high-quality, long-term efficacy evidence in humans is lacking, and it is not considered for chronic occupational noise exposure. Additionally, the WHO classifies hearing loss into mild, moderate, severe, and profound, listing the typical signs and various recommendations for each level of disability ( Box 1). Clinicians can use this classification to educate patients regarding the natural history of NIHL while counseling them on protective measures and the benefits of auditory rehabilitation (i.e., hearing aids or other assistive devices). However, the WHO severity levels are arbitrarily defined, and the system does not address patients with <25 dB hearing level and unilateral hearing loss [ 221]. Additionally, the speech-in-noise test, which is an effective test for measuring noise interference on speech perception skills, is not considered by the WHO system [ 222].

Box 1. WHO grades of hearing loss. WHO grades from the 1991 working group on prevention of deafness and hearing impairment [ 223]. Additional comments on the classifications from Olusanya et al. [ 221]. Abbreviations: dB, decibel; ISO, International Organization for Standardization; WHO, World Health Organization.

0-None

≥25 dB

No or very slight hearing problem.
Can hear whispers.

None

20 dB also recommended. People with 15-20 dB levels
may have hearing problems. People with unilateral hearing
loss may have problems even if the better ear is normal.

1-Slight

26-40 dB

Can hear and repeat words spoken
in a normal voice at 1 m

Counseling. Hearing aids
may be needed

Some difficulty in hearing but can usually hear
normal level of conversation

2-Moderate

41-60 dB

Can hear and repeat words spoken
in raised voice at 1 m

Hearing aids are
usually recommended

None

3-Severe

61-80 dB

Can hear some words when shouted
into better ear

Hearing aids needed. Otherwise
lip-reading and signing should
be taught

Discrepancies between pure-tone thresholds and speech
discrimination score should be noted

4-Profound

≥81 dB

Unable to hear and understand even
a shouted voice

Hearing aids may help understanding
words. Additional rehabilitation needed.
Lip-reading and sometimes signing are
essential.

Speech is distorted, the degree depending on the age at
which hearing was lost

Box 2. Common risk factors for NIHL. Abbreviation: NIHL, noise-induced hearing loss.

Older age, although all ages are at risk

Repeated occupational noise exposure (construction, machine shop/factory, landscaping, mining, agriculture, musician, etc.)

Repeated recreational noise exposure (loud music at concerts, loud volume via earphones/earbuds)

Intense blast or explosion exposure

Shooting firearms (recreational or military)

Lack of hearing protection

Exposure to organic solvents, heavy metals, pesticides, asphyxiants

6.1. Occupational

Occupational NIHL is the most prevalent occupational disease globally [ 229], with approximately 7.0 million years lived with disability attributed to occupational noise exposure in 2019 [ 8]. People employed in construction, manufacturing, mining, agriculture, utility, and transportation industries, military personnel, and musicians are at high risk for NIHL [ 230]. As discussed above, OSHA considers US workers at increased risk of NIHL if noise exposure is at or above 85 dB, averaged over eight working hours or an eight-hour time-weighted average [ 231]. According to a report from the NHANES (1999-2004), 22 million US workers (17%) reported exposure to hazardous workplace noise, with 34% of these workers reporting no use of hearing protection devices [ 232]. Their report identified the highest weighted prevalence of workplace noise exposure for mining (76%) followed by lumber/wood product manufacturing (55%). Other high-risk occupations included repair and maintenance, motor vehicle operators, and construction trades. The position statement from the American College of Occupational and Environmental Medicine (ACOEM) states that occupational and environmental medicine physicians should understand a worker's history of noise exposure and become proficient in the early detection and prevention of NIHL [ 233].

6.2. Military

Hearing loss is common in the military and is particularly disabling as it relates to both safety of the personnel and that of the nation. Personnel are often exposed to continuous as well as intermittent hazardous levels of noise, including gun fire and blast exposure, and increased hearing loss is associated with solvent exposure and longer service [ 234, 235, 236, 237]. Combining acoustic and pressure wave energies can result in rupture of the organ of Corti, separation from the basilar membrane, and fracture and displacement of stereocilia. Indeed, as of 2021, tinnitus is the most prevalent service-connected disability for US veterans while hearing loss is the third-most prevalent, affecting 2.5 and 1.4 million veterans, respectively [ 238]. Individuals with medically disqualifying audiograms or hearing loss at application for service in the US Army and Marine Corp were eight and four times more likely, respectively, to have a hearing loss disability evaluation compared with matched controls [ 239]. Thus, early identification of enlistees at risk of hearing loss and counseling on hearing protection measures may reduce the burden of NIHL in the military. Currently, the post-exposure protocol for acute acoustic trauma in the US military includes removing the individual from the noise hazard and maintaining them in an effectively quiet environment (ambient levels of ≤70 dB) for 21 days [ 88, 240].

6.3. Environmental and Recreational

6.4. Genetic

Multiple studies have found that certain genetic and epigenetic characteristics increase the susceptibility to acoustic trauma in animal models of hearing loss [Cdh23 70, 246, 247, 248]. Transgenic mice expressing genes modeling age-related hearing loss, such as Ahl1 ( 735A>G) in C57BL/6J mice, are more susceptible to further hearing deterioration caused by noise exposure [ 247]. Conversely, mice that lack Ahl1 (i.e., 129/SvEv, Cast/Ei, and MOLF/Ei) are less vulnerable to acoustic injury [ 249, 250, 251, 252]. Studies of knockout mice have detected pathways involving cochlear structures, oxidative stress, potassium recycling (vital for sensory transduction [ 85]), and heat shock proteins (HSPs) which increase the susceptibility of the inner ear to NIHL [ 253]. Some of the mouse genes implicated include Cdh23 [ 254], Pmca2 [ 255], Sod1 [ 83], Gpx1 [ 256], Trpv4 [ 257], Vasp [ 258], Hsf1 [ 259], and mdx [ 249].

Evidence of genetic risk factors in human NIHL is still emerging, although studies have suggested heritability of hearing loss [ 248, 260, 261, 262]. For example, a study of noise sensitivity among 573 twin pairs in a Finnish cohort demonstrated heritability of 36% overall and of 40% after exclusion of hearing-impaired individuals [ 248]. Genes in pathways involving oxidative stress, potassium recycling, and HSPs have also been associated with NIHL in humans. Among the oxidative stress pathway genes, polymorphisms of GSTM1, PON2, SOD2, and CAT have been associated with NIHL, and CAT was independently validated in Swedish and Polish populations [ 263, 264, 265]. GJB1, GJB2, GJB3, GJB4, GJB6, KCNJ10, KCNQ1, KCNQ4, KCNE1, and SLC12A2 are ten genes in the potassium recycling pathway with known or suspected association with syndromic and non-syndromic hearing loss [ 266]. An analysis of 35 small nuclear polymorphisms in these genes from a Swedish population showed associations between KCNE1, KCNQ1, and KCNQ4 with NIHL [ 266], and a Polish study replicating the study found associations between polymorphisms in GJB1, GJB2, GJB4, KCNJ10, and KCNQ1 with NIHL [ 267].

HSPs are involved in the synthesis, folding, assembly, and intracellular transport of many other proteins. HPS expression increases during oxidative or other stress, including that caused by noise exposure, which may have a protective effect against cochlear damage via stabilization of stereocilia or enzyme regulation [ 268, 269]. Three polymorphisms in HSP70 genes have been associated with susceptibility to NIHL: HSP70-1, HSP70-2, and HSP70-hom [ 268, 270, 271]. An association study with 53 candidate genes in two independent noise-exposed populations identified associations between NIHL and two monogenic genes, the deafness genes protocadherin 15 (PCDH15) and myosin 14 (MYH14) [ 272]. Cadherins are responsible for mechanical transduction and form the tip links between hair cells, while myosin regulates cytokinesis, cell motility, and cell polarity in hair cells [ 43, 268]. In addition, noise exposure can result in epigenetic effects (i.e., alternations in gene transcription) via DNA methylation changes [ 273, 274], histone modifications [ 275, 276, 277, 278], and alterations in non-coding microRNAs (miRNAs) [ 279, 280, 281, 282].

Finally, the inner ear has many glucocorticoid receptors (GR), which are affected by acoustic trauma or restraint stress at a transcriptional level [ 283, 284, 285]. In animal models, acoustic trauma increased endogenous corticosterone and decreased cochlear GR mRNA expression [ 283, 284]. This led to a reduction in nuclear translocation of GR in the spiral ganglion neurons and increased activity of NF-κB. Pretreatment with a glucocorticoid agonist (dexamethasone) resulted in a decreased hearing threshold. Conversely, pretreatment with a glucocorticoid synthesis inhibitor (metyrapone) in combination with a GR antagonist (RU 486) exacerbated auditory threshold shifts (25-60 dB) after acoustic trauma [ 283].

7.1. Completed and Ongoing Clinical Trials

The development of novel treatments for NIHL is an area of active research, encompassing interventions with anti-inflammatory, antioxidant, anti-excitatory, anti-apoptotic, or other effects. A search of ClinicalTrials.gov on 20 January 2023 identified 21 registered trials of interventional therapies inclusive of NIHL: one active and not recruiting (NCT05086276 (FX-322)), one not yet recruiting (NCT05511753 (acupuncture)), one recruiting (NCT04766853 (steroids)), two enrolling by invitation only (NCT04768569 and NCT04774250 (zonisamide)), one terminated (NCT02903355 (D-methionine)), one withdrawn (NCT02049073 (zonisamide, steroids)), three of unknown status (NCT02779192 (SPI-1005), NCT04482998 (steroids, hyperbaric oxygen therapy [HBOT]), and NCT01727492 (antioxidants)), and 13 completed (NCT02257983 (EPI-743), NCT01444846 (ebselen), NCT00808470 (micronutrients), NCT00552786 (antioxidant), NCT02951715 (zinc), NCT04120116, NCT04601909, and NCT04629664 (FX-322), NCT02259595 (HPN-07, N-acetylcysteine), NCT03834714 (near infrared light), NCT00802425 (AM-111), and NCT03878875 (sound conditioning)) ( Table S1). Of the 12 completed/terminated clinical trials, just five have reported efficacy results via ClinicalTrials.gov or in publications, and all have focused on agents with antioxidant or anti-inflammatory capacity: micronutrients (i.e., vitamins/minerals), D-methionine, N-acetylcysteine, and ebselen (see details in Table 2 and described below). Additional findings have been published from clinical trials conducted outside of the US registry system, with therapies primarily aimed at preventing or attenuating TTS due to noise exposure ( Table 3).

7.2. Antioxidant Therapy

Beta carotene, vitamins B, C, and E, zinc, and magnesium have antioxidant properties-particularly when combined-and have been shown to reduce vasoconstriction, cochlear cell death, and hearing loss in animal models when administered prior to noise exposure [ 89, 286, 287, 288, 289]. In humans, a 2021 systematic review concluded that certain micronutrients demonstrated protective effects for NIHL but that the results were not consistent [ 290]. A randomized Phase 2 trial (NCT00808470) of micronutrients (beta carotene, vitamins C and E, and magnesium) administered to young adults prior to exposure to 4 h of loud music reported that it was not superior to placebo in preventing TTS at any frequency level [ 291]. However, oral magnesium significantly reduced the magnitude of noise-induced TTS and PTS compared with placebo among an Israeli military personnel [ 292, 293]. Similarly, separate prospective randomized trials demonstrated that vitamin B12 [ 294] and vitamin E (plus inhaled carbogen) [ 295] significantly attenuated noise-induced TTS compared with placebo. However, in an open-label study of oral zinc (NCT02951715) among adults with NIHL-related tinnitus, treatment improved tinnitus symptoms but not hearing thresholds from baseline after 2 months [ 296].

N-acetylcysteine is a thiol which supplies cysteine for intracellular glutathione synthesis. It acts as a free radical scavenger of hydrogen peroxide and hydrogen radicals to promote detoxification of ROS and RNS [ 297, 298, 299]. A randomized Phase 2 crossover trial (NCT00552786) of N-acetylcysteine administered to male Taiwanese workers exposed to loud occupational noise reported that it significantly reduced the magnitude of TTS from baseline (measured with PTA) compared with placebo among some workers [ 300]. Specifically, the benefit was limited to those without polymorphisms in the genes GSTM1 or GSTT1, which code for glutathione S-transferases (mu and theta, respectively) involved in cellular detoxification and nullification of carcinogens. Thus, antioxidant therapy with N-acetylcysteine may help to reduce the magnitude of noise-induced TTS among certain populations, although individuals' genetic profiles influence the effect. D-methionine is the active form of methionine, an essential amino acid needed for tissue repair and selenium/zinc absorption. A randomized, double-blind Phase 3 trial (NCT02903355) of D-methionine administered prior to and during firearms training among US drill sergeant trainees (18 total days) reported in ClinicalTrials.gov that it was not superior to placebo in preventing hearing threshold shift. A separate Phase II-like trial of N-acetylcysteine conducted among a similar US Marines Corp population prior to weapons training also failed to demonstrate superiority of treatment to placebo in preventing noise-induced TTS [ 301].

Sound conditioning, or exposure to low-level noise prior to intense noise, is also aimed at increasing antioxidant activity in the inner ear [ 302]. This benign stimulus is hypothesized to "prime" the stria vascularis and organ of Corti to produce enzymes (i.e., glutathione reductase, gamma-glutamyl cysteine synthetase, and catalase) protective from noise-induced free radical damage [ 303]. A completed prospective clinical trial (NCT03878875) examined whether sound conditioning could attenuate TTS and tinnitus among young adults in the UK, although no results have been posted or published. To date, only studies in animal models have demonstrated any benefit from sound conditioning [ 304, 305].

7.3. Anti-Inflammatory Therapy

Ebselen is a synthetic selenium-containing molecule that has anti-inflammatory properties and has been assessed as a treatment for various forms of SNHL [ 306]. It mimics glutathione peroxidase, the primary antioxidant enzyme in the cochlea and which decreases in activity following noise or ototoxic injury, and activates the Keap1-Nrf2 cytoprotective pathway [ 307, 308]. A Phase 2 randomized clinical trial (NCT01444846) among 83 normal-hearing adults compared a placebo with 200, 400, or 600 mg ebselen administered 2 days prior to and 2 days following a calibrated noise exposure challenge [ 309]. The results indicated that the mean TTS at 4 kHz was significantly reduced (by 68%) in the group receiving 400 mg ebselen compared with placebo.

Table 2. Completed clinical trials of interventions for NIHL registered at ClinicalTrials.gov with reported results.

ClinicalTrial.gov
ID/Name

Intervention

Study Design

Population, N

Active Arm, N

Comparator Arm, N

Primary Outcome

Secondary Outcomes

Results

Publication

Sponsor

NCT02903355: Phase 3 Clinical Trial: D-methionine to Reduce Noise-Induced Hearing Loss (NIHL)

D-methionine to prevent NIHL or tinnitus in a military population

Phase 3 RCT

US drill sergeant instructor trainees (21-45 y) receiving weapons training, N = 266

18 days of oral D-methionine, n = 124

Placebo, n = 142

ASHA shift from baseline to day 29-36 post-drug (day 15-22 post-noise exposure)

Change in DOEHRS-HC, EWS STS, THI

D- methionine was not superior to placebo on any outcome in the interim analysis

None

Metamor, Inc., USA [discontinued development]

NCT00808470: Micronutrients to Prevent Noise-induced Hearing Loss

Micronutrients to reduce magnitude of TTS from 4 h of loud music in young adults

Phase 2 RCT

Adults (18-35 y) with normal hearing, N = 70

4 days of oral beta carotene, vitamins C and E, magnesium, n = 35

Placebo, n = 35

Mean threshold shift at 4 kHz in both ears 15 min post-music vs. baseline

Threshold shift at 0.25, 0.5, 1, 2, 3, 6, and 8 kHz post-music; change in DPOAE amplitude, PMTF thresholds, and tinnitus measures

Micronutrients were not superior to placebo on any outcome in the final analysis

LePrell et al., 2016 [ 291]

University of Michigan, USA

NCT00552786: Antioxidation Medication for Noise-induced Hearing Loss

NAC to prevent TTS in workers exposed to noise in Taiwan

Randomized Phase 2 crossover

Males (25-65 y) with known work noise exposure, N = 53

14 days of 1200 mg NAC

Glucose capsule

Threshold shift from baseline measured with PTA, four time-spaced assessments

Threshold shift from baseline measured with DPOAE, four time-spaced assessments

NAC significantly reduced TTS among men without any GSTIM1 or GSTT1 polymorphisms

Lin et al. (2010) [ 300]

National Taiwan University Hospital, Taiwan

NCT02951715: Improvement of Tinnitus After Oral Zinc on Patients With Noise-induced Hearing Loss

Zine to improve NIHL and tinnitus symptoms

Open label, single arm

Adults with confirmed NIHL-related tinnitus, N = 20

2 months of 40 mg oral zinc daily

None

THI change from baseline

Threshold shift, speech discrimination, DPOAE, tinnitus pitch/loudness from baseline

Zinc did not significantly improve hearing threshold but did improve THI score from baseline

Yeh et al. (2019) [ 296]

Chang Gung Memorial Hospital, China

NCT01444846: Otoprotection With SPI-1005 for Prevention of Temporary Auditory Threshold Shift

Ebselen to prevent TTS

Phase 2 RCT

Adults (18-31 y) with normal hearing, N = 83

4 days of oral 200, 400, or 600 mg ebselen, total n = 63

Placebo capsule, n = 20

Reduction in TTS from baseline (15 min post-sound exposure) at 4 kHz

N/A

Significant reduction in TTS at 4 kHz in 400 mg ebselen vs. placebo groups

Kil et al. (2017) [ 309]

Sound Pharmaceuticals, Inc., USA

Clinical trials have been conducted to assess HBOT and corticosteroids as treatments for NIHL, primarily focusing on acute acoustic trauma (AAT) ( Table 3). Treatment with corticosteroids has been proposed to reduce the inflammation in the inner ear associated with AAT and with intratympanic administration-clinically achieved via laser-assisted myringotomy-resulting in higher perilymph concentrations than systemic administration in animal models [ 240]. However, the therapeutic benefits are largely predicated on very rapid treatment after NIHL onset. A randomized trial of intratympanic plus systemic or just systemic corticosteroids within 3 days of NIHL onset reported that Chinese patients who received intratympanic delivery had significantly better improvement in audiological outcomes and word recognition than the systemic group, although individuals' outcomes varied widely [ 219]. A prospective trial assessed the timing of intravenous corticosteroids and piracetam-a GABA derivative sold outside the US as a nootropic or possible anti-convulsive-as early treatment for AAT among Greek military personnel [ 310]. The results indicated that patients who were treated within 1 h post-noise exposure achieved the best audiological recovery compared with patients treated 16 or 24+ h later, although there was no control group. However, a case-control study of oral corticosteroids after AAT reported that Israeli miliary personnel treated with <24 h of exposure had significantly better hearing outcomes than those who received no treatment [ 311].

Hyperbaric oxygen has been previously used to counteract cochlear hypoxia in sudden idiopathic hearing loss [ 312], including in concert with intratympanic steroids [ 313]. In the context of NIHL, several retrospective studies have noted that HBOT with or without steroid therapy improved hearing recovery after AAT, although the benefits have been limited and inconsistent [ 314, 315, 316, 317]. Additionally, a prospective randomized clinical trial examined three regimens of HBOT and/or corticosteroids and piracetam (i.e., medical therapy), following AAT among Belgian soldiers: (1) 10 days oral medical therapy, (2) intensive (twice daily for 3 days then once daily for 7 days) HBOT plus 5 days intravenous then oral medical therapy, or (3) 10 days once-daily HBOT plus oral medical therapy [ 318]. The results indicated that the audiological outcomes (10 days post-therapy) were superior in the groups that received HBOT versus oral medical therapy alone, although it was not clear if one HBOT regimen was superior to the other. Similar to corticosteroid therapy, the delivery of HBOT treatment very soon after AAT appears crucial to realize benefits [ 319].

Table 3. Additional studies of therapies to prevent or attenuate NIHL (conducted outside of the US).

Study Nation

Author, Year

Intervention

Study Design

Population, N

Active Arm, N

Comparator arm, N

Primary Outcome

Results

Following AAT (attenuation)

Greece

Psillas et al. (2008) [ 310]

Prednisone and piracetam

Randomized cohort study

Male soldiers with firearms-related AAT, N = 52

Therapy in <1 h, n = 20

Therapy in >1-<16 h, n = 17
Therapy in 24+ h, n = 15

Complete or partial recovery in 1 month

Significantly higher recovery rate (65%) and better final threshold shifts if treatment at <1 h vs. with delayed treatment (13-24% recovery)

Belgium

Lafère et al. (2010) [ 318]

HBOT with or without methyl-prednisolone and piracetam (medical therapy)

Cohort study

Belgian soldiers with firearms-related AAT, N = 68

HBOT + oral medical therapy, n = 17
HBOT + IV then oral medical therapy, n = 32

10 days oral medical therapy, N = 17

Average hearing gain and average residual hearing loss 10 days post-treatment vs. baseline pre-AAT

Both regimens of HBOT + medical therapy was superior to medical therapy alone

China

Zhou et al. (2013) [ 219]

Intratympanic steroid (methyl-prednisolone) with or without oral steroid

Prospective RCT

Adults recently diagnosed with NIHL, N = 52

Intratympanic + oral steroid 3 days after NIHL onset, n = 27

Intratympanic placebo + oral steroid 3 days after NIHL onset, n = 26

PTA and speech discrimination score change from baseline

Significantly more of the intratympanic group had ≥15 dB improvement in PTA and ≥15% speech discrimination vs. placebo + oral steroid only

Before noise exposure (prophylaxis)

Israel

Attias et al, (2004) [ 293]

Mg

Prospective RCT

Males (16-37 y) with normal hearing, N = 20

10 days 122 mg oral Mg, n = 10

Placebo, n = 10

TTS immediately following noise exposure
(90 dB for 10 min)

12% of Mg-treated patients experienced TTS ≥ 20 dB, vs. 28% in placebo and no-intake groups; reduced magnitude of TTS was significant for all frequencies between 2 and 8 kHz

Israel

Attias et al, (1994) [ 292]

Mg

Prospective RCT

Male military recruits exposed to noise during 8 weeks of weapons training, N = 255

167 mg oral Mg twice daily during training, n = 125

Placebo, n = 130

PTS 7-10 days post-exposure vs. baseline

PTS was significantly more common and more severe in the placebo vs. Mg-treated group, and negatively correlated with red blood cell Mg level

Italy

Quaranta et al. (2004) [ 294]

Vitamin B12

Prospective RCT

Adults (20-30 y) with normal hearing, N = 20

1 mg B12 daily for 7 days, then 5 mg on day 8, n = 10

Placebo, n = 10

TTS following
112 dB 3 kHz noise for 10 min measured 8 days post-treatment

Significant reduction in TTS at 3 at 4 kHz in B12 group vs. control

India

Kapoor et al. (2011) [ 295]

Vitamin E + inhaled carbogen (5% CO ₂ +95% oxygen)

Prospective RCT

Male industrial workers with exposure to intense occupational noise, N = 40

6 days carbogen, vitamin E only, or combination, total n = 30 (10 each)

Placebo, n = 10

TTS from baseline following 5 h noise exposure
(90-113.5 dB)

Combined carbogen + vitamin E reduced TTS by 1.6-5.1 dB across frequencies; vitamin E groups had reduced serum markers of oxidative stress

This review of the literature described the etiology of and risk factors for NIHL, as well as approaches for screening, prevention, and treatment of affected patients. We also summarized the evidence from publications of experimental therapies which, although promising for prophylaxis or AAT that can be treated very quickly, have yet to address the needs of patients with long-standing or cumulative NIHL. The impact of NIHL is not limited to decreased quality of life of affected individuals but can extend to lower productivity of the workforce and impaired performance of military personnel. Further, NIHL is associated with a substantial economic burden to governments and society at large, expected to increase as the global population ages and experiences increased costs of NIHL-related healthcare and disability. Thus, the prevention of noise-induced cochlear injury, via the use of hearing protection in loud occupational and recreational settings, remains the cornerstone of reducing the enormous burden of NIHL. Governmental regulations and safety-focused organizations play essential roles in advising the public and industry on safe noise exposure levels and in implementing educational programs. For example, a cost-effectiveness analysis of a military hearing conservation program estimated a lifetime savings of USD $10,657 per person in service-related compensation on implementation of the program [ 320]. Additional harm reduction may also result from better alignment of occupational noise exposure limits recommended by NIOSH and OSHA. It is encouraging that there is increased awareness of the need for NIHL prevention compared to decades ago, although there remains a large unmet medical need for therapies beyond prophylaxis or AAT.

Supplementary Materials

This research was funded by the Remondi Foundation, Rich Robbins, Larry Bowman, and the Bertarelli Foundation Endowed Professorship (KMS).

The authors thank Samuel Early for early help with the literature review.

The authors attest they have no conflicts of interest.

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Figure 1. Examples of noise exposure levels in occupational and non-occupational settings. Data from the United States National Institute for Occupational Safety and Health [ 30] and the Hearing Health Foundation [ 31].

Figure 2. Anatomical structures of the inner ear impacted by NIHL. Three-panel diagram illustrating ( a) cross section of gross outer, middle, and inner ear anatomy; ( b) cross-sectional anatomy of the cochlea; ( c) cellular-level anatomy of the sensory epithelium of the cochlea (organ of Corti). Original illustrations by Christine Gralapp and used with permission.

Figure 3. Mechanisms of damage in NIHL. Abbreviations: ROS, reactive oxygen species; SGN, spiral ganglion neurite. Created with BioRender ( www.biorender.com; accessed on 7 February 2023).

Figure 4. Characteristic audiogram of an individual with NIHL. The signature pattern of hearing loss is focused on 3-4 kHz range. Made with Interactive Audiogram Plotter ( https://audprof.com/aud_tools/audiogram/; accessed on 1 February 2023).

Table 1. Occupational noise exposure limits recommended by NIOSH and OSHA.

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# data[].attributes.attachment_link.description
Noise-induced hearing loss (NIHL) is the second most common cause of sensorineural hearing loss, after age-related hearing loss, and affects approximately 5% of the world's population. NIHL is associated with substantial physical, mental, social, and economic impacts at the patient and societal levels.

# data[].attributes.body
Sudden hearing loss

Sudden sensorineural hearing loss.

SSHL happens because there is something wrong with the sensory organs of the inner ear. Sudden deafness frequently affects only one ear.

Something is wrong with the inner ear.

Usually one ear.

Can cause communication difficulties.

Causes:

Some conditions – only 10% of people are diagnosed with an identifiable cause.

Infections.

Head trauma.

Autoimmune diseases.

Exposure to certain drugs that treat cancer or severe infections.

Blood circulation problems.

Neurological disorders, such as multiple sclerosis.

Disorders of the inner ear.

Exposure to loud noises.

Diagnosis:

With pure tone audiometry:

Doctor can measure how loud different frequencies, or pitches, of sounds need to be before you can hear them. One sign of SSHL could be the loss of at least 30 decibels in three connected frequencies within 72 hours.

Make conversational speech sound like a whisper.

Treatment:

The most common treatment for sudden deafness, especially when the cause is unknown, is corticosteroids.

If the cause is an infection, the doctor may prescribe antibiotics.

Hearing aids to amplify sound.

Cochlear implants to directly stimulate the auditory connections in the ear that go to the brain.

Referrals:

Audiologist.

ENT.

Occupational therapist.

Speech pathologist.

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Impact on Communication and Intervention Strategies

Impact on Communication

Noise-induced hearing loss (NIHL) occurs when there is damage to the hair cells in the cochlea due to prolonged exposure to loud noise. The impact on communication can be significant and includes:

1. Difficulty Understanding Speech:

NIHL often affects the ability to hear high-frequency sounds, which are essential for understanding consonants like "s," "t," "f," and "sh." This can make speech sound muffled or unclear, particularly in environments with background noise.

2. Reduced Speech Discrimination:

Individuals with NIHL may struggle to differentiate between similar-sounding words or sounds, especially in noisy environments. This can lead to frequent misunderstandings during conversations.

3. Social Isolation and Communication Avoidance:

The frustration of not being able to understand others can lead to withdrawal from social interactions, contributing to feelings of loneliness and isolation.

4. Increased Listening Effort:

People with NIHL often need to concentrate more to understand conversations, leading to listening fatigue and decreased engagement in communication.

Intervention Strategies

1. Medical Interventions

Hearing Protection:

Preventative measures are critical. Educating patients about the use of hearing protection (e.g., earplugs, earmuffs) in noisy environments can help prevent further damage.

Pharmacological Interventions:

Research into otoprotective agents is ongoing, with some medications under investigation for their potential to protect against NIHL. However, these are not yet widely available.

2. Audiological Interventions

Hearing Aids:

Modern digital hearing aids can amplify specific frequencies affected by NIHL, improving speech understanding. They can be programmed to reduce background noise and enhance speech clarity.

Assistive Listening Devices (ALDs):

ALDs, such as personal amplifiers and FM systems, can be used in specific settings (e.g., classrooms, theatres) to improve the signal-to-noise ratio, making it easier to hear speech.

Tinnitus Management:

Many individuals with NIHL experience tinnitus (ringing in the ears). Audiologists can provide tinnitus retraining therapy (TRT) and sound therapy to manage symptoms.

3. Management by Other Health Professionals

Speech-Language Pathology:

Speech therapists can work with individuals to develop strategies for clearer speech production and improved communication, including lip reading and other compensatory techniques.

Psychological Support:

Psychologists or counsellors can help address the emotional and social consequences of hearing loss, such as depression, anxiety, or social withdrawal.

Occupational Therapy:

Occupational therapists can assist with environmental modifications, such as advising on workplace accommodations or home adjustments to enhance communication.

Vocational Rehabilitation:

Vocational rehabilitation professionals can support individuals in adapting to their hearing loss in the workplace, including the use of technology and adaptive strategies to maintain employment.