How Noise Damage Affects The Hearing Ability

Executive Summary

We are connected to our surroundings by five senses: Sight, smell, taste, touch and hearing. Hearing is more than sounds, it is a biopsychosocial process. There are sounds, with specific features, that can damage our hearing causing Noise Induced Hearing Loss (NIHL); a problem increasing worldwide. It has negative effects that could be avoided, but hearing impairment is not as prioritized as it should be.

Hearing is a complex process. It involves diverse connections and procedures, some visible and some others that are still an enigma. The ear is divided in outer, middle and inner ear. Each of them with specialized organs to complete a function that generates (auditory and balance) information transmitted through specific nerves to our brains. Cochlea, located in the inner ear is the main hearing organ. It is composed by sensitive cells known as outer and inner hair cells.

Sound is processed to reach the Nervous System through mechanoelectrical transduction in the Organ of Corti. A theory describes the possibility of an NIHL caused by a not proportioned production of oxidants and antioxidants within the inner ear that can damage hair cells.

Introduction:

Sight, smell, taste, touch and hearing: five senses. Senses connect us to our environment, from keeping us secure to enriching us. We live in a world that gives us the opportunity to experience a wide range of sounds. From nature sounds to machinery; from a conversation to music; from enjoyable to undesirable noises. Hearing keeps us aware and allows us to communicate. Hearing interacts with conscious and unconscious functions. (Graham and John M. Baguley, 2009) (de Sebastián, 1999)

Some sounds can disturb our nerves and some others can be even harmful. Noise pollution may deteriorate hearing, gradually or suddenly. Sounds, mainly over 85 dB (Lonsbury-Martin and Martin, 2010), can damage the sensitive structures of the inner ear causing noise induced hearing loss (NIHL). Unfortunately, this problem is underestimated; there are no physical manifestations that we can perceive, until a frustrating communication problem arises. Hearing impairment is a health issue to which we are all exposed, reflected in a growth in incidence and prevalence. Hearing loss has negative effects on individuals, people who interact with them and even educational or socioeconomic aspects. Highlighting, NIHL is preventable. To understand how do loud noises can damage hearing ability we need to know the normal function of this process. (Haggard, 1982)

To sum up, three tasks are needed to hear a sound:

1. Arrival of acoustic stimulus to receptors.
2. Transduction of stimulus.
3. Processing electrical signals.

Inner ear

Labyrinth: Bony (perilymph) and membranous (endolymph). Semi-circular canals + Cochlea. Cochlea: Hearing portion of the ear. Receptive cells. Divides sounds according to frequency to activate specific auditory nerve fibres. Non-linear action: amplitude compression of sounds to help auditory nerve codify for various intensities. Active process: records around 50 dB of ear’s sensitivity. (Møller, 2013) Coiled
(2.5 turns) tube, formed by three chambers filled with fluid. Connected at helicotrema à Scala tympani and vestibuli: perilymph Scala media: endolymph (high K+) Oval window: produces pressure wave that travels through scala vestibuli à scala tympani à causes vibration of round window. Scala media: part of membranous labyrinth. Also known as cochlear duct. Contains blood vessels of stria vascularis (producer of endolymph). Embodies Organ of Corti: primary receptor of hearing. (Mala, 2006) Organ of Corti: transforms physical energy into nervous energy –transduction Vibration of structures causing displacement of cochlear fluid à movement of hair cells à electrochemical signals. -Components: key sensory cells (inner and outer hair cells, both with stereocilia at apical surfaces), pillar cells (for rigidity and building the tunnel of Corti that separates inner and outer hair cells) and supporting cells (Deiter’s and Hensen cells). (Graham and John M. Baguley, 2009) (The Open University, 2017)

The receptive cells of the inner ear are known as hair cells. Their name comes from the cilia and stereocilia (or kinocilium, a longer hair) that project from the apex of these cells into the cochlear duct. The apexes of the cilia have protein filaments, which connect to adjacent cilia, associated with ion channels that open with tension.

There are two types of hair cells: Inner Hair Cells (IHC) and Outer Hair Cells (OHC). (Mala, 2006)

Inner Hair cells

About 3500, arranged in one row beneath the tectorial membrane (not attached). Cylindrical shape Sensory transduction. 90-95% of afferent nerves are connected to IHC, providing information about sound stimulation (auditory data) from the ear to the brain (neurotransmitter: glutamate). Steady internal potential: - 45 mV (Owen, 2003b) (Møller, 2013)

Outer Hair Cells

Approximately12000 organized in three to four rows (W or V formation). Located near the centre of basilar membrane. Action depends on sound intensity. Mediate active process of the cochlea à “Cochelar amplifier”.Connected to tectorial membrane by stereocilia. Stereocilia: detect vibrations within the cochlea, composed from actin filaments that generate cross-links between rows. Stereociliary bundles: they open ion channels for K and Ca à converting mechanical into electrical energy. Electromotility: Depolarization leads to contraction in response to mechanical stimuli using prestin (the motor protein). OHC adjust the movement of basilar membrane (amplitude) modifying the stimulation received by IHC, increasing frequency selectivity.Olivocochlear efferent innervation (neurotransmitter: acetylcholine) provides the ability to “fine tune” auditory stimuli. Steady internal potential: -70 mV (Brownell et al., 2018) (Mala, 2006) (Owen, 2003) (Møller, 2013)

Mechanoelectrical transduction

When perilymph stimulates the stereociliary bundle towards the kinocilium it leads to a depolarisation and a propagation of action potential à release of neurotransmitter vesicles

1. Sound waves travel from outer ear à middle ear (stapes hits oval window and generates a wave through the perilymph inside the labyrinth, flowing through helicotrema until round window) à inner ear (wave travels along the cochlea) * High frequencies: base *Low frequencies: apex
2. Pressure wave inside the cochlea: Vibration of the perilymph à movement of the basilar membrane à vibration of the Organ of Corti (Hair Cells)à OHCs enhance the movement of basilar membrane à perilymph stimulates the stereociliary bundle towards the kinocilium. With sufficient fluid movement the hairs are deflected and ion channels open up by stretching the tip links. *Mechanical energy
3. Potassium from endolymph gets into the IHC through ion channels (because of positive electrical charge)àpartial depolarization and propagation of action potential à influx of Ca+ along hair cell body à complete depolarization. *Electrical energy
4. The positive electrical charge modifies the hair cell membrane à Synaptic vesicles containing neurotransmitter
5. Neurotransmitter (glutamate) is released from the base of the hair cell à neuron excitation (synapsis) à signals towards brain (Auditory Cortex of the temporal lobe) *Chemical energy (Graham and John M. Baguley, 2009)(Owen, 2003a)

Noise Induced Hearing Loss

Hearing loss: an incerase in tresholds over 25 dB. Type: conductive, sensorineural or mixed. Degree: moderate, mild, severe, profound. Configuration: high/low frequency, bilateral/unilateral, symmetrical/asymmetrical, progressive/sudden and fluctuating/stable . (WHO Media centre, 2014) (American Speech Language Hearing Association, 2016). Sensorineural hearing loss: damage to the inner ear (cochlea) or nerve pathway (Vestibulocochelar nerve CNVIII or Central Nervous System). Causes: illnesses, medication, genetic, aging, congenital or loud noises. (American Speech Language Hearing Association, 2016) (Kari, Wilkinson and Woodson, 2013)

Noise Induced Hearing Loss - damage caused by (loud) noise exposure. It can be the result of regular or single events. It can be permanent or temporary. (Neeraj N, Vardhman and Guru Gobind, 2012) Generally occurs at: frequency of 2-4 kHz (American Hearing Research Foundation, 2012) and intensity 85 dB or more. (American Academy of Otolaryngology–Head and Neck Surgery., 2017) Hair cells are not capable of regenerating. (University of Texas, 2014)

Mechanism of damage

• Mechanical destruction: changes in hair cells’ rigidity à sensory cells destruction àloss of function
• Excessive metabolic activity at cellular level (oxidative stress): increased levels of energy needed à elevation in oxygen consumption à production of free radicals in the cochlea à insufficient antioxidant defence à cell death (Krug et al., 2015)
• Oxidative stress and NIHL: the reviews. Summaries of previous information reporting descriptive information about oxidative stress in hearingloss.
• Oxidative Stress and Cochlear Damage (Hu and Henderson, 2014) [USA] Oxidative stress is able to generate several cochlear pathogeneses causing inner ear disorders. Antioxidant therapies may be used for treatment. Experimental models and data in human studies support the influence of oxidative stress in inner ear disorders; mainly by signalling pathways that produce cellular damage and cell death. The effect of antioxidants needs further verification.
• Mechanisms of sensorineural cell damage, death and survival in the cochlea (Wong and Ryan, 2015) [USA]: Most of acquired hearing loss cases are caused by irreversible damage of sensorineural tissues of the cochlea. Intracellular mechanisms and survival signalling pathways participate in sensorineural injury. Antioxidants, antiapoptotics and cytokine inhibitors drugs are showing advances but will need further support with evidence-based treatment.
• Cellular mechanisms of noise-induced hearing loss (Kurabi et al., 2017) [USA]: Intense sounds or noises can lead to temporary threshold shift or residual permanent threshold shift with changes in auditory nerve functions. The main cause of NIHL is injury to cochlear hair cells and pathologies involving synapsis. Hair cell damage generates substrates that lead to the collection of reactive oxygen species and activation of intracellular stress pathways producing apoptosis or necrotic cell death. Damage to cochlear neurons is also involved in NIHL.
• A comprehensive study of oxidative stress in sudden hearing loss (Gul et al., 2017) [Turkey]: There is an oxidative imbalance with effects in Idiopathic Sudden Sensorineural Hearing Loss (ISSHL). Authors conducted a study with 50 patients with ISSHL and 50 healthy participants; measuring levels of total oxidant status (TOS), total antioxidant status, paraoxonase and thiol/disulphide in peripheral blood. Furthermore, they calculated a global oxidative stress index. They evaluated the relationship between oxidative markers and severity of HL. Patients woth ISSHL had higher TOS levels than controls and higher oxidative index. There was no significant relation between oxidative markers and severity of HL. Disulphide and TOS showed association with ISSHL according to binary logistic regression model. Findings demonstrated endothelial dysfunction in ISSHL and modifications in oxidants and antioxidants in oxidative stress. Researchers concluded that there is an association between ISSHL with oxidative stress; that a decrease in oxygen can damage endothelium by a dysfunction involving inner ear microcirculation.
• Emerging therapeutic interventions against NIHL (Sha and Schacht, 2017) [USA]: NIHL is one of the principal causes of HL, also notably preventable. It affects quality of life mainly in population between 20 and 69 years old; with an important economic cost to society. Authors exposed a review of animal and human models. These studies leaded to therapies now being tested in trials, highlighting the need of further work to improve protective therapies.

Conclusion

Since the theory of free radicals modifying cell cycle emerged it has been used to explain several issues within human illnesses. This theory has been used to propose an explanation of how loud noises impact our hearing. The most relevant characteristic of this idea is that the production of oxidant substrates can cause injury in hair cells, which are unable to regenerate once they are death, either by apoptosis or necrosis pathways. Nevertheless, further research and information is needed to apply this knowledge in useful therapies to prevent NIHL.

Reviews and studies show research and data on the relationship between oxidative stress and NIHL; they were conducted in the last five years. All of them were supported by referencing recent resource. Arguments are presented encouraging the idea of an inner ear damage by an imbalance in oxidants and antioxidants production. There was just one experimental study, the rest of them analysed information that was already available on how free radicals can damage the hair cells producing hearing impairment.

In fact, all this scientific observations enforce the theory of a disproportion of oxidant and antioxidant substrates production in vulnerable patients with an important exposure to loud noises to end up showing hearing loss.

References:

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