Protect your hearing and stay away from occupational noise-induced hearing loss

Occupational noise-induced hearing loss (noise deafness) is sensory hearing loss caused by noise.

Noise is widely present in people's work process and environment, and noise-induced hearing loss is one of the common occupational diseases. The characteristics of hearing loss caused by noise are that the initial manifestation is hearing loss in the high-frequency band of 3000Hz to 6000Hz, and the cells at the base of the cochlea are damaged, degenerated, and necrotic. As the noise exposure time increases, the condition worsens and develops to the language frequency band of 500, 1000, and 2000Hz, eventually leading to the loss of most or all of the cochlea, especially when the top is damaged, there will be obvious language hearing impairment. Noise hazards have become one of the main hazards in countries around the world today, and noise pollution has been considered the first of the seven major public hazards in the world.

Causes

1. Noise intensity: The noise intensity is the main factor affecting hearing. The greater the intensity, the earlier the hearing loss occurs, the more serious the damage, and the more people are affected.

2. Noise exposure time: Lifetime exposure to noise below 80dB (A) will not cause hearing damage. From 85dB (A), the hearing damage increases with the number of years of exposure. The table also shows the critical exposure years for hearing damage at different noise intensities, that is, the exposure years when the number of people with hearing damage exceeds 5%. At 85dB (A), it is 20 years, at 90dB (A), it is 10 years, at 95dB (A), it is 5 years, and at 100dB (A), it is within 5 years. The time required to cause hearing damage at high intensity varies greatly, ranging from as short as a few days to as long as several years, and is generally about 3 to 4 months.

3. Frequency and spectrum of noise: The human ear is more tolerant to low frequencies than to medium and high frequencies.

Sounds between 2000 and 4000 Hz are most likely to cause damage to the cochlea, and narrowband sounds or pure tones have a greater impact than broadband sounds. In addition, intermittent noise is less harmful than continuous noise, sudden noise is more harmful than gradual noise, and noise with vibration is more damaging to the inner ear than simple noise.

4. Individual differences: People have different sensitivity to noise. About 5% of the population are susceptible to noise. They not only experience a more obvious temporary threshold shift (TTS) after being exposed to noise than the general population, but also recover more slowly. Animals with different genetic types have different sensitivities to noise damage. Peter J Kazel studied the cell membrane-ATPase isoform2 (PMCA2) gene of mice15 and found that homozygous mice with mutations in this gene were more susceptible to noise-induced hearing loss. After excessive noise stimulation, PMCA2 mutant mice showed a significant permanent threshold shift of auditory brainstem response. In addition, mice with superoxide dismutase gene knockout had more severe hearing loss16. Peter M. Rabinowits et al. studied the polymorphism of two metabolic genes (GSTM1, GSTT1) related to glutathione S-convertase in 58 workers and found that workers with the GSTM1 gene had higher frequencies of distortion product otoacoustic emissions, suggesting changes in outer hair cell function. This suggests that this gene may play an important role in protecting cells from noise damage.

5. Noise type and exposure mode: Impulse noise is more harmful than continuous noise, and duration is more harmful than indirect contact.

6. Other factors: For example, age factors. The older you are, the more serious the noise damage is. For ear disease factors, people with sensorineural hearing loss are prone to noise-induced hearing loss. At the same time, it is believed that a diseased auditory organ is more difficult to recover after being injured than a normal person. There are still differences of opinion on the impact of noise stimulation on patients with otitis media. In addition, the speed of onset and severity of noise-induced hearing loss are closely related to personal protection. Long-term use of ear protectors and earplugs in environmental noise will slow down the occurrence and development of hearing damage. The use of sound insulation, soundproofing and sound absorption equipment in the workplace can reduce the impact of noise.

Pathophysiology

In the past, it was believed that the main cause of noise-induced inner ear damage was mechanical vibration. Recent studies have found that many factors, such as changes in the redox state of inner ear cells, the generation of excessive free radicals, and calcium imbalance, are involved in the process of inner ear cell death caused by noise. The death of inner ear hair cells caused by noise can be partially reduced by removing free radicals, improving inner ear blood flow, restoring intracellular calcium ion balance, and reducing glutamate excitotoxic neurotoxicity, which is conducive to the recovery of noise-induced hearing loss. Noise damage to the auditory organ is the basis for noise-induced hearing loss, especially the formation of PTS.

Population data and a large number of animal experiments show that no matter what kind of noise stimulation the hair cells receive (broadband noise, narrowband noise, high-frequency or low-frequency noise, pure tone, etc.), the hair cell damage site of the Corti organ mostly occurs in the basal turn and the second turn of the cochlear basilar membrane. From the process of hair cell damage, the first is the degeneration and loss of outer hair cells, and then the degeneration of synapses between hair cells and auditory nerve fibers. The number and morphological structure of hair cells change, mainly manifested as: ① a decrease in ascending synapses; ② a decrease in vesicles in synapses; ③ a decrease in synaptic volume; ④ a decrease in the accumulation density of vesicles in synapses. Among the three rows of outer hair cells. The third row is most vulnerable to damage because it is located in the center of the basilar membrane. The vibration displacement is the largest, so it is most vulnerable to damage. With the accumulation of noise exposure, the second row of hair cells, Deiter cells, Heine cells and supporting cells such as the outer column are then affected. Because the inner hair cells are close to the bony spiral plate, the displacement amplitude is small when vibrating. Therefore, the damage is relatively small. The noise threshold that causes damage to them is about 20 dBA higher than that of the outer hair cells. When inner hair cells are affected. This is often accompanied by a decrease in the number of spiral ganglion fibers and their cells, and even deformation, destruction and disappearance of the entire Corti organ.

The loss of cochlear hair cells caused by noise in the auditory nerve can lead to the degeneration of auditory nerve fibers. Degeneration of the spiral ganglion can lead to a decrease in the volume of the cochlear nerve nucleus, apoptosis, and a decrease in the number of cells. After studying the cochlea on one side where the entire Corti organ was damaged, it was found that the degree of loss of the auditory nerve varied in different parts: 82% in the middle and lower part, 67% in the middle part, and 49% in the middle and upper part.

The damage caused by noise in the central auditory system mainly occurs in the cochlear nucleus, superior olivary nucleus, medial geniculate body, hypothalamus and auditory cortex. Noise can cause neuronal degeneration in these areas, changes in cell electrophysiological activity and reconstruction of frequency tuning curves, resulting in decreased speech recognition ability and the ability to integrate sound signals. When the stimulus is above the characteristic frequency. And the neuron has an inhibitory area outside the excitation area, the low-frequency area at the tail of the curve will expand, and sometimes the high-frequency area will also expand, causing mild to moderate high-frequency hearing loss. The characteristic frequency decreases a lot in the primary auditory cortex neuron, and does not change much in the pre-auditory area and the second auditory cortex. The average frequency curve width decreases significantly in the second auditory cortex. Spontaneous electrical activity is enhanced in the primary auditory cortex, unchanged in the pre-auditory area, and decreased in the second auditory cortex. This reconstruction of the cortical frequency distribution map may be caused by changes in the subcortical frequency distribution map.

Pathogenic mechanism

1. Mechanical injury theory: It is believed that the damage to the auditory organ is caused by the mechanical impact of sound waves, which mainly includes the following viewpoints: ① After high-intensity noise is transmitted through the ossicular chain or the cochlear window, it can cause strong flow of endolymph and perilymph, forming a vortex. The strong liquid vortex impacts the cochlear duct, which can rupture the vestibular membrane, leading to the mixing of endolitholymph and changes in ion composition, as well as damage to the spiral organ cells, followed by atrophy of the stria vascularis and degeneration of nerve fibers; ② Strong basilar membrane vibration can rupture the vestibular membrane, leading to the mixing of endolitholymph and changes in ion composition, as well as damage to the spiral organ cells, followed by atrophy of the stria vascularis and degeneration of nerve fibers; ③ Strong basilar membrane vibration causes micropores in the reticular layer, causing endolymph to infiltrate around the hair cells, causing excessive potassium ions in the internal environment, exposing the cell membrane of the hair cells to the abnormal high potassium environment, thereby being damaged; ④ The spiral organ is separated from the basilar membrane; ⑤ The tectorial membrane is separated from the hair cells.

2. Vascular theory: Noise exposure can damage the microcirculation in the cochlea, leading to ischemia and hypoxia in the cochlea, and causing degeneration of hair cells and spiral organs. A large number of animal experiments have shown that a series of changes can occur in the cochlear blood vessels under the stimulation of strong noise, causing vasospasm, contraction or dilation, slower blood flow, and reduced local blood perfusion; vascular endothelial swelling, increased permeability, and blood concentration leading to a significant increase in viscosity; platelet and red blood cell aggregation, thrombosis; thus leading to microcirculatory disorders, decreased cochlear blood flow, insufficient blood supply to the inner ear, and decreased oxygen tension in the internal and external lymph. The above-mentioned vascular changes cause local ischemia and hypoxia, resulting in metabolic disorders in the internal environment of the cochlea, reduced hair cell metabolism, energy storage and supply disorders, and dysfunction of the enzyme system, which leads to a series of pathological and physiological changes such as damage to the morphological structure of hair cells including spiral organs and dysfunction of sound-to-electric conversion. The hydrogen clearance method or laser Doppler blood flow measurement method found that high- and medium-frequency pure tones or noise can cause a decrease in cochlear blood flow, and light microscopy results suggest that the degree of microvascular changes is related to hair cell damage.

3. Metabolic theory: Noise can cause serious disorders in the enzyme system of hair cells and supporting cells, leading to oxygen and energy metabolism disorders, cell degeneration and death. Continuous noise stimulation affects the cochlear hair cells, increasing their demand for adenosine triphosphate, increasing the oxygen and glucose consumption of hair cells and supporting cells, causing local relative ischemia, increased free radical content and intracellular Ca overload, causing necrosis and apoptosis of cell structure. In addition, the decrease in oxygen partial pressure and reduced supply of cochlear lymph fluid caused by noise further affects the activity of adenosine triphosphatase. Noise can also directly damage local microcirculation disorders in blood vessels, tissue edema, decreased blood oxygen, and decreased K+-Na+-ATPase activity in the vascular stria, so that the cation concentration gradient in the endolymph and the potential in the cochlea cannot be maintained, thereby leading to dysfunction of the spiral organ and hair cells.

4. Others: Recent studies have found that nitric oxide synthase II (NOS II) is positively expressed in noise-damaged cochlea, especially in the vascular striae and spiral ganglion cells. Animal experiments have shown that there is cell apoptosis in noise-exposed cochleae, and it has been concluded that early cell apoptosis in the damaged cochlea is the main cause of hearing loss. Now noise-induced hearing loss susceptibility genes have become a hot topic in academic research. Most current research results show that the main susceptibility genes are as follows: ① 7.4kb deletion of mitochondrial gene; ② presbycusis gene (AHL); ③ plasma membrane Ca2+-ATPase 2 mutation; ④ superoxide dismutase; ⑤ glutathione S-transferase; ⑥ cadherin 23 (CDH23); ⑦ nuclear transcription factor-KB (NF-KB) deletion.

Clinical manifestations

1. Progressive hearing loss

When you are first exposed to noise, your hearing becomes slightly dull. If you leave the noise, your hearing will recover after a few minutes. This phenomenon is called auditory adaptation. If you are exposed to persistent and strong noise, your hearing will become significantly dull and it will take several hours for your hearing to recover. This is called auditory fatigue. If you are further exposed to noise stimulation, it may lead to hearing damage, which is not easy to recover on its own.

2. Tinnitus

It may appear earlier than deafness, or develop at the same time as deafness. It is high-pitched, with the sound of cicadas being more common. It often disturbs people day and night and worsens in quiet times.

3. Others: headache, dizziness, insomnia, fatigue, memory loss, slow reaction, depression, palpitations, high blood pressure, nausea, loss of appetite, indigestion and other symptoms may occur.

Testing

1. Otological examination: The eardrum of patients with noise-induced hearing loss may be congested or have scattered small bleeding spots. In patients with blast-induced hearing loss, the eardrum may be perforated, and perforation of the flaccid part is rare. When the eardrum ruptures, there is often bleeding, and the edges of the perforation are uneven, often triangular, oval or kidney-shaped.

2. Hearing test: The degree of hearing loss varies according to the degree of damage, but the range of hearing loss is mainly between 3000 and 6000 Hz. Early hearing impairment is shown at 4000 Hz. The hearing curve shows a valley-shaped depression, which gradually deepens, and 2000 Hz and 8000 Hz are also affected, so that the hearing shows a downward slope. Generally, the curves of both ears are symmetrical, and those who are asymmetrical are mostly accompanied by ear diseases or individual special cases. The typical audiological spectrum of occupational noise-induced hearing loss is a "V"-shaped or "U"-shaped depression.

Electrocochlear electrogram and auditory brainstem response audiometry can help understand the location of deafness and objectively evaluate the degree of hearing loss. If necessary, high-resolution CT or magnetic resonance imaging can be performed on patients with severe blast injuries to understand the pathological conditions of the tympanic cavity, internal auditory canal, and temporal bone.

Disease diagnosis

According to a clear history of occupational noise exposure (usually higher than 85 decibels), conscious hearing loss or tinnitus symptoms, pure tone audiometry for sensorineural hearing loss, combined with dynamic observation data, on-site hygiene surveys, and exclusion of hearing loss caused by other reasons, noise-induced hearing loss can be diagnosed. The specific diagnostic classification can refer to the Occupational Health Standard of the People's Republic of China GBZ49-2007 "Diagnostic Standards for Occupational Hearing Impairment".

When one ear has mixed hearing loss, if the bone conduction hearing threshold meets the characteristics of occupational noise-induced hearing loss, the bone conduction hearing threshold of that ear can be used for diagnosis and assessment. If the bone conduction hearing threshold is increased, it may be related to conductive hearing loss, and the pure tone hearing threshold of the contralateral ear should be used for diagnosis and assessment. When both ears have mixed hearing loss, and the bone conduction hearing threshold meets the characteristics of occupational noise-induced hearing loss, the bone conduction hearing threshold can be used for diagnosis and assessment. When the bone conduction hearing threshold is used for diagnosis and assessment, the bone conduction pure tone audiometry results should also be corrected for age and gender according to GB/T 7582. After calculating the average speech frequency hearing threshold of the left and right ears respectively, the average hearing threshold of the better ear is used for diagnosis and grading of noise-induced hearing loss. If the speech frequency hearing loss is greater than or equal to the high-frequency hearing loss, occupational noise-induced hearing loss should not be diagnosed. When the pure tone audiometry hearing curve is horizontal or approximately straight, the authenticity of the hearing test results should be doubted.

If the hearing loss at the language frequency exceeds the moderate noise-induced hearing loss, an objective audiometric examination should be conducted to exclude pseudo-deafness and exaggerated hearing loss. Other causes of deafness that should be excluded during diagnosis mainly include: pseudo-deafness, exaggerated hearing loss, drug (streptomycin, gentamicin, kanamycin, etc.) toxic deafness, traumatic deafness, infectious disease (meningococcal meningitis, mumps, measles, etc.) deafness, familial deafness, Meniere's disease, sudden deafness, and various middle ear diseases.

Differential Diagnosis

1. Hearing loss caused by middle ear disease

Conductive hearing loss caused by various reasons will result in differences in air and bone audiometry and testing, that is, bone conduction is normal, while air conduction has hearing loss. When the tympanic membrane is centrally perforated and the ossicular chain is normal: hearing loss is 10~30 decibels, mainly affecting the low frequency band. Tympanic membrane perforation with ossicular chain interruption: tympanic membrane perforation with ossicular chain interruption accounts for about 60% of cases of chronic suppurative otitis media, with an average hearing loss of 40~60 decibels, mainly affecting the low frequency. Ossicular chain interruption caused by trauma and other reasons, but the tympanic membrane remains intact: hearing loss is 40~60 decibels, and the hearing loss is characterized by a flat curve of average loss. Tympanic membrane and ossicles are completely absent: average hearing loss is 50 decibels. Intact tympanic membrane + ossicular chain interruption + oval window closure: the hearing loss caused by this lesion is an average of 60 decibels. External auditory canal blockage: blockage of the external auditory canal by cerumen can cause a flat hearing loss of 30 decibels.

2. Hearing loss caused by inner ear diseases and audiological characteristics

(1) Congenital deafness: It can be hereditary or non-hereditary; it can occur on one side or both sides, with varying degrees of deafness; it is mostly sensorineural.

(2) Toxic deafness: Generally, toxic deafness refers to hearing loss caused by the use of certain drugs to treat diseases or the human body coming into contact with certain chemicals.

Systemic poisoning damage. Drug-induced deafness is one of the main causes of deafness. Ototoxic drugs include aminoglycoside antibiotics such as streptomycin, gentamicin, kanamycin, neomycin, vancomycin, anticancer drugs, diuretics, antimalarial drugs, salicylic acid drugs (aspirin), heavy metals, ethanol, carbon monoxide, anticonvulsant drugs, etc. It is generally believed that changes in auditory function are chronic, delayed, and progressive. Deafness and tinnitus often develop symptoms 1 to 2 weeks after taking the drug. 30% develop symptoms within one month, 45% develop symptoms within 3 months, and the longest deafness can occur after about 1 year. Characteristics of hearing loss: bilateral hearing loss is symmetrical, starting from high frequencies, gradually worsening, and stopping progress in about half a year. The hearing of susceptible individuals drops sharply to severe deafness or even total deafness. The degree of deafness is not proportional to the amount of medication.

(3) Infectious deafness: Infections caused by many pathogenic microorganisms, such as viruses, bacteria, fungi, chlamydia, and mycoplasma, can directly or indirectly cause damage to the inner ear, leading to varying degrees of sensorineural deafness or vestibular dysfunction in both ears or one ear, which is called infectious deafness. Pathogens that have been confirmed to cause infectious deafness include: rubella, mumps, measles, herpes zoster, epidemic meningitis, epidemic encephalitis B, syphilis, etc.

(4) Presbycusis: The incidence of presbycusis varies greatly from person to person, and the speed of development also varies from person to person. It is generally manifested as: patients over middle age have no other deafness factors, the cause of which is unknown, and bilateral high-frequency hearing loss. Some individuals sometimes develop unilateral deafness first, and then gradually develop bilateral deafness. The course of hearing loss is slow and gradual. The hearing loss is manifested as speech hearing loss, which is more serious than pure tone hearing loss. There is difficulty in understanding and a significant decrease in speech discrimination. There is a phenomenon of re-excitation: that is, the soft voice cannot be heard, the loud voice is annoying, and the hearing field is reduced.

Audiology examination: Pure tone audiometry shows air-bone conduction with equal decline, and the hearing curve is mostly high-frequency drop or steep rise. With age, the hearing threshold increases slowly, with little fluctuation. Speech audiometry shows a significant decline, and the speech recognition rate does not decline in parallel with the pure tone hearing change. Due to the degeneration of the auditory center function, the ability to understand language declines, resulting in the phenomenon of only hearing the sound but not understanding the meaning. There is often a resurgence.

(5) Sudden deafness: Sudden deafness refers to sensorineural deafness of unknown cause. The age of onset is usually between 30 and 60 years old. The male-female ratio is 1:1 to 2:1. Sudden deafness is usually unilateral, and hearing loss generally drops to the lowest point within a few minutes or hours.

(6) Non-organic hearing loss (non-organic hearing impairment) In clinical and occupational health examinations, it is often encountered that the results of pure tone tests are inconsistent with the actual hearing loss. Some subjects consciously exaggerate the degree of hearing loss. This type of situation is often described as "non-organic hearing loss", pseudohypacusis, mental or hysterical, and psychogenic hearing loss. Pseudo-hearing loss, now advocated to use the term "exaggerated hearing loss", is a common problem in hearing examinations involving legal compensation and occupational disease compensation, especially in the diagnosis of occupational hearing loss.

Disease treatment

There is still no effective treatment for noise-induced hearing loss. When symptoms appear, you should leave the noisy environment in time, stop the noise stimulation, promote natural recovery, and emphasize early treatment. Common therapeutic drugs are as follows: drugs that regulate neurotrophy, such as vitamin B drugs; vasodilators, such as puerarin, 654-2, salvia miltiorrhiza, ginkgo leaves, angelica injection and other drugs; biological products that promote metabolism, such as coenzyme A, etc. Tinnitus and vertigo can be treated symptomatically. Acupuncture, physical therapy, acupressure and other methods can alleviate symptoms. Hearing aids can be worn for those with severe hearing loss.

Disease prognosis Occupational noise-induced hearing loss is generally incurable, and hearing loss may occur prematurely with age. Some people may develop personality and other psychological disorders.

Disease prevention: The damage to workers' hearing caused by production noise is often the result of long-term and slow accumulation, which can easily be ignored. Since occupational noise-induced hearing loss is an irreversible and permanent hearing loss, it can only be prevented but not cured, so it is particularly important to prevent it before it happens.

First of all, we need to control the source of noise. We can choose low-noise production equipment and improve the production process, or change the movement mode of the noise source (such as using damping, vibration isolation and other measures to reduce the vibration of solid sound-emitting bodies). Secondly, block the spread of noise, such as using sound absorption, sound insulation, sound barriers, vibration isolation and other measures to control the spread of noise. Third, take personal protective measures; such as wearing ear protectors. Ear protectors mainly include earplugs and earmuffs. Currently, a slow-rebound foam plastic earplug is more popular abroad. This earplug has a high sound insulation value and is comfortable and easy to wear. For workers who are exposed to noisy operations, it is particularly important to have an occupational health examination including a hearing test once a year. If hearing abnormalities are found to meet the national standards, they should be transferred away from noisy operations in a timely manner.

If you experience any of the following, you may be suffering from hearing loss. We recommend that you seek medical attention as soon as possible and leave the noisy environment as soon as possible. (1) You need to speak loudly at work. (2) You need to turn up the volume of the TV when watching TV at home. (3) Your family members often complain about your loud voice. (4) You find that you cannot hear others clearly in a noisy environment. (5) You often experience tinnitus, such as the sound of cicadas, especially in a quiet environment.

The following two types of workers are not suitable for noisy work: (1) Workers who have already experienced hearing loss during pre-job physical examinations should no longer be engaged in noisy work to protect their health and safety. (2) Noise-sensitive workers: Workers who are sensitive to noise will experience irritability, sleep disorders, and tinnitus after exposure to noise. After a short period of exposure to noise, a hearing test will show a decrease in high-frequency hearing. If the average high-frequency hearing threshold of both ears is greater than or equal to 40dB, they are not suitable for continuing to engage in noisy work.

Dietary precautions and disease care

Patients with noise-induced hearing loss should leave the noisy environment as soon as possible and pay attention to proper diet and rest. Sedatives can be used to treat poor sleep caused by tinnitus. Patients should be encouraged and comforted for emotional changes such as depression and anxiety caused by noise.

Expert opinion

1. Definition and types of noise:

Noise is a type of sound. From a physical point of view, noise is the irregular and chaotic mixture of sound waves of different frequencies and intensities that makes people feel bored and unpleasant. From a psychological point of view, all sounds that people don't need can be regarded as noise. From the perspective of audiology, any sound that exceeds a certain intensity and causes damage to human hearing is noise. Noise is divided into industrial noise or production noise, military noise, and environmental noise. Noise generated in the production process is production noise or industrial noise.

2. What is the difference between noise in the living environment and occupational noise?

There are four main sources of environmental noise in modern cities: ① traffic noise ② industrial noise ③ construction noise ④ social life noise. The "Urban Area Noise Standard of the People's Republic of China" clearly stipulates the maximum limits of environmental noise in five types of urban areas: sanatorium areas, high-end villa areas, and high-end hotel areas, 50dB during the day and 40dB at night; areas dominated by residential and cultural and educational institutions, 55dB during the day and 45dB at night; mixed residential, commercial, and industrial areas, 60dB during the day and 50dB at night.

Occupational noise mainly refers to industrial noise, which mainly comes from the noise generated by machines or operating processes. The national occupational health standard stipulates that workers can work for 8 hours in an 85 decibel (dB) noise environment, 4 hours in an 88 decibel (dB) noise environment, and 2 hours in a 91 decibel (dB) noise environment, and so on. Exceeding 140 decibels can cause ear pain. Occupational diseases caused by industrial noise include occupational noise-induced deafness and blast-induced deafness.

3. Occupational noise-induced deafness and occupational hearing loss

Generally speaking, occupational exposure to noise for a period of time (each person's sensitivity is different) will cause high-frequency hearing loss (damage), which means that noise can cause pathological processes such as congestion, edema, and necrosis of hair cells, which means that the scope of occupational hearing loss is wider. However, when diagnosing occupational noise-induced hearing loss, hearing generally suffers irreversible damage, which is particularly important to note. Therefore, the state has formulated some systems to conduct regular health examinations on workers on the job, generally promptly identify workers with hearing loss, and promptly transfer them from work to protect their hearing.