Chapter x. Causes of Hearing Damage. 1. Introduction.

Transcription

1 Chapter x Causes of Hearing Damage 1. Introduction. 2. Noise induced hearing damage. 3. Other causes of hearing loss. 4. Tests and Exercises. 5. References. 1. Introduction. This chapter explains the main adverse health effects of noise: damage to the hearing mechanism, known as noise-induced hearing loss (NIHL); and tinnitus. Also covered are other agents that can damage hearing: ototoxic substances; diseases; and the ageing process. Causes of Hearing Damage 1

2 1.1 Agents of Hearing Damage Hearing damage may result from several agents - both occupational and nonoccupational: 1.2 Describing the Hearing Loss 2.1 Acoustic Trauma Noise - occupational (called occupational noise-induced hearing loss ONIHL) Noise - non-occupational (called sociocusis). Ageing - (called presbyacusis). Diseases and infections, ototoxic medications, trauma (blows) to the head (collectively called nosoacusis). Ototoxic hazardous substances in the workplace (eg organic solvents, lead). ('Ototoxic' means 'toxic to the ear'.) If the agent affects the function of the middle ear, eardrum or blocks the ear canal, the hearing loss is called conductive. If the agent damages the cochlea structures, nerve fibres, auditory nerve or auditory centres of the brain, the hearing loss is called sensorineural. 2. Noise-Induced Hearing Damage Noise can affect hearing in four main ways: Acoustic trauma Temporary threshold shift (TTS) Permanent threshold shift (PTS) Tinnitus Acoustic Trauma is defined as damage to the ear resulting from a single exposure or relatively few exposures to a very intense level of sound (peak levels greater than db), usually impulsive in nature, eg explosions. Acoustic trauma, from the effect of a single exposure or relatively few exposures to a very intense level of sound, may cause: damage to the ear drum; damage to the ossicles; and mechanical damage to the hair cells, supporting cells and tissues of the organ of Corti. 2 The Almond Tree Effect

3 2.2 Temporary Threshold Shift (TTS) Temporary Threshold Shift (TTS) is defined as a temporary change in hearing level that recovers between exposures, resulting from sound levels over about 70 to 75 db(a). A temporary threshold shift (TTS), which recovers between exposures, is commonly experienced. You may have noticed sound seeming muffled after exposure to loud noise or music. If you have to turn the car radio up after a day's noisy work, then find it too loud the next morning, you Plate 1: Growth and recovery of TTS. may be experiencing TTS. This may last, depending on the nature of the exposure and the individual, for minutes, hours, or days, after the sound has stopped. In general, for continuous noise, as the exposure time increases so does the TTS, until after 4 to 12 hours a plateau (or asymptotic level) is reached. For impact noises the asymptotic level of TTS appears after only 1 to 2 hours. The recovery after exposure ceases is at first rapid, but then slows down, with complete recovery taking at least as long as the original exposure time. This is shown in plate 1. Higher levels of noise exposure will produce more TTS, as shown in plate 2. As long as intervals between exposures are long enough for complete recovery, it is unlikely that permanent damage will occur. However, TTS is a warning sign that the hearing mechanism is being overloaded. It is thought that Plate 2: TTS for different noise exposures. Causes of Hearing Damage 3

4 TTS is due to reversible biochemical changes to the stereocilia of the hair cells. 2.3 Permanent Threshold Shift (PTS) Permanent Threshold Shift (PTS) is permanent damage to the ear as a result of continued or repeated exposure to excessive noise over a period of time. A permanent threshold shift (PTS) occurs gradually. Normally, it is the hair cells in the inner ear, which detect the 4-6 khz frequencies, which deteriorate first. As most of the speech frequencies are below this range, the loss may initially go unnoticed. With further excessive noise exposure, the hearing loss increases and extends down to lower frequencies as well and the person begins to have trouble understanding speech. Plate 3 shows how permanent hearing loss typically develops with years of exposure to noise. From this you can see that most of the hearing loss at the high frequencies occurs in the first 10 years of exposure. There have been many proposed mechanisms for permanent hearing damage to the inner ear structures. These have been studied by optical and electronmicroscopy: Stereocilia have been observed to lose their rigidity, probably due to destruction of their actin filaments. Damage to the rootlet anchoring them to the hair cell may also occur. Any damage to the stereocilia will lead to a Plate 3: Progression of NIPTS for 90 and 100dBA. 4 The Almond Tree Effect

5 reduction in ability to translate the vibration from the basilar membrane. The hair cell body itself may suffer "metabolic exhaustion", its internal structures swelling and leading to eventual death of the cell. Outer hair cells are more susceptible to damage than inner hair cells, probably due to their stereocilia being subject to shear forces from the tectorial membrane and the greater displacement they undergo, because of their position on the basilar membrane. The first db of hearing loss is probably caused by the loss of the cochlea amplifier function of the outer hair cells. It has been suggested that excessive noise can damage the vascular system (blood supply), impeding the supply of nutrients to the organ of Corti, hastening the metabolic exhaustion. The synapses (connections) of the nerve fibres to the hair cells may swell and degenerate. However, the relationship between cochlea damage and hearing loss is very complicated and still the subject of research. Numerous animal studies have reported substantial hair cell losses with normal thresholds of hearing. Conversely, a given amount of hearing loss may be attributable to one of several factors. This may account for the clinical observation that individuals, with essentially the same audiograms, can have markedly different successes with the use of hearing aids. 2.4 Biologic Variability Like other human characteristics, susceptibility to NIHL has a wide range of variability. The same exposure to noise can result in responses varying from no NIHL to large, debilitating losses. This has to be kept in mind when setting exposure standards for occupational noise. 2.5 Tinnitus Tinnitus is the term given to noises which are heard 'in the ears' or 'in the head' - ringing, buzzing, hissing, whistling, pulsing or other sounds which do not come from an external source. Plate x: Electron micrograms of stereocilia damaged by excessive noise. Plate x: Electron micrograms of hair cells damaged by excessive noise. Causes of Hearing Damage 5

6 Research into the causes of tinnitus is ongoing. The current theory is that damage to the hair cells of the inner ear (from noise or other agents) causes the generation of weak, abnormal nerve impulses, which are mistakenly perceived by the brain as real external sounds. In the 10% or so of people who are troubled by persistent tinnitus, it is thought that these weak signals are amplified to a disturbing level in the neural pathways that connect the cochlea to the different parts of the brain. This process seems to be made worse by stress or emotional events, which may explain why tinnitus is twice as common in hearing impaired people - straining to hear focuses the subconscious brain to pick up anything coming from the inner ear. 3. Other Causes of Hearing Loss 3.1 Ototoxic Agents Ototoxic means 'toxic to the ear'. Certain medications or chemical agents in the workplace can damage the hair cells in the inner ear. Over 200 agents have been reported as ototoxic. These include: antibiotics such as streptomycin; quinine; and salicylates such as aspirin. Workplace ototoxic agents include: solvents such as benzene, toluene, butanol, trichloroethylene; and arsenic, lead, cobalt, mercury, and lithium. Some agents are synergistic with noise exposure, ie, in circumstances where neither the agent nor the noise exposure alone will produce a hearing loss, the combined occurrence will. Such agents include: carbon disulfide carbon monoxide carbon tetrachloride styrene xylene methyl ethyl ketone methyl isobutyl ketone 6 The Almond Tree Effect

7 3.2 Diseases Nosoacusis is defined as hearing damage resulting from diseases and infections, ototoxic medications, or trauma (blows) to the head. Many systemic and hereditary diseases can cause hearing loss. Among these are: rubella, meningitis, diabetes, renal disease, rheumatoid arthritis and Meniere's disease. 3.3 Ageing Presbyacusis is defined as progressive loss in sensitivity at the high frequencies occurring with increasing age. A series of changes occurs in the auditory system as humans age. These include: Loss of hair cells - mostly those at the basal end of the cochlea - hence affecting high frequency perception. Degeneration of the stria vascularis (lateral walls of the scala media) - responsible for maintaining the ion composition of the fluids and hence the cochlea potential - most pronounced at low and mid frequencies. Loss of spiral ganglion cells in the auditory nerve - more severe in the high frequencies. Degenerative changes in the central auditory nervous system. Plate x: Median audiogram for males. The most common audiometric pattern for presbyacusis is a gently sloping audiogram, affecting the high frequencies more than the low. Plate x: Median audiogram for females. Causes of Hearing Damage 7

8 This shows that, on average, presbyacusis starts at about 30 years of age, but doesn't begin to become noticeable until about 55 years for men and 64years for women. Studies on the interaction between NIHL and presbyacusis are still progressing. 3.4 Sociocusis Sociocusis is defined as noise-induced hearing loss from non-occupational noise, for example high level music, recreational shooting, and other noisy hobbies such as carpentry and drag racing. 8 The Almond Tree Effect