Hearing and Hearing Loss

The human auditory sensory system, usually referred to as simply the Ear, is a remarkably complex system that is usually taken for granted by individuals with unimpaired hearing. It is the main subject of study by audiology, usually with an emphasis on speech perception and a variety of hearing disorders. When we discuss the historical evolution of these issues below, we will suggest that the modern concept of "normal hearing" became defined at the point where hearing ability could be quantified, around 1930, and since then, audiological measurement has determined what that meant.

An audiologist specializes in the study and treatment of hearing impairments (and usually has a Master’s degree), whereas the measurement of hearing ability is termed audiometry and is practiced by a audiometrist who gives what is generally called a “hearing test” and can recommend hearing aid equipment. Due to the rapid evolution of digital hearing aid technology today and the ongoing development of cochlear implants, we will leave those topics aside for the time being.

The branch of medicine that is involved with the ear is called otology, and is usually included with otolaryngology, commonly practiced by an ENT (ear, nose and throat) doctor, who can also be a surgeon. Note that the prefix "oto" (from the Greek word for ear) always refers to the auditory system.

These professional branches associated with the subject of hearing involve a large body of research knowledge, particularly in comparison with what typical public education teaches in schools. Here we can only summarize some of the most relevant terminology and issues that are involved.

A) Anatomy of the ear

B) Auditory analysis in the inner ear

C) Hearing loss and impairment

D) Damage-risk criteria

Q) Review Quiz

A. Anatomy of the ear. The anatomy of the ear is commonly divided into three parts, the outer, middle and inner ear as shown in this diagram.

The outer ear consists of the auricle, which funnels sound waves into the ear canal, a process that we described earlier as kind of impedance matching operation since acoustic energy does not easily pass from open air to a small “tube”. Also when we discussed binaural hearing, we pointed out that the ridges of the outer part of the ear, called the pinna (Latin for "wing" with the plural being pinnae), create small delayed versions of the sound wave. When combined with the direct sound, these delays colour the spectrum above 8 kHz and provide us with directional cues for front-back distinctions, as well as elevation. The auricle and pinna are different for each individual, and can change throughout one's lifespan.

The slightly curved ear canal (or “external auditory canal”), as with any small enclosed space, provides a high frequency resonant boost, as will be shown below. It ends at the eardrum (or tympanic membrane) where the pressure variations in the auditory canal cause it to vibrate.

Care needs to be taken not to allow a wax buildup in the ear canal, and sharp objects have to be avoided. Even using a Q-tip is not recommended, and may simply push the earwax (also called cerumen) deeper where it can become impacted. A healthcare provider may recommend liquid drops or perform an irrigation of the ear canal with water, or a dry microsuction.

Foam earplugs are designed to be flexible enough to fit into the ear canal, but custom-designed earplugs made from other materials (preferably with flat frequency response) can also be purchased. Noise-cancelling headphones are now often used by the public, the principle of which is described in the Sound-Sound Interaction module. These types of protectors are called ear defenders, and in the best cases, they can reduce sound levels by 30-35 dB.

The pressure on either side of the eardrum is assumed to be equal, but when the external atmospheric pressure changes (as with elevation), there can be an imbalance in pressure, most easily relieved by yawning (or “popping” one’s ears). As you can see from the diagram, the Eustachian tube leading to the lungs is what allows that to happen. However, there is also a danger of infection in this closed region beyond the eardrum, particularly with high fever (childhood) illnesses such as German measles and meningitis that can cause serious and even permanent damage to hearing.

Autophony refers to hearing one's own voice too loudly through the occlusion of the ear canal by earwax or other blockage (similar to wearing earplugs). It can also be caused by otitis media in the middle ear (described below), or a disorder in the Eustachian tube (Patulous Eustachian Tube) where it is sometimes open and allows internal sounds to be conducted to the middle ear.

The movement of the eardrum at the threshold of hearing is said to be so small that it cannot be seen with the naked eye as the distance is less than a wavelength of light. And if it were any more sensitive, molecular movement could heard! Given that it can also withstand pressure that is a million times stronger (admittedly with discomfort) this represents a remarkable dynamic range. However, very large pressure transients can perforate or burst an eardrum, though in some cases this can be surgically repaired.

The middle ear consists of three very small bones (the smallest in the body) called the ossicles. Their function is to transfer the energy from the eardrum's response to changes in air pressure through these solid bones as a kind of amplification (up to 22 times their original amplitude) and deliver it to the inner ear. The bones are commonly called the hammer, anvil and stirrup because of their shapes, but their proper names are the malleus, incus and stapes, respectively.

In the above diagram, the very small stapedius muscle (about 1 mm in length) which is attached to the stirrup, is not shown, but its function is to damp a large incoming pressure surge (greater than 85 dB) as a form of hearing protection. However, for the brain to detect such an increase and send a message to this muscle to contract requires a time lag estimated at up to 300 ms. Unfortunately this mechanism cannot react quickly enough to protect against impact sounds with very fast attacks, particularly gunfire, but also some other mechanized sounds, in which case hearing protection must always be used.

The stapedius muscle can also be activated by one's own speaking voice in order to prevent its low frequency components (that become obvious with earplugs) masking other incoming sounds.

Inflammation of the middle ear is called otitis media and can be very painful and often affects young children.

As mentioned above, both the unimpaired outer and inner ear have their own resonant frequencies, as shown here, both in the range of 1-4 kHz. Together they give a 10-20 dB boost to those frequencies prior to entering the cochlea. This explains why the frequency response of the ear, as shown in the Equal Loudness Contours, is always higher in the 1-4 kHz range, at all intensity levels.

Frequency response of outer and middle ear (source: Br

The last bone in the ossicular chain is the stapes, or stirrup (less than the size of your smallest fingernail), and it acts like a piston at the oval window of the cochlea (see the first diagram), transmitting the vibration to the fluid inside. This wave passes through the spiral-shaped cochlea as described in the next section, with the round window at the far end responding to the pressure that it exerts. A small wave called otoacoustic emissions can be emitted from the oval window and pass back through the middle ear and out the ear canal where they can be picked up by a microphone. They are a sign that the cochlea is functioning properly.

Any impairment in the energy transmission through the outer and inner ear results in conductive hearing loss, which can be a mechanical issue caused by calcification of the bones that can be corrected by micro-surgery, or by a tumour. This transmission through the ossicles should not be confused with bone conduction, which refers to sound passing through the bones of the body and reaching the cochlea (which is embedded deep within the bones of the skull) as discussed next.

The inner ear consists of the snail-shell-shaped cochlea (cochlea is Greek for snail), the three semi-circular canals and the auditory nerve passing to and from the brain. Whereas the sound wave changes media from the air, through the bones of the ossicles, and then to the liquid filled cochlea, it is the analysis of the wave inside the cochlea that is crucial – and the most complex part of the system – so we will devote the next section to understanding how it works.

However, before we do that, it is worth noting the function of the three semi-circular canals, named for their horseshoe shape, that are part of the bony labyrinth of the cochlea. They are our balance mechanism, each of the three responding to movement in the x, y and z planes, that is, the three dimensions of possible head movement.

The three canals are filled with endolymph, similar to the cochlea, which responds to movement and acceleration by bending the cilia of the hair cells, also similar to the cochlea. The horizontal canal detects motion when we turn our head left and right, around a vertical axis. The superior canal does the same for nodding the head around the lateral axis, and the posterior canal reacts to a movement of the head towards the shoulder. In other contexts such as flying, these movements are called pitch, roll and yaw. It is important to keep in mind that hearing and the sense of balance are intimately connected.


B. Auditory analysis in the inner ear. The interior structure of the bony cochlea is tricky to understand because it includes a canal filled with perilymph (a fluid similar to plasma and cerebrospinal fluid, rich in sodium and poor in potassium). This canal is called the vestibular canal (scala vestibuli), that starts at the base of the cochlea and the oval window where the stapes is creating a pressure wave. This canal ascends to the apex of the cochlea, spiralling around 2-1/2 times, and then the wave returns down a second canal, the tympanic canal (scala tympani), back to the basal end where the round window is located to relieve the pressure.

In between the two canals is the cochlear duct (scala media), filled with endolymph (a unique kind of fluid rich in potassium and low in sodium, the opposite of the perilymph), within which resides the organ of Corti which is attached to the basilar membrane that separates it from the tympanic canal. A similar membrane called Reissner’s membrane, separates the cochlear duct on the other side, from the vestibular canal. Given the spiral shape of these canals, it is difficult to visualize them, but we will try to do this with two cross-sectional diagrams. You can also look for some of the digital animations of the cochlear structure that are available online.

The organ of Corti was discovered by an Italian anatomist, Alfonso Giacomo Gaspard Corti in 1851. However, the hair cells attached to it cannot be seen in visible light with a microscope, and so it remained until the advent of the electron microscope to make these features visible. In the next diagrams, we can see more of the placement and structure of the organ of Corti on the basilar membrane, including the three rows of outer hair cells, and one row of inner hair cells, all of which can fire in response to the incoming sound wave and send those impulses via the auditory nerve to the brain.

As you can see, the organ of Corti will move in response to the fluid wave that affects the basilar membrane, on its way down the tympanic canal. However, the hair cells are not in contact with that membrane (which would likely result in some damage over time). Instead, they have contact with the tectorial membrane above the cells, which is protected from the two canals and the motion of the fluid wave.

As we have discussed previously in terms of the spectral analysis along the length of the basilar membrane – often referred to as a “bulging” of the membrane, but better understood as an oscillatory motion shown below at the right – there is what is called a tonotopic mapping of the frequency response along the basilar membrane according to position along its length. If the membrane were uncoiled, its length would be 33-34 mm – incredibly small – with the position of resonance going from high frequencies at the basal end to low frequencies at the apical end, as shown.

Notice that the high frequencies are analyzed near the base where the basilar membrane is the stiffest (thereby allowing only high frequencies to resonate), with 4 Khz at the first “turn” of the spiral. It is thought that the mechanics of the fluid vibration in this area might contribute an answer to the naive question: why do we lose high frequency sensitivity with age, and not low?” There are, of course, many factors involved in hearing loss that we will look at in the next section, but it is useful to keep this in mind.

The more important aspect of this spatial arrangement is that the resonances at octave intervals are equally spaced along this length, as shown here. This gives rise to the logarithmic scaling of frequency that we associate with cochlear analysis. This diagram shows the octaves of the pitch A, which double in frequency, as resonating at equal distances from the base of the cochlea.

Frequency distribution along the length of the basilar membrane showing its logarithmic basis

When stimulated with a periodic sound, the hair cells will fire at the same rate as the periodicity, as long as it’s in the low to mid range where there is time for them to regenerate. This ability results in our fine-tuned sensitivity to pitch in those ranges. Above that, groups of nearby hair cells will fire together at the same cumulative periodicity, called volley theory.

We are now ready to examine the hair cells themselves. A healthy ear has over 15,000 such microscopic fibres, which are actually bundles of fibres called stereocilia, plus a singular one called a kinocilium.

There are three outer rows of hair cells in a V-shaped formation. They respond to lower intensity sounds by being displacement sensitive. They are shown at the bottom in an electron microscope photo at the right. Above that is a diagram that shows what “displacement sensitive” means in terms of directionality – a full amplitude range signal is produced when the displacement is to the right, as in the top diagram, and zero amplitude when it is 90° away from that direction, with a proportional diminution in between.

The function of these outer hair cells (found only in mammals) is to amplify quiet sounds, such that a wider dynamic range of amplitudes can be accommodated by a smaller range of hair cell deflections, a process called cochlear amplification. They also improve frequency discrimination which is very important in speech and music. A chemical reaction here also allows cells to adapt to constant level sounds, since the brain is always alert to new information coming in. On the other hand, the outer hair cells are unfortunately also the first to be damaged by noise, as discussed later.

In contrast, the single inner row of hair cells responds to higher intensity levels, and their stimulation is velocity sensitive.

You have probably thought of the hair cells as only sending impulses to the brain along the auditory nerve. This “ascending” pathway is referred to as “afferent” and is well understood. However, the hair cells also receive impulses from the brain along the “descending” pathway, referred to as “efferent”.

These efferent stimulations are less well understood, but in general they influence the behaviour of the hair cells in terms of their response, such as in noisy contexts. The ability to detect signals in a noisy environment is well known to decline with age, for instance. They can also modulate cochlear amplification in the outer hair cells, mediate selective attention, and create an improvement of the signal to noise ratio. This also allows them to support adaptation and frequency selectivity, which shows that the auditory system is a dynamically functioning system, not merely a passive signal processor.


C. Hearing loss and impairment. Instances of hearing impairment have certainly occurred throughout history, but it began to be regarded as a serious medical and social problem in the 19th century as a result of industrialization. In fact, one of the early terms for hearing loss was boilermaker’s disease, because of the high sound levels involved. However, many industries, particularly in Scotland and the industrial north of England were known to produce serious degrees of hearing loss, as in the well documented case of the female jute weavers that will be discussed shortly.

Although noise has been and remains a significant cause of hearing loss (referred to as NIHL, Noise-induced Hearing Loss), there are many other causes and types of degradation of the auditory function, such that it is regarded as a worldwide problem, estimated as affecting over a billion people in various degrees. We will start by giving a brief summary of the major types of hearing loss, and associated issues.

These conditions should be kept separate from deafness (or anacusis) which is a complete lack of hearing ability, with an associated community who have established their own forms of communication such as sign language. The "hard of hearing", on the other hand, are those who use a mix of lipreading and hearing aids.

We will provide brief definitions first, and then discuss some of these categories and conditions more fully. Note that all of them can be unilateral (a single ear) or bilateral (both ears), asymmetrical (affecting each ear differently), and experienced in combination.
- acoustic trauma refers to a sudden and severe sensorineural loss of hearing (over 40 dB loss), often incurred by a single exposure to high sound levels, for instance from an explosion or gunfire, or very high levels over an extended period; the aftermath of the trauma can include ringing in the ears (tinnitus), balancing problems, and hyperacusis, a painful sensitivity to certain frequencies or sound levels which often affects musicians (and may accompany other diseases)

- conductive hearing loss, as referred to above in terms of the transfer of acoustic energy through the outer and inner ear; the causes are quite varied but often can be treated

- sensory-neural (or sensorineural) hearing loss, which refers to a gradual reduction of hearing sensitivity in the cochlea through damage to the hair cells; it can be temporary (that is, recoverable with rest and quiet), chronic or permanent, and is measured with an audiogram, as shown below; it can also be sudden as described above as acoustic trauma, and can be combined with conductive loss

- central hearing loss, which refers to an impairment resulting from defects in the central nervous system, including the auditory cortex, rather than the middle or inner ear; it can be caused by lesions in the auditory pathway or cortex such that sounds are heard but not understood

- presbycusis is age-related hearing loss, always in the high frequencies, and has many contributing factors, as discussed below

- tinnitus refers to a persistent sound in the ears when there is no external source; it can be a byproduct of ototoxic chemical exposure or excessive noise, or it can be an indicator of other medical problems

- recruitment is a non-linear amplification of sounds where normal level sounds are heard as much quieter, but above a certain point, they are heard as much louder, and therefore they can mask other sounds and create sensory-neural hearing loss; the non-linear gain with this condition is similar to hyperacusis, mentioned above

- diplacusis is a loss of frequency sensitivity in one ear that results in pitch being heard differently in each ear, sometimes called double hearing or interaural pitch difference; based on an appreciable delay between the ears, it can also affect rhythm perception
The sources of hearing loss are often divided as follows:
- occupational hearing loss is associated with workplace exposure to noise, for which most industrialized countries have established damage risk criteria (discussed below) and other regulations

- sociocusis is non-occupational hearing loss, and thus harder to regulate; it also makes it more difficult to adjudicate occupational claims for compensation because the measurement of hearing loss cannot distinguish which sources are its cause

Sensory-neural hearing loss. A standard hearing test – which is now usually offered free of charge at most audiology clinics – includes a pure-tone audiometric test and a speech-in-noise test, given to each ear separately since their sensitivity can be quite different. In fact, bilateral differences are quite common.

It may also involve other tests, such as with a typanometer that sends a puff of air to the eardrum to measure its responsiveness, to test if there is any conductive hearing loss. Other tests may involve the cochlear response.

The results of the pure tone tests (i.e. sine waves) for frequencies, usually between 250 Hz and 8 kHz (known as the speech range), are displayed on a graph called an audiogram. Note that the threshold of hearing level is at the top on the 0 dB line. This line has been flattened out to account for the threshold of hearing being variable at all frequencies, as shown on the Equal Loudness Contours.

The vertical axis is called the Hearing Level in positive dB increments (which is referred to as dB HL), and indicates the signal level above the threshold that the subject has been able to just detect. Values for the left and right ears are plotted separately, and together they show the frequency response of the ear.

An audiogram showing the typical notch at 4 kHz associated with noise-induced hearing loss

Values above the 0 dB hearing line are possible for unimpaired hearing, either because of the standard deviation of the measurement (+ or - 5 dB) and the fact that when the test is being done, it may be difficult to determine which is the faintest sound that can be heard (with multiple exposures being required and an average taken of correct responses).

Low frequencies below 250 Hz are not usually measured because there is seldom any hearing loss (HL) in that region, and those frequencies are not important for speech. Likewise there is no test above 8 kHz where the amount of presbycusis could be detected, again because of a bias towards the speech frequencies, ignoring their role in music, and environmental sound localization. In fact, until recently, audiologists have only focussed on speech perception and therapeutic interventions aimed at its improvement.

One advantage of the graphic format of an audiogram is that it shows hearing loss as a vertical decline (compared with other graphs we will present below), and therefore the results are communicated more intuitively. "Normal" hearing is regarded as the range from -10 dB to +15 dB HL, with the range of 16 - 25 dB being a slight loss. A hearing loss of 25-40 dB is regarded as “mild”, 40-60 dB as “moderate”, even though this degree of loss will create serious problems in communication, and below that, “severe” and “profound” loss, the latter being deafness. The complete scale is shown here.

Degrees of hearing loss shown in dB HL (Source: healthyhearing.com)

Another important role of the audiogram with NIHL (noise-induced hearing loss) is that it clearly indicates the effects of noise exposure, which are quite distinct from presbycusis (age-related HL). The old excuse that HL is just because of age, and not noise exposure, is untenable. NIHL occurs with a characteristic notch at 4 kHz, as shown above, and typically deepens on the lower side over time. As we have repeatedly seen throughout the Tutorial, this is the frequency range that is most important for speech and other essential aspects of acoustic communication, particularly because it incorporates both vowel and consonant information.

Here is a sound example where we implement the same severe loss shown in this particular audiogram shown above. Note how muffled and ambiguous the speech is, even on headphones. If significant background noise were present, the intelligibility would be even less, as dicussed below.

Voice heard without and with the hearing loss shown in the audiogram above (Source: Sylvi macCormac)

Temporary Threshold Shift (TTS) shows the same notch pattern in an audiogram, as in the diagram below, on the left for workers at the start and end of a shift, and at right for a rock band rehearsing or performing for three hours at a very dangerous level of 112 dBA. In fact, as discussed below under Damage-Risk Criteria, any exposure above 90-95 dBA for this length of time is regarded as having a high risk of permanent hearing loss.

TTS is the result of the outer hair cells (those that respond to lower levels of sound) becoming saturated and are no longer firing. They are also deprived of a nutrient supply of blood via the very tiny capillaries that service them. One effect of noise, as we will see in the next module, is an increase of blood pressure and decrease in blood flow to the “extremities” which normally means the hands and feet, but it can also affect the hair cells and the semicircular canals for balance.

It should also be noted that, whereas TTS as a formal definition refers to noise exposure, there are other conditions, such as even the common cold or earwax buildup, that can reduce hearing acuity on a temporary basis. As discussed in the Magnitude module, hearing is constantly adapting to the ambient sound level, such that our impressions of loudness are relative, not absolute. We are generally unaware of these shifts, unless we go from a relatively high to low ambient situation, or vice versa.

The key difference is that TTS puts the emphasis on a change that may become permanent, unlike this continuous change in hearing sensitivity that we experience every day.
19. Personal Listening Experiment. Buy a pair of foam earplugs at a drugstore (they are good to have on hand), make sure they are fitting snugly in your ears and are comfortable. Leave them in for at least a half hour, or longer if possible, as you go about some daily walking activities (but not driving or biking). What sounds become magnified, and which sounds that you normally expect become muted or absent? When you eventually remove the plugs, you will have a threshold shift where everything will sound louder than normal. Estimate how long it takes to adapt to the ambient level where you are. The effects you experience are based in the occlusion (blocking) of the ear canal, and increased awareness of bone conduction.
Sometimes audiologists and others, trying to explain TTS, use a comparison to trampled grass which can “recover” if not walked on further. Admittedly, the stereocilia of the hair cells might be comparable to grass, but the cause of TTS is not a physical one of being crushed. Overstimulation and a lack of blood supply is a better explanation.

Another side-effect of more severe noise exposure is a ringing in the ears, called tinnitus, which is caused by the hair cells firing spontaneously after the overstimulation. This should in fact be an “early warning signal” that over-exposure has occurred and future exposure should be avoided. It can also occur as a side-effect of, most commonly, aspirin and similar pain management drugs which also constrict the blood vessels and reduce flow to the hair cells. However, there are many other causes of tinnitus as noted below.

If there is insufficient time for recovery, TTS can become chronic, and eventually a permanent threshold shift (PTS). If this is the result of noise it is called NIPTS (Noise-induced Permanent Threshold Shift). PTS and NIPTS mean that some of the hair cells are dead and, as is typical in mammals (but not fish or birds), they cannot be regenerated.

These graphs, generated from lab experiments, show that there will be approximately a 25 dB TTS after an hour’s exposure to a 4 kHz noise at 90 dB, and the shift will be in the range of possible acoustic trauma (leading to PTS) after 8 hours. The righthand diagram shows recovery times for a full 7 days of exposure which will lead to PTS. However, the dotted line shows that a 95 dB exposure for just under 2 hours will require a full day for recovery. This indicates how noise exposure can become chronic if there is not at least 16 hours of non-exposure, and result in permanent loss of course with higher levels.

The Jute Weavers. The long-term effect of NIPTS, as to how it keeps worsening, has been well established since the original publication in 1965 of the case of the “jute weavers” and their audiograms. What has not always made clear, is that these were all women who had worked in the mills of Scotland for anywhere from 1 to 40 years in a constant, high intensity level factory setting measured at around 100 dB, without hearing protection.

The sad truth about their existence is only mitigated by the contribution the knowledge of their plight has served for audiology. The clarity of the data was supported by the fact that these women had little or no exposure to gunfire, or other high level noise other than their workplace. And most had never worked anywhere else, so the cause and effect paradigm was near “perfect”.

Audiograms for the jute weavers after multi-year noise exposure

The curves from top to bottom, then left to right, show that the sensory-neural HL in the first 10 years keeps growing around the 4 kHz notch, but after that, it starts digging more deeply into the 1-3 kHz range – all of which are important speech frequencies. The old excuse not to wear hearing protection in older workers (because their hearing was already gone) is not valid.

The data also suggests why the relatively slow but steady deterioration can lead to denial and some forms of adaptation by the worker’s family and friends. Lipreading will likely be practiced more, friends and family may learn to “speak up” (even though it’s clarity, not loudness that matters), but in the end there is greater social isolation.

Most of us have no experience, luckily, of working in such a high intensity industrial situation, and in developed Western countries such conditions would not be allowed without hearing protection. But in the rest of world, there are usually few such measures being enforced. Here is a recording made in a German textile manufacturing factory of a room with 100 weaving machines whose output was measured at 100 dBA, similar to that of the jute weavers. This excerpt only lasts a minute, but if you have a Sound Level Meter and turn up the volume to even 90 dB you can experience how intolerable the loudness of the sound is. Ironically, since the recordist was moving about the room, it has been commented on that the rhythms of the machine are aurally interesting.

100 weaving machines at 100 dB, Kolb & Schüle textile factory, Bissingen, Germany
Source: WSP Eur 17 take 9

This next diagram is a graph that shows more or less the same data, but in a reverse format in terms of the “growth” of the hearing loss, which is less intuitive but still quite telling. It shows that the 3 and 4 kHz loss occurs fairly quickly over the first 10 years, and after that, there is still steady growth at 1 and 2 kHz.

Lastly, we should clarify another myth about sensory-neural hearing loss. Speaking more loudly to someone with this kind of impairment is not the right thing to do (and certainly no one likes be shouted at). It is better to (1) face the person and allow them to lipread, once you have their attention, and (2) to speak more clearly and enunciate words properly.

The other implication of this kind of HL is that the person will avoid noisy situations because they are less able to pick out conversation and other sounds from the background din. Over time, this tendency promotes social isolation. We can try to understand the reason for both of these situations with the following graphs that shows how impaired hearing (in different subjects) differs from normal hearing in the frequency resolution of the ear.

Frequency resolution in normal and impaired ears at 1 kHz

The “normal” graphs for the 1 kHz centre frequency are sharp and well defined. Therefore, information in adjacent bands, and across the frequency spectrum, are more detailed via the distribution of resonances along the basilar membrane in the cochlea. For impaired ears, the filter bands are much broader and even less well defined for lower frequencies below the centre. Hearing with this type of reduced sensitivity would be like seeing through a blurry window - nothing would be well defined, and distinguishing a sound in the presence of noise would be degraded.

Presbycusis. The deterioration of hearing with age is called Age-related Hearing Impairment (ARHI), but it is also known as presbycucis and regarded as a non-occupational type of loss. It normally takes the form of a roll-off of high frequencies above 8 kHz, similar to a low-pass filter, with higher frequencies attenuated first, then progressively lower ones with age. As we saw with the audiogram above, the very high frequencies are not normally measured in a standard hearing test, as they do not directly affect speech comprehension. Speech and music with such a high frequency roll-off merely sounds duller.

However, these diagrams show a typical presbycusis loss in men and women for the critical speech frequencies of 1-4 kHz, according to age. The loss is always greater for men than women? Why would you suppose that to be true?

Typical presbycusis curves for men and women
in the most critical speech frequency range

If you answered the above question by thinking that men would be more likely to be exposed to noise in the workplace, that doesn’t fit the definition of presbycusis which is non-occupational. Other gender specific factors are more likely to be the explanation; for instance, female estrogen has a protective effect on hearing. However, presbycusis can also combine with the more common NIHL sensory-neural hearing loss (with the 4 kHz notch) and can affect detection of both the consonants and higher vowel formants.

There are many other factors in ARHI, such as exposure to toxic chemicals, and various types of medication that are ototoxic (i.e. damaging to hearing), such as aminoglycosides, cisplatin, salicylate and loop diuretics which are sometimes prescribed for older people. Medical conditions such as diabetes, renal failure, immune function impairment and cardiovascular disease may also play a factor.

When we are considering a life-long set of factors that can affect health, it should not be surprising that hearing impairment with age is mainly correlated with overall health, as well as noise exposure. Hearing loss is widely thought to be “natural”, but it is more likely to be a reflection of one’s overall health.

This type of question about presbycusis being inevitable or not received a great deal of public attention in the 1960s when the American otologist Dr. Samuel Rosen studied a group of people known as the Mabaan in the Sudan south of Khartoum. The environment was essentially noise-free (with typical levels below 40 dB), except during celebrations.

In Rosen’s autobiography he says that “they walked along the trails single file, sometimes separated by as much as 100 yards, the length of a football field. Yet they conversed in normal tones. The one in front did not even turn around to reply!”.

Once audiometric tests began, he noticed much less high frequency decline with both older men and women, including testing the very high frequencies of 14, 16 and 18 kHz which Western adults can seldom hear. But it was his remark that “Mabaans aged fifty to fifty-nine had much better hearing than Americans aged twenty to twenty-nine” that caught the public’s attention through media reports. In fact for years later, a general idea that “some African tribe didn’t lose their hearing with age” still circulated widely.

One of the graphs in his research publication (in Transactions, American Otological Society, vol. 50, 1962) did show this comparison between the Mabaan men aged 50-59 and American men aged 20-29 being similar, but the American data was Aram Glorig’s 1954 Wisconsin State Fair data with noise-exposed subjects, one of the worst set of findings ever reported. However, to be fair, Rosen also showed a comparison with non-noise exposed American men, also by Glorig (1960), in this diagram.

Although Rosen thought the noise-free environment of the Mabaan played a role, he was more impressed by the fact that they had low blood pressure that did not rise significantly with age, as did American data. They also had no incidence of hypertension, coronary thrombosis, ulcerative colitis, duodenal ulcer and bronchial asthma. As noted above, high blood pressure constricts the blood supply getting to the hair cells, and therefore it is plausible to regard that as an important factor in the lesser level of ARHI among these people. It was also a good reminder that everything involved in human health is connected, and we should be careful about seeking single causes for any health-related issue.

Recruitment. Auditory recruitment is dysfunction of the inner ear that distorts the dynamic range of the sounds being heard. Low level sounds seem quieter than normal, but past a certain threshold their intensity becomes magnified by a non-linear amplification and they become overly loud. This effect, which can be made worse with a hearing aid, means that quieter sounds are masked and the person experiences a threshold shift after each burst of loudness that is similar to permanent hearing loss.

Non-linear dynamic response associated with recruitment

This diagram compares a normal dynamic response (dashed line) which is quite linear, with a non-linear response pattern typical of recruitment (solid line). For instance, a 60 dB tone in the impaired ear was matched in loudness to a 30 dB tone in a normal ear (basically turning normal speech loudness into a whisper). Normal speech at 60 dB sounded with equal loudness as a shouted 80 dB, and so on. This distortion can occur even at the phonemic level where louder phonemes will mask quieter ones, making speech very problematic to understand.

Tinnitus is the experience of a persistent sound in one or both ears when there is no external source. It is often described as a ringing, buzzing, hiss or roaring. The term can be pronounced with the emphasis on the first or second syllable.

Tinnitus is generally regarded as an indicator, not a cause, of another condition, most commonly NIHL and presbycusis, but it can also be a side-effect of many other medical conditions as well. As noted above, a transient version of a “ringing in your ears” (in the 5 - 10 kHz range) can be experienced as a response to excessive noise exposure, or medications such as aspirin which constrict blood flow, and result in a spontaneous firing of the hair cells.

However, with various chronic diseases it can become a nearly constant presence and therefore create psychological and other problems such as depression anxiety and stress, depending on its severity. It is estimated to affect 10-15% of the population, and despite the search for some form of medical relief, there are no proven medicines that can be prescribed. However, a variety of therapies can be tried, such as introducing sound to mask the tinnitus or distract from it, and notching out frequencies close to the tinnitus frequency.

Ototoxins in history. Chemicals and drugs that have the potential to damage hearing have been mentioned several times in this module. However, they have a much longer history. Historian Hillel Schwartz’s encyclopedic tome Making Noise (Zone Books, 2011) documents the long history of noise (which his subtitle alliteratively reminds us is “from Babel to the Big Bang and Beyond”), and provides amazing detail about the Industrial Revolution’s introduction of countless sources of noise.

However, he also points out that in the 19th century, exposure to ototoxic chemicals (such as lead, mercury and solvents) was widespread, high fever diseases were common and produced hearing loss in both children and adults, and that the medicines that were available (quinine, morphine, cocaine in its alkaloid form, and by the end of the century, aspirin), all of them could be ototoxic and result in tinnitus, depending on the dosage (pp. 368 ff). So what if anything constituted “normal hearing” at that time?

Audiometers and sound level meters were not invented until the late 1920s and early 30s with the electrical developments at Bell Labs that we have mentioned several times. So, at that point of the ability to quantify sound (and hearing), the modern concept of what was “normal” and “impaired” began to be solidified. Likewise, noise abatement measures began to be put in place, as documented for Europe and North America by Karin Bijsterveld in her comprehensive Mechanical Sound (MIT Press, 2008). However, damage risk criteria for industry, at least in North America, had to wait until the 1970s.


D. Damage-risk criteria. The institutionalized approach to risk management usually involves establishing risk criteria and appropriate standards to guide exposure. In North America, these criteria for the workplace were slow to be adopted in terms of risk to hearing, but in 1971 the Occupational Safety and Health Act in the U.S. came into effect for noisy industrial environments, to be administered by the OSHA (Occupational Safety and Health Administration) in the Department of Labor. As might be expected, the initial guidelines were a compromise between industry, worried about costs, and audiologists who were more concerned about aural health. These first guidelines were stated as shown here.

The main two characteristics of the criteria were the 8-hour exposure limit (set to 90 dB, whereas audiologists recommended 85 dB) and the “exchange rate” of 5 dB increase for half the amount of time (whereas audiologists would have preferred a 3 dB rate). There was also a general reference to impact noise measured at peak levels.

The other problem with this initial set of criteria is that it was labelled as “permissible” levels, but which were clearly not “safe” levels. In other words, they did not guarantee a lack of occupational hearing loss, as some might have assumed. Some commentators have suggested something along the lines that at these exposure levels, a hearing loss of no more than 15 dB would be experienced by 1/3 of those exposed.

A larger issue that has been raised by some critics, such as Raymond Hétu from Québec, is that this approach solidified hearing loss as the main basis for regulation and compensation, as administered by audiologists using audiometric methods. Given the range of noise effects that will be outlined in the next module, there are many more consequences of noise in the workplace, many of which can increase the risk of accidents, as in Hétu’s diagram here.

Outline of the effects of occupational noise exposure (source:

In more recent decades, there has been a move by regulators towards hearing conservation programs. This involves providing annual hearing tests for workers (in medium to large business and industrial operations), and prescribed levels of hearing protection based on the time-averaged noise levels that have been measured.

Many jurisdictions now follow the standard of 85 dBA time-weighted exposure over 8 hours, and a 3 dB exchange rate (that is, halving the duration of exposure for each 3 dB increase in sound level, as recommended by the NIOSH (National Institute for Occupational Safety and Health). The aim is to reduce the risk of occupational NIHL, and a comparison of OSHA and NIOSH criteria is shown here. Note that the time-weighted level Leq will be explained in the next module.

The effectiveness of personalized hearing protection is measured as a NRR value (Noise Reduction Rating), although its actual effectiveness depends on the fit and pattern of use by the user. Some estimates show that actual use is often about half of the maximum value. The following chart shows how to calculate the estimated noise exposure level using the NRR value, for earmuffs, earplugs and their combination (“dual protection").

For instance, with a Leq of 98 dBA and a NRR of 30 for earplugs, the estimated noise exposure is 80 dBA, with an effective rating of 50%. With earmuffs, that value would be reduced to around 74 dBA (effective rating of 70%). Of course these values assume an ideal fit for the protection and 100% use.

The best protectors are the closed over the ear headphone or earmuff type protectors (class A), with soft foam earplugs or fitted plugs as class B if they can reduce levels by 30 dB. It is important that the reduction is fairly uniform across the entire range of frequencies so that speech can still be understood, given that high frequencies are easy to attenuate, but low and mid-range ones are not. There are some misconceptions about hearing speech or other signals when using earplugs. Research shows that it is easier to detect and comprehend these sounds when the ambience is lower, particularly if all frequencies are reduced by about the same amount, and therefore it is better to use earplugs in those situations, as speech may be better understood.

Impulse content of noise. The criteria described above are solely based on a dosage model, which is basically averaged noise level plus duration of exposure. In the past, a dosimeter (or "dosemeter" in the UK) was sometimes used, attached to the worker’s clothing, to determine the dosage of the exposure, a procedure that could easily produce a flawed result as the worker moved about.

Today, the Equivalent Energy Level, or Leq, can do a better job and is incorporated into many portable sound level meters and apps, and the averaged result can be measured over any length of time. It is usually A-weighted (in dBA) and therefore discriminates against low frequencies, with the traditional justification that dBA “reflects how we hear”, a non-technical reference to the Equal Loudness Contours from which the A-weighting scale was derived for low intensities (the 40 phon curve) as described in the Magnitude module. However, you can see a reference to dBC levels in the chart above, which does include low-frequencies, but that weighting network isn’t always available and cannot be used in windy conditions outdoors.

On the other hand, it has been known for several decades that industries where impulsive noise content is prevalent, such as with a punch press, or in the impact sounds made by glass and metal hitting each other, or other types of mechanical operations, average risk limits for 50% hearing loss are lower and therefore the risk can be greater, as shown here from a report in the 1970s in Europe.

Risk limits for different industries with impulsive content (source: Brüel)

Note that the lower the line, the higher the risk because of impulsive content in the typical sounds of that industry (that is, the risk of hearing loss is the same at a lower level). It is a small comfort that amplified pop music (which the Europeans call “beat music”) is less risky because the audio equipment cannot reproduce the brief transients that are the problem. However, the same dosage model (level plus duration) still makes amplified music as dangerous to the ears as any other industrial noise.

What has not become generally integrated into risk criteria today is the impulsive content of sounds. Everything we have described so far relates to steady noise levels. Admittedly the Leq measurement will include the energy of brief transient sounds, but it is not clear what time-scale should be used, as many of these transients can last under 100 µs (microseconds). In the following diagram, we can see examples of these short transients in a beer bottling plant. Note that the strongest spectral energy is in the 2-3 kHz range.

Spectrum and waveform from a bottling plant showing brief impulsive transients (source: Brüel)

Of course, it has been long known that gunfire of any kind can produce acoustic trauma (permanent hearing loss) with even a single exposure, and as described above, the stapedius muscle that has the capability of damping an incoming pressure transient in the ossicles, cannot do so fast enough to prevent this kind of damage. Peak levels that can range from 140 to 175 dBA will cause permanent damage.

Traditionally, the sound level meter (SLM) has had two settings for its temporal response, slow (for visually averaging a time-varying sound with a 1 second averaging time), the fast response for tracking rapid transient sound levels, and the impulse response for peaks. The fast response of the meter at 125 ms is closer to the brain’s own averaging time, which also determines the apparent loudness of a sound, as demonstrated in the demo with short clicks. The impulse meter (now seldom used) has the time constant of 35 ms.

In fact, if you watch a SLM fluctuate on the fast scale, it is easy to see the correlation between what you are hearing and what is being measured. However, the danger with impulsive sounds arises because there is nothing preventing them from going directly into the inner ear and causing damage. The averaging times for the outer and middle ear are in the microsecond range. Moreover, as documented above, the natural amplification of the sound wave in the outer and middle ear is 10-12 dB, and as we just saw in the above diagram, that frequency range is where most impulsive energy lies.
20. A personal listening experiment for this effect (but don’t do it for very long) is when you hear bottles hitting each other, or a series of metallic impacts, or even hammering at close range. They won’t sound that loud, but you can often feel an after-effect of discomfort or a Temporary Threshold Shift. If you have to work in such an environment, use hearing protection!
Of even greater concern is that some children’s toys, such as a toy “cap pistol”, or fireworks, can also produce very strong pressure transients.

A peak sound level measurement represents the true maximum pressure of a sound wave, so for instance, a sine wave’s peak (as opposed to its RMS value) is 3 dB higher than its SPL (sound pressure level). In a digital meter, there is no time weighting involved, but keep in mind we are dealing with time values near the sampling period (e.g. 20.8 µsec for a 48 kHz sampling rate), so higher sampling rates will need to be used.

In terms of damage risk criteria, there are some guidelines about impulsive content, such as an upper limit of 135-140 dB peak levels, but as yet, there is no agreement on exactly how the true peak levels should be measured and how the threshold of risk for hearing loss is determined. There is also no satisfactory way of combining the measurement of steady state noise with impulsive content.


Q. Try this review quiz to test your comprehension of the above material, and perhaps to clarify some distinctions you may have missed.